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PARP activation promotes nuclear AID accumulation in lymphoma cells.
Oncotarget 7, 13197-13208 (2016)
Activation-induced cytidine deaminase (AID) initiates immunoglobulin diversification in germinal center B cells by targeted introduction of DNA damage. As aberrant nuclear AID action contributes to the generation of B cell lymphoma, the protein's activity is tightly regulated, e.g. by nuclear/cytoplasmic shuttling and nuclear degradation. In the present study, we asked whether DNA damage may affect regulation of the AID protein. We show that exogenous DNA damage that mainly activates base excision repair leads to prevention of proteasomal degradation of AID and hence its nuclear accumulation. Inhibitor as well as knockout studies indicate that activation of poly (ADP-ribose) polymerase (PARP) by DNA damaging agents promotes both phenomena. These findings suggest that PARP inhibitors influence DNA damage dependent AID regulation, with interesting implications for the regulation of AID function and chemotherapy of lymphoma.
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Publikationstyp
Artikel: Journalartikel
Dokumenttyp
Wissenschaftlicher Artikel
Schlagwörter
Dna Damage ; Activation-induced Cytidine Deaminase ; Lymphoma ; Poly (adp-ribose) Polymerase ; Protein Stability; Induced Cytidine Deaminase; Class-switch Recombination; Dna-damage Response; Protein-kinase-a; Somatic Hypermutation; Homologous Recombination; Genomic Uracil; B-cells; Phosphorylation; Mechanisms
ISSN (print) / ISBN
1949-2553
e-ISSN
1949-2553
Zeitschrift
OncoTarget
Quellenangaben
Band: 7,
Heft: 11,
Seiten: 13197-13208
Verlag
Impact Journals LLC
Nichtpatentliteratur
Publikationen
Begutachtungsstatus
Peer reviewed