Angiotensin II receptor type 2

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Lua error in Module:Infobox_gene at line 33: attempt to index field 'wikibase' (a nil value). Angiotensin II receptor type 2, also known as the AT2 receptor is a protein that in humans is encoded by the AGTR2 gene.[1]

Function

Angiotensin II is a potent pressor hormone and a primary regulator of aldosterone secretion. It is an important effector controlling blood pressure and volume in the cardiovascular system. It acts through at least two types of receptors termed AT1 and AT2. AGTR2 belongs to a family 1 of G protein-coupled receptors. It is an integral membrane protein. It plays a role in the central nervous system and cardiovascular functions that are mediated by the renin-angiotensin system. This receptor mediates programmed cell death (apoptosis). In adults, it is highly expressed in myometrium with lower levels in adrenal gland and fallopian tube. It is highly expressed in fetal kidney and intestine. The human AGTR2 gene is composed of three exons and spans at least 5 kb. Exons 1 and 2 encode for 5' untranslated mRNA sequence and exon 3 harbors the entire uninterrupted open reading frame.[1]

Stimulation of AT2 by the selective agonist CGP 42112A increases mucosal nitric oxide production.[2]

Model organisms

Model organisms have been used in the study of AGTR2 function. A conditional knockout mouse line, called Agtr2tm1a(EUCOMM)Wtsi[5][6] was generated as part of the International Knockout Mouse Consortium program — a high-throughput mutagenesis project to generate and distribute animal models of disease to interested scientists — at the Wellcome Trust Sanger Institute.[7][8][9]

Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion.[3][10] Twenty one tests were carried out on mutant mice, but no significant abnormalities were observed.[3]

Interactions

Angiotensin II receptor type 2 has been shown to interact with MTUS1.[11]

See also

References

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  4. Mouse Resources Portal, Wellcome Trust Sanger Institute.
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External links

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Further reading

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This article incorporates text from the United States National Library of Medicine, which is in the public domain.