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Hivan1  -  HIV-associated nephropathy 1

Mus musculus

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Disease relevance of Hivan1


High impact information on Hivan1


Chemical compound and disease context of Hivan1


Biological context of Hivan1


Anatomical context of Hivan1

  • The immunohistochemical staining pattern of podocan protein in normal kidney glomeruli was consistent with that of the glomerular basement membrane, and staining was markedly increased in sclerotic glomerular lesions in the transgenic HIVAN model [12].
  • HIV-1 has recently been shown to infect renal tubular epithelial cells in patients with HIVAN [5].
  • It was demonstrated that HIV-1 mRNA is expressed in renal epithelium of the transgenic mouse and in patients with HIVAN, suggesting a direct role for HIV-1 in disease pathogenesis in both humans and the murine model [3].
  • Protease inhibitors modulate apoptosis in mesangial cells derived from a mouse model of HIVAN [13].
  • These results demonstrate that the mechanical properties of WT and HIVAN podocytes are markedly different in a manner that is consistent with differences in the composition and arrangement of their cytoskeletons [14].

Associations of Hivan1 with chemical compounds


Other interactions of Hivan1


Analytical, diagnostic and therapeutic context of Hivan1


  1. Mapping a locus for susceptibility to HIV-1-associated nephropathy to mouse chromosome 3. Gharavi, A.G., Ahmad, T., Wong, R.D., Hooshyar, R., Vaughn, J., Oller, S., Frankel, R.Z., Bruggeman, L.A., D'Agati, V.D., Klotman, P.E., Lifton, R.P. Proc. Natl. Acad. Sci. U.S.A. (2004) [Pubmed]
  2. Nephropathy in human immunodeficiency virus-1 transgenic mice is due to renal transgene expression. Bruggeman, L.A., Dikman, S., Meng, C., Quaggin, S.E., Coffman, T.M., Klotman, P.E. J. Clin. Invest. (1997) [Pubmed]
  3. Human immunodeficiency virus-1 induces loss of contact inhibition in podocytes. Schwartz, E.J., Cara, A., Snoeck, H., Ross, M.D., Sunamoto, M., Reiser, J., Mundel, P., Klotman, P.E. J. Am. Soc. Nephrol. (2001) [Pubmed]
  4. Nef stimulates proliferation of glomerular podocytes through activation of Src-dependent Stat3 and MAPK1,2 pathways. He, J.C., Husain, M., Sunamoto, M., D'Agati, V.D., Klotman, M.E., Iyengar, R., Klotman, P.E. J. Clin. Invest. (2004) [Pubmed]
  5. Microcyst formation and HIV-1 gene expression occur in multiple nephron segments in HIV-associated nephropathy. Ross, M.J., Bruggeman, L.A., Wilson, P.D., Klotman, P.E. J. Am. Soc. Nephrol. (2001) [Pubmed]
  6. Amelioration of nephropathy in mice expressing HIV-1 genes by the cyclin-dependent kinase inhibitor flavopiridol. Nelson, P.J., D'Agati, V.D., Gries, J.M., Suarez, J.R., Gelman, I.H. J. Antimicrob. Chemother. (2003) [Pubmed]
  7. HIV-associated renal disorders: recent insights into pathogenesis and treatment. Berggren, R., Batuman, V. Current HIV/AIDS reports. (2005) [Pubmed]
  8. NF-kappaB regulates Fas-mediated apoptosis in HIV-associated nephropathy. Ross, M.J., Martinka, S., D'Agati, V.D., Bruggeman, L.A. J. Am. Soc. Nephrol. (2005) [Pubmed]
  9. 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]
  10. Persistent NF-kappaB activation in renal epithelial cells in a mouse model of HIV-associated nephropathy. Martinka, S., Bruggeman, L.A. Am. J. Physiol. Renal Physiol. (2006) [Pubmed]
  11. HIV-associated nephropathy. Winston, J., Klotman, P.E. Mt. Sinai J. Med. (1998) [Pubmed]
  12. Podocan, a novel small leucine-rich repeat protein expressed in the sclerotic glomerular lesion of experimental HIV-associated nephropathy. Ross, M.D., Bruggeman, L.A., Hanss, B., Sunamoto, M., Marras, D., Klotman, M.E., Klotman, P.E. J. Biol. Chem. (2003) [Pubmed]
  13. Protease inhibitors modulate apoptosis in mesangial cells derived from a mouse model of HIVAN. Mongia, A., Bhaskaran, M., Reddy, K., Manjappa, N., Baqi, N., Singhal, P.C. Kidney Int. (2004) [Pubmed]
  14. HIV infection changes glomerular podocyte cytoskeletal composition and results in distinct cellular mechanical properties. Tandon, R., Levental, I., Huang, C., Byfield, F.J., Ziembicki, J., Schelling, J.R., Bruggeman, L.A., Sedor, J.R., Janmey, P.A., Miller, R.T. Am. J. Physiol. Renal Physiol. (2007) [Pubmed]
  15. Captopril prevents nephropathy in HIV-transgenic mice. Bird, J.E., Durham, S.K., Giancarli, M.R., Gitlitz, P.H., Pandya, D.G., Dambach, D.M., Mozes, M.M., Kopp, J.B. J. Am. Soc. Nephrol. (1998) [Pubmed]
  16. 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]
  17. Fibroblast growth factor-2 increases the renal recruitment and attachment of HIV-infected mononuclear cells to renal tubular epithelial cells. Tang, P., Jerebtsova, M., Przygodzki, R., Ray, P.E. Pediatr. Nephrol. (2005) [Pubmed]
  18. Suppression of HIV-1 expression by inhibitors of cyclin-dependent kinases promotes differentiation of infected podocytes. Nelson, P.J., Gelman, I.H., Klotman, P.E. J. Am. Soc. Nephrol. (2001) [Pubmed]
  19. Transgenic models of HIV-1. Klotman, P.E., Rappaport, J., Ray, P., Kopp, J.B., Franks, R., Bruggeman, L.A., Notkins, A.L. AIDS (1995) [Pubmed]
  20. HIV-1 infection initiates an inflammatory cascade in human renal tubular epithelial cells. Ross, M.J., Fan, C., Ross, M.D., Chu, T.H., Shi, Y., Kaufman, L., Zhang, W., Klotman, M.E., Klotman, P.E. J. Acquir. Immune Defic. Syndr. (2006) [Pubmed]
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