Document Detail


Galpha12 and Galpha13 mediate differentiation of P19 mouse embryonal carcinoma cells in response to retinoic acid.
MedLine Citation:
PMID:  9305907     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
P19 mouse embryonal carcinoma cells can be stimulated to differentiate into endodermal-like, mesodermal-like, and neuronal-like phenotypes in response to specific morphogens. At low concentrations, retinoic acid stimulates P19 embryonal cells to differentiate to cells displaying an endodermal phenotype, whereas at higher concentrations it stimulates differentiation to neuroectoderm. The Galpha12 and Galpha13 subunits of heterotrimeric G-proteins are expressed in the embryonal P19 cells and stimulated in response to retinoic acid as the cells differentiate to endodermal or neuroectodermal phenotypes. Suppression of the expression of either Galpha12 or Galpha13 by antisense RNA is shown to promote cell detachment from substratum and apoptosis. Expression of the constitutively active, mutant form of Galpha12 (Q229L), in contrast, stimulates loss of the embryonal phenotype. Expression of the constitutively active form of Galpha13 (Q226L) stimulates differentiation of the cells from embryonal to endodermal, in the absence of retinoic acid. Thus, both Galpha12 and Galpha13 are essential to stimulation of cell differentiation by retinoic acid. Deficiency of either Galpha12 or Galpha13 increases programmed cell death.
Authors:
E H Jho; C C Malbon
Related Documents :
18442987 - Cardiac differentiation in xenopus requires the cyclin-dependent kinase inhibitor, p27x...
12592337 - The protein tyrosine phosphatase heptp regulates nuclear translocation of erk2 and can ...
18313397 - Profiling tra-1-81 antigen distribution on a human embryonic stem cell.
2265407 - Berberine-induced morphologic differentiation and down-regulation of c-ki-ras2 protoonc...
11542787 - Induction of chromosomal damage in cho-k1 cells and their repair-deficient mutant xrs5 ...
19299557 - Positioning cytokinesis.
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The Journal of biological chemistry     Volume:  272     ISSN:  0021-9258     ISO Abbreviation:  J. Biol. Chem.     Publication Date:  1997 Sep 
Date Detail:
Created Date:  1997-10-23     Completed Date:  1997-10-23     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  2985121R     Medline TA:  J Biol Chem     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  24461-7     Citation Subset:  IM    
Affiliation:
Department of Molecular Pharmacology, Diabetes & Metabolic Diseases Research Center, School of Medicine, State University of New York, Stony Brook, New York 11794-8651, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis
Calcium-Calmodulin-Dependent Protein Kinases / metabolism
Carcinoma, Embryonal / pathology*
Cell Differentiation / drug effects*,  physiology
GTP-Binding Proteins / genetics,  physiology*
Mice
RNA, Messenger / genetics,  metabolism
Signal Transduction
Tretinoin / pharmacology*
Grant Support
ID/Acronym/Agency:
DK-30111/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/RNA, Messenger; 302-79-4/Tretinoin; EC 2.7.11.17/Calcium-Calmodulin-Dependent Protein Kinases; EC 3.6.1.-/GTP-Binding Proteins

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Purification and partial characterization of a cellular carotenoid-binding protein from ferret liver...
Next Document:  c-Jun amino-terminal kinase is regulated by Galpha12/Galpha13 and obligate for differentiation of P1...