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
<?xml version='1.0' encoding='utf-8'?> <resource xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns="http://datacite.org/schema/kernel-4" xsi:schemaLocation="http://datacite.org/schema/kernel-4 http://schema.datacite.org/meta/kernel-4.1/metadata.xsd"> <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> </resource>
Görüntülenme | 27 |
İndirme | 6 |
Veri hacmi | 1.7 kB |
Tekil görüntülenme | 24 |
Tekil indirme | 6 |