Source:http://linkedlifedata.com/resource/pubmed/id/15729333
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
7028
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pubmed:dateCreated |
2005-2-24
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pubmed:abstractText |
Development of immature T-cell precursors (thymocytes) to either the CD4 helper or CD8 killer T-cell lineages correlates precisely with their T-cell receptor specificity for major histocompatibility complex class II or class I molecules, respectively, indicating that the process is carefully regulated. Although intensively studied owing to its importance in determining the composition of the mature T-cell compartment and as a general model of binary lineage decisions, the underlying molecular pathways remain obscure. We have previously reported a spontaneous mouse mutant (HD (helper deficient) mice) in which lineage commitment is specifically perturbed without affecting positive selection. Here we show that a point mutation in the zinc finger transcription factor Th-POK (T-helper-inducing POZ/Krüppel-like factor) is responsible for redirection of class-II-restricted thymocytes to the CD8 lineage in HD mice. Furthermore, we demonstrate that constitutive expression of this factor during thymic development leads to redirection of class-I-restricted thymocytes to the CD4 lineage, indicating that Th-POK is a master regulator of lineage commitment.
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pubmed:commentsCorrections | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Histocompatibility Antigens Class I,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, T-Cell,
http://linkedlifedata.com/resource/pubmed/chemical/Th-POK protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
1476-4687
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:day |
24
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pubmed:volume |
433
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
826-33
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:15729333-Amino Acid Sequence,
pubmed-meshheading:15729333-Animals,
pubmed-meshheading:15729333-CD4-Positive T-Lymphocytes,
pubmed-meshheading:15729333-CD8-Positive T-Lymphocytes,
pubmed-meshheading:15729333-Cell Lineage,
pubmed-meshheading:15729333-Genetic Complementation Test,
pubmed-meshheading:15729333-Histocompatibility Antigens Class I,
pubmed-meshheading:15729333-Mice,
pubmed-meshheading:15729333-Mice, Inbred Strains,
pubmed-meshheading:15729333-Mice, Mutant Strains,
pubmed-meshheading:15729333-Molecular Sequence Data,
pubmed-meshheading:15729333-Receptors, Antigen, T-Cell,
pubmed-meshheading:15729333-Signal Transduction,
pubmed-meshheading:15729333-Thymus Gland,
pubmed-meshheading:15729333-Transcription Factors,
pubmed-meshheading:15729333-Zinc Fingers
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pubmed:year |
2005
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pubmed:articleTitle |
The zinc finger transcription factor Th-POK regulates CD4 versus CD8 T-cell lineage commitment.
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pubmed:affiliation |
Fox Chase Cancer Center, 7701 Burholme Avenue, Philadelphia, Pennsylvania 19111, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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