| pubmed-article:9794389 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9794389 | lifeskim:mentions | umls-concept:C0021761 | lld:lifeskim |
| pubmed-article:9794389 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
| pubmed-article:9794389 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
| pubmed-article:9794389 | lifeskim:mentions | umls-concept:C0439064 | lld:lifeskim |
| pubmed-article:9794389 | lifeskim:mentions | umls-concept:C1879746 | lld:lifeskim |
| pubmed-article:9794389 | lifeskim:mentions | umls-concept:C1547011 | lld:lifeskim |
| pubmed-article:9794389 | pubmed:issue | 9 | lld:pubmed |
| pubmed-article:9794389 | pubmed:dateCreated | 1998-11-18 | lld:pubmed |
| pubmed-article:9794389 | pubmed:abstractText | The mechanism by which early lymphoid cells are selectively transformed by v-Abl is currently unknown. Previous studies have shown constitutive activation of IL-4 and IL-7 signaling pathways, as measured by activation of Janus protein kinase (JAK)1, JAK3, STAT5, and STAT6, in pre-B cells transformed by v-Abl. To determine whether activation of these cytokine signaling pathways by v-Abl is important in the cellular events induced by the Abelson murine leukemia virus, the effects of IL-4 and IL-7 on pre-B cells transformed with a temperature-sensitive v-Abl mutant were examined. Whereas IL-4 had little or no effect, IL-7 delayed both the apoptosis and cell cycle arrest that occur upon v-Abl kinase inactivation. IL-7 also delayed the decreases in the levels of c-Myc, Bcl-2, and Bcl-xL that occur upon loss of v-Abl kinase activity. IL-7 did not maintain v-Abl-mediated differentiation arrest of the pre-B cells, as activation of NF-kappaB and RAG gene transcription was unaffected by IL-7. These results identify a potential role for IL-7 signaling pathways in transformation by v-Abl while demonstrating that a combination of IL-4 and IL-7 signaling cannot substitute for an active v-Abl kinase in transformed pre-B cells. | lld:pubmed |
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| pubmed-article:9794389 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:9794389 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:9794389 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9794389 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:9794389 | pubmed:issn | 0022-1767 | lld:pubmed |
| pubmed-article:9794389 | pubmed:author | pubmed-author:BanerjeeAA | lld:pubmed |
| pubmed-article:9794389 | pubmed:author | pubmed-author:RothmanPP | lld:pubmed |
| pubmed-article:9794389 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9794389 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:9794389 | pubmed:volume | 161 | lld:pubmed |
| pubmed-article:9794389 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9794389 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9794389 | pubmed:pagination | 4611-7 | lld:pubmed |
| pubmed-article:9794389 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:9794389 | pubmed:year | 1998 | lld:pubmed |
| pubmed-article:9794389 | pubmed:articleTitle | IL-7 reconstitutes multiple aspects of v-Abl-mediated signaling. | lld:pubmed |
| pubmed-article:9794389 | pubmed:affiliation | Integrated Program in Cellular, Molecular, and Biophysical Studies, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA. | lld:pubmed |
| pubmed-article:9794389 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9794389 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:9794389 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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