Source:http://linkedlifedata.com/resource/pubmed/id/20969596
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
|
pubmed:dateCreated |
2010-10-25
|
pubmed:abstractText |
Current research suggests that a number of newly identified T-helper cell subsets retain a degree of context-dependent plasticity in their signature cytokine expression patterns. To understand this process, a major challenge is to determine the molecular mechanisms by which lineage-defining transcription factors regulate gene expression profiles in T-helper cells. This mechanistic information will aid in our interpretation of whether a T-helper cell state that expresses or retains the capacity to re-express a combination of lineage-defining transcription factors will have a stable or more flexible gene expression profile. Studies examining the developmental T-box transcription factor T-bet demonstrate the powerful information that is gained from combining in vivo analysis with basic biochemical and molecular mechanism approaches. Significantly, T-bet's ability to physically recruit epigenetic modifying complexes, in particular a Jmjd3 H3K27-demethylase and a Set7/9 H3K4-methyltransferase complex, to its target genes allows T-bet to effectively reverse and establish new epigenetic states. This observation suggests that until T-bet is permanently extinguished, T-helper cells will retain some plasticity toward a T-helper 1-like program. Therefore, insight into the complexity of T-helper cell commitment decisions will be aided by determining the molecular mechanisms for lineage-defining transcription factors.
|
pubmed:grant |
http://linkedlifedata.com/resource/pubmed/grant/2T32 GM007270,
http://linkedlifedata.com/resource/pubmed/grant/AI061061,
http://linkedlifedata.com/resource/pubmed/grant/AI07272-061A,
http://linkedlifedata.com/resource/pubmed/grant/R01 AI061061-07,
http://linkedlifedata.com/resource/pubmed/grant/R01 AI071272-10
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Histone Demethylases,
http://linkedlifedata.com/resource/pubmed/chemical/Histone-Lysine N-Methyltransferase,
http://linkedlifedata.com/resource/pubmed/chemical/T-Box Domain Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/T-box transcription factor TBX21
|
pubmed:status |
MEDLINE
|
pubmed:month |
Nov
|
pubmed:issn |
1600-065X
|
pubmed:author | |
pubmed:copyrightInfo |
© 2010 John Wiley & Sons A/S.
|
pubmed:issnType |
Electronic
|
pubmed:volume |
238
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
233-46
|
pubmed:dateRevised |
2011-11-1
|
pubmed:meshHeading |
pubmed-meshheading:20969596-Animals,
pubmed-meshheading:20969596-Cell Differentiation,
pubmed-meshheading:20969596-Cell Lineage,
pubmed-meshheading:20969596-Epigenesis, Genetic,
pubmed-meshheading:20969596-Gene Expression Regulation, Developmental,
pubmed-meshheading:20969596-Histone Demethylases,
pubmed-meshheading:20969596-Histone-Lysine N-Methyltransferase,
pubmed-meshheading:20969596-Humans,
pubmed-meshheading:20969596-T-Box Domain Proteins,
pubmed-meshheading:20969596-Th1 Cells
|
pubmed:year |
2010
|
pubmed:articleTitle |
Molecular mechanisms by which T-bet regulates T-helper cell commitment.
|
pubmed:affiliation |
Molecular and Cellular Biology Program, University of Washington, Seattle, WA, USA.
|
pubmed:publicationType |
Journal Article,
Review,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
|