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Gene Review

Agt  -  angiotensinogen (serpin peptidase...

Mus musculus

Synonyms: AI265500, AngI, AngII, Angiotensinogen, Aogen, ...
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Disease relevance of Agt

  • The importance of K for the hyperaldosteronism during dietary Na restriction was verified by the observation that superimposition of K restriction led to hypotension in Agt+/+ and uniform death in Agt-/- mice along with a reduction in P(aldo) by 75 and 90%, respectively [1].
  • This genetic manipulation overcame the hypotension of AOGEN-deficient mice and even caused hypertension indistinguishable in its extent from the parent transgenic mice with an intact endogenous AOGEN gene [2].

High impact information on Agt

  • In all Agt genotypes, UUO reduced ipsilateral renal mass and increased that of the opposite kidney [3].
  • These abnormal phenotypes are quantitatively similar to those found in mutant mice homozygous for the angiotensinogen gene (Agt-/-), indicating that major biological functions of endogenous Ang elucidated by the abnormal phenotypes of Agt-/- are mediated by the AT1 receptors [4].
  • Plasma aldosterone levels (P(aldo)) were comparable during NS, and similarly elevated during LS in Agt+/+ and Agt-/-. Moreover, in both, the elevation in P(aldo) was accompanied by marked increase in adrenal zona glomerulosa cells and adrenal P450aldo mRNA [1].
  • The marked gender differences in gene expression in wild-type mice and the changes induced by moderate alterations in Agt expression and BP emphasize the need to look for similar differences in humans [5].
  • A highly significant correlation between renal expression of the angiotensin type 1a receptor and kallikrein, independent of Agt genotype, is present in females (P < 0.0001) but not males (P = 0.4) [5].

Biological context of Agt

  • This phenotype is virtually identical to that seen in angiotensinogen-deficient (Agt-/-) and angiotensin-converting enzyme-deficient (Ace -/-) mice that are unable to synthesize angiotensin II [6].
  • The downregulation of Aogen in myocytes from FVB.Igf+/- mice was characterized by a reduction in Ang II [7].
  • Thus plasma angiotensin is maintained or considerably increased following BNx in mice and the change is consistent with first-order kinetics with respect to renin and aogen in the circulation [8].
  • These "gene titration" experiments establish that changes in Agt gene expression cause changes in the blood pressures of mice [9].
  • The ratio of postcoital plugs to subsequent litters was 4.0 and 1.2 for Agt(-/-) and Agt(+/+) breedings, respectively (P = 0.03) [10].

Anatomical context of Agt

  • In the present study, we examined mechanical stretch-induced activation of mitogen-activated protein kinases (MAP kinases) using cultured cardiac myocytes derived from neonatal angiotensinogen gene deficient mice (Agt-/-) and neonatal wild type mice (Agt+/+) [11].
  • RESULT(S): The mean number of oocytes harvested was greatest in wild-type mice (two copies of Agt, 39.9 +/- 14) with a reduction of ovulatory capacity in mice overexpressing Agt (three copies [34.8 +/- 11.7] and four copies [31.2 +/- 12.4], P =.026) [12].
  • Mice bearing one, two, three, or four copies of the Agt gene underwent renal artery clipping to induce high-renin two-kidney, one-clip renovascular hypertension (2K1C), or uninephrectomy, salt loading, and application of deoxycorticosterone-acetate (DOCA) pellets to induce low-renin mineralocorticoid hypertension [13].

Associations of Agt with chemical compounds


Regulatory relationships of Agt

  • Furthermore, hypertension-induced alterations in kidney histology and function were less pronounced in crossbred mice than in equally hypertensive animals expressing AOGEN locally [2].

Other interactions of Agt


Analytical, diagnostic and therapeutic context of Agt

  • We have used gene targeting to vary the amounts of angiotensinogen and angiotensin-converting enzyme (ACE) synthesized from their genes (Agt and Ace) [9].


  1. Angiotensin-independent mechanism for aldosterone synthesis during chronic extracellular fluid volume depletion. Okubo, S., Niimura, F., Nishimura, H., Takemoto, F., Fogo, A., Matsusaka, T., Ichikawa, I. J. Clin. Invest. (1997) [Pubmed]
  2. Reduced hypertension-induced end-organ damage in mice lacking cardiac and renal angiotensinogen synthesis. Kang, N., Walther, T., Tian, X.L., Bohlender, J., Fukamizu, A., Ganten, D., Bader, M. J. Mol. Med. (2002) [Pubmed]
  3. Reduced angiotensinogen expression attenuates renal interstitial fibrosis in obstructive nephropathy in mice. Fern, R.J., Yesko, C.M., Thornhill, B.A., Kim, H.S., Smithies, O., Chevalier, R.L. J. Clin. Invest. (1999) [Pubmed]
  4. Murine double nullizygotes of the angiotensin type 1A and 1B receptor genes duplicate severe abnormal phenotypes of angiotensinogen nullizygotes. Tsuchida, S., Matsusaka, T., Chen, X., Okubo, S., Niimura, F., Nishimura, H., Fogo, A., Utsunomiya, H., Inagami, T., Ichikawa, I. J. Clin. Invest. (1998) [Pubmed]
  5. Molecular phenotyping for analyzing subtle genetic effects in mice: application to an angiotensinogen gene titration. Kim, H.S., Lee, G., John, S.W., Maeda, N., Smithies, O. Proc. Natl. Acad. Sci. U.S.A. (2002) [Pubmed]
  6. Reduced growth, abnormal kidney structure, and type 2 (AT2) angiotensin receptor-mediated blood pressure regulation in mice lacking both AT1A and AT1B receptors for angiotensin II. Oliverio, M.I., Kim, H.S., Ito, M., Le, T., Audoly, L., Best, C.F., Hiller, S., Kluckman, K., Maeda, N., Smithies, O., Coffman, T.M. Proc. Natl. Acad. Sci. U.S.A. (1998) [Pubmed]
  7. Overexpression of insulin-like growth factor-1 attenuates the myocyte renin-angiotensin system in transgenic mice. Leri, A., Liu, Y., Wang, X., Kajstura, J., Malhotra, A., Meggs, L.G., Anversa, P. Circ. Res. (1999) [Pubmed]
  8. Plasma angiotensin in binephrectomised mice. Skinner, S., Bouhnik, J., Huang, H., Gonzalez, M.F., Ménard, J., Corvol, P. Clin. Exp. Hypertens. (1995) [Pubmed]
  9. Theodore Cooper Memorial Lecture. A mouse view of hypertension. Smithies, O. Hypertension (1997) [Pubmed]
  10. Genetic control of fertility and embryonic waste in the mouse: A rolefor angiotensinogen. Tempfer, C.B., Moreno, R.M., Gregg, A.R. Biol. Reprod. (2000) [Pubmed]
  11. Stretch-induced MAP kinase activation in cardiomyocytes of angiotensinogen-deficient mice. Nyui, N., Tamura, K., Mizuno, K., Ishigami, T., Hibi, K., Yabana, M., Kihara, M., Fukamizu, A., Ochiai, H., Umemura, S., Murakami, K., Ohno, S., Ishii, M. Biochem. Biophys. Res. Commun. (1997) [Pubmed]
  12. Influence of the angiotensinogen gene on the ovulatory capacity of mice. Hefler, L.A., Gregg, A.R. Fertil. Steril. (2001) [Pubmed]
  13. Effect of the angiotensinogen genotype on experimental hypertension in mice. Handtrack, C., Cordasic, N., Klanke, B., Veelken, R., Hilgers, K.F. J. Mol. Med. (2007) [Pubmed]
  14. Endothelial-derived nitric oxide and angiotensinogen: blood pressure and metabolism during mouse pregnancy. Hefler, L.A., Tempfer, C.B., Moreno, R.M., O'Brien, W.E., Gregg, A.R. Am. J. Physiol. Regul. Integr. Comp. Physiol. (2001) [Pubmed]
  15. Linkage of Agt and Actsk-1 to distal mouse chromosome 8 loci: a new conserved linkage. Abonia, J.P., Abel, K.J., Eddy, R.L., Elliott, R.W., Chapman, V.M., Shows, T.B., Gross, K.W. Mamm. Genome (1993) [Pubmed]
  16. The angiotensinogen gene of Swiss mice is closely linked to a retrovirus-like element. Clouston, W.M. DNA Cell Biol. (1990) [Pubmed]
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