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> Guinea Pig Polyclonal Anti-Nephrin

Guinea Pig Polyclonal Anti-Nephrin

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Referentie GP-N2

Formaat : 100µL

Merk : Progen

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anti-Nephrin guinea pig polyclonal, serum

anti-Nephrin guinea pig polyclonal, serum
anti-Nephrin guinea pig polyclonal, serum
anti-Nephrin guinea pig polyclonal, serum
anti-Nephrin guinea pig polyclonal, serum
anti-Nephrin guinea pig polyclonal, serum
anti-Nephrin guinea pig polyclonal, serum
Role of the polarity protein Scribble for podocyte differentiation and maintenance.
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Role of the polarity protein Scribble for podocyte differentiation and maintenance.
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Role of the polarity protein Scribble for podocyte differentiation and maintenance.
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Early-onset diabetic E1-DN mice develop albuminuria and glomerular injury typical of diabetic nephropathy.
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Early-onset diabetic E1-DN mice develop albuminuria and glomerular injury typical of diabetic nephropathy.
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Podocyte-Specific Deletion of Murine CXADR Does Not Impair Podocyte Development, Function or Stress Response.
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Podocyte-Specific Deletion of Murine CXADR Does Not Impair Podocyte Development, Function or Stress Response.
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Podocyte-Specific Deletion of Murine CXADR Does Not Impair Podocyte Development, Function or Stress Response.
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Podocyte-Specific Deletion of Murine CXADR Does Not Impair Podocyte Development, Function or Stress Response.
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Podocyte-Specific Deletion of Murine CXADR Does Not Impair Podocyte Development, Function or Stress Response.
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Podocyte-Specific Deletion of Murine CXADR Does Not Impair Podocyte Development, Function or Stress Response.
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Podocyte-Specific Deletion of Murine CXADR Does Not Impair Podocyte Development, Function or Stress Response.
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Microtubule Associated Protein 1b (MAP1B) Is a Marker of the Microtubular Cytoskeleton in Podocytes but Is Not Essential for the Function of the Kidney Filtration Barrier in Mice.
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Microtubule Associated Protein 1b (MAP1B) Is a Marker of the Microtubular Cytoskeleton in Podocytes but Is Not Essential for the Function of the Kidney Filtration Barrier in Mice.
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Loss of endogenous thymosin β4 accelerates glomerular disease.
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Loss of endogenous thymosin β4 accelerates glomerular disease.
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Loss of endogenous thymosin β4 accelerates glomerular disease.
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Loss of endogenous thymosin β4 accelerates glomerular disease.
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Angiotensin II increases glomerular permeability by β-arrestin mediated nephrin endocytosis.
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Angiotensin II increases glomerular permeability by β-arrestin mediated nephrin endocytosis.
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Angiotensin II increases glomerular permeability by β-arrestin mediated nephrin endocytosis.
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Diacylglycerol Kinase alpha is Involved in the Vitamin E-Induced Amelioration of Diabetic Nephropathy in Mice.
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A novel in vivo method to quantify slit diaphragm protein abundance in murine proteinuric kidney disease.
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A novel in vivo method to quantify slit diaphragm protein abundance in murine proteinuric kidney disease.
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A novel in vivo method to quantify slit diaphragm protein abundance in murine proteinuric kidney disease.
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A novel in vivo method to quantify slit diaphragm protein abundance in murine proteinuric kidney disease.
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PAX2 is dispensable for in vitro nephron formation from human induced pluripotent stem cells.
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Studying the role of fascin-1 in mechanically stressed podocytes.
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Studying the role of fascin-1 in mechanically stressed podocytes.
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Studying the role of fascin-1 in mechanically stressed podocytes.
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Studying the role of fascin-1 in mechanically stressed podocytes.
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Studying the role of fascin-1 in mechanically stressed podocytes.
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ARF6 mediates nephrin tyrosine phosphorylation-induced podocyte cellular dynamics.
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ARF6 mediates nephrin tyrosine phosphorylation-induced podocyte cellular dynamics.
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ARF6 mediates nephrin tyrosine phosphorylation-induced podocyte cellular dynamics.
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ARF6 mediates nephrin tyrosine phosphorylation-induced podocyte cellular dynamics.
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ARF6 mediates nephrin tyrosine phosphorylation-induced podocyte cellular dynamics.
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ARF6 mediates nephrin tyrosine phosphorylation-induced podocyte cellular dynamics.
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Structured illumination microscopy and automatized image processing as a rapid diagnostic tool for podocyte effacement.
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Structured illumination microscopy and automatized image processing as a rapid diagnostic tool for podocyte effacement.
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Structured illumination microscopy and automatized image processing as a rapid diagnostic tool for podocyte effacement.
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Hmox1 Deficiency Sensitizes Mice to Peroxynitrite Formation and Diabetic Glomerular Microvascular Injuries.
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Role of c-Abl and nephrin in podocyte cytoskeletal remodeling induced by angiotensin II.
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Role of c-Abl and nephrin in podocyte cytoskeletal remodeling induced by angiotensin II.
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Role of c-Abl and nephrin in podocyte cytoskeletal remodeling induced by angiotensin II.
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Role of c-Abl and nephrin in podocyte cytoskeletal remodeling induced by angiotensin II.
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Progenitor Renin Lineage Cells are not involved in the regeneration of glomerular endothelial cells during experimental renal thrombotic microangiopathy.
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Repeated administration of alpha-galactosylceramide ameliorates experimental lupus nephritis in mice.
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Novel Microscopic Techniques for Podocyte Research.
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Novel Microscopic Techniques for Podocyte Research.
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Novel Microscopic Techniques for Podocyte Research.
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Differentiation of human iPSCs into functional podocytes.
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Reconstitution of the embryonic kidney identifies a donor cell contribution to the renal vasculature upon transplantation.
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Reconstitution of the embryonic kidney identifies a donor cell contribution to the renal vasculature upon transplantation.
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Reconstitution of the embryonic kidney identifies a donor cell contribution to the renal vasculature upon transplantation.
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Reconstitution of the embryonic kidney identifies a donor cell contribution to the renal vasculature upon transplantation.
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Reconstitution of the embryonic kidney identifies a donor cell contribution to the renal vasculature upon transplantation.
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Reconstitution of the embryonic kidney identifies a donor cell contribution to the renal vasculature upon transplantation.
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Reconstitution of the embryonic kidney identifies a donor cell contribution to the renal vasculature upon transplantation.
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Reconstitution of the embryonic kidney identifies a donor cell contribution to the renal vasculature upon transplantation.
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Reconstitution of the embryonic kidney identifies a donor cell contribution to the renal vasculature upon transplantation.
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Reconstitution of the embryonic kidney identifies a donor cell contribution to the renal vasculature upon transplantation.
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Reconstitution of the embryonic kidney identifies a donor cell contribution to the renal vasculature upon transplantation.
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Reconstitution of the embryonic kidney identifies a donor cell contribution to the renal vasculature upon transplantation.
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Reconstitution of the embryonic kidney identifies a donor cell contribution to the renal vasculature upon transplantation.
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Reconstitution of the embryonic kidney identifies a donor cell contribution to the renal vasculature upon transplantation.
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Reconstitution of the embryonic kidney identifies a donor cell contribution to the renal vasculature upon transplantation.
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Reconstitution of the embryonic kidney identifies a donor cell contribution to the renal vasculature upon transplantation.
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CD36-Mediated Lipid Accumulation and Activation of NLRP3 Inflammasome Lead to Podocyte Injury in Obesity-Related Glomerulopathy.
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CD36-Mediated Lipid Accumulation and Activation of NLRP3 Inflammasome Lead to Podocyte Injury in Obesity-Related Glomerulopathy.
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CD36-Mediated Lipid Accumulation and Activation of NLRP3 Inflammasome Lead to Podocyte Injury in Obesity-Related Glomerulopathy.
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Angiotensin II-mediated MYH9 downregulation causes structural and functional podocyte injury in diabetic kidney disease.
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CCR2 knockout ameliorates obesity-induced kidney injury through inhibiting oxidative stress and ER stress.
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The mechanisms of ameliorating effect of a green tea polyphenol on diabetic nephropathy based on diacylglycerol kinase α.
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An HIV-Tat inducible mouse model system of childhood HIV-associated nephropathy.
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Protective Role of Tangshen Formula on the Progression of Renal Damage in db/db Mice by TRPC6/Talin1 Pathway in Podocytes.
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Protective Role of Tangshen Formula on the Progression of Renal Damage in db/db Mice by TRPC6/Talin1 Pathway in Podocytes.
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Protective Role of Tangshen Formula on the Progression of Renal Damage in db/db Mice by TRPC6/Talin1 Pathway in Podocytes.
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Protective Role of Tangshen Formula on the Progression of Renal Damage in db/db Mice by TRPC6/Talin1 Pathway in Podocytes.
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Inhibiting calpain 1 and 2 in cyclin G associated kinase-knockout mice mitigates podocyte injury.
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Inhibiting calpain 1 and 2 in cyclin G associated kinase-knockout mice mitigates podocyte injury.
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Metformin ameliorates the severity of experimental Alport syndrome.
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Super-resolved local recruitment of CLDN5 to filtration slits implicates a direct relationship with podocyte foot process effacement.
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Super-resolved local recruitment of CLDN5 to filtration slits implicates a direct relationship with podocyte foot process effacement.
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A Novel Model for Nephrotic Syndrome Reveals Associated Dysbiosis of the Gut Microbiome and Extramedullary Hematopoiesis.
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Glomerular endothelial cell senescence drives age-related kidney disease through PAI-1.
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BET Proteins Regulate Expression of Osr1 in Early Kidney Development.
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Beneficial Impact of Interspecies Chimeric Renal Organoids Against a Xenogeneic Immune Response.
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Beneficial Impact of Interspecies Chimeric Renal Organoids Against a Xenogeneic Immune Response.
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Beneficial Impact of Interspecies Chimeric Renal Organoids Against a Xenogeneic Immune Response.
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Beneficial Impact of Interspecies Chimeric Renal Organoids Against a Xenogeneic Immune Response.
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Beneficial Impact of Interspecies Chimeric Renal Organoids Against a Xenogeneic Immune Response.
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Beneficial Impact of Interspecies Chimeric Renal Organoids Against a Xenogeneic Immune Response.
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Beneficial Impact of Interspecies Chimeric Renal Organoids Against a Xenogeneic Immune Response.
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Beneficial Impact of Interspecies Chimeric Renal Organoids Against a Xenogeneic Immune Response.
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Beneficial Impact of Interspecies Chimeric Renal Organoids Against a Xenogeneic Immune Response.
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Product: anti-Nephrin guinea pig polyclonal, serum
Art.No.: GP-N2

Quantity 100 µl
Antibody Type Polyclonal
Host Guinea pig
Conjugate Unconjugated
Application ICC/IF, IHC, WB
Purification Stabilized antiserum
Reactivity Human, Mouse
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 Synthetic peptide of mouse Nephrin (intracellular domain, aa1243-1256, EPGSLPFELRGHLV)
Formulation Contains 0.09% sodium azide
UniprotID O60500 (Human), Q9QZS7 (Mouse)
Synonym Nephrin, Renal glomerulus-specific cell adhesion receptor, NPHS1, NPHN
Note Centrifuge prior to opening
Tested applications Tested dilutions
Immunocytochemistry (ICC)/ Immunofluorescence (IF) Assay dependent
Immunohistochemistry (IHC) - frozen 1:50
Immunohistochemistry (IHC) - paraffin 1:50 (microwave treatment recommended)
Western Blot (WB) 1:500

The antibody reacts specifically with nephrin, first described as a kidney podocyte marker protein (MW 135,000 calculated from aa sequence data; apparent Mr 185,000 after SDS-PAGE).
Nephrin is a transmembrane cell adhesion molecule located at the slit diaphragm.
Immunolocalization: the antibody stains positively podocytes of the kidney, radial glial cells of the brain, Sertoli cells of testis, and beta islet cells of the pancreas.
Tested cultured cell lines: PCL (podocyte cell line), M-1 (cortical collecting duct cells).

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