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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  <identifier identifierType="URL">https://aperta.ulakbim.gov.tr/record/232808</identifier>
  <creators>
    <creator>
      <creatorName>Gundogdu, Ramazan</creatorName>
      <givenName>Ramazan</givenName>
      <familyName>Gundogdu</familyName>
    </creator>
    <creator>
      <creatorName>Erdogan, M. Kadir</creatorName>
      <givenName>M. Kadir</givenName>
      <familyName>Erdogan</familyName>
      <affiliation>Bingol Univ, Dept Biol, TR-12000 Bingol, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Ditsiou, Angeliki</creatorName>
      <givenName>Angeliki</givenName>
      <familyName>Ditsiou</familyName>
    </creator>
    <creator>
      <creatorName>Spanswick, Victoria</creatorName>
      <givenName>Victoria</givenName>
      <familyName>Spanswick</familyName>
      <affiliation>UCL, UCL Canc Inst, London WC1E 6DD, England</affiliation>
    </creator>
    <creator>
      <creatorName>Garcia-Gomez, Juan Jose</creatorName>
      <givenName>Juan Jose</givenName>
      <familyName>Garcia-Gomez</familyName>
      <affiliation>UCL, UCL Canc Inst, London WC1E 6DD, England</affiliation>
    </creator>
    <creator>
      <creatorName>Hartley, John A.</creatorName>
      <givenName>John A.</givenName>
      <familyName>Hartley</familyName>
      <affiliation>UCL, UCL Canc Inst, London WC1E 6DD, England</affiliation>
    </creator>
    <creator>
      <creatorName>Esashi, Fumiko</creatorName>
      <givenName>Fumiko</givenName>
      <familyName>Esashi</familyName>
      <affiliation>Univ Oxford, Sir William Dunn Sch Pathol, Oxford OX1 3RE, England</affiliation>
    </creator>
    <creator>
      <creatorName>Hergovich, Alexander</creatorName>
      <givenName>Alexander</givenName>
      <familyName>Hergovich</familyName>
    </creator>
    <creator>
      <creatorName>Gomez, Valenti</creatorName>
      <givenName>Valenti</givenName>
      <familyName>Gomez</familyName>
    </creator>
  </creators>
  <titles>
    <title>Hmob2 Deficiency Impairs Homologous Recombination-Mediated Dna Repair And Sensitises Cancer Cells To Parp Inhibitors</title>
  </titles>
  <publisher>Aperta</publisher>
  <publicationYear>2021</publicationYear>
  <dates>
    <date dateType="Issued">2021-01-01</date>
  </dates>
  <resourceType resourceTypeGeneral="Text">Journal article</resourceType>
  <alternateIdentifiers>
    <alternateIdentifier alternateIdentifierType="url">https://aperta.ulakbim.gov.tr/record/232808</alternateIdentifier>
  </alternateIdentifiers>
  <relatedIdentifiers>
    <relatedIdentifier relatedIdentifierType="DOI" relationType="IsIdenticalTo">10.1016/j.cellsig.2021.110106</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">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.</description>
  </descriptions>
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