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Gene Review

Havcr1  -  hepatitis A virus cellular receptor 1

Rattus norvegicus

Synonyms: HAVcr-1, Hepatitis A virus cellular receptor 1 homolog, KIM-1, Kidney injury molecule 1, Kim1, ...
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Disease relevance of Havcr1

  • When rats were subjected to increasing periods (10, 20, 30, or 45 min) of bilateral ischemia, there was an increasing amount of urinary Kim-1 detected [1].
  • We studied Kim-1 in a nontoxic, nonischemic, model of tubulointerstitial damage caused by acute proteinuria [2].
  • The mRNA and protein for Kim-1 are expressed at very low levels in normal rodent kidney, but expression increases dramatically after injury in proximal tubule epithelial cells in postischemic rodent kidney and in humans during ischemic acute renal failure [3].
  • Kim-1 expression was limited to areas with inflammation (MØ), fibrosis (alpha-smooth muscle actin), and tubular damage (osteopontin), and only occasionally with tubular dedifferentiation (vimentin) [2].

High impact information on Havcr1


Chemical compound and disease context of Havcr1

  • After only 10 min of bilateral ischemia, Kim-1 levels on day 1 were 10-fold higher (5 ng/ml) than control levels, whereas plasma creatinine and BUN were not increased and there was no glycosuria, increased proteinuria, or increased urinary NAG levels [1].

Biological context of Havcr1

  • The upregulation of expression of Kim-1 and its presence in the urine in response to exposure to various types of nephrotoxicants suggest that this protein may serve as a general biomarker for tubular injury and repair processes [3].

Anatomical context of Havcr1

  • The following markers were used to assess the temporal aspects of renal damage: (a) urea nitrogen (BUN) and creatinine in blood serum, (b) kidney injury molecule (KIM-1) mRNA levels, and (c) tubular necrotic damage [5].

Associations of Havcr1 with chemical compounds


Other interactions of Havcr1

  • The expression of KIM-1 and AQP-2 was similar among the treatment groups [6].
  • These include several transporters (Slc21a2, Slc15, Slc34a2), Kim 1, IGFbp-1, osteopontin, alpha-fibrinogen, and Gstalpha [8].

Analytical, diagnostic and therapeutic context of Havcr1


  1. Urinary kidney injury molecule-1: a sensitive quantitative biomarker for early detection of kidney tubular injury. Vaidya, V.S., Ramirez, V., Ichimura, T., Bobadilla, N.A., Bonventre, J.V. Am. J. Physiol. Renal Physiol. (2006) [Pubmed]
  2. Tubular kidney injury molecule-1 in protein-overload nephropathy. van Timmeren, M.M., Bakker, S.J., Vaidya, V.S., Bailly, V., Schuurs, T.A., Damman, J., Stegeman, C.A., Bonventre, J.V., van Goor, H. Am. J. Physiol. Renal Physiol. (2006) [Pubmed]
  3. Kidney injury molecule-1: a tissue and urinary biomarker for nephrotoxicant-induced renal injury. Ichimura, T., Hung, C.C., Yang, S.A., Stevens, J.L., Bonventre, J.V. Am. J. Physiol. Renal Physiol. (2004) [Pubmed]
  4. Kidney injury molecule-1 (KIM-1), a putative epithelial cell adhesion molecule containing a novel immunoglobulin domain, is up-regulated in renal cells after injury. Ichimura, T., Bonventre, J.V., Bailly, V., Wei, H., Hession, C.A., Cate, R.L., Sanicola, M. J. Biol. Chem. (1998) [Pubmed]
  5. Evaluation of oxidative stress in d-serine induced nephrotoxicity. Orozco-Ibarra, M., Medina-Campos, O.N., S??nchez-Gonz??lez, D.J., Mart??nez-Mart??nez, C.M., Floriano-S??nchez, E., Santamar??a, A., Ramirez, V., Bobadilla, N.A., Pedraza-Chaverri, J. Toxicology (2007) [Pubmed]
  6. Correlation between cyclosporine-induced nephrotoxicity in reduced nephron mass and expression of kidney injury molecule-1 and aquaporin-2 gene. Hong, M.E., Hong, J.C., Stepkowski, S., Kahan, B.D. Transplant. Proc. (2005) [Pubmed]
  7. Kidney injury molecule-1 is a phosphatidylserine receptor that confers a phagocytic phenotype on epithelial cells. Ichimura, T., Asseldonk, E.J., Humphreys, B.D., Gunaratnam, L., Duffield, J.S., Bonventre, J.V. J. Clin. Invest. (2008) [Pubmed]
  8. Prediction of nephrotoxicant action and identification of candidate toxicity-related biomarkers. Thukral, S.K., Nordone, P.J., Hu, R., Sullivan, L., Galambos, E., Fitzpatrick, V.D., Healy, L., Bass, M.B., Cosenza, M.E., Afshari, C.A. Toxicologic pathology. (2005) [Pubmed]
  9. Animal models of acute tubular necrosis. Heyman, S.N., Lieberthal, W., Rogiers, P., Bonventre, J.V. Current opinion in critical care. (2002) [Pubmed]
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