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Role of PARP‐14 in B cell survival signaling
Author(s) -
Cho Sung Hoon,
Goenka Shreevrat,
Gudapati Prathyusha,
Henttinen Tiina,
Reinikainen Arja,
Lahesmaa Riitta,
Boothby Mark
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.662.16
Subject(s) - poly adp ribose polymerase , biology , dna repair , nad+ kinase , transcription factor , microbiology and biotechnology , dna damage , apoptosis , gene expression , gene , cancer research , polymerase , dna , enzyme , biochemistry
Poly‐(ADP‐Ribose) Polymerases (PARPs) catalyze formation of branched ADP‐ribose polymers by transfer of ADP‐ribose residues from NAD+ to target protein. PARPs are involved in a wide range of biological processes including inflammation, regulation of gene expression, and DNA damage repair. Although there are 17 PARP superfamily members, very little is known about their function except that of PARP‐1. PARP‐14, a member of macrodomain‐containing PARP subfamily, is highly expressed in lymphoid organs and interacts with the IL‐4‐activated transcription factor Stat6. To elucidate physiological functions of PARP‐14, we have generated and analyzed PARP‐14 deficient mice. IL‐4 was unable to enhance the proliferation of anti‐IgM‐stimulated PARP‐14 KO B cells, and the Ag‐specific IgA response was reduced in mice lacking this enzyme. In addition, PARP‐14 mediates IL‐4‐induced protection against apoptosis following irradiation or growth factor withdrawal, and regulates IL‐4 effect on the levels of gene products related to cell survival. Collectively, the results establish that PARP‐14 plays a crucial role in IL‐4 regulation of gene expression and lymphocyte functions.