Linked Life Data

16375601

Source:http://linkedlifedata.com/resource/pubmed/id/16375601

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2005-12-26
pubmed:abstractText
The high-affinity binding interactions between interferons (IFNs) and their cognate cell surface receptors lead to the activation of receptor-associated Janus protein tyrosine kinases (Jaks) and subsequent phosphorylation and activation of a group of transcription factors, the signal transducers and activators of transcription (Stats). Upon IFN-induced activation, these Stat proteins form homodimeric and heterodimeric complexes that translocate to the nucleus and bind specific elements within the promoters of IFN-stimulated genes (ISGs). In addition to the well-studied IFN-induced ISG factor 3 (ISGF3) and Stat1:1 complexes, IFNs induce the formation of a number of other Stat-containing complexes, including Stat3:3 and Stat5:5 homodimers, as well as Stat2:1 and Stat5:CrkL heterodimers, that also mediate gene transcription. Moreover, emerging evidence suggests that particular amino acid residues within the individual Stat proteins contribute to different aspects of Stat function. These residues modulate the transcriptional activation potential of Stat-containing complexes and thereby influence the expression of ISGs. Indeed, the Stat proteins function in a multifaceted manner to regulate the expression of proteins that mediate IFN responses.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1079-9907
pubmed:author
pubmed:issnType
Print
pubmed:volume
25
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
733-44
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Stats: multifaceted regulators of transcription.
pubmed:affiliation
Division of Cell & Molecular Biology, Toronto General Research Institute, University Health Network, University of Toronto, Toronto, Ontario M5G 2M1, Canada.
pubmed:publicationType
Journal Article, Review