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MyD88-5 links mitochondria, microtubules, and JNK3 in neurons and regulates neuronal survival.

MyD88-5 links mitochondria, microtubules, and JNK3 in neurons and regulates neuronal survival. Research Abstract Details 

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  • MyD88-5 links mitochondria, microtubules, and JNK3 in neurons and regulates neuronal survival. Abstract Text:

    younghwa kimYounghwa Kim,ping zhouPing Zhou,liping qianLiping Qian,jen-zen chuangJen-Zen Chuang,jessica leeJessica Lee,chenjian liChenjian Li,costantino iadecolaCostantino Iadecola,carl nathanCarl Nathan,aihao dingAihao Ding,

    The innate immune system relies on evolutionally conserved Toll-like receptors (TLRs) to recognize diverse microbial molecular structures. Most TLRs depend on a family of adaptor proteins termed MyD88s to transduce their signals. Critical roles of MyD88-1-4 in host defense were demonstrated by defective immune responses in knockout mice. In contrast, the sites of expression and functions of vertebrate MyD88-5 have remained elusive. We show that MyD88-5 is distinct from other MyD88s in that MyD88-5 is preferentially expressed in neurons, colocalizes in part with mitochondria and JNK3, and regulates neuronal death. We prepared MyD88-5/GFP transgenic mice via a bacterial artificial chromosome to preserve its endogenous expression pattern. MyD88-5/GFP was detected chiefly in the brain, where it associated with punctate structures within neurons and copurified in part with mitochondria. In vitro, MyD88-5 co-immunoprecipitated with JNK3 and recruited JNK3 from cytosol to mitochondria. Hippocampal neurons from MyD88-5-deficient mice were protected from death after deprivation of oxygen and glucose. In contrast, MyD88-5-null macrophages behaved like wild-type cells in their response to microbial products. Thus, MyD88-5 appears unique among MyD88s in functioning to mediate stress-induced neuronal toxicity.

    MyD88-5 links mitochondria, microtubules, and JNK3 in neurons and regulates neuronal survival. Publishing Authors By Initials

    y kimY Kim,p zhouP Zhou,l qianL Qian,jz chuangJZ Chuang,j leeJ Lee,c liC Li,c iadecolaC Iadecola,c nathanC Nathan,a dingA Ding,

    For similar biochemical phenomena, metabolism, and nutrition: metabolism: biological transport: protein transport research abstracts see: biochemical phenomena, metabolism, and nutrition: metabolism: biological transport: protein transport research

    PUBMED ID PMID:

    MEDLINE DATE:

    MyD88-5 links mitochondria, microtubules, and JNK3 in neurons and regulates neuronal survival. Journal Published:

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

    Journal: The Journal of experimental medicine

    VOLUME: 204

    Page Numbers: 2063-74

    Journal Abbreviation: J. Exp. Med.

    ISSN: 0022-1007

    DAY: 27

    MONTH: 08

    YEAR: 2007

    MyD88-5 links mitochondria, microtubules, and JNK3 in neurons and regulates neuronal survival. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 2985109

    MyD88-5 links mitochondria, microtubules, and JNK3 in neurons and regulates neuronal survival. Keywords Mesh Terms:

    KEYWORDS: Protein Transport

    MESH TERMS: enzymology

    Chemical & Substance for Abstract: MyD88-5 links mitochondria, microtubules, and JNK3 in neurons and regulates neuronal survival. Information

    Substance Name: Mitogen-Activated Protein Kinase 10

    Registry Number: EC 2.7.1.-

    Grant and Affiliation Information for MyD88-5 links mitochondria, microtubules, and JNK3 in neurons and regulates neuronal survival.

    AFFILIATION: Department of Microbiology and Immunology, Weill Medical College of Cornell University, New York, NY 10021, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NINDS

    GRANT: NS 35806

    ACRONYM: NS

    MEDLINETA: J Exp Med

    REFSOURCE:

    DATABASENAME:

    ACCESSION NUMBER:

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