Alternative splicing: a novel mechanism to fine-tune the expression and function of the human AT1 receptor.
Activation of the angiotensin II type 1 (AT(1)) receptor is closely involved in the pathogenesis of cardiovascular diseases; therefore, aberrant regulation of the production of this receptor might play a role in these disorders. Currently, there is strong evidence to suggest that the predominant mechanism regulating the number of AT(1) receptors is the modulation of mRNA stability. Here, we discuss the importance of alternative splicing as an additional post-transcriptional mechanism regulating human AT(1) receptor number and function.
Elton
Terry S
TS
Department of Chemistry and Biochemistry, Brigham Young University, C100 Benson Science Building, Provo, UT 84602-5700, USA. terry_elton@byu.edu
Martin
Mickey M
MM
D017398:Alternative Splicing; D000595:Amino Acid Sequence / Q000235:genetics; D000818:Animals; D001483:Base Sequence / Q000235:genetics; D005091:Exons; D014644:Genetic Variation; D006801:Humans; D008969:Molecular Sequence Data; D012333:RNA, Messenger / Q000378:metabolism; D044140:Receptor, Angiotensin, Type 1; D011945:Receptors, Angiotensin / Q000235:genetics* / Q000378:metabolism*; D014018:Tissue Distribution
D012333:RNA, Messenger; D044140:Receptor, Angiotensin, Type 1; D011945:Receptors, Angiotensin