| pubmed-article:11228417 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11228417 | lifeskim:mentions | umls-concept:C0040113 | lld:lifeskim |
| pubmed-article:11228417 | lifeskim:mentions | umls-concept:C0036576 | lld:lifeskim |
| pubmed-article:11228417 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
| pubmed-article:11228417 | lifeskim:mentions | umls-concept:C0808080 | lld:lifeskim |
| pubmed-article:11228417 | lifeskim:mentions | umls-concept:C1881379 | lld:lifeskim |
| pubmed-article:11228417 | lifeskim:mentions | umls-concept:C1705922 | lld:lifeskim |
| pubmed-article:11228417 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:11228417 | pubmed:dateCreated | 2001-3-6 | lld:pubmed |
| pubmed-article:11228417 | pubmed:abstractText | During development, alphabeta T cells undergo positive or negative selection and CD4(+)/CD8(+) lineage commitment-events that have a major impact on the functionality of the T cell repertoire. The precise mechanisms of these differentiative steps remain elusive. Research this year has focused on quantitative models of signaling. For positive selection, the timing and extent of ERK activation may be important. For lineage commitment, the extent of Lck recruitment and activation may be the decisive factor. Next, the search is on for the genes that commit the cell to the fate determined by these quantitative differences in signals. | lld:pubmed |
| pubmed-article:11228417 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11228417 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11228417 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:11228417 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11228417 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:11228417 | pubmed:issn | 0952-7915 | lld:pubmed |
| pubmed-article:11228417 | pubmed:author | pubmed-author:HogquistK AKA | lld:pubmed |
| pubmed-article:11228417 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11228417 | pubmed:volume | 13 | lld:pubmed |
| pubmed-article:11228417 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11228417 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11228417 | pubmed:pagination | 225-31 | lld:pubmed |
| pubmed-article:11228417 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
| pubmed-article:11228417 | pubmed:meshHeading | pubmed-meshheading:11228417... | lld:pubmed |
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| pubmed-article:11228417 | pubmed:meshHeading | pubmed-meshheading:11228417... | lld:pubmed |
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| pubmed-article:11228417 | pubmed:meshHeading | pubmed-meshheading:11228417... | lld:pubmed |
| pubmed-article:11228417 | pubmed:meshHeading | pubmed-meshheading:11228417... | lld:pubmed |
| pubmed-article:11228417 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11228417 | pubmed:articleTitle | Signal strength in thymic selection and lineage commitment. | lld:pubmed |
| pubmed-article:11228417 | pubmed:affiliation | Center for Immunology, University of Minnesota, MMC 334, 420 Delaware Street SE, Minneapolis, MN 55455, USA. hogqu001@tc.umn.edu | lld:pubmed |
| pubmed-article:11228417 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11228417 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:11228417 | pubmed:publicationType | Review | lld:pubmed |
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