Ignet

Gene Information

Gene symbol: PARP1

Gene name: poly (ADP-ribose) polymerase 1

HGNC ID: 270

Synonyms: PARP

Related Genes

#	Gene Symbol	Number of hits
1	ACO2	1 hits
2	AIFM1	1 hits
3	AKR1B1	1 hits
4	AKT1	1 hits
5	ALB	1 hits
6	BAX	1 hits
7	BRCA1	1 hits
8	CASP3	1 hits
9	CAT	1 hits
10	CCND1	1 hits
11	CTGF	1 hits
12	EGFR	1 hits
13	EP300	1 hits
14	EXTL3	1 hits
15	GAPDH	1 hits
16	GORASP1	1 hits
17	GSTA1	1 hits
18	IFNG	1 hits
19	IL6	1 hits
20	INS	1 hits
21	ITGAL	1 hits
22	KLRG1	1 hits
23	MAPK14	1 hits
24	MAPK8	1 hits
25	NFKB1	1 hits
26	NOS2A	1 hits
27	NOTCH1	1 hits
28	NR1I2	1 hits
29	PARG	1 hits
30	PDX1	1 hits
31	PPARGC1A	1 hits
32	PTGS2	1 hits
33	SOD2	1 hits
34	TNF	1 hits
35	TP53	1 hits
36	TSC2	1 hits
37	UCP1	1 hits
38	YY1	1 hits

Related Sentences

#	PMID	Sentence
1	11134536	In this study, we found that the combined addition of IL-6 and dexamethasone induced the expression of Reg gene in beta cells and that PARP inhibitors enhanced the expression.
2	11134536	Thus, PARP inhibitors enhance the DNA/protein complex formation for Reg gene transcription and stabilize the complex by inhibiting the autopoly(ADP-ribosyl)ation of PARP.
3	11590148	However, PARP-1 interacted in vitro directly with both subunits of NF-kappa B (p50 and p65), and mapping of the interaction domains revealed that both subunits bind to different PARP-1 domains.
4	11991201	More recently, we showed that the combined addition of IL-6 and dexamethasone induces the Reg gene expression in beta-cells and that PARP inhibitors enhance the expression.
5	11991201	Therefore, PARP inhibitors prevent beta-cell necrosis, induce beta-cell replication and maintain insulin secretion.
6	12829633	These results suggest that PARP inhibition protects against autoimmune beta-cell destruction in NOD mice by inducing apoptosis of islet-infiltrating leukocytes and decreasing IFN-gamma expression in the islets.
7	12941777	In contrast, diabetic sensory neurons had elevated expression of the DNA repair enzyme poly(ADP-ribose) polymerase (PARP) in their nuclei, cytoplasm, and proximal axonal segments not overlapping with caspase-3 localization.
8	14523042	Overexpression of UCP-1 or MnSOD also prevented hyperglycemia-induced DNA strand breaks and activation of PARP.
9	14523042	Elevated glucose increased poly(ADP-ribosyl)ation of GAPDH in WT aortae, but not in the aortae from PARP-1-deficient mice.
10	14529360	Microglial migration is strongly controlled in living brain tissue by expression of the integrin CD11a, which is regulated in turn by PARP-1, proposing that PARP-1 downregulation may therefore be a promising strategy in protecting neurons from this secondary damage, as well.
11	14529360	PARP(s) might regulate cell fate as essential modulators of death and survival transcriptional programs with relation to NF-kappaB and p53, proposing that inhibitors of poly(ADP-ribosyl)ation could therefore prevent the deleterious consequences of neuroinflammation by reducing NF-kappaB activity.
12	15054118	The role of PARP in regulating AIF translocation in myocytes also was confirmed in an isolated perfused heart preparation.
13	15054118	Overall, the current results demonstrate the importance of the PARP pathway in diabetic rats subjected to myocardial infarction and demonstrate the role of PARP in regulating AIF translocation in MI/R.
14	15077172	In the absence of PARP-1, NF-kappaB activation and induction kappaB-target genes did not take place during the promotion of tumor development.
15	15448084	Here we present novel evidence that early interventions aimed at reducing oxidative stress of pancreatic cells and islets through the use of the catalytic antioxidant probe AEOL10150 (manganese [III] 5,10,15,20-tetrakis [1,3,-diethyl-2imidazoyl] manganese-porphyrin pentachloride [TDE-2,5-IP]) effectively reduces NF-kappaB binding to DNA, the release of cytokines and chemokines, and PARP activation in islet cells, resulting in higher survival and better insulin release.
16	15953818	The PARP-1 through interaction with nuclear factor-kappaB, p53, and other transcription factors might significantly modulate cell survival and death and a type of death pathway.
17	15965083	We report that curcumin prevented MG-induced cell death and apoptotic biochemical changes such as mitochondrial release of cytochrome c, caspase-3 activation, and cleavage of PARP (poly [ADP-ribose] polymerase).
18	16181138	Fifthly, PARP activity can be inhibited in cells by inhibition of poly(ADP-ribose)-glycohydrolase (PARG); will this be a viable strategy for future drug design?
19	16505238	Nicotinamide and other low-potency poly(ADP-ribose) polymerase (PARP) inhibitors were thus tested for their ability to restore insulin promoter activity.
20	16505238	The low-potency PARP inhibitors nicotinamide, 3-aminobenzamide, or PD128763 increased expression of a human insulin reporter gene suppressed by elevated glucose.
21	16505238	Low-potency PARP inhibitors restored MafA mRNA and protein levels, but they had no affect on PDX-1 protein levels or binding activity.
22	16505238	These data suggest that low-potency PARP inhibitors increase insulin biosynthesis, in part, through a mechanism involving increased MafA gene transcription.
23	16906222	However, a report published in a recent issue of the International Journal of Biological Sciences revealed that PARP-1 inhibitors, although able to kill na�ve BRCA1 mutant cells with high specificity both in vitro and in vivo, exhibit minimal specificity in inhibiting the growth of mouse mammary tumor cells irrespective of their BRCA1 status in allograft nude mice.
24	16906222	Non-specific inhibition in human BRCA1+/+, BRCA1+/-, and BRCA1-/- breast cancer cells by PARP-1 inhibitors was also observed.
25	16981139	Mitochondrial aconitase was reduced; the activities of NAPDH-oxidase and PARP were enhanced.
26	16981139	Activation of PARP by ROS may be an important mediator of vascular dysfunction in insulin resistance.
27	17065349	We have previously shown that nuclear factor-kappaB (NF-kappaB) mediates fibronectin expression in endothelial cells and in organs affected by diabetes complications. p300, a transcription coactivator, may regulate NF-kappaB activity via poly(ADP-ribose) polymerase (PARP) activation.
28	17065349	High glucose induced fibronectin expression in the endothelial cells, which was associated with increased p300, PARP activity, and NF-kappaB activation.
29	17065349	We then used p300 small interfering RNA (siRNA) and showed decreased fibronectin and PARP expression, as well as NF-kappaB activation, in the endothelial cells.
30	19440038	At the molecular level, metformin increases P-AMPK, reduces P-EGFR, EGFR, P-MAPK, P-Src, cyclin D1 and cyclin E (but not cyclin A or B, p27 or p21), and induces PARP cleavage in a dose- and time-dependent manner.
31	19175688	Myocardial XO, p22(phox), p40(phox), p47(phox), gp91(phox), iNOS, eNOS mRNA and/or protein levels, ROS and nitrotyrosine (NT) formation, caspase3/7 and PARP activity, chromatin fragmentation and various markers of fibrosis (collagen-1, TGF-beta, CTGF, fibronectin) were measured using molecular biology and biochemistry methods or immunohistochemistry.
32	19900402	Further, the combination also reduced the overactivation of PARP as evident from increased NAD levels and decreased PAR immunopositivity in sciatic nerve microsections.
33	20422335	The activities of the antioxidant enzymes superoxide dismutase (SOD), catalase (CAT) and glutathione S-transferase (GST), the incidence of DNA damage, the activation of poly (ADP-ribose) polymerase-1 (PARP-1), a marker of DNA repair, and connective tissue growth factor (CTGF), a marker of tissue fibrosis, were examined in the hearts of rats for 16 weeks after diabetes induction by streptozotocin (STZ) administration.
34	20566666	Simvastatin significantly upregulated PGC-1alpha (P < 0.01), subsequently decreased Deltapsim (P < 0.05) and ROS generation (P < 0.01), inhibited PARP activation (P < 0.01), and further reduced VEGF expression (P < 0.01) and p38 MAPK activity (P < 0.01).
35	20824098	In the present study, we found MyD88-deficient mice fed a HFD had increased circulating levels of insulin, leptin and cholesterol, as well as liver dysfunction (increased induction of ALT levels, increased activation of JNK and cleavage of PARP), which were linked to the onset of severe diabetes.
36	20621183	PARP-1 gene deficiency reduced urinary albumin (ELISA) and protein excretion prevented diabetes-induced kidney hypertrophy, and decreased mesangial expansion and collagen deposition (both assessed by histochemistry) as well as fibronectin expression.
37	20868648	Furthermore, overexpression of PARP-1 significantly inhibited promoter activity and decreased COX-2 expression.
38	20868648	These data suggest that PARP-1 plays an important role in the regulation of COX-2 expression via binding to the inhibitory element.
39	21289215	Induction of diabetes also increased phosphorylation of tuberin in association with mTOR activation (measured by p70S6K phosphorylation), inactivation of Bcl-2, increased cytosolic cytochrome c expression, activation of caspase 3, and cleavage of PARP; insulin treatment prevented these changes.
40	21289215	High glucose induced translocation of the caspase substrate YY1 from the cytoplasm to the nucleus and enhanced cleavage of PARP.
41	21289215	These data show that the tuberin/mTOR pathway promotes apoptosis of tubular epithelial cells in diabetes, mediated in part by cleavage of PARP by YY1.
42	21496888	To investigate whether overactivated Poly (ADP-ribose) polymerase (PARP) and subsequent activation of nuclear factor kappa B (NF-?B) correlate with the development of diabetic cystopathy via induction of bladder apoptosis.
43	20357221	This study evaluated poly(ADP-ribose) polymerase (PARP) inhibition as a new therapeutic approach for peripheral diabetic neuropathy using clinically relevant animal model and endpoints, and nitrotyrosine (NT), TNF-alpha, and nitrite/nitrate as potential biomarkers of the disease.
44	11511974	In addition to the direct cytotoxic pathway regulated by DNA injury and PARP activation, PARP also appears to modulate the course of inflammation by regulating the activation of nuclear factor kappaB, and the expression of a number of genes, including the gene for intercellular adhesion molecule 1 and the inducible nitric oxide synthase.
45	21813561	We found that apoptosis was increased in both STZ-induced diabetic mice and high-glucose-treated HRVECs, which was due to increased activation of PARP, cleaved caspase3, and reduced expression of Notch1 and p-Akt.
46	21813561	Thus, our study demonstrated that Notch1 signaling protects cells from PARP- and NF-?B-induced apoptosis under high glucose through the activation of Akt.
47	21617845	Neuroprotective and nephroprotective effects of PARP inhibition were not due to alleviation of diabetic hyperglycemia, or peripheral nerve p38 mitogen-activated protein kinase activation.
48	15616034	This study evaluated the effects of aldose reductase inhibition on diabetes-induced oxidative-nitrosative stress and poly(ADP-ribose) polymerase (PARP) activation.
49	15616034	In conclusion, aldose reductase inhibition counteracts diabetes-induced nitrosative stress and PARP activation in sciatic nerve and retina.
50	22061042	Increased oxidative stress, mitochondrial membrane depolarization, activation of caspase-3, and PARP observed in diabetic groups indicated bax triggered mitochondrial mediated cellular apoptosis.