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

JSON-LD (schema.org)

{
  "@context": "https://schema.org/", 
  "@id": 99259, 
  "@type": "ScholarlyArticle", 
  "creator": [
    {
      "@type": "Person", 
      "affiliation": "Karolinska Inst, KI Alzheimer Dis Res Ctr, SE-14186 Huddinge, Sweden", 
      "name": "Tang, Zhi"
    }, 
    {
      "@type": "Person", 
      "affiliation": "Istanbul Medipol Univ, Sch Med, Dept Med Biochem, TR-34083 Unkapani, Fatih Istanbul, Turkey", 
      "name": "Baykal, Ahmet Tank"
    }, 
    {
      "@type": "Person", 
      "affiliation": "Karolinska Inst, Dept Biosci & Nutr, SE-14157 Huddinge, Sweden", 
      "name": "Gao, Hui"
    }, 
    {
      "@type": "Person", 
      "affiliation": "Karolinska Inst Hosp, Ctr Infect Med, Dept Med, Huddinge, Sweden", 
      "name": "Quezada, Hernan Concha"
    }, 
    {
      "@type": "Person", 
      "affiliation": "Karolinska Inst, KI Alzheimer Dis Res Ctr, SE-14186 Huddinge, Sweden", 
      "name": "Zhang, Haiyan"
    }, 
    {
      "@type": "Person", 
      "affiliation": "Karolinska Inst, KI Alzheimer Dis Res Ctr, SE-14186 Huddinge, Sweden", 
      "name": "Bereczki, Erika"
    }, 
    {
      "@type": "Person", 
      "affiliation": "TUBITAK, Marmara Res Ctr, Genet Engn & Biotechnol Inst, TR-41470 Gebze, Turkey", 
      "name": "Serhatli, Muge"
    }, 
    {
      "@type": "Person", 
      "affiliation": "TUBITAK, Marmara Res Ctr, Genet Engn & Biotechnol Inst, TR-41470 Gebze, Turkey", 
      "name": "Baykal, Betul"
    }, 
    {
      "@type": "Person", 
      "affiliation": "TUBITAK, Marmara Res Ctr, Genet Engn & Biotechnol Inst, TR-41470 Gebze, Turkey", 
      "name": "Acioglu, Cigdem"
    }, 
    {
      "@type": "Person", 
      "affiliation": "Karolinska Inst, KI Alzheimer Dis Res Ctr, SE-14186 Huddinge, Sweden", 
      "name": "Wang, Shan"
    }, 
    {
      "@type": "Person", 
      "affiliation": "Karolinska Inst, KI Alzheimer Dis Res Ctr, SE-14186 Huddinge, Sweden", 
      "name": "Ioja, Eniko"
    }, 
    {
      "@type": "Person", 
      "affiliation": "Henan Univ, Sch Med, Inst Immunol, Henan Prov Key Med Lab Cellular & Mol Immunol, Kaifeng 475004, Henan, Peoples R China", 
      "name": "Ji, Xinying"
    }, 
    {
      "@type": "Person", 
      "affiliation": "Karolinska Inst, KI Alzheimer Dis Res Ctr, SE-14186 Huddinge, Sweden", 
      "name": "Zhang, Yan"
    }, 
    {
      "@type": "Person", 
      "name": "Guan, Zhizhong"
    }, 
    {
      "@type": "Person", 
      "affiliation": "Karolinska Inst, KI Alzheimer Dis Res Ctr, SE-14186 Huddinge, Sweden", 
      "name": "Winblad, Bengt"
    }, 
    {
      "@type": "Person", 
      "affiliation": "Karolinska Inst, KI Alzheimer Dis Res Ctr, SE-14186 Huddinge, Sweden", 
      "name": "Pei, Jin-Jing"
    }
  ], 
  "datePublished": "2014-01-01", 
  "description": "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.", 
  "headline": "mTor Is a Signaling Hub in Cell Survival: A Mass-Spectrometry-Based Proteomics Investigation", 
  "identifier": 99259, 
  "image": "https://aperta.ulakbim.gov.tr/static/img/logo/aperta_logo_with_icon.svg", 
  "license": "http://www.opendefinition.org/licenses/cc-by", 
  "name": "mTor Is a Signaling Hub in Cell Survival: A Mass-Spectrometry-Based Proteomics Investigation", 
  "url": "https://aperta.ulakbim.gov.tr/record/99259"
}