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Activation of ERK1/2 and TNF-alpha production are mediated by calcium/calmodulin, and PKA signaling pathways during Mycobacterium bovis infection.

Activation of ERK1/2 and TNF-alpha production are mediated by calcium/calmodulin, and PKA signaling pathways during Mycobacterium bovis infection. Research Abstract Details 

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  • Activation of ERK1/2 and TNF-alpha production are mediated by calcium/calmodulin, and PKA signaling pathways during Mycobacterium bovis infection. Abstract Text:

    p P ,a trejoA Trejo,e mirandaE Miranda,

    Mycobacterium bovis bacillus Calmette-Guérin (BCG)-induced tumor necrosis factor (TNF)-alpha secretion via an extracellular signal-regulated kinase (ERK) mitogen-activated protein kinase-dependent mechanism is an important host defence mechanism against Mycobacterium tuberculosis in human monocytes. We now define distinct signaling pathways that regulate induction of TNF-alpha and activation of ERK1/2 by intracellular signaling mechanisms during M. bovis infection. We determined that M. bovis BCG-induced ERK 1/2 activation occurs through a mechanism that requires intracellular calcium and likely involves a calmodulin-sensitive step. In contrast, M. bovis BCG can induce p38 mapk activation by a calcium (Ca2+)/calmodulin-independent mechanism. Interestingly, we present evidence that M. bovis BCG activates protein kinase A (PKA), since pretreatment of monocytes with H-89, a inhibitor of PKA activity, blocked the ability of M. bovis BCG to induce ERK1/2 activation. These results were further supported by the fact that treatment of cells with KT5720, another well-described inhibitor of PKA activity, significantly diminished the effect of M. bovis BCG on ERK1/2 activation. Furthermore, secretion of TNF-alpha in M. bovis-infected human monocytes was also dependent on Ca2+/calmodulin, and PKA pathways. Finally, addition of H-89 significantly diminished TNF-alpha mRNA expression in M. bovis-infected human monocytes. These results indicate that the Ca2+/calmodulin, and PKA pathways play important regulatory roles in monocyte signaling upon M. bovis infection.

    Activation of ERK1/2 and TNF-alpha production are mediated by calcium/calmodulin, and PKA signaling pathways during Mycobacterium bovis infection. Publishing Authors By Initials

    p P ,a trejoA Trejo,e mirandaE Miranda,

    For similar peptides: intercellular signaling peptides and proteins: cytokines: monokines: tumor necrosis factor-alpha research abstracts see: peptides: intercellular signaling peptides and proteins: cytokines: monokines: tumor necrosis factor-alpha research

    PUBMED ID PMID:

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    Activation of ERK1/2 and TNF-alpha production are mediated by calcium/calmodulin, and PKA signaling pathways during Mycobacterium bovis infection. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: The Journal of infection

    VOLUME: 52

    Page Numbers: 147-53

    Journal Abbreviation: J. Infect.

    ISSN: 1532-2742

    DAY: 14

    MONTH: Feb

    YEAR: 2006

    Activation of ERK1/2 and TNF-alpha production are mediated by calcium/calmodulin, and PKA signaling pathways during Mycobacterium bovis infection. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 7908424

    Activation of ERK1/2 and TNF-alpha production are mediated by calcium/calmodulin, and PKA signaling pathways during Mycobacterium bovis infection. Keywords Mesh Terms:

    KEYWORDS: Tumor Necrosis Factor-alpha

    MESH TERMS: metabolism

    Chemical & Substance for Abstract: Activation of ERK1/2 and TNF-alpha production are mediated by calcium/calmodulin, and PKA signaling pathways during Mycobacterium bovis infection. Information

    Substance Name: Mitogen-Activated Protein Kinase 3

    Registry Number: EC 2.7.1.37

    Grant and Affiliation Information for Activation of ERK1/2 and TNF-alpha production are mediated by calcium/calmodulin, and PKA signaling pathways during Mycobacterium bovis infection.

    AFFILIATION: Departamento de Inmunología, Escuela Nacional de Ciencias Biológicas, IPN, Carpio y Plan de Ayala, 11340 México, DF, México. pmendezs@bios.encb.ipn.mx

    Country: England

    England Research Publication

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    ACRONYM:

    MEDLINETA: J Infect

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