|
rdf:type |
|
|
lifeskim:mentions |
|
|
pubmed:issue |
3
|
|
pubmed:dateCreated |
2005-5-31
|
|
pubmed:abstractText |
Dexras1/AGS1/RasD1 is a member of the Ras superfamily of monomeric G proteins and has been suggested to disrupt receptor-G protein signaling. We examined the ability of Dexras1 to modulate dopamine D(2L) receptor regulation of adenylyl cyclase (AC) type 1 in HEK293 cells. Acute D(2L) receptor-mediated inhibition of A23187-stimulated AC1 activity (IC50, 4.0+/-1.4 nM; 50+/-3% inhibition) was not altered in the presence of Dexras1 (IC50, 2.4+/-1.3 nM, 50+/-1% inhibition); however, Dexras1 blocked acute D(2L) receptor-mediated activation of ERK 1/2 by approximately 50%. Heterologous sensitization of AC1 induced by persistent activation of D(2L) receptors was completely blocked by Dexras1 under basal and A23187-stimulated conditions. The block of sensitization was concentration-dependent and was not observed with a nucleotide binding-deficient Dexras1G31V mutant. Sensitization of AC1 was Gbetagamma-dependent as demonstrated using the C-terminus of beta-adrenergic receptor kinase (betaARK-ct). These data suggest that Dexras1 selectively regulates receptor-mediated Gbetagamma signaling pathways.
|
|
pubmed:grant |
|
|
pubmed:language |
eng
|
|
pubmed:journal |
|
|
pubmed:citationSubset |
IM
|
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adenylate Cyclase,
http://linkedlifedata.com/resource/pubmed/chemical/Calcimycin,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP,
http://linkedlifedata.com/resource/pubmed/chemical/Extracellular Signal-Regulated MAP...,
http://linkedlifedata.com/resource/pubmed/chemical/G-protein Beta gamma,
http://linkedlifedata.com/resource/pubmed/chemical/GTP-Binding Protein alpha...,
http://linkedlifedata.com/resource/pubmed/chemical/GTP-Binding Protein beta Subunits,
http://linkedlifedata.com/resource/pubmed/chemical/GTP-Binding Protein gamma Subunits,
http://linkedlifedata.com/resource/pubmed/chemical/GTP-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Quinpirole,
http://linkedlifedata.com/resource/pubmed/chemical/RASD1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Dopamine D2,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/dopamine D2L receptor,
http://linkedlifedata.com/resource/pubmed/chemical/ras Proteins
|
|
pubmed:status |
MEDLINE
|
|
pubmed:month |
Jul
|
|
pubmed:issn |
0006-291X
|
|
pubmed:author |
|
|
pubmed:issnType |
Print
|
|
pubmed:day |
8
|
|
pubmed:volume |
332
|
|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
|
|
pubmed:pagination |
913-20
|
|
pubmed:dateRevised |
2009-11-19
|
|
pubmed:meshHeading |
pubmed-meshheading:15913563-Adenylate Cyclase,
pubmed-meshheading:15913563-Binding Sites,
pubmed-meshheading:15913563-Calcimycin,
pubmed-meshheading:15913563-Cell Line,
pubmed-meshheading:15913563-Cyclic AMP,
pubmed-meshheading:15913563-Extracellular Signal-Regulated MAP Kinases,
pubmed-meshheading:15913563-GTP-Binding Protein alpha Subunits, Gi-Go,
pubmed-meshheading:15913563-GTP-Binding Protein beta Subunits,
pubmed-meshheading:15913563-GTP-Binding Protein gamma Subunits,
pubmed-meshheading:15913563-GTP-Binding Proteins,
pubmed-meshheading:15913563-Humans,
pubmed-meshheading:15913563-Kinetics,
pubmed-meshheading:15913563-Mutagenesis, Site-Directed,
pubmed-meshheading:15913563-Quinpirole,
pubmed-meshheading:15913563-Receptors, Dopamine D2,
pubmed-meshheading:15913563-Recombinant Proteins,
pubmed-meshheading:15913563-Signal Transduction,
pubmed-meshheading:15913563-Transfection,
pubmed-meshheading:15913563-ras Proteins
|
|
pubmed:year |
2005
|
|
pubmed:articleTitle |
Dexras1 blocks receptor-mediated heterologous sensitization of adenylyl cyclase 1.
|
|
pubmed:affiliation |
Department of Medicinal Chemistry and Molecular Pharmacology, Purdue University, West Lafayette, IN 47909, USA.
|
|
pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
|
