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One or more keywords matched the following items that are connected to Remold, Heinz
Item TypeName
Academic Article Enhancement of antimycobacterial activity of macrophages by stabilization of inner mitochondrial membrane potential.
Academic Article Mycobacterium tuberculosis evades macrophage defenses by inhibiting plasma membrane repair.
Academic Article Cytokines enhance neutrophils from human immunodeficiency virus-negative donors and AIDS patients to inhibit the growth of Mycobacterium avium in vitro.
Academic Article Immunization of healthy adult subjects in the United States with inactivated Mycobacterium vaccae administered in a three-dose series.
Academic Article Cytosolic phospholipase A2 participates with TNF-alpha in the induction of apoptosis of human macrophages infected with Mycobacterium tuberculosis H37Ra.
Academic Article Pathogenic Mycobacterium tuberculosis evades apoptosis of host macrophages by release of TNF-R2, resulting in inactivation of TNF-alpha.
Academic Article Virulent Mycobacterium tuberculosis strains evade apoptosis of infected alveolar macrophages.
Academic Article Infection by Mycobacterium tuberculosis promotes human alveolar macrophage apoptosis.
Academic Article Efferocytosis is an innate antibacterial mechanism.
Academic Article Plasminogen activator inhibitor type 2 prevents programmed cell death of human macrophages infected with Mycobacterium avium, serovar 4.
Academic Article Antigen-dependent heterogeneity of human migration inhibitory factor.
Academic Article Interleukin 10 produced by macrophages inoculated with Mycobacterium avium attenuates mycobacteria-induced apoptosis by reduction of TNF-alpha activity.
Academic Article Critical role of mitochondrial damage in determining outcome of macrophage infection with Mycobacterium tuberculosis.
Academic Article Evasion of innate immunity by Mycobacterium tuberculosis: is death an exit strategy?
Academic Article IL-1ß promotes antimicrobial immunity in macrophages by regulating TNFR signaling and caspase-3 activation.
Academic Article Apoptosis is an innate defense function of macrophages against Mycobacterium tuberculosis.
Academic Article Human macrophages acquire a hyporesponsive state of tumor necrosis factor alpha production in response to successive Mycobacterium avium serovar 4 stimulation.
Academic Article A mechanism of virulence: virulent Mycobacterium tuberculosis strain H37Rv, but not attenuated H37Ra, causes significant mitochondrial inner membrane disruption in macrophages leading to necrosis.
Academic Article Programmed cell death of Mycobacterium avium serovar 4-infected human macrophages prevents the mycobacteria from spreading and induces mycobacterial growth inhibition by freshly added, uninfected macrophages.
Academic Article Interleukin-12 enhances antigen-specific proliferation of peripheral blood mononuclear cells from HIV-positive and negative donors in response to Mycobacterium avium.
Academic Article Survival of human macrophages infected with Mycobacterium avium intracellulare correlates with increased production of tumor necrosis factor-alpha and IL-6.
Academic Article TNF-alpha response of human monocyte-derived macrophages to Mycobacterium avium, serovar 4, is of brief duration and protein kinase C dependent.
Academic Article Dying to live: how the death modality of the infected macrophage affects immunity to tuberculosis.
Academic Article Macrophage apoptosis in response to high intracellular burden of Mycobacterium tuberculosis is mediated by a novel caspase-independent pathway.
Academic Article Mycobacterium tuberculosis blocks crosslinking of annexin-1 and apoptotic envelope formation on infected macrophages to maintain virulence.
Academic Article Eicosanoid pathways regulate adaptive immunity to Mycobacterium tuberculosis.
Academic Article Concurrent infection of human macrophages with HIV-1 and Mycobacterium avium results in decreased cell viability, increased M. avium multiplication and altered cytokine production.
Academic Article A macrophage invasion mechanism for mycobacteria implicating the extracellular domain of CD43.
Academic Article Identification of Mycobacterium avium DNA sequences that encode exported proteins by using phoA gene fusions.
Academic Article Lipid mediators in innate immunity against tuberculosis: opposing roles of PGE2 and LXA4 in the induction of macrophage death.
Academic Article Macrophage apoptosis in mycobacterial infections.
Academic Article Lipids, apoptosis, and cross-presentation: links in the chain of host defense against Mycobacterium tuberculosis.
Concept Mycobacterium leprae
Concept Mycobacterium
Concept Mycobacterium avium-intracellulare Infection
Concept Mycobacterium avium
Concept Mycobacterium Infections
Concept Mycobacterium tuberculosis
Concept Mycobacterium kansasii
Concept Mycobacterium avium Complex
Academic Article The prostaglandin E2 receptor EP4 is integral to a positive feedback loop for prostaglandin E2 production in human macrophages infected with Mycobacterium tuberculosis.
Grant A Novel Mechanism of Innate Immunity Against TB
Grant A Novel Mechanism of Innate Immunity Against TB
Grant Escape of Mycobacterium tuberculosis from the macrophage is regulated by eicosano
Grant MYCOBACTERIUM AVIUM/INTRACELLULARE INFECTIONS AND AIDS
Grant Investigating the Role of the GTPase Arl8b in Plasma Membrane Repair of Mtb-Infected Macrophages
Grant Role of lipid mediators in host resistance to Mycobacterium tuberculosis
Grant VIRULENCE AND GENOTYPE/PHENOTYPE OF MYCOBACTERIUM AVIUM
Grant Regulation of Apoptotic Envelope Formation by MTB in the Host Macrophage
Academic Article Bcl-xL mediates RIPK3-dependent necrosis in M. tuberculosis-infected macrophages.
Academic Article Lysosome-Mediated Plasma Membrane Repair Is Dependent on the Small GTPase Arl8b and Determines Cell Death Type in Mycobacterium tuberculosis Infection.
Academic Article Sirtuin 3 Downregulation in Mycobacterium tuberculosis-Infected Macrophages Reprograms Mitochondrial Metabolism and Promotes Cell Death.
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  • Mycobacterium
Funded by the NIH National Center for Advancing Translational Sciences through its Clinical and Translational Science Awards Program, grant number UL1TR002541.