Collaborator of Stat6 (CoaSt6)-associated Poly(ADP-ribose) Polymerase Activity Modulates Stat6-dependent Gene Transcription

Goenka, Shreevrat; Cho, Sung Hoon; Boothby, Mark

doi:10.1074/jbc.m611283200

Cited by 83 publications

(110 citation statements)

References 39 publications

(71 reference statements)

Supporting

Mentioning

105

Contrasting

Order By: Relevance

“…Substrates could also include the transcription factors that RCD1 and SRO1 bind to, histones, transcriptional coactivators, and/or chromatin-remodeling factors. Examples of such activity by PARPs in other systems are abundant in the literature (Goenka et al, 2007;Krishnakumar et al, 2008;Sala et al, 2008). Given the pleiotropic nature of the rcd1-3; sro1-1 mutant phenotype, it is likely that the RCD1 and SRO1 proteins have multiple targets that vary both temporally and spatially.…”

Section: Genotypementioning

confidence: 99%

The Paralogous GenesRADICAL-INDUCED CELL DEATH1andSIMILAR TO RCD ONE1Have Partially Redundant Functions during Arabidopsis Development

2009

View full text Add to dashboard Cite

RADICAL-INDUCED CELL DEATH1 (RCD1) and SIMILAR TO RCD ONE1 (SRO1) are the only two proteins encoded in the Arabidopsis (Arabidopsis thaliana) genome containing both a putative poly(ADP-ribose) polymerase catalytic domain and a WWE protein-protein interaction domain, although similar proteins have been found in other eukaryotes. Poly(ADP-ribose) polymerases mediate the attachment of ADP-ribose units from donor NAD + molecules to target proteins and have been implicated in a number of processes, including DNA repair, apoptosis, transcription, and chromatin remodeling. We have isolated mutants in both RCD1 and SRO1, rcd1-3 and sro1-1, respectively. rcd1-3 plants display phenotypic defects as reported for previously isolated alleles, most notably reduced stature. In addition, rcd1-3 mutants display a number of additional developmental defects in root architecture and maintenance of reproductive development. While single mutant sro1-1 plants are relatively normal, loss of a single dose of SRO1 in the rcd1-3 background increases the severity of several developmental defects, implying that these genes do share some functions. However, rcd1-3 and sro1-1 mutants behave differently in several developmental events and abiotic stress responses, suggesting that they also have distinct functions. Remarkably, rcd1-3; sro1-1 double mutants display severe defects in embryogenesis and postembryonic development. This study shows that RCD1 and SRO1 are at least partially redundant and that they are essential genes for plant development.

show abstract

Section: Genotypementioning

confidence: 99%

The Paralogous GenesRADICAL-INDUCED CELL DEATH1andSIMILAR TO RCD ONE1Have Partially Redundant Functions during Arabidopsis Development

2009

View full text Add to dashboard Cite

show abstract

“…Along with the three tandem ÒmacroÓ domains, PARP14 contains a WWE domain and a catalytic PARP domain at the C-terminal. 38, 48 The WWE domain is predicted to mediate protein-protein interactions in ubiquitination and ADP-ribose conjugation systems. 49 Indeed, it has been shown that PARP14 associates with Stat6 and phosphoglucose isomerase through its C-terminus.…”

Section: Discussionmentioning

confidence: 99%

Poly(ADP-ribose) polymerase family member 14 (PARP14) is a novel effector of the JNK2-dependent pro-survival signal in multiple myeloma

et al. 2012

View full text Add to dashboard Cite

Regulation of cell survival is a key part of the pathogenesis of multiple myeloma (MM). JNK signaling has been implicated in MM pathogenesis, but its function is unclear. To elucidate the role of JNK in MM, we evaluated the specific functions of the two major JNK proteins, JNK1 and JNK2. We show here that JNK2 is constitutively activated in a panel of MM cell lines and primary tumors. Using loss-of-function studies, we demonstrate that JNK2 is required for the survival of myeloma cells and constitutively suppresses JNK1-mediated apoptosis by affecting expression of poly(ADP-ribose) polymerase (PARP)14, a key regulator of B-cell survival.Strikingly, we found that PARP14 is highly expressed in myeloma plasma cells and associated with disease progression and poor survival. Overexpression of PARP14 completely rescued myeloma cells from apoptosis induced by JNK2 knockdown, indicating that PARP14 is critically involved in JNK2-dependent survival. Mechanistically, PARP14 was found to promote the survival of myeloma cells by binding and inhibiting JNK1. Moreover, inhibition of PARP14 enhances the sensitization of MM cells to anti-myeloma agents. Our findings reveal a novel regulatory pathway in myeloma cells through which JNK2 signals cell survival via PARP14, and identify PARP14 as a potential therapeutic target in myeloma.

show abstract

“…PARP14 is too large for efficient retrovirion generation, but the middle (three tandem "macrodomains") and C-terminal (catalytic ADP ribosyltransferase) portions (PARP14-MC) sufficed for its transcriptional function (13,14). Bone marrow cells lacking PARP14 were transduced with PARP14-MC cDNA or empty vector ("MiT"), and then used to reconstitute recipients ( S4B).…”

Section: Parp14mentioning

confidence: 99%

“…This partner of Stat6 encodes an ADP ribosyltransferase whose activity can participate in amplifying Stat6-mediated promoter induction (13)(14)(15). Mice lacking this protein, renamed PARP14 (13), contained normal numbers of B and T lymphocytes, but the proliferative response of anti-IgM-stimulated PARP14-null B cells to IL-4 was decreased, as was the induction of two genes that encode prosurvival proteins (15).…”

mentioning

confidence: 99%

Glycolytic rate and lymphomagenesis depend on PARP14, an ADP ribosyltransferase of the B aggressive lymphoma (BAL) family

Cho¹,

Ahn²,

Bhargava

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

128

View full text Add to dashboard Cite

Poly(ADP-ribose)polymerase (PARP)14-a member of the B aggressive lymphoma (BAL) family of macrodomain-containing PARPs-is an ADP ribosyltransferase that interacts with Stat6, enhances induction of certain genes by IL-4, and is expressed in B lymphocytes. We now show that IL-4 enhancement of glycolysis in B cells requires PARP14 and that this process is central to a role of PARP14 in IL-4-induced survival. Thus, enhancements of AMP-activated protein kinase activity restored both IL-4-induced glycolytic activity in Parp14 −/− B cells and prosurvival signaling by this cytokine. Suppression of apoptosis is central to B-lymphoid oncogenesis, and elevated macro-PARP expression has been correlated with lymphoma aggressiveness. Strikingly, PARP14 deficiency delayed B lymphomagenesis and reversed the block to B-cell maturation driven by the Myc oncogene. Collectively, these findings reveal links between a mammalian ADP ribosyltransferase, cytokine-regulated metabolic activity, and apoptosis; show that PARP14 influences Myc-induced oncogenesis; and suggest that the PARP14-dependent capacity to increase cellular metabolic rates may be an important determinant of lymphoma pathobiology.

show abstract

Collaborator of Stat6 (CoaSt6)-associated Poly(ADP-ribose) Polymerase Activity Modulates Stat6-dependent Gene Transcription

Cited by 83 publications

References 39 publications

The Paralogous GenesRADICAL-INDUCED CELL DEATH1andSIMILAR TO RCD ONE1Have Partially Redundant Functions during Arabidopsis Development

The Paralogous GenesRADICAL-INDUCED CELL DEATH1andSIMILAR TO RCD ONE1Have Partially Redundant Functions during Arabidopsis Development

Poly(ADP-ribose) polymerase family member 14 (PARP14) is a novel effector of the JNK2-dependent pro-survival signal in multiple myeloma

Glycolytic rate and lymphomagenesis depend on PARP14, an ADP ribosyltransferase of the B aggressive lymphoma (BAL) family

Contact Info

Product

Resources

About