| pubmed-article:17062731 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17062731 | lifeskim:mentions | umls-concept:C0027950 | lld:lifeskim |
| pubmed-article:17062731 | lifeskim:mentions | umls-concept:C0024432 | lld:lifeskim |
| pubmed-article:17062731 | lifeskim:mentions | umls-concept:C0033684 | lld:lifeskim |
| pubmed-article:17062731 | lifeskim:mentions | umls-concept:C0038952 | lld:lifeskim |
| pubmed-article:17062731 | lifeskim:mentions | umls-concept:C1366587 | lld:lifeskim |
| pubmed-article:17062731 | lifeskim:mentions | umls-concept:C0205224 | lld:lifeskim |
| pubmed-article:17062731 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:17062731 | pubmed:dateCreated | 2007-2-7 | lld:pubmed |
| pubmed-article:17062731 | pubmed:abstractText | The antiapoptotic protein Mcl-1, a member of the Bcl-2 family, plays critical roles in promoting the survival of lymphocytes and hematopoietic stem cells. Although previous studies have implicated Mcl-1 in regulating the survival of neutrophils and macrophages, the in vivo function of Mcl-1 in these 2 cell lineages remained unclear. To address this, we have generated mice conditionally lacking Mcl-1 expression in neutrophils and macrophages. We show that Mcl-1 conditional knockout mice had a severe defect in neutrophil survival, whereas macrophage survival was normal. The granulocyte compartment in the blood, spleen, and bone marrow of Mcl-1 conditional knockout mice exhibited an approximately 2- to 3-fold higher apoptotic rate than control cells. In contrast, resting and activated macrophages from Mcl-1-deficient mice exhibited normal survival and contained up-regulated expression of Bcl-2 and Bcl-xL. These data suggest that Mcl-1 plays a nonredundant role in promoting the survival of neutrophils but not macrophages. | lld:pubmed |
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| pubmed-article:17062731 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:17062731 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:17062731 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17062731 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:17062731 | pubmed:issn | 0006-4971 | lld:pubmed |
| pubmed-article:17062731 | pubmed:author | pubmed-author:HeYou-WenYW | lld:pubmed |
| pubmed-article:17062731 | pubmed:author | pubmed-author:DzhagalovIvan... | lld:pubmed |
| pubmed-article:17062731 | pubmed:author | pubmed-author:St... | lld:pubmed |
| pubmed-article:17062731 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17062731 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:17062731 | pubmed:volume | 109 | lld:pubmed |
| pubmed-article:17062731 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17062731 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17062731 | pubmed:pagination | 1620-6 | lld:pubmed |
| pubmed-article:17062731 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:17062731 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:17062731 | pubmed:articleTitle | The antiapoptotic protein Mcl-1 is essential for the survival of neutrophils but not macrophages. | lld:pubmed |
| pubmed-article:17062731 | pubmed:affiliation | Department of Immunology, Duke University Medical Center, Durham, NC 27710, USA. | lld:pubmed |
| pubmed-article:17062731 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17062731 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:17062731 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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