{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Pfeifer M"],"funding":["National Institute for Health Research (NIHR)","Marie Curie"],"pagination":["3423-3433"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6545462"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["202(12)"],"pubmed_abstract":["Induction of programmed DNA damage and its recognition and repair are fundamental for B cell development. The ssDNA-binding protein SSB1 has been described in human cells as essential for the recognition and repair of DNA damage. To study its relevance for B cells, we recently developed <i>Ssb1</i> <sup>-/-</sup> and conditional <i>Ssb1</i> <sup>-/-</sup> mice. Although SSB1 loss did not affect B cell development, <i>Ssb1</i> <sup>-/-</sup> cells exhibited compensatory expression of its homolog SSB2. We have now generated <i>Ssb2</i> <sup>-/-</sup> mice and show in this study that SSB2 is also dispensable for B cell development and DNA damage response activation. In contrast to the single loss of <i>Ssb1</i> or <i>Ssb2</i>, however, combined SSB1/2 deficiency caused a defect in early B cel"],"journal":["Journal of immunology (Baltimore, Md. : 1950)"],"pubmed_title":["SSB1/SSB2 Proteins Safeguard B Cell Development by Protecting the Genomes of B Cell Precursors."],"pmcid":["PMC6545462"],"funding_grant_id":["NIHR-RP-011-053","P49318"],"pubmed_authors":["Robinson ME","Boulianne B","Lippert TP","Ho HN","Feldhahn N","Stebbing J","Pfeifer M","Brem R"],"additional_accession":[]},"is_claimable":false,"name":"SSB1/SSB2 Proteins Safeguard B Cell Development by Protecting the Genomes of B Cell Precursors.","description":"Induction of programmed DNA damage and its recognition and repair are fundamental for B cell development. The ssDNA-binding protein SSB1 has been described in human cells as essential for the recognition and repair of DNA damage. To study its relevance for B cells, we recently developed <i>Ssb1</i> <sup>-/-</sup> and conditional <i>Ssb1</i> <sup>-/-</sup> mice. Although SSB1 loss did not affect B cell development, <i>Ssb1</i> <sup>-/-</sup> cells exhibited compensatory expression of its homolog SSB2. We have now generated <i>Ssb2</i> <sup>-/-</sup> mice and show in this study that SSB2 is also dispensable for B cell development and DNA damage response activation. In contrast to the single loss of <i>Ssb1</i> or <i>Ssb2</i>, however, combined SSB1/2 deficiency caused a defect in early B cel","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Jun","modification":"2025-04-18T14:12:10.53Z","creation":"2019-07-24T07:08:11Z"},"accession":"S-EPMC6545462","cross_references":{"pubmed":["31085591"],"doi":["10.4049/jimmunol.1801618"]}}