| pubmed-article:8895560 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8895560 | lifeskim:mentions | umls-concept:C0023449 | lld:lifeskim |
| pubmed-article:8895560 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
| pubmed-article:8895560 | lifeskim:mentions | umls-concept:C0054846 | lld:lifeskim |
| pubmed-article:8895560 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:8895560 | pubmed:issue | 19 | lld:pubmed |
| pubmed-article:8895560 | pubmed:dateCreated | 1996-12-16 | lld:pubmed |
| pubmed-article:8895560 | pubmed:abstractText | Ectopic activation of the TAL-1 gene in T lymphocytes occurs in the majority of cases of human T cell acute lymphoblastic leukemia (T-ALL), yet experiments to date have failed to demonstrate a direct transforming capability for tal-1. The tal-1 gene product is a serine phosphoprotein and basic helix-loop-helix (bHLH) transcription factor known to regulate embryonic hematopoiesis. We have established a transgenic mouse model in which tal-1 mis-expression in the thymus results in the development of clonal T cell lymphoblastic leukemia/lymphoma. Thus, overexpression of tal-1 alone can be transforming, verifying its pathogenic role in human T-ALL. In addition, leukemogenesis is accelerated dramatically by transgenic co-expression of tal-1 and the catalytic subunit of casein kinase IIalpha (CKIIalpha), a serine/threonine protein kinase known to modulate the activity of other bHLH transcription factors. Although tal-1 is a substrate for CKII, the synergy of the tal-1 and CKIIalpha transgenes appears to be indirect, perhaps mediated through the E protein heterodimeric partners of tal-1. These studies prove that dysregulated tal-1 is oncogenic, providing a direct molecular explanation for the malignancies associated with TAL-1 activation in human T-ALL. | lld:pubmed |
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| pubmed-article:8895560 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:8895560 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:8895560 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8895560 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:8895560 | pubmed:issn | 0261-4189 | lld:pubmed |
| pubmed-article:8895560 | pubmed:author | pubmed-author:LederPP | lld:pubmed |
| pubmed-article:8895560 | pubmed:author | pubmed-author:SeldinD CDC | lld:pubmed |
| pubmed-article:8895560 | pubmed:author | pubmed-author:KelliherM AMA | lld:pubmed |
| pubmed-article:8895560 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8895560 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:8895560 | pubmed:volume | 15 | lld:pubmed |
| pubmed-article:8895560 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8895560 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8895560 | pubmed:pagination | 5160-6 | lld:pubmed |
| pubmed-article:8895560 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:8895560 | pubmed:year | 1996 | lld:pubmed |
| pubmed-article:8895560 | pubmed:articleTitle | Tal-1 induces T cell acute lymphoblastic leukemia accelerated by casein kinase IIalpha. | lld:pubmed |
| pubmed-article:8895560 | pubmed:affiliation | Department of Genetics, Harvard Medical School, Howard Hughes Medical Institute, Boston, MA 02115, USA. | lld:pubmed |
| pubmed-article:8895560 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8895560 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:8895560 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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