Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1997-1-7
pubmed:abstractText
Induction of many primary-response genes by a variety of stimuli occurs in a transient manner. The precise mechanism responsible for these transient kinetics is not completely understood. We report here that the orphan nuclear receptor, TIS1, which is a potent sequence-specific transcription factor, was transiently induced by the adrenergic agonist isoprenaline in the C2C12 skeletal-muscle cell line. Moreover, we showed that the rapid decline in mRNA level after peak induction was due in part to a specific desensitization of the isoprenaline-mediated induction pathway. Desensitization of the induction response presumably occurred at the level of the receptor, as agents that either bypass the adrenergic receptor or activate alternative signalling pathways were able to induce TIS1 expression in the desensitized cells. However, stimulation by agents that directly activate intracellular enzymes also resulted in the signal-transduction-pathway-specific desensitization of TIS1 inducibility. Our results suggest that the pathway-specific nature of the desensitization process may be important for directing an integrated response to multiple physiological stimuli.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/8948433-1346465, http://linkedlifedata.com/resource/pubmed/commentcorrection/8948433-1352481, http://linkedlifedata.com/resource/pubmed/commentcorrection/8948433-1645447, http://linkedlifedata.com/resource/pubmed/commentcorrection/8948433-1883198, http://linkedlifedata.com/resource/pubmed/commentcorrection/8948433-1922099, http://linkedlifedata.com/resource/pubmed/commentcorrection/8948433-1925541, http://linkedlifedata.com/resource/pubmed/commentcorrection/8948433-2115122, http://linkedlifedata.com/resource/pubmed/commentcorrection/8948433-2283997, http://linkedlifedata.com/resource/pubmed/commentcorrection/8948433-2440339, http://linkedlifedata.com/resource/pubmed/commentcorrection/8948433-2471069, http://linkedlifedata.com/resource/pubmed/commentcorrection/8948433-2479823, http://linkedlifedata.com/resource/pubmed/commentcorrection/8948433-2549263, http://linkedlifedata.com/resource/pubmed/commentcorrection/8948433-2555161, http://linkedlifedata.com/resource/pubmed/commentcorrection/8948433-2898731, http://linkedlifedata.com/resource/pubmed/commentcorrection/8948433-3185562, http://linkedlifedata.com/resource/pubmed/commentcorrection/8948433-3186734, http://linkedlifedata.com/resource/pubmed/commentcorrection/8948433-3272167, http://linkedlifedata.com/resource/pubmed/commentcorrection/8948433-3330774, http://linkedlifedata.com/resource/pubmed/commentcorrection/8948433-3543027, http://linkedlifedata.com/resource/pubmed/commentcorrection/8948433-3841511, http://linkedlifedata.com/resource/pubmed/commentcorrection/8948433-487428, http://linkedlifedata.com/resource/pubmed/commentcorrection/8948433-7692969, http://linkedlifedata.com/resource/pubmed/commentcorrection/8948433-8164692, http://linkedlifedata.com/resource/pubmed/commentcorrection/8948433-8380897, http://linkedlifedata.com/resource/pubmed/commentcorrection/8948433-8384301, http://linkedlifedata.com/resource/pubmed/commentcorrection/8948433-8386317, http://linkedlifedata.com/resource/pubmed/commentcorrection/8948433-8473354
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0264-6021
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
308 ( Pt 3)
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
785-9
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Signal-transduction-pathway-specific desensitization of expression of orphan nuclear receptor TIS1.
pubmed:affiliation
Department of Pharmacology, University of Missouri-Columbia 65212, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't