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PARP1 is acting as a coactivator of HIF-1alpha-dependent gene expression in B cells, and this co-activation is enhanced by LMP1-mediated activation of PARP1.
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Interaction among susceptibility genotypes of PARP1 SNPs in thyroid carcinoma.
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Here, the show that PARP1 association with DNA is diffusion-limited, and release of PARP1 from DNA is promoted by binding of an additional DNA molecule that facilitates a 'monkey bar' mechanism, also known as intersegment transfer.
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miR-31-5p prevents the nuclear location of PARP1 detected by immunofluorescence, histological analysis and Western blotting analysis.
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inhibition of poly(ADP-ribose) polymerase (PARP) increases the speed of fork elongation and does not cause fork stalling, which is in contrast to the accepted model in which inhibitors of PARP induce fork stalling and collapse(3); findings contribute to a better understanding of the mechanism of fork speed control, with implications for genomic (in)stability and rational cancer treatment
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genomic ribonucleotides are a hitherto unappreciated source of PARP-trapping DNA lesions, and that the frequent deletion of RNASEH2B in metastatic prostate cancer and chronic lymphocytic leukaemia could provide an opportunity to exploit these findings therapeutically.
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elevated expression of PARP-1 mRNA and miR-223, with a reduction of PARP-1 protein level and enzyme activity in colonic tissue of pediatric patients with Crohn's disease
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miR-7-5p reduced energy consumption via inhibiting PARP-1 expression, and miR-7-5p increased energy generation by suppressing the expression of Bcl-2.
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Study finds that PARP1 mutations caused a distinct set of drug sensitivities when compared to other known forms of PARPi resistance (loss of REV7 (MAD2L2) or TP53BP1, or BRCA1 reversion mutants), suggesting that knowledge of the molecular mechanism of resistance in individual patients could inform decisions on further treatment.
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Results suggest that RNF168 acts as a counterpart of PARP1 in DDR and regulates the HR/NHEJ repair processes through the ubiquitination of PARP1.
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two-step mechanism activates and then stabilizes PARP-1 on a DNA break, indicating that PARP-1 allostery influences persistence on DNA damage, with important implications for PARP inhibitors that engage the NAD(+) binding site
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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.
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Cell proliferation determines PARP1 transcription and production of electrophiles. PARP1 contributes to cell protection against electrophiles. PARP1 controls transcription of redox-sensitive kinases, antioxidants and detoxifying enzymes. [review]
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interactive domains between Ets-1 and PARP-1 have been mapped to the C-terminal region of Ets-1 and the BRCA1 carboxy-terminal (BRCT) domain of PARP-1
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depletion of NOX1 and NOX4 partially rescued the growth inhibition of PARP1-deficient tumor xenografts. Our findings suggest that in addition to compromising the repair of DNA damage, PARP inhibition or depletion may exert extra antitumor effect by elevating oxidative stress in ovarian cancer cells
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CDK4/6 inhibitors also lead to accumulation of DNA damage by repressing PARP1 in oxidatively stressed cells. Thus, CDK4/6 inhibitors sensitize G1-arrested cells to anticancer drugs, since these cells require PARP1-OGG1 functional interaction for cell survival
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Low PARP expression is associated with mouth Cancer.
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The dysfunction of PARP1 in esophageal epithelial cells increases the levels of ROS and oxidative DNA damage in Barrett's esophagus.
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results suggest that PARP-1 overexpression may define an important risk factor in non-M3 AML patients and PARP-1 is a potential therapeutic target for AML treatment
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polymorphism of PARP-1 gene is more likely responsible for development of GD in Chinese individuals
