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A novel 165-kDa Golgin protein induced by brain ischemia and phosphorylated by Akt protects against apoptosis.

A novel 165-kDa Golgin protein induced by brain ischemia and phosphorylated by Akt protects against apoptosis. Research Abstract Details 

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  • A novel 165-kDa Golgin protein induced by brain ischemia and phosphorylated by Akt protects against apoptosis. Abstract Text:

    ruiqiong ranRuiqiong Ran,ruiqin panRuiqin Pan,aigang luAigang Lu,huichun xuHuichun Xu,ryan r davisRyan R Davis,frank r sharpFrank R Sharp,ruiqiong ranRuiqiong Ran,ruiqin panRuiqin Pan,aigang luAigang Lu,huichun xuHuichun Xu,ryan r davisRyan R Davis,frank r sharpFrank R Sharp,

    A cDNA encoding a novel protein was cloned from ischemic rat brain and found to be homologous to testis Mea-2 Golgi-associated protein (Golga3). The sequence predicted a 165-kDa protein, and in vitro translated protein exhibited a molecular mass of 165-170 kDa. Because brain ischemia induced the mRNA, and the protein localized to the Golgi apparatus, this protein was designated Ischemia-Inducible Golgin Protein 165 (IIGP165). In HeLa cells, serum and glucose deprivation-induced caspase-dependent cleavage of the IIGP165 protein, after which the IIGP165 fragments translocated to the nucleus. The C-terminus of IIGP165, which contains a LXXLL motif, appears to function as a transcriptional co-regulator. Akt co-localizes with IIGP165 protein in the Golgi in vivo, and phosphorylates IIGP165 on serine residues 345 and 134. Though transfection of IIGP165 cDNA alone does not protect HeLa cells from serum deprivation or Brefeldin-A-triggered cell death, co-transfection of both Akt and IIGP165 cDNA or combined IIGP165-transfection with PDGF treatment significantly protects HeLa cells better than either treatment alone. These data show that Akt phosphorylation of IIGP165 protects against apoptotic cell death, and add to evidence that the Golgi apparatus also plays a role in regulating apoptosis.

    A novel 165-kDa Golgin protein induced by brain ischemia and phosphorylated by Akt protects against apoptosis. Publishing Authors By Initials

    r ranR Ran,r panR Pan,a luA Lu,h xuH Xu,rr davisRR Davis,fr sharpFR Sharp,r ranR Ran,r panR Pan,a luA Lu,h xuH Xu,rr davisRR Davis,fr sharpFR Sharp,

    For similar abstracts research abstracts see: abstracts research

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    A novel 165-kDa Golgin protein induced by brain ischemia and phosphorylated by Akt protects against apoptosis. Journal Published:

    PUBLICATION TYPE: Research Support, N.I.H., Extr

    Journal: Molecular and cellular neurosciences

    VOLUME: 36

    Page Numbers: 392-407

    Journal Abbreviation: Mol. Cell. Neurosci.

    ISSN: 1044-7431

    DAY: 9

    MONTH: 08

    YEAR: 2007

    A novel 165-kDa Golgin protein induced by brain ischemia and phosphorylated by Akt protects against apoptosis. Information

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    LANGUAGE: eng

    NlmUniqueID: 9100095

    A novel 165-kDa Golgin protein induced by brain ischemia and phosphorylated by Akt protects against apoptosis. Keywords Mesh Terms:

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    Chemical & Substance for Abstract: A novel 165-kDa Golgin protein induced by brain ischemia and phosphorylated by Akt protects against apoptosis. Information

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    Grant and Affiliation Information for A novel 165-kDa Golgin protein induced by brain ischemia and phosphorylated by Akt protects against apoptosis.

    AFFILIATION: M.I.N.D. Institute and Department of Neurology, University of California at Davis Medical Center, University of California at Davis, Sacramento, CA 95817, USA. ruiqiong.ran@ucdmc.ucdavis.edu

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NINDS

    GRANT: NS056302

    ACRONYM: NS

    MEDLINETA: Mol Cell Neurosci

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