1 Ocak 2014 Dergi makalesi Açık Erişim

Tang, Zhi; Baykal, Ahmet Tank; Gao, Hui; Quezada, Hernan Concha; Zhang, Haiyan; Bereczki, Erika; Serhatli, Muge; Baykal, Betul; Acioglu, Cigdem; Wang, Shan; Ioja, Eniko; Ji, Xinying; Zhang, Yan; Guan, Zhizhong; Winblad, Bengt; Pei, Jin-Jing

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  <identifier identifierType="URL">https://aperta.ulakbim.gov.tr/record/99259</identifier>
  <creators>
    <creator>
      <creatorName>Tang, Zhi</creatorName>
      <givenName>Zhi</givenName>
      <familyName>Tang</familyName>
      <affiliation>Karolinska Inst, KI Alzheimer Dis Res Ctr, SE-14186 Huddinge, Sweden</affiliation>
    </creator>
    <creator>
      <creatorName>Baykal, Ahmet Tank</creatorName>
      <givenName>Ahmet Tank</givenName>
      <familyName>Baykal</familyName>
      <affiliation>Istanbul Medipol Univ, Sch Med, Dept Med Biochem, TR-34083 Unkapani, Fatih Istanbul, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Gao, Hui</creatorName>
      <givenName>Hui</givenName>
      <familyName>Gao</familyName>
      <affiliation>Karolinska Inst, Dept Biosci &amp; Nutr, SE-14157 Huddinge, Sweden</affiliation>
    </creator>
    <creator>
      <creatorName>Quezada, Hernan Concha</creatorName>
      <givenName>Hernan Concha</givenName>
      <familyName>Quezada</familyName>
      <affiliation>Karolinska Inst Hosp, Ctr Infect Med, Dept Med, Huddinge, Sweden</affiliation>
    </creator>
    <creator>
      <creatorName>Zhang, Haiyan</creatorName>
      <givenName>Haiyan</givenName>
      <familyName>Zhang</familyName>
      <affiliation>Karolinska Inst, KI Alzheimer Dis Res Ctr, SE-14186 Huddinge, Sweden</affiliation>
    </creator>
    <creator>
      <creatorName>Bereczki, Erika</creatorName>
      <givenName>Erika</givenName>
      <familyName>Bereczki</familyName>
      <affiliation>Karolinska Inst, KI Alzheimer Dis Res Ctr, SE-14186 Huddinge, Sweden</affiliation>
    </creator>
    <creator>
      <creatorName>Serhatli, Muge</creatorName>
      <givenName>Muge</givenName>
      <familyName>Serhatli</familyName>
      <affiliation>TUBITAK, Marmara Res Ctr, Genet Engn &amp; Biotechnol Inst, TR-41470 Gebze, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Baykal, Betul</creatorName>
      <givenName>Betul</givenName>
      <familyName>Baykal</familyName>
      <affiliation>TUBITAK, Marmara Res Ctr, Genet Engn &amp; Biotechnol Inst, TR-41470 Gebze, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Acioglu, Cigdem</creatorName>
      <givenName>Cigdem</givenName>
      <familyName>Acioglu</familyName>
      <affiliation>TUBITAK, Marmara Res Ctr, Genet Engn &amp; Biotechnol Inst, TR-41470 Gebze, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Wang, Shan</creatorName>
      <givenName>Shan</givenName>
      <familyName>Wang</familyName>
      <affiliation>Karolinska Inst, KI Alzheimer Dis Res Ctr, SE-14186 Huddinge, Sweden</affiliation>
    </creator>
    <creator>
      <creatorName>Ioja, Eniko</creatorName>
      <givenName>Eniko</givenName>
      <familyName>Ioja</familyName>
      <affiliation>Karolinska Inst, KI Alzheimer Dis Res Ctr, SE-14186 Huddinge, Sweden</affiliation>
    </creator>
    <creator>
      <creatorName>Ji, Xinying</creatorName>
      <givenName>Xinying</givenName>
      <familyName>Ji</familyName>
      <affiliation>Henan Univ, Sch Med, Inst Immunol, Henan Prov Key Med Lab Cellular &amp; Mol Immunol, Kaifeng 475004, Henan, Peoples R China</affiliation>
    </creator>
    <creator>
      <creatorName>Zhang, Yan</creatorName>
      <givenName>Yan</givenName>
      <familyName>Zhang</familyName>
      <affiliation>Karolinska Inst, KI Alzheimer Dis Res Ctr, SE-14186 Huddinge, Sweden</affiliation>
    </creator>
    <creator>
      <creatorName>Guan, Zhizhong</creatorName>
      <givenName>Zhizhong</givenName>
      <familyName>Guan</familyName>
    </creator>
    <creator>
      <creatorName>Winblad, Bengt</creatorName>
      <givenName>Bengt</givenName>
      <familyName>Winblad</familyName>
      <affiliation>Karolinska Inst, KI Alzheimer Dis Res Ctr, SE-14186 Huddinge, Sweden</affiliation>
    </creator>
    <creator>
      <creatorName>Pei, Jin-Jing</creatorName>
      <givenName>Jin-Jing</givenName>
      <familyName>Pei</familyName>
      <affiliation>Karolinska Inst, KI Alzheimer Dis Res Ctr, SE-14186 Huddinge, Sweden</affiliation>
    </creator>
  </creators>
  <titles>
    <title>Mtor Is A Signaling Hub In Cell Survival: A Mass-Spectrometry-Based Proteomics Investigation</title>
  </titles>
  <publisher>Aperta</publisher>
  <publicationYear>2014</publicationYear>
  <dates>
    <date dateType="Issued">2014-01-01</date>
  </dates>
  <resourceType resourceTypeGeneral="Text">Journal article</resourceType>
  <alternateIdentifiers>
    <alternateIdentifier alternateIdentifierType="url">https://aperta.ulakbim.gov.tr/record/99259</alternateIdentifier>
  </alternateIdentifiers>
  <relatedIdentifiers>
    <relatedIdentifier relatedIdentifierType="DOI" relationType="IsIdenticalTo">10.1021/pr500192g</relatedIdentifier>
  </relatedIdentifiers>
  <rightsList>
    <rights rightsURI="http://www.opendefinition.org/licenses/cc-by">Creative Commons Attribution</rights>
    <rights rightsURI="info:eu-repo/semantics/openAccess">Open Access</rights>
  </rightsList>
  <descriptions>
    <description descriptionType="Abstract">mTor plays a central role in controlling protein homeostasis and cell survival. Recently, we have demonstrated that perturbations of mTor signaling are implicated in Alzheimer's disease (AD) and that mTor complex 1 (mTorC1) is involved in the formation of toxic phospho-tau. Therefore, we employed mass-spectrometry-based proteomics to identify specific protein expression changes in relation with cell survival in human neuroblastoma SH-SYSY cells expressing genetically modified mTor. Cell death in SH-SYSY cells was induced by moderate serum deprivation. Using flow cytometry we observed that up-regulated mTor complex 2 (mTorC2) increases the number of viable cells. By using a combination approach of proteomic and enrichment analysis we have identified several proteins (Thioredoxin-dependent peroxide reductase, Peroxiredoxin-5, Cofilin 1 (non-muscle), Annexin A5, Mortalin, and 14-3-3 protein zeta/delta) involved in mitochondrial integrity, apoptotosis, and pro-survival functions (caspase inhibitor activity and anti-apoptosis) that were significantly altered by mTor activity modulation. The major findings of this study are the implication of mTorC2 but not mTorC1 in cell viability modulation by activating the pro-survival machinery. Taken together, these results suggest that up-regulated mTorC2 might be playing an important role in promoting cell survival by suppressing the mitochondria-caspase-apoptotic pathway in vitro.</description>
  </descriptions>
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