Angiotensin II receptor type 2

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AGTR2
Identifiers
AliasesAGTR2, AT2, ATGR2, MRX88, Angiotensin II receptor type 2
External IDsOMIM: 300034 MGI: 87966 HomoloGene: 20172 GeneCards: AGTR2
Gene location (Human)
X chromosome (human)
Chr.X chromosome (human)[1]
X chromosome (human)
Genomic location for AGTR2
Genomic location for AGTR2
BandXq23Start116,170,744 bp[1]
End116,174,974 bp[1]
RNA expression pattern
PBB GE AGTR2 222321 at fs.png

PBB GE AGTR2 207294 at fs.png

PBB GE AGTR2 207293 s at fs.png
More reference expression data
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_000686

NM_007429

RefSeq (protein)

NP_000677

NP_031455

Location (UCSC)Chr X: 116.17 – 116.17 MbChr X: 21.48 – 21.49 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Angiotensin II receptor type 2, also known as the AT2 receptor is a protein that in humans is encoded by the AGTR2 gene.[5]

Function[edit]

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.[5]

Stimulation of AT2 by the selective agonist CGP 42112A increases mucosal nitric oxide production.[6]

Model organisms[edit]

Model organisms have been used in the study of AGTR2 function. A conditional knockout mouse line, called Agtr2tm1a(EUCOMM)Wtsi[9][10] 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.[11][12][13]

Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion.[7][14] Twenty one tests were carried out on mutant mice, but no significant abnormalities were observed.[7]

Interactions[edit]

Angiotensin II receptor type 2 has been shown to interact with MTUS1.[15]

See also[edit]

References[edit]

  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000180772 - Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000068122 - Ensembl, May 2017
  3. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. ^ a b "Entrez Gene: AGTR2 angiotensin II receptor, type 2".
  6. ^ Ewert S, Laesser M, Johansson B, Holm M, Aneman A, Fandriks L (March 2003). "The angiotensin II receptor type 2 agonist CGP 42112A stimulates NO production in the porcine jejunal mucosa". BMC Pharmacology. 3: 2. doi:10.1186/1471-2210-3-2. PMC 153509. PMID 12689346.
  7. ^ a b c Gerdin AK (2010). "The Sanger Mouse Genetics Programme: High throughput characterisation of knockout mice". Acta Ophthalmologica. 88 (S248): 0. doi:10.1111/j.1755-3768.2010.4142.x.
  8. ^ Mouse Resources Portal, Wellcome Trust Sanger Institute.
  9. ^ "International Knockout Mouse Consortium".
  10. ^ "Mouse Genome Informatics".
  11. ^ Skarnes WC, Rosen B, West AP, Koutsourakis M, Bushell W, Iyer V, Mujica AO, Thomas M, Harrow J, Cox T, Jackson D, Severin J, Biggs P, Fu J, Nefedov M, de Jong PJ, Stewart AF, Bradley A (June 2011). "A conditional knockout resource for the genome-wide study of mouse gene function". Nature. 474 (7351): 337–42. doi:10.1038/nature10163. PMC 3572410. PMID 21677750.
  12. ^ Dolgin E (June 2011). "Mouse library set to be knockout". Nature. 474 (7351): 262–3. doi:10.1038/474262a. PMID 21677718.
  13. ^ Collins FS, Rossant J, Wurst W (January 2007). "A mouse for all reasons". Cell. 128 (1): 9–13. doi:10.1016/j.cell.2006.12.018. PMID 17218247.
  14. ^ van der Weyden L, White JK, Adams DJ, Logan DW (June 2011). "The mouse genetics toolkit: revealing function and mechanism". Genome Biology. 12 (6): 224. doi:10.1186/gb-2011-12-6-224. PMC 3218837. PMID 21722353.
  15. ^ Nouet S, Amzallag N, Li JM, Louis S, Seitz I, Cui TX, Alleaume AM, Di Benedetto M, Boden C, Masson M, Strosberg AD, Horiuchi M, Couraud PO, Nahmias C (July 2004). "Trans-inactivation of receptor tyrosine kinases by novel angiotensin II AT2 receptor-interacting protein, ATIP". The Journal of Biological Chemistry. 279 (28): 28989–97. doi:10.1074/jbc.M403880200. PMID 15123706.


Further reading[edit]

External links[edit]