Effect of Mycobacterium tuberculosis-derived sulfolipid I on human phagocytic cells
about
Evolutionary landscape of the Mycobacterium tuberculosis complex from the viewpoint of PhoPR: implications for virulence regulation and application to vaccine developmentBacterial iron-sulfur cluster sensors in mammalian pathogensFunction and Structure of a Prokaryotic Formylglycine-generating EnzymeA sulfated metabolite produced by stf3 negatively regulates the virulence of Mycobacterium tuberculosisPapA1 and PapA2 are acyltransferases essential for the biosynthesis of the Mycobacterium tuberculosis virulence factor sulfolipid-1MmpL8 is required for sulfolipid-1 biosynthesis and Mycobacterium tuberculosis virulenceElucidation and chemical modulation of sulfolipid-1 biosynthesis in Mycobacterium tuberculosis.Biosynthesis and translocation of unsulfated acyltrehaloses in Mycobacterium tuberculosis.The cell envelope glycoconjugates of Mycobacterium tuberculosisNew targets and inhibitors of mycobacterial sulfur metabolism.Sulfolipid deficiency does not affect the virulence of Mycobacterium tuberculosis H37Rv in mice and guinea pigsLipid metabolism and Type VII secretion systems dominate the genome scale virulence profile of Mycobacterium tuberculosis in human dendritic cells.Sulfolipid-1 biosynthesis restricts Mycobacterium tuberculosis growth in human macrophagesMonocyte responses to sulfatide from Mycobacterium tuberculosis: inhibition of priming for enhanced release of superoxide, associated with increased secretion of interleukin-1 and tumor necrosis factor alpha, and altered protein phosphorylation.Mechanisms involved in mycobacterial growth inhibition by gamma interferon-activated bone marrow macrophages: role of reactive nitrogen intermediatesSynthetic studies toward Mycobacterium tuberculosis sulfolipid-I.Deciphering the virulence factors of the opportunistic pathogen Mycobacterium colombiense.Virulence factors of the Mycobacterium tuberculosis complexCharacterization of sulfolipids of Mycobacterium tuberculosis H37Rv by multiple-stage linear ion-trap high-resolution mass spectrometry with electrospray ionization reveals that the family of sulfolipid II predominates.Mycobacterium tuberculosis inhibits human innate immune responses via the production of TLR2 antagonist glycolipids.
P2860
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P2860
Effect of Mycobacterium tuberculosis-derived sulfolipid I on human phagocytic cells
description
1988 nî lūn-bûn
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1988年の論文
@ja
1988年学术文章
@wuu
1988年学术文章
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1988年学术文章
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1988年学术文章
@zh-my
1988年学术文章
@zh-sg
1988年學術文章
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1988年學術文章
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1988年學術文章
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name
Effect of Mycobacterium tuberculosis-derived sulfolipid I on human phagocytic cells
@en
Effect of Mycobacterium tuberculosis-derived sulfolipid I on human phagocytic cells.
@nl
type
label
Effect of Mycobacterium tuberculosis-derived sulfolipid I on human phagocytic cells
@en
Effect of Mycobacterium tuberculosis-derived sulfolipid I on human phagocytic cells.
@nl
prefLabel
Effect of Mycobacterium tuberculosis-derived sulfolipid I on human phagocytic cells
@en
Effect of Mycobacterium tuberculosis-derived sulfolipid I on human phagocytic cells.
@nl
P2093
P2860
P1476
Effect of Mycobacterium tuberculosis-derived sulfolipid I on human phagocytic cells
@en
P2093
P2860
P304
P407
P577
1988-11-01T00:00:00Z