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Nphs2  -  nephrosis 2, podocin

Mus musculus

Synonyms: AI790225, PDCN, Podocin, SRN1, podocin
 
 
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Disease relevance of Nphs2

  • Nphs2-/- mice developed proteinuria during the antenatal period and died a few days after birth from renal failure caused by massive mesangial sclerosis [1].
  • We generated podocin-deficient (Nphs2-/-) mice to investigate the function of podocin, a protein expressed at the insertion of the slit diaphragm in podocytes and defective in a subset of patients with steroid-resistant nephrotic syndrome and focal and segmental glomerulosclerosis [1].
  • Podocyte-specific antigens, including WT-1, synaptopodin, nephrin, and podocin, were not expressed by any cells in glomerular crescents, suggesting that podocytes underwent profound phenotypic changes in this nephritis model [2].
  • Recently generated were conditional transgenic mice (podocin/Vpr) that express one of the HIV-1 accessory genes, vpr, selectively in podocytes using podocin promoter and Tet-on system [3].
  • Glomerular expression of nephrin and synaptopodin, but not podocin, is decreased in kidney sections from women with preeclampsia [4].
 

High impact information on Nphs2

  • Moreover, GST pull-down experiments reveal that podocin associates via its COOH-terminal domain with CD2AP, a cytoplasmic binding partner of nephrin, and with nephrin itself [5].
  • Here we show, by immunoelectron microscopy, that podocin localizes to the podocyte foot process membrane, at the insertion site of the slit diaphragm [5].
  • Our findings reveal a novel role for the slit diaphragm proteins nephrin, CD2AP, and podocin and demonstrate that these three proteins, in addition to their structural functions, initiate PI3K/AKT-dependent signal transduction in glomerular podocytes [6].
  • Like Nephrin and Podocin, Neph1 was enriched in Triton X-100 detergent-resistant membrane fractions [7].
  • During the calcium switch, there were reversible changes in localization and detergent solubility of the slit diaphragm protein ZO-1 and alpha-actinin-4, whereas nephrin and podocin solubility were unchanged [8].
 

Chemical compound and disease context of Nphs2

 

Biological context of Nphs2

 

Anatomical context of Nphs2

  • On the cellular level--using immunostaining--we detected cells expressing podocin, nephrin and wt-1, characteristic for differentiated podocytes and other cells, which expressed Tamm-Horsfall protein, a marker for distal tubule epithelial cells of kidney tissue [14].
 

Associations of Nphs2 with chemical compounds

 

Regulatory relationships of Nphs2

 

Other interactions of Nphs2

 

Analytical, diagnostic and therapeutic context of Nphs2

  • Early glomerular filtration defect and severe renal disease in podocin-deficient mice [1].

References

  1. Early glomerular filtration defect and severe renal disease in podocin-deficient mice. Roselli, S., Heidet, L., Sich, M., Henger, A., Kretzler, M., Gubler, M.C., Antignac, C. Mol. Cell. Biol. (2004) [Pubmed]
  2. Podocytes populate cellular crescents in a murine model of inflammatory glomerulonephritis. Moeller, M.J., Soofi, A., Hartmann, I., Le Hir, M., Wiggins, R., Kriz, W., Holzman, L.B. J. Am. Soc. Nephrol. (2004) [Pubmed]
  3. Angiotensin II Type 1 Receptor Blockade Inhibits the Development and Progression of HIV-Associated Nephropathy in a Mouse Model. Hiramatsu, N., Hiromura, K., Shigehara, T., Kuroiwa, T., Ideura, H., Sakurai, N., Takeuchi, S., Tomioka, M., Ikeuchi, H., Kaneko, Y., Ueki, K., Kopp, J.B., Nojima, Y. J. Am. Soc. Nephrol. (2007) [Pubmed]
  4. Glomerular expression of nephrin and synaptopodin, but not podocin, is decreased in kidney sections from women with preeclampsia. Garovic, V.D., Wagner, S.J., Petrovic, L.M., Gray, C.E., Hall, P., Sugimoto, H., Kalluri, R., Grande, J.P. Nephrol. Dial. Transplant. (2007) [Pubmed]
  5. Podocin, a raft-associated component of the glomerular slit diaphragm, interacts with CD2AP and nephrin. Schwarz, K., Simons, M., Reiser, J., Saleem, M.A., Faul, C., Kriz, W., Shaw, A.S., Holzman, L.B., Mundel, P. J. Clin. Invest. (2001) [Pubmed]
  6. Nephrin and CD2AP associate with phosphoinositide 3-OH kinase and stimulate AKT-dependent signaling. Huber, T.B., Hartleben, B., Kim, J., Schmidts, M., Schermer, B., Keil, A., Egger, L., Lecha, R.L., Borner, C., Pavenstädt, H., Shaw, A.S., Walz, G., Benzing, T. Mol. Cell. Biol. (2003) [Pubmed]
  7. Nephrin and Neph1 co-localize at the podocyte foot process intercellular junction and form cis hetero-oligomers. Barletta, G.M., Kovari, I.A., Verma, R.K., Kerjaschki, D., Holzman, L.B. J. Biol. Chem. (2003) [Pubmed]
  8. Cultured podocytes establish a size-selective barrier regulated by specific signaling pathways and demonstrate synchronized barrier assembly in a calcium switch model of junction formation. Hunt, J.L., Pollak, M.R., Denker, B.M. J. Am. Soc. Nephrol. (2005) [Pubmed]
  9. CD2-associated protein and glomerular disease. Wolf, G., Stahl, R.A. Lancet (2003) [Pubmed]
  10. Retinoic Acid Inhibits HIV-1-Induced Podocyte Proliferation through the cAMP Pathway. He, J.C., Lu, T.C., Fleet, M., Sunamoto, M., Husain, M., Fang, W., Neves, S., Chen, Y., Shankland, S., Iyengar, R., Klotman, P.E. J. Am. Soc. Nephrol. (2007) [Pubmed]
  11. HIV-1 Nef induces dedifferentiation of podocytes in vivo: a characteristic feature of HIVAN. Husain, M., D'Agati, V.D., He, J.C., Klotman, M.E., Klotman, P.E. AIDS (2005) [Pubmed]
  12. Autocrine VEGF-A system in podocytes regulates podocin and its interaction with CD2AP. Guan, F., Villegas, G., Teichman, J., Mundel, P., Tufro, A. Am. J. Physiol. Renal Physiol. (2006) [Pubmed]
  13. Effect of the knockdown of podocin mRNA on nephrin and alpha-actinin in mouse podocyte. Fan, Q., Ding, J., Zhang, J., Guan, N., Deng, J. Exp. Biol. Med. (Maywood) (2004) [Pubmed]
  14. Cells differentiated from mouse embryonic stem cells via embryoid bodies express renal marker molecules. Kramer, J., Steinhoff, J., Klinger, M., Fricke, L., Rohwedel, J. Differentiation (2006) [Pubmed]
 
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