| First Author | Cho SH | Year | 2009 |
| Journal | Blood | Volume | 113 |
| Issue | 11 | Pages | 2416-25 |
| PubMed ID | 19147789 | Mgi Jnum | J:146533 |
| Mgi Id | MGI:3837883 | Doi | 10.1182/blood-2008-03-144121 |
| Citation | Cho SH, et al. (2009) PARP-14, a member of the B aggressive lymphoma family, transduces survival signals in primary B cells. Blood 113(11):2416-25 |
| abstractText | Poly(ADP-ribos)ylation is one of the longest-known but most enigmatic posttranslational modifications transducing specific signals. The enzyme responsible for the majority of poly(ADP-ribose) polymerization in cells, PARP-1, promotes DNA repair but also mediates a caspase-independent form of apoptosis in response to stressors such as irradiation. However, the biologic function of most other PARPs is not known. Macro-PARPs constitute one branch of the large family of PARP-like proteins also designated as B aggressive lymphoma proteins (BAL1, 2a/2b, 3, or PARP-9, PARP-14, and PARP-15). To elucidate biologic role(s) of a BAL-family macro-PARP, we analyzed mice deficient in PARP-14, a binding partner of the IL-4-induced transcription factor Stat6. We show here that PARP-14 plays a fundamental role mediating protection against apoptosis in IL-4-treated B cells, including that after DNA damage, and mediates IL-4 effects on the levels of gene products that regulate cell survival, proliferation, and lymphomagenesis. Collectively, the results establish that PARP-14 mediates regulation of gene expression and lymphocyte physiology by IL-4 and has a function distinct from PARP-1. Furthermore, the findings suggest mechanisms by which BAL-family proteins might influence pathologic processes involving B lymphocytes. |
