Source:http://linkedlifedata.com/resource/pubmed/id/12496428
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2002-12-23
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pubmed:abstractText |
Mcl-1 protein expression was found to be up-regulated during infection with virulent Mycobacterium tuberculosis strain H37Rv. Mcl-1 induction in THP-1 cells was optimal at a multiplicity of infection of 0.8-1.2 bacilli per macrophage and was independent of opsonin coating of the bacteria. Mcl-1 expression was elevated as early as 4 h, peaked at 5.8-fold above control cells at 24 h, and remained elevated at 48 h after infection. In THP-1 cells, mMcl-1 mRNA was induced by infection with live H37Rv but not with attenuated M. tuberculosis strain H37Ra, heat-killed H37Rv, or latex beads. In THP-1 cells and monocyte-derived macrophages (MDMs), Mcl-1 protein was induced by infection with live H37Rv but not with attenuated M. tuberculosis strain H37Ra, heat-killed H37Rv, or latex beads. Treatment of uninfected, H37Ra-infected, and H37Rv-infected THP-1 cells and MDMs with antisense oligonucleotides to mcl-1 reduced Mcl-1 expression by >84%. This resulted in an increase in apoptosis of both MDMs and THP-1 cells that were infected with H37Rv, but not cells that were uninfected or infected with H37Ra. Increased apoptosis correlated with a decrease in M. tuberculosis CFUs recovered from antisense-treated, H37Rv-infected cells at 4 and 7 days after infection. In contrast, CFU recoveries from sense-treated, H37Rv-infected cells or from antisense- or sense-treated, H37Ra-infected cells were unchanged from controls. Thus, the antiapoptotic effect of the induction of Mcl-1 expression in H37Rv-infected macrophages promotes the survival of virulent M. tuberculosis.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Neoplasm Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Oligonucleotides, Antisense,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-bcl-2,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/myeloid cell leukemia sequence 1...
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
170
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
430-7
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:12496428-Apoptosis,
pubmed-meshheading:12496428-Cells, Cultured,
pubmed-meshheading:12496428-Humans,
pubmed-meshheading:12496428-Immunity, Innate,
pubmed-meshheading:12496428-Intracellular Fluid,
pubmed-meshheading:12496428-Macrophages,
pubmed-meshheading:12496428-Mycobacterium tuberculosis,
pubmed-meshheading:12496428-Neoplasm Proteins,
pubmed-meshheading:12496428-Oligonucleotides, Antisense,
pubmed-meshheading:12496428-Proto-Oncogene Proteins c-bcl-2,
pubmed-meshheading:12496428-RNA, Messenger,
pubmed-meshheading:12496428-Tumor Cells, Cultured,
pubmed-meshheading:12496428-Up-Regulation,
pubmed-meshheading:12496428-Virulence
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pubmed:year |
2003
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pubmed:articleTitle |
Survival of Mycobacterium tuberculosis in host macrophages involves resistance to apoptosis dependent upon induction of antiapoptotic Bcl-2 family member Mcl-1.
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pubmed:affiliation |
Immunity and Infection Research Center, Vancouver Hospital and Health Sciences Center, University of British Columbia, Vancouver, British Columbia, Canada.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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