PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 34166935-9 2021 Finally, we found that low-dose antimony(0.8uM) inhibited mitophagy by deregulating expression of PINK1, Parkin, and p(ser65)-Parkin, and activation of PINK1-Parkin pathway by CCCP could inhibit antimony-induced tumor cell growth. Carbonyl Cyanide m-Chlorophenyl Hydrazone 176-180 PTEN induced kinase 1 Homo sapiens 152-157 25404737-4 2015 In this study, we show that PINK1-dependent Parkin mitochondrial recruitment in response to global mitochondrial damage by carbonyl cyanide m-chlorophenylhydrazine (CCCP) requires active glucose metabolism. Carbonyl Cyanide m-Chlorophenyl Hydrazone 165-169 PTEN induced kinase 1 Homo sapiens 28-33 24660806-2 2014 Using phosphoproteomic analysis, we identified a novel ubiquitin phosphopeptide phosphorylated at Ser65 that was enriched 14-fold in HEK (human embryonic kidney)-293 cells overexpressing wild-type PINK1 stimulated with the mitochondrial uncoupling agent CCCP (carbonyl cyanide m-chlorophenylhydrazone), to activate PINK1, compared with cells expressing kinase-inactive PINK1. Carbonyl Cyanide m-Chlorophenyl Hydrazone 254-258 PTEN induced kinase 1 Homo sapiens 197-202 24660806-2 2014 Using phosphoproteomic analysis, we identified a novel ubiquitin phosphopeptide phosphorylated at Ser65 that was enriched 14-fold in HEK (human embryonic kidney)-293 cells overexpressing wild-type PINK1 stimulated with the mitochondrial uncoupling agent CCCP (carbonyl cyanide m-chlorophenylhydrazone), to activate PINK1, compared with cells expressing kinase-inactive PINK1. Carbonyl Cyanide m-Chlorophenyl Hydrazone 254-258 PTEN induced kinase 1 Homo sapiens 315-320 24660806-2 2014 Using phosphoproteomic analysis, we identified a novel ubiquitin phosphopeptide phosphorylated at Ser65 that was enriched 14-fold in HEK (human embryonic kidney)-293 cells overexpressing wild-type PINK1 stimulated with the mitochondrial uncoupling agent CCCP (carbonyl cyanide m-chlorophenylhydrazone), to activate PINK1, compared with cells expressing kinase-inactive PINK1. Carbonyl Cyanide m-Chlorophenyl Hydrazone 254-258 PTEN induced kinase 1 Homo sapiens 315-320 24660806-2 2014 Using phosphoproteomic analysis, we identified a novel ubiquitin phosphopeptide phosphorylated at Ser65 that was enriched 14-fold in HEK (human embryonic kidney)-293 cells overexpressing wild-type PINK1 stimulated with the mitochondrial uncoupling agent CCCP (carbonyl cyanide m-chlorophenylhydrazone), to activate PINK1, compared with cells expressing kinase-inactive PINK1. Carbonyl Cyanide m-Chlorophenyl Hydrazone 260-300 PTEN induced kinase 1 Homo sapiens 197-202 24660806-2 2014 Using phosphoproteomic analysis, we identified a novel ubiquitin phosphopeptide phosphorylated at Ser65 that was enriched 14-fold in HEK (human embryonic kidney)-293 cells overexpressing wild-type PINK1 stimulated with the mitochondrial uncoupling agent CCCP (carbonyl cyanide m-chlorophenylhydrazone), to activate PINK1, compared with cells expressing kinase-inactive PINK1. Carbonyl Cyanide m-Chlorophenyl Hydrazone 260-300 PTEN induced kinase 1 Homo sapiens 315-320 24660806-2 2014 Using phosphoproteomic analysis, we identified a novel ubiquitin phosphopeptide phosphorylated at Ser65 that was enriched 14-fold in HEK (human embryonic kidney)-293 cells overexpressing wild-type PINK1 stimulated with the mitochondrial uncoupling agent CCCP (carbonyl cyanide m-chlorophenylhydrazone), to activate PINK1, compared with cells expressing kinase-inactive PINK1. Carbonyl Cyanide m-Chlorophenyl Hydrazone 260-300 PTEN induced kinase 1 Homo sapiens 315-320 24184327-3 2014 In this study, we report that increased mitochondrial PINK1 levels observed in human neuroblastoma SH-SY5Y cells after carbonyl cyanide m-chlorophelyhydrazone (CCCP) treatment were due to de novo protein synthesis, and not just increased stabilization of full length PINK1 (FL-PINK1). Carbonyl Cyanide m-Chlorophenyl Hydrazone 160-164 PTEN induced kinase 1 Homo sapiens 54-59 24184327-3 2014 In this study, we report that increased mitochondrial PINK1 levels observed in human neuroblastoma SH-SY5Y cells after carbonyl cyanide m-chlorophelyhydrazone (CCCP) treatment were due to de novo protein synthesis, and not just increased stabilization of full length PINK1 (FL-PINK1). Carbonyl Cyanide m-Chlorophenyl Hydrazone 160-164 PTEN induced kinase 1 Homo sapiens 267-272 24184327-3 2014 In this study, we report that increased mitochondrial PINK1 levels observed in human neuroblastoma SH-SY5Y cells after carbonyl cyanide m-chlorophelyhydrazone (CCCP) treatment were due to de novo protein synthesis, and not just increased stabilization of full length PINK1 (FL-PINK1). Carbonyl Cyanide m-Chlorophenyl Hydrazone 160-164 PTEN induced kinase 1 Homo sapiens 267-272 21860779-5 2011 The PINK1-parkin pathway is associated with quality control of the mitochondria, as determined in cultured cells treated with the mitochondrial uncoupler carbonyl cyanide m-chlorophenylhydrazone (CCCP), which causes mitochondrial depolarization. Carbonyl Cyanide m-Chlorophenyl Hydrazone 154-194 PTEN induced kinase 1 Homo sapiens 4-9 21860779-5 2011 The PINK1-parkin pathway is associated with quality control of the mitochondria, as determined in cultured cells treated with the mitochondrial uncoupler carbonyl cyanide m-chlorophenylhydrazone (CCCP), which causes mitochondrial depolarization. Carbonyl Cyanide m-Chlorophenyl Hydrazone 196-200 PTEN induced kinase 1 Homo sapiens 4-9 31862413-6 2020 Furthermore, NRF-1 over-expression (OE) up-regulated the protein level of full-length PINK1 in CCCP-treated cells, indicating the enhanced PINK1/Parkin-mediated mitophagy. Carbonyl Cyanide m-Chlorophenyl Hydrazone 95-99 PTEN induced kinase 1 Homo sapiens 86-91 34295842-6 2021 Rapamycin or carbonyl cyanide m-chlorophenyl hydrazone (CCCP) treatment led to increased CVB3 RNA copy number in a dose-dependent manner, suggesting enhanced viral replication via autophagy/mitophagy activation, whereas knockdown of PTEN-induced putative kinase protein 1(PINK1) led to impaired mitophagy and subsequent reduction in viral replication. Carbonyl Cyanide m-Chlorophenyl Hydrazone 13-54 PTEN induced kinase 1 Homo sapiens 272-277 34127073-4 2021 These cells were treated with a protonophore carbonyl cyanide m-chlorophenylhydrazone (CCCP) to induce the PINK1/Parkin-mediated mitophagy, which was assessed using biochemical and microscopy approaches. Carbonyl Cyanide m-Chlorophenyl Hydrazone 45-85 PTEN induced kinase 1 Homo sapiens 107-112 34127073-4 2021 These cells were treated with a protonophore carbonyl cyanide m-chlorophenylhydrazone (CCCP) to induce the PINK1/Parkin-mediated mitophagy, which was assessed using biochemical and microscopy approaches. Carbonyl Cyanide m-Chlorophenyl Hydrazone 87-91 PTEN induced kinase 1 Homo sapiens 107-112 35068334-6 2022 BCL2-associated X (BAX), B-cell lymphoma-2 (Bcl-2), Beclin1, Parkin and PTEN Induced Kinase 1 (Pink1) expression was detected by Western blot, immunohistochemistry, and immunofluorescence in thoracic aorta, HG- and CCCP-induced HUVECs. Carbonyl Cyanide m-Chlorophenyl Hydrazone 215-219 PTEN induced kinase 1 Homo sapiens 72-93 35068334-6 2022 BCL2-associated X (BAX), B-cell lymphoma-2 (Bcl-2), Beclin1, Parkin and PTEN Induced Kinase 1 (Pink1) expression was detected by Western blot, immunohistochemistry, and immunofluorescence in thoracic aorta, HG- and CCCP-induced HUVECs. Carbonyl Cyanide m-Chlorophenyl Hydrazone 215-219 PTEN induced kinase 1 Homo sapiens 95-100 35068334-10 2022 In diabetic thoracic aorta, HG- and CCCP-induced HUVECs, Sal B distinctly increased Bcl-2 expression and reduced BAX, Beclin1, Parkin and Pink1 expression, thereby protecting endothelial cells from apoptosis and mitophagy. Carbonyl Cyanide m-Chlorophenyl Hydrazone 36-40 PTEN induced kinase 1 Homo sapiens 138-143 32779864-2 2020 The proton ionophores, like carbonyl cyanide m-chlorophenylhydrazone (CCCP) and carbonyl cyanide-4-(trifluoromethoxy)phenylhydrazone (FCCP), inhibit PINK1 import into mitochondrial matrix and induce PINK1 OMM accumulation. Carbonyl Cyanide m-Chlorophenyl Hydrazone 28-68 PTEN induced kinase 1 Homo sapiens 149-154 32779864-2 2020 The proton ionophores, like carbonyl cyanide m-chlorophenylhydrazone (CCCP) and carbonyl cyanide-4-(trifluoromethoxy)phenylhydrazone (FCCP), inhibit PINK1 import into mitochondrial matrix and induce PINK1 OMM accumulation. Carbonyl Cyanide m-Chlorophenyl Hydrazone 28-68 PTEN induced kinase 1 Homo sapiens 199-204 32154065-4 2020 Moreover, the induction of PINK1-dependent mitophagy with carbonylcyanide-m-chlorophenylhydrazone (CCCP) or salinomycin, or overexpression of PINK1 leads to inhibition of transwell migration, suppression of myeloma cell homing to calvarium, and decreased osteolytic bone lesions. Carbonyl Cyanide m-Chlorophenyl Hydrazone 58-97 PTEN induced kinase 1 Homo sapiens 27-32 32154065-4 2020 Moreover, the induction of PINK1-dependent mitophagy with carbonylcyanide-m-chlorophenylhydrazone (CCCP) or salinomycin, or overexpression of PINK1 leads to inhibition of transwell migration, suppression of myeloma cell homing to calvarium, and decreased osteolytic bone lesions. Carbonyl Cyanide m-Chlorophenyl Hydrazone 99-103 PTEN induced kinase 1 Homo sapiens 27-32 30558471-5 2019 We observed no discernable presence of Pink1 in isolated mitochondria from skeletal muscle at any time point following acute exercise, in contrast to clear evidence of stabilization of Pink1 on mitochondria in HeLa cells following treatment with the uncoupler carbonyl cyanide m-chlorophenyl hydrazone (CCCP). Carbonyl Cyanide m-Chlorophenyl Hydrazone 260-301 PTEN induced kinase 1 Homo sapiens 185-190 30133157-6 2018 Furthermore, mitochondria from PINK1 knockdown cells, in which motility was most impaired, had increased levels of GSK3betaSer9 and higher release of mitochondrial Ca2+ when exposed to CCCP-induced mitochondrial uncoupling. Carbonyl Cyanide m-Chlorophenyl Hydrazone 185-189 PTEN induced kinase 1 Homo sapiens 31-36 29241732-13 2018 In conclusion, we demonstrated that PGAM5 regulates PINK1-Parkin-mediated mitophagy, which can exert a neuroprotective effect against CCCP-induced apoptosis. Carbonyl Cyanide m-Chlorophenyl Hydrazone 134-138 PTEN induced kinase 1 Homo sapiens 52-57 31332166-4 2019 First, strongly downregulated PARKIN and the mitophagic adaptor protein SQSTM1/p62 delays PINK1 activation to impair mitophagy induction after mitochondrial depolarization by CCCP or antimycin A plus oligomycin. Carbonyl Cyanide m-Chlorophenyl Hydrazone 175-179 PTEN induced kinase 1 Homo sapiens 90-95 28848050-5 2017 Supporting this, combinatorial treatment with N-acetyl-l-cysteine and catalase substantially inhibited the ROS upsurge and PINK1-dependent Parkin translocation to mitochondria in response to carbonyl cyanide m-chlorophenylhydrazone treatment. Carbonyl Cyanide m-Chlorophenyl Hydrazone 191-231 PTEN induced kinase 1 Homo sapiens 123-128 26631732-3 2016 The binding between the UBL domain and the R1 domain was suppressed by carbonyl cyanide m-chlorophenyl hydrazone treatment or by expression of PTEN-induced putative kinase 1 (PINK1), an upstream kinase that phosphorylates Parkin at the Ser-65 residue of the UBL domain. Carbonyl Cyanide m-Chlorophenyl Hydrazone 71-112 PTEN induced kinase 1 Homo sapiens 143-173 26631732-3 2016 The binding between the UBL domain and the R1 domain was suppressed by carbonyl cyanide m-chlorophenyl hydrazone treatment or by expression of PTEN-induced putative kinase 1 (PINK1), an upstream kinase that phosphorylates Parkin at the Ser-65 residue of the UBL domain. Carbonyl Cyanide m-Chlorophenyl Hydrazone 71-112 PTEN induced kinase 1 Homo sapiens 175-180