Journal
MOLECULAR AND CELLULAR BIOLOGY
Volume 26, Issue 18, Pages 6870-6879Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/MCB.00314-06
Keywords
-
Categories
Funding
- NCI NIH HHS [P30 CA046592, P30 CA 046592] Funding Source: Medline
- NHLBI NIH HHS [T32 HL007853, T32 HL 07853-06] Funding Source: Medline
- NIAMS NIH HHS [P30 AR 0483] Funding Source: Medline
- NIDDK NIH HHS [P60 DK020572, P30 DK 034933, P30 DK034933, P60 DK 20572] Funding Source: Medline
- NIGMS NIH HHS [R01 GM039561, R01 GM 39561] Funding Source: Medline
Ask authors/readers for more resources
Signal transduction via guanine nucleotide binding proteins (G proteins) is involved in cardiovascular, neural, endocrine, and immune cell function. Regulators of G protein signaling (RGS proteins) speed the turn-off of G protein signals and inhibit signal transduction, but the in vivo roles of RGS proteins remain poorly defined. To overcome the redundancy of RGS functions and reveal the total contribution of RGS regulation at the G alpha(i2) subunit, we prepared a genomic knock-in of the RGS-insensitive G184S Gnai2 allele. The G alpha(G184S)(i2) knock-in mice show a dramatic and complex phenotype affecting multiple organ systems (heart, myeloid, skeletal, and central nervous system). Both homozygotes and heterozygotes demonstrate reduced viability and decreased body weight. Other phenotypes include shortened long bones, a markedly enlarged spleen, elevated neutrophil counts, an enlarged heart, and behavioral hyperactivity. Heterozygous G alpha(+/G184S)(i2) mice show some but not all of these abnormalities. Thus, loss of RGS actions at G alpha(i2) produces a dramatic and pleiotropic phenotype which is more evident than the phenotype seen for individual RGS protein knockouts.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available