RAD51D splice variants and cancer-associated mutations reveal XRCC2 interaction to be critical for homologous recombination

•Only RAD51D isoform 1 rescues HR-deficiency observed in RAD51D knock-out cell lines.•The RAD51D Walker A motif is important for its HR-function and interaction with XRCC2.•Phosphorylation near the Walker A motif is unlikely to regulate RAD51D function. The proficiency of cancer cells to repair DNA...

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Veröffentlicht in:	DNA repair Jg. 76; S. 99 - 107
Hauptverfasser:	Baldock, Robert A., Pressimone, Catherine A., Baird, Jared M., Khodakov, Anton, Luong, Thong T., Grundy, McKenzie K., Smith, Chelsea M., Karpenshif, Yoav, Bratton-Palmer, Dominique S., Prakash, Rohit, Jasin, Maria, Garcin, Edwige B., Gon, Stéphanie, Modesti, Mauro, Bernstein, Kara A.
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	Netherlands Elsevier B.V 01.04.2019 Elsevier
Schlagworte:	Cell Line, Tumor DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism Double-strand break repair Homologous Recombination Humans Life Sciences Mutation Protein Binding Protein Isoforms - genetics Protein Isoforms - metabolism Protein Processing, Post-Translational RAD51 paralogs RAD51D Walker A motif XRCC2 RAD51 paralogs RAD51D Double-strand break repair Walker A motif Homologous recombination XRCC2 Double-strand break repair, Homologous recombination, RAD51 paralogs, RAD51D, Walker A motif, XRCC2
ISSN:	1568-7864, 1568-7856, 1568-7856
Online-Zugang:	Volltext
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