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The results demonstrate that PARylation process in Drosophila is tightly regulated in the context of strands-breaks repair; PARP is essential during the maintenance of DNA integrity, but dispensable in the DNA repair process.
A mutation of Parp also increases NAD+ levels; although, this was only observed in parkin (显示 PARK2 ELISA试剂盒) mutant flies and not in the heterozygous Parp mutants, possibly owing to an increased PARP activity in the parkin (显示 PARK2 ELISA试剂盒) mutants.
chromatin loosening and associated initiation of gene expression is activated by phosphorylation of H2Av (显示 H2AFV ELISA试剂盒) in a nucleosome positioned in promoter regions of PARP-1-dependent genes
Based on these findings, we propose a model that explains how PARP1 activity impacts nucleolar functions and, consequently, ribosomal biogenesis
PARP is associated with the 5' end of Hsp70, and its enzymatic activity is rapidly induced by heat shock leading to nucleosome loss.
Activation of PARP-1 overexpression in the imago results in extension of the lifespan in females and males. The lifespan increase in females with PARP-1 conditional overexpression was accompanied by decrease of fertility.
PARP1 is targeted to chromatin by association with the histone H2A variant (H2Av).
demonstrate that this alteration specifically excludes PARP1 protein from heterochromatin and makes PARP1 unable to maintain repression of retrotransposable elements.
PARP-e autoregulates Parp transcription
propose that chromosomal PARP molecules become activated by developmental or environmental cues and strip nearby chromatin proteins off DNA to generate a puff
PARP1 recruits KLF4 (显示 KLF4 ELISA试剂盒) to activate telomerase expression and stem cell pluripotency, indicating a positive regulatory role of the PARP1-KLF4 (显示 KLF4 ELISA试剂盒) complex in telomerase expression in cancer and stem cells.
The results suggest that ATRX (显示 ATRX ELISA试剂盒) is required to limit replication stress during cellular proliferation, whereas upregulation of PARP-1 activity functions as a compensatory mechanism to protect stalled forks, limiting genomic damage, and facilitating late-born neuron production.
Epithelial-mesenchymal-transition integrated with mesenchymal PARP-1 expression, predicts prostate cancer radioresistance.
this work indicates that suppression of JNK1 (显示 MAPK8 ELISA试剂盒)/2 activity by MKP-1 (显示 DUSP1 ELISA试剂盒) maintains PARP-1 levels and suggests that MKP-1 (显示 DUSP1 ELISA试剂盒)-mediated cisplatin resistance can be bypassed by PARP-1 inhibition.
we report that AIF-independent PARP-1-dependent necrosis constitutes a major mechanism of RPE cell death leading to retinal degeneration in dry age-related macular degeneration .
Data show that poly(ADP-ribose) polymerase 1 (PARP1)-mediated senescence rescue was accompanied by transcriptional activation of the melanocyte-lineage survival oncogene (显示 RAB1A ELISA试剂盒) MITF (显示 MITF ELISA试剂盒), indicating a role for PARP1 in melanomagenesis.
PARP1 is activated in the non-alcoholic fatty liver of mice and patients.
This study reports the novel findings that HER2 (显示 ERBB2 ELISA试剂盒) increases PARP1 protein via suppression of the let-7a miRNA, which regulates the PARP1 3'-UTR (显示 UTS2R ELISA试剂盒). Moreover, HER2 (显示 ERBB2 ELISA试剂盒) status correlates with high PARP1 and low let-7a in breast cancer clinical specimens.
Results show that PARP1 mediates 14-3-3s regulation of non-homologous end joining repair.
Identification of PARP-1 as a unique regulator of Il12b (显示 IL12B ELISA试剂盒) transcription in response to inflammatory insults in an allele-differentiating manner
no difference was found in the level of SBDP145 between muscles, while SBDP120 and PARP-1 cleavage products were not detected
ADPRT Val762Ala and APE1 (显示 APEX1 ELISA试剂盒) Asp148Glu polymorphisms are not associated with increased breast cancer risk
analysis of poly(ADP-ribose) polymerase 1 interaction with apurinic/apyrimidinic sites
FGF2 (显示 FGF2 ELISA试剂盒) stimulates poly(ADP-ribose) polymerase activity by a DNA strand breaks-independent manner which involves a mitogen-activated protein kinases (MAPK (显示 MAPK1 ELISA试剂盒))-dependent pathway
Data show that Tp53 (显示 TP53 ELISA试剂盒)- and Atm (显示 ATM ELISA试剂盒)-defective Chronic lymphocytic leukemia (CLL) mimicking the high-risk form of human disease and that Atm (显示 ATM ELISA试剂盒)-deficient CLL is sensitive to PARP1 inhibition.
No increase of axonal regeneration was observed in Parp1(-/-) mice after optic nerve crush injury or dorsal hemisection of the thoracic spinal cord, and there was no improvement in motor function recovery. Comprehensive in vivo analysis reveals no indication that clinical PARP inhibitors will on their own provide benefit for recovery from central nervous system trauma.
MEIS2 (显示 MEIS2 ELISA试剂盒) associates with chromatin-bound PBX1 (显示 PBX1 ELISA试剂盒), recruits PARP1/ARTD1, and initiates PARP1-mediated eviction of H1 from the chromatin fiber.
Activation of either PARP-1 or -2 is likely to play a role in muscle protein catabolism via oxidative stress, NF-kappaB (显示 NFKB1 ELISA试剂盒) signaling, and enhanced proteasomal degradation in cancer-induced cachexia.
PARP-1 attenuates adipogenesis by PARylating C/EBPb (显示 CEBPB ELISA试剂盒), a pro-adipogenic transcription factor, on three residues in its regulatory domain.
The findings suggest that PARP1 inhibition protects against long-term ethanol-induced liver injury, as indicated by limited hepatocytes steatosis, apoptosis, inflammation levels, and neutrophil infiltration, mainly by limiting KC activation during the initiation of ALD.
PARP-1 knockout resulted in lowered arginase II (显示 ARG2 ELISA试剂盒) expression in macrophages and aortic endothelial cells.
PARP-1 stabilizes Sox2 (显示 SOX2 ELISA试剂盒) binding to nucleosomes at suboptimal sites through cooperative interactions on DNA to regulate Sox2 (显示 SOX2 ELISA试剂盒) pioneer activity at intractable genomic loci.
This gene encodes a chromatin-associated enzyme, poly(ADP-ribosyl)transferase, which modifies various nuclear proteins by poly(ADP-ribosyl)ation. The modification is dependent on DNA and is involved in the regulation of various important cellular processes such as differentiation, proliferation, and tumor transformation and also in the regulation of the molecular events involved in the recovery of cell from DNA damage. In addition, this enzyme may be the site of mutation in Fanconi anemia, and may participate in the pathophysiology of type I diabetes.
ADP-ribosyltransferase (NAD+; poly (ADP-ribose) polymerase)
, ADP-ribosyltransferase NAD(+)
, ADP-ribosyltransferase diphtheria toxin-like 1
, NAD(+) ADP-ribosyltransferase 1
, poly (ADP-ribose) polymerase family, member 1
, poly [ADP-ribose] polymerase 1
, poly(ADP-ribose) polymerase
, poly(ADP-ribose) synthetase
, poly[ADP-ribose] synthase 1
, ADP-ribosyltransferase (NAD+
, ADP-ribosyltransferase 1
, ADPRT 1
, poly (ADP-ribose) polymerase)
, poly(ADP-ribose) polymerase PARP-1
, poly[ADP-ribose] synthetase 1
, ADP-ribosyltransferase (NAD+, poly (ADP-ribose) polymerase) 1
, ADP-ribosyltransferase (NAD+; poly (ADP-ribose) polymerase) 1
, Poly(ADP ribose) polymerase 1
, Poly(ADP)-Ribose polymerase
, Poly(ADP-)Ribose polymerase
, Poly(ADP-ribose) polymerase
, Poly(ADP-ribose) polymerase 1
, ADP-ribosyltransferase (NAD+) poly (ADP-ribose) polymerase)
, Poly[ADP-ribose] synthase 1
, LOW QUALITY PROTEIN: poly [ADP-ribose] polymerase 1