PARG, poly(ADP-ribose) glycohydrolase, 8505

N. diseases: 50; N. variants: 2
Source: ALL
Disease Score gda Association Type Type Original DB Sentence supporting the association PMID PMID Year
CUI: C0007621
Disease: Neoplastic Cell Transformation
Neoplastic Cell Transformation
0.300 Therapeutic phenotype CTD_human Poly(ADP-Ribose) Glycohydrolase (PARG) Silencing Suppresses Benzo(a)pyrene Induced Cell Transformation. 27003318 2016
CUI: C0007621
Disease: Neoplastic Cell Transformation
Neoplastic Cell Transformation
0.300 Biomarker phenotype CTD_human Poly(ADP-Ribose) Glycohydrolase (PARG) Silencing Suppresses Benzo(a)pyrene Induced Cell Transformation. 27003318 2016
CUI: C0007621
Disease: Neoplastic Cell Transformation
Neoplastic Cell Transformation
0.300 Biomarker phenotype CTD_human Poly(ADP-ribose) glycohydrolase silencing down-regulates TCTP and Cofilin-1 associated with metastasis in benzo(a)pyrene carcinogenesis. 25628927 2015
CUI: C0007621
Disease: Neoplastic Cell Transformation
Neoplastic Cell Transformation
0.300 Therapeutic phenotype CTD_human Poly(ADP-ribose) glycohydrolase silencing down-regulates TCTP and Cofilin-1 associated with metastasis in benzo(a)pyrene carcinogenesis. 25628927 2015
CUI: C0012684
Disease: Blastocyst Disintegration
Blastocyst Disintegration
0.300 Biomarker phenotype CTD_human Failure to degrade poly(ADP-ribose) causes increased sensitivity to cytotoxicity and early embryonic lethality. 15591342 2004
CUI: C0013937
Disease: Embryo Resorption
Embryo Resorption
0.300 Biomarker phenotype CTD_human Failure to degrade poly(ADP-ribose) causes increased sensitivity to cytotoxicity and early embryonic lethality. 15591342 2004
CUI: C0752350
Disease: Embryo Death
Embryo Death
0.300 Biomarker phenotype CTD_human Failure to degrade poly(ADP-ribose) causes increased sensitivity to cytotoxicity and early embryonic lethality. 15591342 2004
CUI: C0752351
Disease: Embryo Loss
Embryo Loss
0.300 Biomarker phenotype CTD_human Failure to degrade poly(ADP-ribose) causes increased sensitivity to cytotoxicity and early embryonic lethality. 15591342 2004
CUI: C1136082
Disease: Embryo Disintegration
Embryo Disintegration
0.300 Biomarker phenotype CTD_human Failure to degrade poly(ADP-ribose) causes increased sensitivity to cytotoxicity and early embryonic lethality. 15591342 2004
CUI: C0006023
Disease: Borna Disease
Borna Disease
0.200 Biomarker disease RGD Hippocampal poly(ADP-Ribose) polymerase 1 and caspase 3 activation in neonatal bornavirus infection. 18057239 2008
CUI: C0751955
Disease: Brain Infarction
Brain Infarction
0.200 Biomarker disease RGD We demonstrate that either pre- or post-ischemia treatment with 40 mg/kg of N-bis-(3-phenyl-propyl)9-oxo-fluorene-2,7-diamide, a novel PARG inhibitor, significantly reduces brain infarct volumes by 40-53% in a rat model of focal cerebral ischemia. 12834903 2003
CUI: C0017654
Disease: Glomerular Filtration Rate
Glomerular Filtration Rate
0.100 GeneticVariation phenotype GWASCAT A catalog of genetic loci associated with kidney function from analyses of a million individuals. 31152163 2019
CUI: C0006826
Disease: Malignant Neoplasms
Malignant Neoplasms
0.090 Biomarker group BEFREE Poly(ADP-ribose)ylation (PARylation) by PAR polymerase 1 (PARP1) and PARylation removal by poly(ADP-ribose) glycohydrolase (PARG) critically regulate DNA damage responses; yet, conflicting reports obscure PARG biology and its impact on cancer cell resistance to PARP1 inhibitors. 31827085 2019
CUI: C0006826
Disease: Malignant Neoplasms
Malignant Neoplasms
0.090 Biomarker group BEFREE Taken together, these results indicate that <i>DUSP22</i> deficiency exerts a synthetic lethal effect when combined with PARG dysfunction, suggesting that DUSP22 dysfunction could be a useful biomarker for cancer therapy using PARG inhibitors. 31142510 2019
CUI: C0006826
Disease: Malignant Neoplasms
Malignant Neoplasms
0.090 Biomarker group BEFREE Furthermore, the induction of apoptosis code of DNA replication catastrophe by synthetic lethality of PARG inhibition and the recent progresses regarding the development of small molecule PARG inhibitors and their therapeutic potentials in cancer chemotherapy are highlighted in this review. 31176615 2019
CUI: C0006826
Disease: Malignant Neoplasms
Malignant Neoplasms
0.090 Biomarker group BEFREE Our results highlight the HuR-PARG axis as an opportunity to enhance PARPi-based therapies.<i>Cancer Res; 77(18); 5011-25.©2017 AACR</i>. 28687616 2017
CUI: C0006826
Disease: Malignant Neoplasms
Malignant Neoplasms
0.090 Biomarker group BEFREE This was the first study that reported evidences to support an oncogenic role of PARG in BaP induced carcinogenesis, which provided a new perspective for our understanding in BaP exposure induced cancer. 27003318 2016
CUI: C0006826
Disease: Malignant Neoplasms
Malignant Neoplasms
0.090 Biomarker group BEFREE Hence, this study emphasizes and converges on the relevance of silencing PARG which inhibits growth of human colonic cancer cells via PI3K/Akt/NFκ-B pathway; as colon carcinoma remains to be amongst one of the commonest cancers throughout the world with high morbidity and mortality rates. 21713600 2012
CUI: C0006826
Disease: Malignant Neoplasms
Malignant Neoplasms
0.090 Biomarker group BEFREE Furthermore, accumulating experimental evidence supports the utility of PARP and PARG inhibitors in cancer therapy and several clinical trials are now ongoing. 17645773 2007
CUI: C0006826
Disease: Malignant Neoplasms
Malignant Neoplasms
0.090 Biomarker group BEFREE In this brief review on PARP and PARG enzymes, emphasis is placed on PARP-1, the best understood member of the PARP family and on the relationship of poly(ADP-ribosyl)ation to cancer and other diseases of aging. 15743666 2005
CUI: C0006826
Disease: Malignant Neoplasms
Malignant Neoplasms
0.090 Biomarker group BEFREE Further analysis of PARP-1, PARG and other PARP family genes should extend our understanding of the pathogenesis of cancer and autoimmune diseases. 15868402 2005
CUI: C1306459
Disease: Primary malignant neoplasm
Primary malignant neoplasm
0.080 Biomarker group BEFREE Taken together, these results indicate that <i>DUSP22</i> deficiency exerts a synthetic lethal effect when combined with PARG dysfunction, suggesting that DUSP22 dysfunction could be a useful biomarker for cancer therapy using PARG inhibitors. 31142510 2019
CUI: C1306459
Disease: Primary malignant neoplasm
Primary malignant neoplasm
0.080 Biomarker group BEFREE Poly(ADP-ribose)ylation (PARylation) by PAR polymerase 1 (PARP1) and PARylation removal by poly(ADP-ribose) glycohydrolase (PARG) critically regulate DNA damage responses; yet, conflicting reports obscure PARG biology and its impact on cancer cell resistance to PARP1 inhibitors. 31827085 2019
CUI: C1306459
Disease: Primary malignant neoplasm
Primary malignant neoplasm
0.080 Biomarker group BEFREE Furthermore, the induction of apoptosis code of DNA replication catastrophe by synthetic lethality of PARG inhibition and the recent progresses regarding the development of small molecule PARG inhibitors and their therapeutic potentials in cancer chemotherapy are highlighted in this review. 31176615 2019
CUI: C1306459
Disease: Primary malignant neoplasm
Primary malignant neoplasm
0.080 Biomarker group BEFREE Our results highlight the HuR-PARG axis as an opportunity to enhance PARPi-based therapies.<i>Cancer Res; 77(18); 5011-25.©2017 AACR</i>. 28687616 2017