Browse our anti-PARP1 (PARP1) Antibodies

Human Poly (ADP-Ribose) Polymerase 1 (PARP1) interaction partners

1. Studied increased sensitivity to alkylating antineoplastic agents thru down-regulation of poly(ADP-ribose) polymerase 1 (PARP1) by miR-891b in a human breast cancer cell line. Found MiR-891b increases sensitivity of breast cancer cell line to N-methyl-N-nitro-N-nitrosoguanidine by suppressing PARP1 expression.

2. We show that prior to heat shock, the HSF1-PARP13-PARP1 complex binds to the HSP70 promoter. In response to heat shock, activated and auto-PARylated PARP1 dissociates from HSF1-PARP13 and is redistributed throughout the HSP70 locus.

3. MM express elevated MALAT1 and involve in alternative non-homozygous end joining (A-NHEJ) pathway by binding to PARP1 and LIG3, two key components of the A-NHEJ protein complex.

4. These data first uncovered potentially pathogenic miR-379-5p and two novel targets PARP1 and XRCC6 in biochemical premature ovarian insufficiency.

5. macroH2A1.1 mediates an isoform-specific effect through its ability to suppress PARP1 activity. Second, the unstructured linker region exerts an additional repressive effect that is common to all macroH2A proteins. In the absence of DNA damage, the macroH2A linker is also sufficient for rescuing heterochromatin architecture in cells deficient for macroH2A

6. Increased BRCA1 mRNA expression (but not PARP1 mRNA) occurs early in the development of breast cancer. Ductal carcinoma in situ and normal breast tissue share highly similar BRCA1 and PARP1 expression level.

7. PARP-1 may serve not only as a biomarker at initial biopsies for a disease that may become aggressive but also as a new therapeutic target of advanced mycosis fungoides and Sezary syndrome

8. Authors developed a functional ex-vivo approach to detect repair switch to an alternative end-joining pathway, PARP1-EJ, and cancer cell-specific effects in fresh specimens from prostate cancer patients. One-third of tumor samples exhibited a switch to PARP1-EJ, while normal prostate tissues from the same patients showed no repair switch.

9. Niraparib (MK-4827), a novel poly(ADP-Ribose) polymerase inhibitor, radiosensitizes human lung and breast cancer cells.

10. Polymorphism in PARP-1 rs2271347 was significantly associated with increased ischemic stroke risk (additive model: OR: 1.74; 95% CI: 1.03-2.93; p = 0.037). Patients harboring the PARP-1 rs2271347 GA/AA genotype had a worse initial stroke (additive model: OR: 1.85; 95% CI: 1.10-3.11; p = 0.021). Our study suggests that genetic variant of rs2271347 may contribute to the etiology of ischemic stroke.

11. a model whereby PARP1 localizes to ssDNA breaks and recruits Cockayne syndrome protein B to participate in DNA repair.

12. PARP1 promotes Runx2 expression, and Runx2 deficiency offsets the pro-calcifying effects of PARP1. Activated PARP1 suppresses miRNA-204 expression via the IL-6/STAT3 pathway and thus relieves the repression of its target, Runx2, resulting in increased Runx2 protein.

13. DNA damage-induced PARP1 activation confers cardiomyocyte dysfunction through NAD(+) depletion in experimental atrial fibrillation.

14. The findings from our present study indicate that PARP-1 expression negatively impacts the prognosis of AML patients.

15. The role of PARP-1 in response to DNA damage is reviewed.

16. FBXL10-RNF68-RNF2 ubiquitin ligase complex (FRRUC) is rapidly and transiently recruited to sites of DNA damage in a PARP1- and TIMELESS-dependent manner to promote mono-ubiquitylation of H2A at Lys119.

17. PARP1 enzymatic activity did not significantly reverse the effect of TNF on the human PHEX gene expression.

18. Via interference with XRCC1/PARP1-mediated base excision repair.

19. These findings suggest that as a risk-associated lncRNA, FOXD3-AS1 inhibits the progression of NB through repressing PARP1-mediated CTCF activation.

20. The work demonstrated the vital connection of PARP-1 and autophagy in the activation of CFs, and provided solid evidence supporting PARP-1 inhibition as a feasible strategy for the treatment of post-MI heart failure.

Mouse (Murine) Poly (ADP-Ribose) Polymerase 1 (PARP1) interaction partners

1. DNA damage-induced PARP1 activation confers cardiomyocyte dysfunction through NAD(+) depletion in experimental atrial fibrillation.

2. PARP-1 played a critical role in hydrogen peroxide-mediated autophagy and both of them were involved in apoptosis of vascular smooth muscle cell.

3. The present results demonstrated that the lack of PARP1 enzyme only disturbed the microbial flora of the duodenum, where the biodiversity increased in the knockout animals on the species level but decreased on the order level.

4. PARP-1, via manipulating the binding of NF-kB/AP-1 at the MMP-9 promoter, regulates MMP-9 expression, which helps maintain mitochondrial homeostasis.

5. PARP1 interacts with HuR, resulting in its PARylation, primarily at site D226. PARP inhibition and the D226 mutation impair HuR's PARylation, nucleocytoplasmic shuttling and mRNA binding.

6. Peripheral T-cell number was not affected in single PARP1-deficient mice. Double-deficiency in PARP-1/PARP-2 in T-cells led to highly aggressive T-cell lymphomas.

7. The dysfunction of PARP1 in esophageal epithelial cells increases the levels of ROS and oxidative DNA damage in Barrett's esophagus.

8. pharmacological inhibition of PARP-1 reversed both particulate matter-induced Abeta increase and glial activation.

9. The functional consequence of Parp1 heterozygosity on BRCA2 loss is demonstrated by a significant increase in tumorigenesis in Brca2 knockout mice.

10. findings reveal PARP-1 as a double-edged sword in colorectal carcinogenesis, which suppresses tumor initiation following DNA alkylation in a MGMT-dependent manner, but promotes inflammation-driven tumor progression.

11. an immunoprecipitation assay indicated that hypoxia triggered activation of the binding activity of Sp1 to the promoters of PARP-1 and caspase-3, which is abrogated by miR-7a/b. In summary, these findings identified miR-7a/b as protectors of cardiac remodeling and hypoxia-induced injury in H9c2 cardiomyoblasts involving Sp1 and PARP-1.

12. PARP-1 mediated microgial responses can directly reduce blood brain barrier integrity by increasing endothelial cell permeability.

13. A stimulation induced PARP1 binding to phosphorylated Erk2 in the chromatin of cerebral neurons caused Erk-induced PARP1 activation, rendering transcription factors and promoters of immediate early genes (IEG) accessible to PARP1-bound phosphorylated Erk2.

14. The present work identifies several microglial responses to the endogenous alarmin S100B, including release of the cytotoxic protease MMP9 and shows that these effects are modulated by PARP-1.

15. flavonoids of Rosa roxburghii Tratt enhanced radioprotection at least partially by regulating PARP-1/AIF to reduce apoptosis.

16. These data demonstrate the presence of an FAF1-PARP1 axis that is involved in oxidative stress-induced necrosis and in the pathology of Parkinson's disease.

17. Data indicate that poly(ADP-ribose)polymerase 1 (PARP1) D993A/D993A mice and cells are viable and show no obvious abnormalities.

18. Telomere-internal double-strand breaks (DSBs) are also repaired by a PARP1- and Ligase3-dependent reaction, suggesting alternative non-homologous end-joining (alt-NHEJ), which relies on microhomology at DSBs.

19. post-translational modification facilitates the mobilization of SIRT6 to DNA damage sites and is required for efficient recruitment of poly (ADP-ribose) polymerase 1 (PARP1) to DNA break sites and for efficient repair of double-strand break.

20. Data show that Tp53- and Atm-defective Chronic lymphocytic leukemia (CLL) mimicking the high-risk form of human disease and that Atm-deficient CLL is sensitive to PARP1 inhibition.

Fruit Fly (Drosophila melanogaster) Poly (ADP-Ribose) Polymerase 1 (PARP1) interaction partners

1. 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.

2. A mutation of Parp also increases NAD+ levels; although, this was only observed in parkin mutant flies and not in the heterozygous Parp mutants, possibly owing to an increased PARP activity in the parkin mutants.

3. chromatin loosening and associated initiation of gene expression is activated by phosphorylation of H2Av in a nucleosome positioned in promoter regions of PARP-1-dependent genes

4. Based on these findings, we propose a model that explains how PARP1 activity impacts nucleolar functions and, consequently, ribosomal biogenesis

5. PARP is associated with the 5' end of Hsp70, and its enzymatic activity is rapidly induced by heat shock leading to nucleosome loss.

6. 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.

7. PARP1 is targeted to chromatin by association with the histone H2A variant (H2Av).

8. inhibits transcription by contributing to the condensation of chromatin, which creates a barrier against gene transcription

9. demonstrate that this alteration specifically excludes PARP1 protein from heterochromatin and makes PARP1 unable to maintain repression of retrotransposable elements.

10. PARP-e autoregulates Parp transcription

11. propose that chromosomal PARP molecules become activated by developmental or environmental cues and strip nearby chromatin proteins off DNA to generate a puff

12. PARP1 is required for protein targeting to Cajal body.

Cow (Bovine) Poly (ADP-Ribose) Polymerase 1 (PARP1) interaction partners

1. no difference was found in the level of SBDP145 between muscles, while SBDP120 and PARP-1 cleavage products were not detected

2. ADPRT Val762Ala and APE1 Asp148Glu polymorphisms are not associated with increased breast cancer risk

3. analysis of poly(ADP-ribose) polymerase 1 interaction with apurinic/apyrimidinic sites

4. FGF2 stimulates poly(ADP-ribose) polymerase activity by a DNA strand breaks-independent manner which involves a mitogen-activated protein kinases (MAPK)-dependent pathway

Pig (Porcine) Poly (ADP-Ribose) Polymerase 1 (PARP1) interaction partners

1. The transcript levels of autophagy-related genes and poly(ADP-ribose) polymerase 1 (PARP1), were transiently up-regulated by fertilization, decreased at the late 1-cell stage, and maintained until the blastocyst stage.

2. The PARP1 signaling pathway is involved in oocyte nest breakdown and primordial follicle formation in fetal and neonatal porcine ovaries, but is different from follicular atresia in adult porcine ovaries that involves cellular apoptosis.

3. Cleavage of PARP-1 by activated (cleaved) caspase-3 may serve a key role in controlling follicular atresia through granulosa cell degeneration.