◀ Back to RELA

PARP1 — RELA

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: PARP1 — RELA (direct interaction, pull down) Hassa et al., J Biol Chem 2001*
• IRef Biogrid Interaction: PARP1 — RELA (physical association, affinity chromatography technology) Hassa et al., J Biol Chem 2001*
• IRef Biogrid Interaction: PARP1 — RELA (direct interaction, pull down) Hassa et al., J Biol Chem 2005
• IRef Biogrid Interaction: PARP1 — RELA (physical association, affinity chromatography technology) Hassa et al., J Mol Biol 2008*
• IRef Hprd Interaction: PARP1 — RELA (in vitro) Hassa et al., J Biol Chem 2001*
• IRef Hprd Interaction: PARP1 — RELA (in vivo) Hassa et al., J Biol Chem 2001*
• IRef Intact Interaction: PARP1 — RELA (physical association, tandem affinity purification) Bouwmeester et al., Nat Cell Biol 2004
• IRef Ophid Interaction: PARP1 — RELA (aggregation, interologs mapping) Brown et al., Bioinformatics 2005

Text-mined interactions from Literome

Payne et al., Cell Death Differ 1998 : The pre-treatment of cells with specific inhibitors of these proteins [ pyrrolidine dithiocarbamate ( NF-kappaB inhibitor ) and 3-aminobenzamide ( PARP inhibitor ) ] sensitizes cells to the induction of apoptosis by NaDOC, indicating that these stress response pathways are protective in nature
Hassa et al., Biol Chem 1999 : Here we show that poly ( ADP ribose ) polymerase ( PARP ) is required for specific NF-kappaB transcriptional activation in vivo
Kameoka et al., Biochem J 2000 (Leukemia L1210) : Taken together, these results strongly suggest that PARP is involved in the regulation of NF-kappaB through the protein modification
Chang et al., J Biol Chem 2001 : Here, we report the molecular mechanism by which PARP-1 activates the sequence-specific binding of NF-kappaB to its oligodeoxynucleotide
Ibuki et al., Biochim Biophys Acta 2003 : We concluded that ( 1 ) the increase in NO production was due to direct DNA damage by gamma-irradiation, and that ( 2 ) PARP activation through DNA damage induced NF-kappaB activation, leading to iNOS expression and NO production
Chiarugi et al., J Neurochem 2003 (Neurodegenerative Diseases) : Our findings build on prior published reports in PARP-1 null mice and highlight the importance of PARP-1 enzymatic activity in transcriptional control during glial activation, identifying PARP-1 activity dependent regulation of NF-kappaB as a novel pharmacological target for therapeutic intervention in the treatment of acute and chronic neurodegenerative disorders
Hassa et al., J Biol Chem 2003 : Furthermore, PARP-1 interacted directly with p300 and enhanced the interaction of NF-kappaB1/p50 to p300 ... Furthermore, PARP-1 interacted directly with p300 and enhanced the interaction of NF-kappaB1/p50 to p300
Nakajima et al., J Biol Chem 2004 (Inflammation) : Electrophoretic mobility shift assay revealed that PARP-1 inhibitors and the antisense RNA for PARP-1 mRNA reduced the LPS induced DNA binding of NF-kappaB ... Non modified PARP-1 also reduced the DNA binding of NF-kappaB via its physical association with NF-kappaB, whereas AM-PARP had no effect
Virág et al., Curr Vasc Pharmacol 2005 (Necrosis) : Besides serving as a cytotoxic mediator, PARP-1 is also involved in transcriptional regulation, most notably in the NF kappaB and AP-1 driven expression of inflammatory mediators ... Besides serving as a cytotoxic mediator, PARP-1 is also involved in transcriptional regulation, most notably in the NF kappaB and AP-1 driven expression of inflammatory mediators
Koh et al., Toxicology 2005 (Brain Ischemia...) : Therefore, the PARP inhibitor reduces the expression of MMP-9 and NF-kappaB and the infiltration of neutrophils in ischemic stroke ... We investigated the effect of poly ( ADP-ribose ) polymerase ( PARP ) inhibitor on the levels of plasma and brain matrix metalloproteinase-9 (MMP-9) and the expression of nuclear factor kappa B (NF-kappaB) during experimental focal cerebral ischemia
Takahashi et al., Genes Cells 2005 (Pancreatic Neoplasms) : We found that both NF-kappaB activation and Bcl-2 family proteins could prevent the 53BP2S mediated depression of mitochondrial transmembrane potential, activation of caspase-9, cleavage of poly ADP ribose polymerase ( PARP ) , and cell death
Martin-Oliva et al., Cancer Res 2006 (Cell Transformation, Neoplastic...) : Inhibition of PARP also affected activator protein-1 (AP-1) activation but not nuclear factor-kappaB (NF-kappaB)
Amiri et al., Oncogene 2006 (Melanoma) : In its inactive state, PARP-1 binds to the CXCL1 promoter in a sequence-specific manner and prevents binding of NF-kappaB ( p65/p50 ) to its element
Szabó et al., Diabetes 2006 (Body Weight...) : PARP blockade by INO-1001 and PJ-34 prevented hyperglycemia induced nuclear factor-kappaB (NFkappaB) activation of podocytes, and it was made evident by the inhibitor of kappaBalpha phosphorylation and NFkappaB p50 nuclear translocation
García et al., Ann Rheum Dis 2008 (Arthritis, Rheumatoid) : PARP inhibition reduced TNF induced JNK phosphorylation and AP-1 and NF kappaB binding activities were partially impaired by treatment with PARP inhibitors or by PARP-1 knockdown
El Kihel et al., Bioorg Med Chem 2008 (Colonic Neoplasms...) : This activity was associated with Mcl-1 and PARP-1 cleavage, inhibition of NFkappaB signaling, and DNA fragmentation, demonstrating an apoptotic cell death signaling pathway
Pacurari et al., Environ Health Perspect 2008 (Neoplasms, Mesothelial) : In the present study, we exposed mesothelial cells to SWCNTs and investigated reactive oxygen species ( ROS ) generation, cell viability, DNA damage, histone H2AX phosphorylation, activation of poly(ADP-ribose) polymerase 1 ( PARP-1 ), stimulation of extracellular signal regulated kinase ( ERKs ), Jun N-terminal kinases (JNKs), protein p38, and activation of activator protein-1 (AP-1), nuclear factor kappaB (NF-kappaB) , and protein serine-threonine kinase ( Akt )
Madinier et al., PloS one 2009 (Brain Infarction...) : Indeed, PARP-1 contributes to the activation of the transcription factor NF-kB , which is essential to the upregulation of proinflammatory genes, in particular responsible for microglial activation/proliferation
Zerfaoui et al., J Immunol 2010 : However, the mechanism by which PARP-1 affects NF-kappaB activation has been elusive ... In this study, we show that PARP-1 inhibition by gene knockout, knockdown, or pharmacologic blockade prevented p65 NF-kappaB nuclear translocation in smooth muscle cells upon TLR4 stimulation, NF-kappaB DNA binding activity, and subsequent inducible NO synthase and ICAM-1 expression ... PARP-1 was dispensable for LPS induced IkappaBalpha phosphorylation and subsequent degradation but was required for p65 NF-kappaB phosphorylation ... Pharmacologic inhibition of PARP-1 increased p65 NF-kappaB-Crm1 interaction in LPS treated smooth muscle cells
Teo et al., Nat Cell Biol 2010 : NF-kappaB is induced by ectopic expression of Rap1 , whereas its activity is inhibited by Rap1 depletion ... Furthermore, levels of Rap1 are positively regulated by NF-kappaB , and human breast cancers with NF-kappaB hyperactivity show elevated levels of cytoplasmic Rap1
Shaposhnikov et al., Adv Gerontol 2011 (Inflammation) : No synergic effect between conditionally activated PARP-1 expression and NF-kB inhibition is observed