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Gene Review

Akr1b7  -  aldo-keto reductase family 1, member B7

Mus musculus

Synonyms: AR, Aldehyde reductase, Aldo-keto reductase family 1 member B7, Aldose reductase-related protein 1, Avdp, ...
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Disease relevance of Akr1b7


Psychiatry related information on Akr1b7

  • The effects of dexmedetomidine, a subtype-nonselective alpha 2-AR agonist, on monoamine turnover in brain and on locomotor activity were similar in mice with targeted inactivation of the alpha 2C-AR gene and in their controls, but the hypothermic effect of the alpha 2-AR agonist was significantly attenuated by the receptor gene inactivation [3].
  • These results suggest that androgens may interact with either AR or PR, and perhaps both receptors, in E2 + TP-induced mammary glands and the induced tumors to effect the reduction in latency period, enhance tumor size, and increase incidence to 100% [4].

High impact information on Akr1b7

  • Estrens directly activated transcription in several cell lines, albeit at much higher concentrations than estradiol or the SERM, and acted for the most part through the AR [5].
  • In this study, we compared the effects of a SERM (PSK3471) and 2 estrens (estren-alpha and estren-beta) on bone and reproductive organs to determine whether estrens are safe and act via the estrogen receptors and/or the androgen receptor (AR) [5].
  • Sexually dimorphic behaviors are likely to involve neural pathways that express the androgen receptor (AR) [6].
  • Spinal and bulbar muscular atrophy (SBMA) is a polyglutamine disease caused by the expansion of a CAG repeat in the androgen receptor (AR) gene [7].
  • The results provide clear in vivo evidence that androgen/AR signaling in Sertoli cells plays a direct important role in spermatogenesis and in Leydig cells plays an autocrine regulatory role to modulate Leydig cell steroidogenic function [8].

Chemical compound and disease context of Akr1b7

  • In cells stably transfected with MVDP antisense cDNA, NADH-linked ICR activity was abolished even in the presence of forskolin, and the isocaproaldehyde toxicity was increased compared with that of intact Y1 cells, as measured by isocaproaldehyde LD(50) [9].
  • Taken together, increased polyol pathway flux through AR is a major contributing factor in the early signs of diabetic neuropathy, possibly through depletion of glutathione, increased superoxide accumulation, increased JNK activation, and DNA damage [10].
  • In Y1 cells transfected with MVDP antisense cDNA, forskolin-induced toxicity was abolished by aminoglutethimide [9].
  • Recent evidence demonstrates that the androgen receptor (AR) continues to influence prostate cancer growth despite medical therapies that reduce circulating androgen ligands to castrate levels and/or block ligand binding [11].
  • It is not affected by the AR blockers cyproterone and flutamide, whereas it is completely inhibited by the phospholipase C inhibitor U-73122 and pertussis toxin [12].

Biological context of Akr1b7

  • The major gene expression pattern for FR-1 was slightly different from that of MVDP, with the highest levels of mRNA detected in testis, heart, adrenal gland, and ovary; less was found in the lung and it was barely detectable in eye, intestine, liver and seminal vesicle tissue [13].
  • The closely related genes Fgfrp and Avdp were also mapped in this region of the chromosome, suggesting that these three genes may have arisen by a gene duplication event [14].
  • Inhibition of AR prevented growth factor-induced COX-2 activity, protein, and mRNA and significantly decreased activation of nuclear factor-kappaB and protein kinase C (PKC) and phosphorylation of PKC-beta2 as well as progression of Caco-2 cell growth but had no effect on COX-1 activity [2].
  • Cell cycle analysis suggests that inhibition of AR prevents growth factor-induced proliferation of Caco-2 cells at S phase [2].
  • To better understand androgenregulated MVDP gene expression, the location and sequences of androgen response elements (AREs) in the 5'-flanking DNA were determined [15].

Anatomical context of Akr1b7

  • Contrary to previous reports, MVDP was detected in a variety of tissues besides the vas deferens [13].
  • High levels of MVDP mRNA were found in the adrenal glands, and low levels of expression were detected in eye, intestine, seminal vesicle, kidney, liver, testis and lung [13].
  • The structural abnormalities observed in the sural nerve of diabetic AR(+/+) mice were less severe in the diabetic AR(-/-) mice, although it was only mildly protected by AR deficiency under short-term diabetic conditions [10].
  • Sorbitol levels in the sciatic nerves of diabetic AR(+/+) mice were increased significantly, whereas sorbitol levels in the diabetic AR(-/-) mice were significantly lower than those in diabetic AR(+/+) mice [10].
  • In this study, we report that ligand-bound AR, but not ligand-bound ER, directly suppressed activity of the bovine LHbeta promoter when examined in a gonadotrope-derived cell line [16].

Associations of Akr1b7 with chemical compounds

  • In steroidogenic organs, AKR1B7/MVDP scavenges isocaproaldehyde produced from the cholesterol side-chain cleavage reaction [17].
  • Treatment of neonatal animals with furosemide dramatically reduced expression of TonEBP, AR, and UT-A1 [18].
  • When inhibitors of AR were applied during the pre-ischemic phase, they significantly improved deranged cardiac function, creatine kinase release, and ATP content [1].
  • AR besides reducing aldo-sugars efficiently reduces toxic lipid aldehydes and their conjugates with glutathione [2].
  • For MVDP, isocaproaldehyde, a product of side-chain cleavage of cholesterol generated during steroidogenesis, is the best natural substrate identified so far [9].

Regulatory relationships of Akr1b7

  • We show that in adrenals, the pituitary hormone ACTH regulates MVDP gene expression in a coordinate fashion with steroidogenic genes [19].
  • Furthermore, we report that MVDP gene regulation is impaired in stably transfected Y1 clones expressing DAX-1 [19].

Other interactions of Akr1b7


Analytical, diagnostic and therapeutic context of Akr1b7


  1. Aldose reductase inhibitors improve myocardial reperfusion injury in mice by a dual mechanism. Iwata, K., Matsuno, K., Nishinaka, T., Persson, C., Yabe-Nishimura, C. J. Pharmacol. Sci. (2006) [Pubmed]
  2. Aldose reductase regulates growth factor-induced cyclooxygenase-2 expression and prostaglandin e2 production in human colon cancer cells. Tammali, R., Ramana, K.V., Singhal, S.S., Awasthi, S., Srivastava, S.K. Cancer Res. (2006) [Pubmed]
  3. Genetic alteration of alpha 2C-adrenoceptor expression in mice: influence on locomotor, hypothermic, and neurochemical effects of dexmedetomidine, a subtype-nonselective alpha 2-adrenoceptor agonist. Sallinen, J., Link, R.E., Haapalinna, A., Viitamaa, T., Kulatunga, M., Sjöholm, B., Macdonald, E., Pelto-Huikko, M., Leino, T., Barsh, G.S., Kobilka, B.K., Scheinin, M. Mol. Pharmacol. (1997) [Pubmed]
  4. Promotion of estrogen-induced mammary gland carcinogenesis by androgen in the male Noble rat: probable mediation by steroid receptors. Liao, D.Z., Pantazis, C.G., Hou, X., Li, S.A. Carcinogenesis (1998) [Pubmed]
  5. Bone protection by estrens occurs through non-tissue-selective activation of the androgen receptor. Windahl, S.H., Galien, R., Chiusaroli, R., Clément-Lacroix, P., Morvan, F., Lepescheux, L., Nique, F., Horne, W.C., Resche-Rigon, M., Baron, R. J. Clin. Invest. (2006) [Pubmed]
  6. Visualizing sexual dimorphism in the brain. Shah, N.M., Pisapia, D.J., Maniatis, S., Mendelsohn, M.M., Nemes, A., Axel, R. Neuron (2004) [Pubmed]
  7. Testosterone reduction prevents phenotypic expression in a transgenic mouse model of spinal and bulbar muscular atrophy. Katsuno, M., Adachi, H., Kume, A., Li, M., Nakagomi, Y., Niwa, H., Sang, C., Kobayashi, Y., Doyu, M., Sobue, G. Neuron (2002) [Pubmed]
  8. Differential effects of spermatogenesis and fertility in mice lacking androgen receptor in individual testis cells. Tsai, M.Y., Yeh, S.D., Wang, R.S., Yeh, S., Zhang, C., Lin, H.Y., Tzeng, C.R., Chang, C. Proc. Natl. Acad. Sci. U.S.A. (2006) [Pubmed]
  9. Product of side-chain cleavage of cholesterol, isocaproaldehyde, is an endogenous specific substrate of mouse vas deferens protein, an aldose reductase-like protein in adrenocortical cells. Lefrançois-Martinez, A.M., Tournaire, C., Martinez, A., Berger, M., Daoudal, S., Tritsch, D., Veyssière, G., Jean, C. J. Biol. Chem. (1999) [Pubmed]
  10. Aldose reductase-deficient mice are protected from delayed motor nerve conduction velocity, increased c-Jun NH2-terminal kinase activation, depletion of reduced glutathione, increased superoxide accumulation, and DNA damage. Ho, E.C., Lam, K.S., Chen, Y.S., Yip, J.C., Arvindakshan, M., Yamagishi, S., Yagihashi, S., Oates, P.J., Ellery, C.A., Chung, S.S., Chung, S.K. Diabetes (2006) [Pubmed]
  11. Mutation of the androgen receptor causes oncogenic transformation of the prostate. Han, G., Buchanan, G., Ittmann, M., Harris, J.M., Yu, X., Demayo, F.J., Tilley, W., Greenberg, N.M. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
  12. Testosterone signaling through internalizable surface receptors in androgen receptor-free macrophages. Benten, W.P., Lieberherr, M., Stamm, O., Wrehlke, C., Guo, Z., Wunderlich, F. Mol. Biol. Cell (1999) [Pubmed]
  13. Tissue-specific expression of two aldose reductase-like genes in mice: abundant expression of mouse vas deferens protein and fibroblast growth factor-regulated protein in the adrenal gland. Lau, E.T., Cao, D., Lin, C., Chung, S.K., Chung, S.S. Biochem. J. (1995) [Pubmed]
  14. Comparisons of genomic structures and chromosomal locations of the mouse aldose reductase and aldose reductase-like genes. Ho, H.T., Jenkins, N.A., Copeland, N.G., Gilbert, D.J., Winkles, J.A., Louie, H.W., Lee, F.K., Chung, S.S., Chung, S.K. Eur. J. Biochem. (1999) [Pubmed]
  15. Identification of a functional androgen response element in the promoter of the gene for the androgen-regulated aldose reductase-like protein specific to the mouse vas deferens. Fabre, S., Manin, M., Pailhoux, E., Veyssière, G., Jean, C. J. Biol. Chem. (1994) [Pubmed]
  16. AR suppresses transcription of the LHbeta subunit by interacting with steroidogenic factor-1. Jorgensen, J.S., Nilson, J.H. Mol. Endocrinol. (2001) [Pubmed]
  17. Steroidogenic factor-1 controls the aldose reductase akr1b7 gene promoter in transgenic mice through an atypical binding site. Martinez, A., Val, P., Sahut-Barnola, I., Aigueperse, C., Veyssière, G., Lefrançois-Martinez, A.M. Endocrinology (2003) [Pubmed]
  18. Sequential expression of NKCC2, TonEBP, aldose reductase, and urea transporter-A in developing mouse kidney. Lee, H.W., Kim, W.Y., Song, H.K., Yang, C.W., Han, K.H., Kwon, H.M., Kim, J. Am. J. Physiol. Renal Physiol. (2007) [Pubmed]
  19. SF-1 (steroidogenic factor-1), C/EBPbeta (CCAAT/enhancer binding protein), and ubiquitous transcription factors NF1 (nuclear factor 1) and Sp1 (selective promoter factor 1) are required for regulation of the mouse aldose reductase-like gene (AKR1B7) expression in adrenocortical cells. Aigueperse, C., Val, P., Pacot, C., Darne, C., Lalli, E., Sassone-Corsi, P., Veyssiere, G., Jean, C., Martinez, A. Mol. Endocrinol. (2001) [Pubmed]
  20. Androgen suppression of GnRH-stimulated rat LHbeta gene transcription occurs through Sp1 sites in the distal GnRH-responsive promoter region. Curtin, D., Jenkins, S., Farmer, N., Anderson, A.C., Haisenleder, D.J., Rissman, E., Wilson, E.M., Shupnik, M.A. Mol. Endocrinol. (2001) [Pubmed]
  21. Androgens augment the mitogenic effects of oocyte-secreted factors and growth differentiation factor 9 on porcine granulosa cells. Hickey, T.E., Marrocco, D.L., Amato, F., Ritter, L.J., Norman, R.J., Gilchrist, R.B., Armstrong, D.T. Biol. Reprod. (2005) [Pubmed]
  22. Androgen regulation of the mRNA encoding a major protein of the mouse vas deferens. Martinez, A., Pailhoux, E., Berger, M., Jean, C. Mol. Cell. Endocrinol. (1990) [Pubmed]
  23. Androgens regulate expression of the gene coding for a mouse vas deferens protein related to the aldo-keto reductase superfamily in epithelial cell subcultures. Dassouli, A., Manin, M., Veyssiere, G., Jean, C. J. Steroid Biochem. Mol. Biol. (1994) [Pubmed]
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