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> Anti-p62 / SQSTM1 (C-terminus) guinea pig polyclonal, serum

Anti-p62 / SQSTM1 (C-terminus) guinea pig polyclonal, serum

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Cat# GP62-C

Size : 100µL

Brand : Progen

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Phone : +1 850 650 7790

anti-p62/ SQSTM1 (C-terminus) guinea pig polyclonal, serum

anti-p62/ SQSTM1 (C-terminus) guinea pig polyclonal, serum
anti-p62/ SQSTM1 (C-terminus) guinea pig polyclonal, serum
anti-p62/ SQSTM1 (C-terminus) guinea pig polyclonal, serum
anti-p62/ SQSTM1 (C-terminus) guinea pig polyclonal, serum
anti-p62/ SQSTM1 (C-terminus) guinea pig polyclonal, serum
anti-p62/ SQSTM1 (C-terminus) guinea pig polyclonal, serum
anti-p62/ SQSTM1 (C-terminus) guinea pig polyclonal, serum
anti-p62/ SQSTM1 (C-terminus) guinea pig polyclonal, serum
anti-p62/ SQSTM1 (C-terminus) guinea pig polyclonal, serum
anti-p62/ SQSTM1 (C-terminus) guinea pig polyclonal, serum
anti-p62/ SQSTM1 (C-terminus) guinea pig polyclonal, serum
anti-p62/ SQSTM1 (C-terminus) guinea pig polyclonal, serum
Inhibition of mTOR by rapamycin abolishes cognitive deficits and reduces amyloid-beta levels in a mouse model of Alzheimer's disease.
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Cell loss and autophagy in the extra-adrenal chromaffin organ of Zuckerkandl are regulated by glucocorticoid signalling.
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Cell loss and autophagy in the extra-adrenal chromaffin organ of Zuckerkandl are regulated by glucocorticoid signalling.
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Rapamycin attenuates the progression of tau pathology in P301S tau transgenic mice.
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A novel acylaminoimidazole derivative, WN1316, alleviates disease progression via suppression of glial inflammation in ALS mouse model.
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A novel acylaminoimidazole derivative, WN1316, alleviates disease progression via suppression of glial inflammation in ALS mouse model.
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Rotavirus increases levels of lipidated LC3 supporting accumulation of infectious progeny virus without inducing autophagosome formation.
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Rotavirus increases levels of lipidated LC3 supporting accumulation of infectious progeny virus without inducing autophagosome formation.
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Ribosomal protein mutations induce autophagy through S6 kinase inhibition of the insulin pathway.
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Ribosomal protein mutations induce autophagy through S6 kinase inhibition of the insulin pathway.
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Ribosomal protein mutations induce autophagy through S6 kinase inhibition of the insulin pathway.
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Ribosomal protein mutations induce autophagy through S6 kinase inhibition of the insulin pathway.
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Disrupted autophagy after spinal cord injury is associated with ER stress and neuronal cell death.
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Disrupted autophagy after spinal cord injury is associated with ER stress and neuronal cell death.
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Disrupted autophagy after spinal cord injury is associated with ER stress and neuronal cell death.
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Disrupted autophagy after spinal cord injury is associated with ER stress and neuronal cell death.
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Disrupted autophagy after spinal cord injury is associated with ER stress and neuronal cell death.
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Disrupted autophagy after spinal cord injury is associated with ER stress and neuronal cell death.
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Cucurbitacin E has neuroprotective properties and autophagic modulating activities on dopaminergic neurons.
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The unexpected role of polyubiquitin chains in the formation of fibrillar aggregates.
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The unexpected role of polyubiquitin chains in the formation of fibrillar aggregates.
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The unexpected role of polyubiquitin chains in the formation of fibrillar aggregates.
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The unexpected role of polyubiquitin chains in the formation of fibrillar aggregates.
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The unexpected role of polyubiquitin chains in the formation of fibrillar aggregates.
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Proteotoxic stress induces phosphorylation of p62/SQSTM1 by ULK1 to regulate selective autophagic clearance of protein aggregates.
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Proteotoxic stress induces phosphorylation of p62/SQSTM1 by ULK1 to regulate selective autophagic clearance of protein aggregates.
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Proteotoxic stress induces phosphorylation of p62/SQSTM1 by ULK1 to regulate selective autophagic clearance of protein aggregates.
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Proteotoxic stress induces phosphorylation of p62/SQSTM1 by ULK1 to regulate selective autophagic clearance of protein aggregates.
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Proteotoxic stress induces phosphorylation of p62/SQSTM1 by ULK1 to regulate selective autophagic clearance of protein aggregates.
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Proteotoxic stress induces phosphorylation of p62/SQSTM1 by ULK1 to regulate selective autophagic clearance of protein aggregates.
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Proteotoxic stress induces phosphorylation of p62/SQSTM1 by ULK1 to regulate selective autophagic clearance of protein aggregates.
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Proteotoxic stress induces phosphorylation of p62/SQSTM1 by ULK1 to regulate selective autophagic clearance of protein aggregates.
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Proteotoxic stress induces phosphorylation of p62/SQSTM1 by ULK1 to regulate selective autophagic clearance of protein aggregates.
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Proteotoxic stress induces phosphorylation of p62/SQSTM1 by ULK1 to regulate selective autophagic clearance of protein aggregates.
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Proteotoxic stress induces phosphorylation of p62/SQSTM1 by ULK1 to regulate selective autophagic clearance of protein aggregates.
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Autophagic signaling and proteolytic enzyme activity in cardiac and skeletal muscle of spontaneously hypertensive rats following chronic aerobic exercise.
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Estrogen receptor α regulates non-canonical autophagy that provides stress resistance to neuroblastoma and breast cancer cells and involves BAG3 function.
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Frontotemporal dementia caused by CHMP2B mutation is characterised by neuronal lysosomal storage pathology.
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Frontotemporal dementia caused by CHMP2B mutation is characterised by neuronal lysosomal storage pathology.
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Frontotemporal dementia caused by CHMP2B mutation is characterised by neuronal lysosomal storage pathology.
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Frontotemporal dementia caused by CHMP2B mutation is characterised by neuronal lysosomal storage pathology.
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All-trans retinoic acid and rapamycin normalize Hutchinson Gilford progeria fibroblast phenotype.
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Sqstm1-GFP knock-in mice reveal dynamic actions of Sqstm1 during autophagy and under stress conditions in living cells.
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Sqstm1-GFP knock-in mice reveal dynamic actions of Sqstm1 during autophagy and under stress conditions in living cells.
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Sqstm1-GFP knock-in mice reveal dynamic actions of Sqstm1 during autophagy and under stress conditions in living cells.
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Sqstm1-GFP knock-in mice reveal dynamic actions of Sqstm1 during autophagy and under stress conditions in living cells.
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Autophagy and endosomal trafficking inhibition by Vibrio cholerae MARTX toxin phosphatidylinositol-3-phosphate-specific phospholipase A1 activity.
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Identification of p62/SQSTM1 as a component of non-canonical Wnt VANGL2-JNK signalling in breast cancer.
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Identification of p62/SQSTM1 as a component of non-canonical Wnt VANGL2-JNK signalling in breast cancer.
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Identification of p62/SQSTM1 as a component of non-canonical Wnt VANGL2-JNK signalling in breast cancer.
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Identification of p62/SQSTM1 as a component of non-canonical Wnt VANGL2-JNK signalling in breast cancer.
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Identification of p62/SQSTM1 as a component of non-canonical Wnt VANGL2-JNK signalling in breast cancer.
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Identification of p62/SQSTM1 as a component of non-canonical Wnt VANGL2-JNK signalling in breast cancer.
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Identification of p62/SQSTM1 as a component of non-canonical Wnt VANGL2-JNK signalling in breast cancer.
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Identification of p62/SQSTM1 as a component of non-canonical Wnt VANGL2-JNK signalling in breast cancer.
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Identification of p62/SQSTM1 as a component of non-canonical Wnt VANGL2-JNK signalling in breast cancer.
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mTOR Hyperactivation by Ablation of Tuberous Sclerosis Complex 2 in the Mouse Heart Induces Cardiac Dysfunction with the Increased Number of Small Mitochondria Mediated through the Down-Regulation of Autophagy.
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mTOR Hyperactivation by Ablation of Tuberous Sclerosis Complex 2 in the Mouse Heart Induces Cardiac Dysfunction with the Increased Number of Small Mitochondria Mediated through the Down-Regulation of Autophagy.
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mTOR Hyperactivation by Ablation of Tuberous Sclerosis Complex 2 in the Mouse Heart Induces Cardiac Dysfunction with the Increased Number of Small Mitochondria Mediated through the Down-Regulation of Autophagy.
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mTOR Hyperactivation by Ablation of Tuberous Sclerosis Complex 2 in the Mouse Heart Induces Cardiac Dysfunction with the Increased Number of Small Mitochondria Mediated through the Down-Regulation of Autophagy.
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mTOR Hyperactivation by Ablation of Tuberous Sclerosis Complex 2 in the Mouse Heart Induces Cardiac Dysfunction with the Increased Number of Small Mitochondria Mediated through the Down-Regulation of Autophagy.
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mTOR Hyperactivation by Ablation of Tuberous Sclerosis Complex 2 in the Mouse Heart Induces Cardiac Dysfunction with the Increased Number of Small Mitochondria Mediated through the Down-Regulation of Autophagy.
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A Founder Mutation in VPS11 Causes an Autosomal Recessive Leukoencephalopathy Linked to Autophagic Defects.
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p62/Sqstm1 promotes malignancy of HCV-positive hepatocellular carcinoma through Nrf2-dependent metabolic reprogramming.
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p62/Sqstm1 promotes malignancy of HCV-positive hepatocellular carcinoma through Nrf2-dependent metabolic reprogramming.
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p62/Sqstm1 promotes malignancy of HCV-positive hepatocellular carcinoma through Nrf2-dependent metabolic reprogramming.
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p62/Sqstm1 promotes malignancy of HCV-positive hepatocellular carcinoma through Nrf2-dependent metabolic reprogramming.
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p62/Sqstm1 promotes malignancy of HCV-positive hepatocellular carcinoma through Nrf2-dependent metabolic reprogramming.
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p62/Sqstm1 promotes malignancy of HCV-positive hepatocellular carcinoma through Nrf2-dependent metabolic reprogramming.
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TSC but not PTEN loss in starving cones of retinitis pigmentosa mice leads to an autophagy defect and mTORC1 dissociation from the lysosome.
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TSC but not PTEN loss in starving cones of retinitis pigmentosa mice leads to an autophagy defect and mTORC1 dissociation from the lysosome.
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TSC but not PTEN loss in starving cones of retinitis pigmentosa mice leads to an autophagy defect and mTORC1 dissociation from the lysosome.
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TSC but not PTEN loss in starving cones of retinitis pigmentosa mice leads to an autophagy defect and mTORC1 dissociation from the lysosome.
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Intracellular glutathione determines bortezomib cytotoxicity in multiple myeloma cells.
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Effect of Exendin-4 on Autophagy Clearance in Beta Cell of Rats with Tacrolimus-induced Diabetes Mellitus.
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Oleuropein Prevents Neuronal Death, Mitigates Mitochondrial Superoxide Production and Modulates Autophagy in a Dopaminergic Cellular Model.
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Hydroxychloroquine potentiates carfilzomib toxicity towards myeloma cells.
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Hydroxychloroquine potentiates carfilzomib toxicity towards myeloma cells.
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Differential roles of NF-Y transcription factor in ER chaperone expression and neuronal maintenance in the CNS.
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Differential roles of NF-Y transcription factor in ER chaperone expression and neuronal maintenance in the CNS.
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Differential roles of NF-Y transcription factor in ER chaperone expression and neuronal maintenance in the CNS.
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Activation of the Keap1/Nrf2 stress response pathway in autophagic vacuolar myopathies.
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Activation of the Keap1/Nrf2 stress response pathway in autophagic vacuolar myopathies.
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Activation of the Keap1/Nrf2 stress response pathway in autophagic vacuolar myopathies.
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Activation of the Keap1/Nrf2 stress response pathway in autophagic vacuolar myopathies.
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Autophagy dysregulation in Danon disease.
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Autophagy dysregulation in Danon disease.
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Autophagy dysregulation in Danon disease.
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Gastrin activates autophagy and increases migration and survival of gastric adenocarcinoma cells.
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Gastrin activates autophagy and increases migration and survival of gastric adenocarcinoma cells.
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Gastrin activates autophagy and increases migration and survival of gastric adenocarcinoma cells.
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Gastrin activates autophagy and increases migration and survival of gastric adenocarcinoma cells.
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Propagation of pathological α-synuclein in marmoset brain.
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Sarcolipin deletion exacerbates soleus muscle atrophy and weakness in phospholamban overexpressing mice.
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Exploiting macrophage autophagy-lysosomal biogenesis as a therapy for atherosclerosis.
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Exploiting macrophage autophagy-lysosomal biogenesis as a therapy for atherosclerosis.
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Exploiting macrophage autophagy-lysosomal biogenesis as a therapy for atherosclerosis.
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Exploiting macrophage autophagy-lysosomal biogenesis as a therapy for atherosclerosis.
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Exploiting macrophage autophagy-lysosomal biogenesis as a therapy for atherosclerosis.
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Exploiting macrophage autophagy-lysosomal biogenesis as a therapy for atherosclerosis.
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Exploiting macrophage autophagy-lysosomal biogenesis as a therapy for atherosclerosis.
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Exploiting macrophage autophagy-lysosomal biogenesis as a therapy for atherosclerosis.
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Impaired autophagosome clearance contributes to neuronal death in a piglet model of neonatal hypoxic-ischemic encephalopathy.
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Cryptic amyloidogenic elements in mutant NEFH causing Charcot-Marie-Tooth 2 trigger aggresome formation and neuronal death.
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Cryptic amyloidogenic elements in mutant NEFH causing Charcot-Marie-Tooth 2 trigger aggresome formation and neuronal death.
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Cryptic amyloidogenic elements in mutant NEFH causing Charcot-Marie-Tooth 2 trigger aggresome formation and neuronal death.
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Centriolar Satellites Control GABARAP Ubiquitination and GABARAP-Mediated Autophagy.
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Centriolar Satellites Control GABARAP Ubiquitination and GABARAP-Mediated Autophagy.
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Centriolar Satellites Control GABARAP Ubiquitination and GABARAP-Mediated Autophagy.
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Centriolar Satellites Control GABARAP Ubiquitination and GABARAP-Mediated Autophagy.
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Centriolar Satellites Control GABARAP Ubiquitination and GABARAP-Mediated Autophagy.
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Centriolar Satellites Control GABARAP Ubiquitination and GABARAP-Mediated Autophagy.
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Centriolar Satellites Control GABARAP Ubiquitination and GABARAP-Mediated Autophagy.
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Hypoxia ameliorates intestinal inflammation through NLRP3/mTOR downregulation and autophagy activation.
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Lysosomotropism depends on glucose: a chloroquine resistance mechanism.
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Selective degradation of PU.1 during autophagy represses the differentiation and antitumour activity of TH9 cells.
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Selective degradation of PU.1 during autophagy represses the differentiation and antitumour activity of TH9 cells.
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Selective degradation of PU.1 during autophagy represses the differentiation and antitumour activity of TH9 cells.
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Selective degradation of PU.1 during autophagy represses the differentiation and antitumour activity of TH9 cells.
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Selective degradation of PU.1 during autophagy represses the differentiation and antitumour activity of TH9 cells.
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Selective degradation of PU.1 during autophagy represses the differentiation and antitumour activity of TH9 cells.
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Standard Assays for the Study of Autophagy in the Ex Vivo Retina.
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Phosphorylation and degradation of αB-crystallin during enterovirus infection facilitates viral replication and induces viral pathogenesis.
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L-leucine and SPNS1 coordinately ameliorate dysfunction of autophagy in mouse and human Niemann-Pick type C disease.
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L-leucine and SPNS1 coordinately ameliorate dysfunction of autophagy in mouse and human Niemann-Pick type C disease.
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Sequestosome 1 Deficiency Delays, but Does Not Prevent Brain Damage Formation Following Acute Brain Injury in Adult Mice.
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Sequestosome 1 Deficiency Delays, but Does Not Prevent Brain Damage Formation Following Acute Brain Injury in Adult Mice.
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Sequestosome 1 Deficiency Delays, but Does Not Prevent Brain Damage Formation Following Acute Brain Injury in Adult Mice.
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Negative Regulation of the Keap1-Nrf2 Pathway by a p62/Sqstm1 Splicing Variant.
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Negative Regulation of the Keap1-Nrf2 Pathway by a p62/Sqstm1 Splicing Variant.
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Negative Regulation of the Keap1-Nrf2 Pathway by a p62/Sqstm1 Splicing Variant.
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Negative Regulation of the Keap1-Nrf2 Pathway by a p62/Sqstm1 Splicing Variant.
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Negative Regulation of the Keap1-Nrf2 Pathway by a p62/Sqstm1 Splicing Variant.
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Negative Regulation of the Keap1-Nrf2 Pathway by a p62/Sqstm1 Splicing Variant.
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Negative Regulation of the Keap1-Nrf2 Pathway by a p62/Sqstm1 Splicing Variant.
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Negative Regulation of the Keap1-Nrf2 Pathway by a p62/Sqstm1 Splicing Variant.
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Negative Regulation of the Keap1-Nrf2 Pathway by a p62/Sqstm1 Splicing Variant.
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Negative Regulation of the Keap1-Nrf2 Pathway by a p62/Sqstm1 Splicing Variant.
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Oxidation of SQSTM1/p62 mediates the link between redox state and protein homeostasis.
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Oxidation of SQSTM1/p62 mediates the link between redox state and protein homeostasis.
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Oxidation of SQSTM1/p62 mediates the link between redox state and protein homeostasis.
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Oxidation of SQSTM1/p62 mediates the link between redox state and protein homeostasis.
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Oxidation of SQSTM1/p62 mediates the link between redox state and protein homeostasis.
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Oxidation of SQSTM1/p62 mediates the link between redox state and protein homeostasis.
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Oxidation of SQSTM1/p62 mediates the link between redox state and protein homeostasis.
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Loss of autophagy in dopaminergic neurons causes Lewy pathology and motor dysfunction in aged mice.
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Loss of autophagy in dopaminergic neurons causes Lewy pathology and motor dysfunction in aged mice.
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Loss of autophagy in dopaminergic neurons causes Lewy pathology and motor dysfunction in aged mice.
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Loss of autophagy in dopaminergic neurons causes Lewy pathology and motor dysfunction in aged mice.
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Loss of autophagy in dopaminergic neurons causes Lewy pathology and motor dysfunction in aged mice.
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Loss of autophagy in dopaminergic neurons causes Lewy pathology and motor dysfunction in aged mice.
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Loss of autophagy in dopaminergic neurons causes Lewy pathology and motor dysfunction in aged mice.
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Loss of autophagy in dopaminergic neurons causes Lewy pathology and motor dysfunction in aged mice.
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AMPK Inhibits ULK1-Dependent Autophagosome Formation and Lysosomal Acidification via Distinct Mechanisms.
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Live-Cell Mesothelioma Biobank to Explore Mechanisms of Tumor Progression.
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Mfn2 ubiquitination by PINK1/parkin gates the p97-dependent release of ER from mitochondria to drive mitophagy.
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Mfn2 ubiquitination by PINK1/parkin gates the p97-dependent release of ER from mitochondria to drive mitophagy.
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Lysosomal damage after spinal cord injury causes accumulation of RIPK1 and RIPK3 proteins and potentiation of necroptosis.
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Lysosomal damage after spinal cord injury causes accumulation of RIPK1 and RIPK3 proteins and potentiation of necroptosis.
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Lysosomal damage after spinal cord injury causes accumulation of RIPK1 and RIPK3 proteins and potentiation of necroptosis.
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Lysosomal damage after spinal cord injury causes accumulation of RIPK1 and RIPK3 proteins and potentiation of necroptosis.
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Lysosomal damage after spinal cord injury causes accumulation of RIPK1 and RIPK3 proteins and potentiation of necroptosis.
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Lysosomal damage after spinal cord injury causes accumulation of RIPK1 and RIPK3 proteins and potentiation of necroptosis.
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Lysosomal damage after spinal cord injury causes accumulation of RIPK1 and RIPK3 proteins and potentiation of necroptosis.
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Lysosomal damage after spinal cord injury causes accumulation of RIPK1 and RIPK3 proteins and potentiation of necroptosis.
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Systemic overexpression of SQSTM1/p62 accelerates disease onset in a SOD1H46R-expressing ALS mouse model.
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Systemic overexpression of SQSTM1/p62 accelerates disease onset in a SOD1H46R-expressing ALS mouse model.
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Systemic overexpression of SQSTM1/p62 accelerates disease onset in a SOD1H46R-expressing ALS mouse model.
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The ubiquitin ligase UBR5 suppresses proteostasis collapse in pluripotent stem cells from Huntington's disease patients.
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Autophagy mediates epithelial cancer chemoresistance by reducing p62/SQSTM1 accumulation.
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Autophagy mediates epithelial cancer chemoresistance by reducing p62/SQSTM1 accumulation.
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Autophagy mediates epithelial cancer chemoresistance by reducing p62/SQSTM1 accumulation.
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Autophagy mediates epithelial cancer chemoresistance by reducing p62/SQSTM1 accumulation.
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NADPH Oxidase and Guanylate Binding Protein 5 Restrict Survival of Avirulent Type III Strains of Toxoplasma gondii in Naive Macrophages.
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The PPARα Agonist Fenofibrate Prevents Formation of Protein Aggregates (Mallory-Denk bodies) in a Murine Model of Steatohepatitis-like Hepatotoxicity.
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The PPARα Agonist Fenofibrate Prevents Formation of Protein Aggregates (Mallory-Denk bodies) in a Murine Model of Steatohepatitis-like Hepatotoxicity.
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The PPARα Agonist Fenofibrate Prevents Formation of Protein Aggregates (Mallory-Denk bodies) in a Murine Model of Steatohepatitis-like Hepatotoxicity.
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The PPARα Agonist Fenofibrate Prevents Formation of Protein Aggregates (Mallory-Denk bodies) in a Murine Model of Steatohepatitis-like Hepatotoxicity.
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A short isoform of ATG7 fails to lipidate LC3/GABARAP.
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Deubiquitinase Usp12 functions noncatalytically to induce autophagy and confer neuroprotection in models of Huntington's disease.
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Resveratrol Ameliorates Mitophagy Disturbance and Improves Cardiac Pathophysiology of Dystrophin-deficient mdx Mice.
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Resveratrol Ameliorates Mitophagy Disturbance and Improves Cardiac Pathophysiology of Dystrophin-deficient mdx Mice.
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USP10 Is a Driver of Ubiquitinated Protein Aggregation and Aggresome Formation to Inhibit Apoptosis.
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USP10 Is a Driver of Ubiquitinated Protein Aggregation and Aggresome Formation to Inhibit Apoptosis.
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USP10 Is a Driver of Ubiquitinated Protein Aggregation and Aggresome Formation to Inhibit Apoptosis.
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USP10 Is a Driver of Ubiquitinated Protein Aggregation and Aggresome Formation to Inhibit Apoptosis.
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USP10 Is a Driver of Ubiquitinated Protein Aggregation and Aggresome Formation to Inhibit Apoptosis.
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USP10 Is a Driver of Ubiquitinated Protein Aggregation and Aggresome Formation to Inhibit Apoptosis.
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USP10 Is a Driver of Ubiquitinated Protein Aggregation and Aggresome Formation to Inhibit Apoptosis.
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USP10 Is a Driver of Ubiquitinated Protein Aggregation and Aggresome Formation to Inhibit Apoptosis.
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USP10 Is a Driver of Ubiquitinated Protein Aggregation and Aggresome Formation to Inhibit Apoptosis.
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USP10 Is a Driver of Ubiquitinated Protein Aggregation and Aggresome Formation to Inhibit Apoptosis.
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USP10 Is a Driver of Ubiquitinated Protein Aggregation and Aggresome Formation to Inhibit Apoptosis.
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USP10 Is a Driver of Ubiquitinated Protein Aggregation and Aggresome Formation to Inhibit Apoptosis.
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USP10 Is a Driver of Ubiquitinated Protein Aggregation and Aggresome Formation to Inhibit Apoptosis.
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USP10 Is a Driver of Ubiquitinated Protein Aggregation and Aggresome Formation to Inhibit Apoptosis.
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USP10 Is a Driver of Ubiquitinated Protein Aggregation and Aggresome Formation to Inhibit Apoptosis.
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USP10 Is a Driver of Ubiquitinated Protein Aggregation and Aggresome Formation to Inhibit Apoptosis.
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USP10 Is a Driver of Ubiquitinated Protein Aggregation and Aggresome Formation to Inhibit Apoptosis.
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Resveratrol Decreases Oxidative Stress by Restoring Mitophagy and Improves the Pathophysiology of Dystrophin-Deficient mdx Mice.
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Resveratrol Decreases Oxidative Stress by Restoring Mitophagy and Improves the Pathophysiology of Dystrophin-Deficient mdx Mice.
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RGS9-2 rescues dopamine D2 receptor levels and signaling in DYT1 dystonia mouse models.
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Autophagy attenuates tubulointerstital fibrosis through regulating transforming growth factor-β and NLRP3 inflammasome signaling pathway.
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Autophagy inhibition specifically promotes epithelial-mesenchymal transition and invasion in RAS-mutated cancer cells.
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Autophagy inhibition specifically promotes epithelial-mesenchymal transition and invasion in RAS-mutated cancer cells.
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Autophagy inhibition specifically promotes epithelial-mesenchymal transition and invasion in RAS-mutated cancer cells.
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Autophagy inhibition specifically promotes epithelial-mesenchymal transition and invasion in RAS-mutated cancer cells.
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Atg7-dependent canonical autophagy regulates the degradation of aquaporin 2 in prolonged hypokalemia.
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Atg7-dependent canonical autophagy regulates the degradation of aquaporin 2 in prolonged hypokalemia.
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Atg7-dependent canonical autophagy regulates the degradation of aquaporin 2 in prolonged hypokalemia.
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Brain tyrosinase overexpression implicates age-dependent neuromelanin production in Parkinson's disease pathogenesis.
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Brain tyrosinase overexpression implicates age-dependent neuromelanin production in Parkinson's disease pathogenesis.
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Myoglobinopathy is an adult-onset autosomal dominant myopathy with characteristic sarcoplasmic inclusions.
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Autophagy regulates lipid metabolism through selective turnover of NCoR1.
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Autophagy regulates lipid metabolism through selective turnover of NCoR1.
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Autophagy regulates lipid metabolism through selective turnover of NCoR1.
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Autophagy regulates lipid metabolism through selective turnover of NCoR1.
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Autophagy regulates lipid metabolism through selective turnover of NCoR1.
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Autophagy regulates lipid metabolism through selective turnover of NCoR1.
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Autophagy regulates lipid metabolism through selective turnover of NCoR1.
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Autophagy regulates lipid metabolism through selective turnover of NCoR1.
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Autophagy regulates lipid metabolism through selective turnover of NCoR1.
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Autophagy regulates lipid metabolism through selective turnover of NCoR1.
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The FMRpolyGlycine Protein Mediates Aggregate Formation and Toxicity Independent of the CGG mRNA Hairpin in a Cellular Model for FXTAS.
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Hyperosmotic Stress Induces Unconventional Autophagy Independent of the Ulk1 Complex.
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Hyperosmotic Stress Induces Unconventional Autophagy Independent of the Ulk1 Complex.
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Hyperosmotic Stress Induces Unconventional Autophagy Independent of the Ulk1 Complex.
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Hyperosmotic Stress Induces Unconventional Autophagy Independent of the Ulk1 Complex.
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m6A mRNA demethylase FTO regulates melanoma tumorigenicity and response to anti-PD-1 blockade.
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Fibril-induced glutamine-/asparagine-rich prions recruit stress granule proteins in mammalian cells.
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Fibril-induced glutamine-/asparagine-rich prions recruit stress granule proteins in mammalian cells.
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Fibril-induced glutamine-/asparagine-rich prions recruit stress granule proteins in mammalian cells.
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Fibril-induced glutamine-/asparagine-rich prions recruit stress granule proteins in mammalian cells.
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Fibril-induced glutamine-/asparagine-rich prions recruit stress granule proteins in mammalian cells.
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Fibril-induced glutamine-/asparagine-rich prions recruit stress granule proteins in mammalian cells.
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Autophagy regulates inflammatory programmed cell death via turnover of RHIM-domain proteins.
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Autophagy regulates inflammatory programmed cell death via turnover of RHIM-domain proteins.
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Autophagy regulates inflammatory programmed cell death via turnover of RHIM-domain proteins.
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Autophagy regulates inflammatory programmed cell death via turnover of RHIM-domain proteins.
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Autophagy regulates inflammatory programmed cell death via turnover of RHIM-domain proteins.
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cPLA2 activation contributes to lysosomal defects leading to impairment of autophagy after spinal cord injury.
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mTORC1 and PKB/Akt control the muscle response to denervation by regulating autophagy and HDAC4.
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mTORC1 and PKB/Akt control the muscle response to denervation by regulating autophagy and HDAC4.
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mTORC1 and PKB/Akt control the muscle response to denervation by regulating autophagy and HDAC4.
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mTORC1 and PKB/Akt control the muscle response to denervation by regulating autophagy and HDAC4.
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mTORC1 and PKB/Akt control the muscle response to denervation by regulating autophagy and HDAC4.
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Lysosomal degradation of newly formed insulin granules contributes to β cell failure in diabetes.
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Altered adipocyte differentiation and unbalanced autophagy in type 2 Familial Partial Lipodystrophy: an in vitro and in vivo study of adipose tissue browning.
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Altered adipocyte differentiation and unbalanced autophagy in type 2 Familial Partial Lipodystrophy: an in vitro and in vivo study of adipose tissue browning.
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Altered adipocyte differentiation and unbalanced autophagy in type 2 Familial Partial Lipodystrophy: an in vitro and in vivo study of adipose tissue browning.
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Altered adipocyte differentiation and unbalanced autophagy in type 2 Familial Partial Lipodystrophy: an in vitro and in vivo study of adipose tissue browning.
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Autophagy inhibition-mediated epithelial-mesenchymal transition augments local myofibroblast differentiation in pulmonary fibrosis.
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Autophagy inhibition-mediated epithelial-mesenchymal transition augments local myofibroblast differentiation in pulmonary fibrosis.
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Autophagy inhibition-mediated epithelial-mesenchymal transition augments local myofibroblast differentiation in pulmonary fibrosis.
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Autophagy inhibition-mediated epithelial-mesenchymal transition augments local myofibroblast differentiation in pulmonary fibrosis.
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Autophagy inhibition-mediated epithelial-mesenchymal transition augments local myofibroblast differentiation in pulmonary fibrosis.
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Autophagy inhibition-mediated epithelial-mesenchymal transition augments local myofibroblast differentiation in pulmonary fibrosis.
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Autophagy inhibition-mediated epithelial-mesenchymal transition augments local myofibroblast differentiation in pulmonary fibrosis.
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Autophagy inhibition-mediated epithelial-mesenchymal transition augments local myofibroblast differentiation in pulmonary fibrosis.
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Cytoplasmic DAXX drives SQSTM1/p62 phase condensation to activate Nrf2-mediated stress response.
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Cytoplasmic DAXX drives SQSTM1/p62 phase condensation to activate Nrf2-mediated stress response.
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Cytoplasmic DAXX drives SQSTM1/p62 phase condensation to activate Nrf2-mediated stress response.
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Cytoplasmic DAXX drives SQSTM1/p62 phase condensation to activate Nrf2-mediated stress response.
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Cytoplasmic DAXX drives SQSTM1/p62 phase condensation to activate Nrf2-mediated stress response.
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Cytoplasmic DAXX drives SQSTM1/p62 phase condensation to activate Nrf2-mediated stress response.
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Cytoplasmic DAXX drives SQSTM1/p62 phase condensation to activate Nrf2-mediated stress response.
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Buffering of cytosolic calcium plays a neuroprotective role by preserving the autophagy-lysosome pathway during MPP+-induced neuronal death.
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Buffering of cytosolic calcium plays a neuroprotective role by preserving the autophagy-lysosome pathway during MPP+-induced neuronal death.
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Buffering of cytosolic calcium plays a neuroprotective role by preserving the autophagy-lysosome pathway during MPP+-induced neuronal death.
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Buffering of cytosolic calcium plays a neuroprotective role by preserving the autophagy-lysosome pathway during MPP+-induced neuronal death.
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G3BP1 inhibits ubiquitinated protein aggregations induced by p62 and USP10.
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G3BP1 inhibits ubiquitinated protein aggregations induced by p62 and USP10.
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G3BP1 inhibits ubiquitinated protein aggregations induced by p62 and USP10.
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G3BP1 inhibits ubiquitinated protein aggregations induced by p62 and USP10.
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G3BP1 inhibits ubiquitinated protein aggregations induced by p62 and USP10.
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G3BP1 inhibits ubiquitinated protein aggregations induced by p62 and USP10.
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G3BP1 inhibits ubiquitinated protein aggregations induced by p62 and USP10.
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G3BP1 inhibits ubiquitinated protein aggregations induced by p62 and USP10.
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G3BP1 inhibits ubiquitinated protein aggregations induced by p62 and USP10.
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G3BP1 inhibits ubiquitinated protein aggregations induced by p62 and USP10.
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G3BP1 inhibits ubiquitinated protein aggregations induced by p62 and USP10.
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G3BP1 inhibits ubiquitinated protein aggregations induced by p62 and USP10.
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SQSTM-1/p62 potentiates HTLV-1 Tax-mediated NF-κB activation through its ubiquitin binding function.
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SQSTM-1/p62 potentiates HTLV-1 Tax-mediated NF-κB activation through its ubiquitin binding function.
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SQSTM-1/p62 potentiates HTLV-1 Tax-mediated NF-κB activation through its ubiquitin binding function.
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SQSTM-1/p62 potentiates HTLV-1 Tax-mediated NF-κB activation through its ubiquitin binding function.
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SQSTM-1/p62 potentiates HTLV-1 Tax-mediated NF-κB activation through its ubiquitin binding function.
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SQSTM-1/p62 potentiates HTLV-1 Tax-mediated NF-κB activation through its ubiquitin binding function.
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SQSTM-1/p62 potentiates HTLV-1 Tax-mediated NF-κB activation through its ubiquitin binding function.
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SQSTM-1/p62 potentiates HTLV-1 Tax-mediated NF-κB activation through its ubiquitin binding function.
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SQSTM-1/p62 potentiates HTLV-1 Tax-mediated NF-κB activation through its ubiquitin binding function.
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SQSTM-1/p62 potentiates HTLV-1 Tax-mediated NF-κB activation through its ubiquitin binding function.
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SQSTM-1/p62 potentiates HTLV-1 Tax-mediated NF-κB activation through its ubiquitin binding function.
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SQSTM-1/p62 potentiates HTLV-1 Tax-mediated NF-κB activation through its ubiquitin binding function.
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SQSTM-1/p62 potentiates HTLV-1 Tax-mediated NF-κB activation through its ubiquitin binding function.
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SQSTM-1/p62 potentiates HTLV-1 Tax-mediated NF-κB activation through its ubiquitin binding function.
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Autophagy protein NRBF2 has reduced expression in Alzheimer's brains and modulates memory and amyloid-beta homeostasis in mice.
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Autophagy protein NRBF2 has reduced expression in Alzheimer's brains and modulates memory and amyloid-beta homeostasis in mice.
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Loss of autophagy impairs physiological steatosis by accumulation of NCoR1.
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Loss of autophagy impairs physiological steatosis by accumulation of NCoR1.
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Loss of autophagy impairs physiological steatosis by accumulation of NCoR1.
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Autophagy Deficiency in Renal Proximal Tubular Cells Leads to an Increase in Cellular Injury and Apoptosis under Normal Fed Conditions.
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Autophagy Deficiency in Renal Proximal Tubular Cells Leads to an Increase in Cellular Injury and Apoptosis under Normal Fed Conditions.
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Autophagy Deficiency in Renal Proximal Tubular Cells Leads to an Increase in Cellular Injury and Apoptosis under Normal Fed Conditions.
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AMPK-dependent activation of the Cyclin Y/CDK16 complex controls autophagy.
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AMPK-dependent activation of the Cyclin Y/CDK16 complex controls autophagy.
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AMPK-dependent activation of the Cyclin Y/CDK16 complex controls autophagy.
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Microglia clear neuron-released α-synuclein via selective autophagy and prevent neurodegeneration.
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Microglia clear neuron-released α-synuclein via selective autophagy and prevent neurodegeneration.
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Microglia clear neuron-released α-synuclein via selective autophagy and prevent neurodegeneration.
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Microglia clear neuron-released α-synuclein via selective autophagy and prevent neurodegeneration.
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Microglia clear neuron-released α-synuclein via selective autophagy and prevent neurodegeneration.
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Microglia clear neuron-released α-synuclein via selective autophagy and prevent neurodegeneration.
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Microglia clear neuron-released α-synuclein via selective autophagy and prevent neurodegeneration.
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Microglia clear neuron-released α-synuclein via selective autophagy and prevent neurodegeneration.
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Microglia clear neuron-released α-synuclein via selective autophagy and prevent neurodegeneration.
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Microglia clear neuron-released α-synuclein via selective autophagy and prevent neurodegeneration.
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Microglia clear neuron-released α-synuclein via selective autophagy and prevent neurodegeneration.
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Microglia clear neuron-released α-synuclein via selective autophagy and prevent neurodegeneration.
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Microglia clear neuron-released α-synuclein via selective autophagy and prevent neurodegeneration.
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Microglia clear neuron-released α-synuclein via selective autophagy and prevent neurodegeneration.
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Microglia clear neuron-released α-synuclein via selective autophagy and prevent neurodegeneration.
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Myocardial cathepsin D is downregulated in sudden cardiac death.
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Inhibition of striatonigral autophagy as a link between cannabinoid intoxication and impairment of motor coordination.
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Inhibition of striatonigral autophagy as a link between cannabinoid intoxication and impairment of motor coordination.
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Inhibition of striatonigral autophagy as a link between cannabinoid intoxication and impairment of motor coordination.
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Inhibition of striatonigral autophagy as a link between cannabinoid intoxication and impairment of motor coordination.
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Inhibition of striatonigral autophagy as a link between cannabinoid intoxication and impairment of motor coordination.
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Inhibition of striatonigral autophagy as a link between cannabinoid intoxication and impairment of motor coordination.
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A Scaffold-Free 3-D Co-Culture Mimics the Major Features of the Reverse Warburg Effect In Vitro.
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A Scaffold-Free 3-D Co-Culture Mimics the Major Features of the Reverse Warburg Effect In Vitro.
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ISG15 Connects Autophagy and IFN-γ-Dependent Control of Toxoplasma gondii Infection in Human Cells.
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ISG15 Connects Autophagy and IFN-γ-Dependent Control of Toxoplasma gondii Infection in Human Cells.
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Novel Insights into the Cellular Localization and Regulation of the Autophagosomal Proteins LC3A, LC3B and LC3C.
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Novel Insights into the Cellular Localization and Regulation of the Autophagosomal Proteins LC3A, LC3B and LC3C.
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Novel Insights into the Cellular Localization and Regulation of the Autophagosomal Proteins LC3A, LC3B and LC3C.
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Novel Insights into the Cellular Localization and Regulation of the Autophagosomal Proteins LC3A, LC3B and LC3C.
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Novel Insights into the Cellular Localization and Regulation of the Autophagosomal Proteins LC3A, LC3B and LC3C.
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Novel Insights into the Cellular Localization and Regulation of the Autophagosomal Proteins LC3A, LC3B and LC3C.
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Novel Insights into the Cellular Localization and Regulation of the Autophagosomal Proteins LC3A, LC3B and LC3C.
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Novel Insights into the Cellular Localization and Regulation of the Autophagosomal Proteins LC3A, LC3B and LC3C.
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The Polyphenol Pterostilbene Ameliorates the Myopathic Phenotype of Collagen VI Deficient Mice via Autophagy Induction.
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Degradation of connexin 50 protein causes waterclefts in human lens.
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Prodigiosin Sensitizes Sensitive and Resistant Urothelial Carcinoma Cells to Cisplatin Treatment.
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Prodigiosin Sensitizes Sensitive and Resistant Urothelial Carcinoma Cells to Cisplatin Treatment.
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Prodigiosin Sensitizes Sensitive and Resistant Urothelial Carcinoma Cells to Cisplatin Treatment.
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Prodigiosin Sensitizes Sensitive and Resistant Urothelial Carcinoma Cells to Cisplatin Treatment.
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Prodigiosin Sensitizes Sensitive and Resistant Urothelial Carcinoma Cells to Cisplatin Treatment.
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Autophagy of the m6A mRNA demethylase FTO is impaired by low-level arsenic exposure to promote tumorigenesis.
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Autophagy of the m6A mRNA demethylase FTO is impaired by low-level arsenic exposure to promote tumorigenesis.
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N-Acetyl-L-leucine improves functional recovery and attenuates cortical cell death and neuroinflammation after traumatic brain injury in mice.
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High-throughput screening for natural compound-based autophagy modulators reveals novel chemotherapeutic mode of action for arzanol.
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High-throughput screening for natural compound-based autophagy modulators reveals novel chemotherapeutic mode of action for arzanol.
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An essential role of the autophagy activating kinase ULK1 in snRNP biogenesis.
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Phosphoproteomic identification of ULK substrates reveals VPS15-dependent ULK/VPS34 interplay in the regulation of autophagy.
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Phosphoproteomic identification of ULK substrates reveals VPS15-dependent ULK/VPS34 interplay in the regulation of autophagy.
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Phosphoproteomic identification of ULK substrates reveals VPS15-dependent ULK/VPS34 interplay in the regulation of autophagy.
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Phosphoproteomic identification of ULK substrates reveals VPS15-dependent ULK/VPS34 interplay in the regulation of autophagy.
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Phosphoproteomic identification of ULK substrates reveals VPS15-dependent ULK/VPS34 interplay in the regulation of autophagy.
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Phosphoproteomic identification of ULK substrates reveals VPS15-dependent ULK/VPS34 interplay in the regulation of autophagy.
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Phosphoproteomic identification of ULK substrates reveals VPS15-dependent ULK/VPS34 interplay in the regulation of autophagy.
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Phosphoproteomic identification of ULK substrates reveals VPS15-dependent ULK/VPS34 interplay in the regulation of autophagy.
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FIP200 controls the TBK1 activation threshold at SQSTM1/p62-positive condensates.
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Lack of Cathepsin D in the central nervous system results in microglia and astrocyte activation and the accumulation of proteinopathy-related proteins.
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Malin restoration as proof of concept for gene therapy for Lafora disease.
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BALB.NCT-Cpox nct is a unique mouse model of hereditary coproporphyria.
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Product: anti-p62/ SQSTM1 (C-terminus) guinea pig polyclonal, serum
Art.No.: GP62-C

Quantity 100 µl
Antibody Type Polyclonal
Host Guinea pig
Conjugate Unconjugated
Application IHC, WB
Purification Stabilized antiserum
Reactivity Bovine, Human, Mouse, Rat
Storage Short term at 2-8°C; long term storage in aliquots at -20°C; avoid freeze/thaw cycles
Intended use Research use only
Immunogen C-terminal domain (20 amino acids: C-NYD IGA ALD TIQ YSK HPP PL) of human p62 protein, coupled to KLH. This peptide sequence is identical in human, monkey, bovine, mouse, and rat.
Formulation Contains 0.09% sodium azide
Note Centrifuge prior to opening
Tested applications Tested dilutions
Immunohistochemistry (IHC) - frozen 1:100-1:600
Immunohistochemistry (IHC) - paraffin 1:100-1:600 (microwave treatment recommended)
Western Blot (WB) 1:1,000-1:3,000

Human 62 kDa (p62) protein, is present in intracytoplasmic inclusions (e.g. hyaline bodies) of hepatocellular carcinoma.
p62 protein (also described as ubiqutin-binding protein; sequestosome 1; SQSTM1) has been found in many tissues and cells, including lymphoid cells, serving probably a common cellular signal transduction mechanism (e.g. ubiquitin-associated degradation and autophagy).
The antiserum stains also neurofibrillary tangles in the brain of patients suffering from Alzheimer's disease.

The GP62-C antibody is knockout validated (Waguri & Komatsu, 2009).

Waguri, S. & Komatsu, M. Chapter 9 Biochemical and Morphological Detection of Inclusion Bodies in Autophagy-Deficient Mice. Methods in Enzymology 453, 181-196 (2009).


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