TY - JOUR
T1 - Regulation of atrial natriuretic peptide secretion by a novel Ras-like protein
AU - Rybkin, Igor I.
AU - Kim, Mi Sung
AU - Bezprozvannaya, Svetlana
AU - Qi, Xiaoxia
AU - Richardson, James A
AU - Plato, Craig F.
AU - Hill, Joseph A
AU - Bassel-Duby, Rhonda S
AU - Olson, Eric N
PY - 2007/11/5
Y1 - 2007/11/5
N2 - A trial cardiomyocytes, neurons, and endocrine tissues secrete neurotransmitters and peptide hormones via large dense-core vesicles (LDCVs). We describe a new member of the Ras family of G-proteins, named RRP17, which is expressed specifically in cardiomyocytes, neurons, and the pancreas. RRP17 interacts with Ca2+-activated protein for secretion-1 (CAPS1), one of only a few proteins known to be associated exclusively with LDCV exocytosis. Ectopic expression of RRP17 in cardiomyocytes enhances secretion of atrial natriuretic peptide (ANP), a regulator of blood pressure and natriuresis. Conversely, genetic deletion of RRP17 in mice results in dysmorphic LDCVs, impaired ANP secretion, and hypertension. These findings identify RRP17 as a component of the cellular machinery involved in regulated secretion within the heart and potential mediator of the endocrine influence of the heart on other tissues.
AB - A trial cardiomyocytes, neurons, and endocrine tissues secrete neurotransmitters and peptide hormones via large dense-core vesicles (LDCVs). We describe a new member of the Ras family of G-proteins, named RRP17, which is expressed specifically in cardiomyocytes, neurons, and the pancreas. RRP17 interacts with Ca2+-activated protein for secretion-1 (CAPS1), one of only a few proteins known to be associated exclusively with LDCV exocytosis. Ectopic expression of RRP17 in cardiomyocytes enhances secretion of atrial natriuretic peptide (ANP), a regulator of blood pressure and natriuresis. Conversely, genetic deletion of RRP17 in mice results in dysmorphic LDCVs, impaired ANP secretion, and hypertension. These findings identify RRP17 as a component of the cellular machinery involved in regulated secretion within the heart and potential mediator of the endocrine influence of the heart on other tissues.
UR - http://www.scopus.com/inward/record.url?scp=35948934236&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=35948934236&partnerID=8YFLogxK
U2 - 10.1083/jcb.200707101
DO - 10.1083/jcb.200707101
M3 - Article
C2 - 17984325
AN - SCOPUS:35948934236
SN - 0021-9525
VL - 179
SP - 527
EP - 537
JO - Journal of Cell Biology
JF - Journal of Cell Biology
IS - 3
ER -