1 Ocak 2021 Dergi makalesi Açık Erişim

Gundogdu, Ramazan; Erdogan, M. Kadir; Ditsiou, Angeliki; Spanswick, Victoria; Garcia-Gomez, Juan Jose; Hartley, John A.; Esashi, Fumiko; Hergovich, Alexander; Gomez, Valenti

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{
  "@context": "https://schema.org/", 
  "@id": 232808, 
  "@type": "ScholarlyArticle", 
  "creator": [
    {
      "@type": "Person", 
      "name": "Gundogdu, Ramazan"
    }, 
    {
      "@type": "Person", 
      "affiliation": "Bingol Univ, Dept Biol, TR-12000 Bingol, Turkey", 
      "name": "Erdogan, M. Kadir"
    }, 
    {
      "@type": "Person", 
      "name": "Ditsiou, Angeliki"
    }, 
    {
      "@type": "Person", 
      "affiliation": "UCL, UCL Canc Inst, London WC1E 6DD, England", 
      "name": "Spanswick, Victoria"
    }, 
    {
      "@type": "Person", 
      "affiliation": "UCL, UCL Canc Inst, London WC1E 6DD, England", 
      "name": "Garcia-Gomez, Juan Jose"
    }, 
    {
      "@type": "Person", 
      "affiliation": "UCL, UCL Canc Inst, London WC1E 6DD, England", 
      "name": "Hartley, John A."
    }, 
    {
      "@type": "Person", 
      "affiliation": "Univ Oxford, Sir William Dunn Sch Pathol, Oxford OX1 3RE, England", 
      "name": "Esashi, Fumiko"
    }, 
    {
      "@type": "Person", 
      "name": "Hergovich, Alexander"
    }, 
    {
      "@type": "Person", 
      "name": "Gomez, Valenti"
    }
  ], 
  "datePublished": "2021-01-01", 
  "description": "Monopolar spindle-one binder (MOBs) proteins are evolutionarily conserved and contribute to various cellular signalling pathways. Recently, we reported that hMOB2 functions in preventing the accumulation of endogenous DNA damage and a subsequent p53/p21-dependent G1/S cell cycle arrest in untransformed cells. However, the question of how hMOB2 protects cells from endogenous DNA damage accumulation remained enigmatic. Here, we uncover hMOB2 as a regulator of double-strand break (DSB) repair by homologous recombination (HR). hMOB2 supports the phosphorylation and accumulation of the RAD51 recombinase on resected single-strand DNA (ssDNA) overhangs. Physiologically, hMOB2 expression supports cancer cell survival in response to DSBinducing anti-cancer compounds. Specifically, loss of hMOB2 renders ovarian and other cancer cells more vulnerable to FDA-approved PARP inhibitors. Reduced MOB2 expression correlates with increased overall survival in patients suffering from ovarian carcinoma. Taken together, our findings suggest that hMOB2 expression may serve as a candidate stratification biomarker of patients for HR-deficiency targeted cancer therapies, such as PARP inhibitor treatments.", 
  "headline": "hMOB2 deficiency impairs homologous recombination-mediated DNA repair and sensitises cancer cells to PARP inhibitors", 
  "identifier": 232808, 
  "image": "https://aperta.ulakbim.gov.tr/static/img/logo/aperta_logo_with_icon.svg", 
  "license": "http://www.opendefinition.org/licenses/cc-by", 
  "name": "hMOB2 deficiency impairs homologous recombination-mediated DNA repair and sensitises cancer cells to PARP inhibitors", 
  "url": "https://aperta.ulakbim.gov.tr/record/232808"
}