Mycobacterium tuberculosis induces an atypical cell death mode to escape from infected macrophages. - Wikidata - awgldk - TriplyDB

Mycobacterium tuberculosis induces an atypical cell death mode to escape from infected macrophages.

Mycobacterium tuberculosis induces an atypical cell death mode to escape from infected macrophages.

http://www.wikidata.org/entity/Q33869756

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Interaction of Mycobacterium tuberculosis with host cell death pathways ESX-1-induced apoptosis during mycobacterial infection: to be or not to be, that is the question Cell death and autophagy in tuberculosis Identification of a Transcription Factor That Regulates Host Cell Exit and Virulence of Mycobacterium tuberculosis A blast without power - cell death induced by the tuberculosis-necrotizing toxin fails to elicit adequate immune responses.Intracellular bacillary burden reflects a burst size for Mycobacterium tuberculosis in vivo.An outer membrane channel protein of Mycobacterium tuberculosis with exotoxin activity.Pathogenicity of Mycobacterium tuberculosis is expressed by regulating metabolic thresholds of the host macrophage.Bim is a crucial regulator of apoptosis induced by Mycobacterium tuberculosis.Beyond macrophages: the diversity of mononuclear cells in tuberculosis.Attenuated Mycobacterium tuberculosis SO2 vaccine candidate is unable to induce cell death.The balance of apoptotic and necrotic cell death in Mycobacterium tuberculosis infected macrophages is not dependent on bacterial virulence.Characterizing virulence-specific perturbations in the mitochondrial function of macrophages infected with Mycobacterium tuberculosis.Transcriptome Analysis Reveals Novel Entry Mechanisms and a Central Role of SRC in Host Defense during High Multiplicity Mycobacterial Infection Cytokine and lipid mediator networks in tuberculosis Caspase-3-independent apoptotic pathways contribute to interleukin-32γ-mediated control of Mycobacterium tuberculosis infection in THP-1 cells Autophagy in the fight against tuberculosis.Wnt/β-catenin signaling reduces Bacillus Calmette-Guerin-induced macrophage necrosis through a ROS -mediated PARP/AIF-dependent pathway.Interactions between naïve and infected macrophages reduce Mycobacterium tuberculosis viability microRNA-17-5p Modulates Bacille Calmette-Guerin Growth in RAW264.7 Cells by Targeting ULK1.Bacillary replication and macrophage necrosis are determinants of neutrophil recruitment in tuberculosis.The tuberculosis necrotizing toxin kills macrophages by hydrolyzing NAD Temporal Expression of Peripheral Blood Leukocyte Biomarkers in a Macaca fascicularis Infection Model of Tuberculosis; Comparison with Human Datasets and Analysis with Parametric/Non-parametric Tools for Improved Diagnostic Biomarker Identification Mycobacteria Clumping Increase Their Capacity to Damage Macrophages.Postprimary Tuberculosis and Macrophage Necrosis: Is There a Big ConNECtion?Mycobacterium tuberculosis PPE68 and Rv2626c genes contribute to the host cell necrosis and bacterial escape from macrophages Caspase-independent apoptosis in infected macrophages triggered by sulforaphane via Nrf2/p38 signaling pathways Mycobacterium tuberculosis Zinc Metalloprotease-1 Assists Mycobacterial Dissemination in Zebrafish.PknE, a serine/threonine protein kinase of Mycobacterium tuberculosis initiates survival crosstalk that also impacts HIV coinfection.Cell death paradigms in the pathogenesis of Mycobacterium tuberculosis infection.A caspase-dependent pathway is involved in Wnt/β-catenin signaling promoted apoptosis in Bacillus Calmette-Guerin infected RAW264.7 macrophages.Notch signaling regulates expression of Mcl-1 and apoptosis in PPD-treated macrophages.Escape from the Phagosome: The Explanation for MHC-I Processing of Mycobacterial Antigens?Mycobacterium tuberculosis effectors interfering host apoptosis signaling.Innate and Adaptive Cellular Immune Responses to Mycobacterium tuberculosis Infection.Mycobacterial escape from macrophage phagosomes to the cytoplasm represents an alternate adaptation mechanism.Tumour necrosis factor receptors and apoptosis of alveolar macrophages during early infection with attenuated and virulent Mycobacterium bovis.Role of apoptosis and autophagy in tuberculosis.Differences between Mycobacterium-Host Cell Relationships in Latent Tuberculous Infection of Mice Ex Vivo and Mycobacterial Infection of Mouse Cells In Vitro.Susceptibility of M. tuberculosis-infected host cells to phospho-MLKL driven necroptosis is dependent on cell type and presence of TNFα.

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P2860

Mycobacterium tuberculosis induces an atypical cell death mode to escape from infected macrophages.

http://www.wikidata.org/entity/Q33869756

description

2011 nî lūn-bûn

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2011 թուականի Մարտին հրատարակուած գիտական յօդուած

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2011 թվականի մարտին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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Mycobacterium tuberculosis ind ...... ape from infected macrophages.

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Mycobacterium tuberculosis ind ...... ape from infected macrophages.

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Mycobacterium tuberculosis ind ...... ape from infected macrophages.

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Mycobacterium tuberculosis ind ...... ape from infected macrophages.

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Christopher Sassetti

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Hardy Kornfeld

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Jinhee Lee

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Kadamba Papavinasasundaram

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Teresa Repasy

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P2860

Differential regulation of caspase-1 activation, pyroptosis, and autophagy via Ipaf and ASC in Shigella-infected macrophages

Bax interacts with the permeability transition pore to induce permeability transition and cytochrome c release in isolated mitochondria

Sphingosine-induced apoptosis is dependent on lysosomal proteases

Mycobacterium tuberculosis nuoG is a virulence gene that inhibits apoptosis of infected host cells

Iron-cofactored superoxide dismutase inhibits host responses to Mycobacterium tuberculosis

The Mycobacterium tuberculosis PhoPR two-component system regulates genes essential for virulence and complex lipid biosynthesis

Mutually dependent secretion of proteins required for mycobacterial virulence.

The combined functions of proapoptotic Bcl-2 family members bak and bax are essential for normal development of multiple tissues

Mitochondrial membrane permeabilization in cell death

Pyroptosis: host cell death and inflammation

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Mycobacterium tuberculosis

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