PMID-sentid Pub_year Sent_text comp_official_name comp_offset protein_name organism prot_offset 26967250-7 2016 We further show that DNA damage, such as exposure to methyl methanesulfonate (MMS), etoposide or arsenic, increases Cdc25A acetylation. Methyl Methanesulfonate 53-76 cell division cycle 25A Homo sapiens 116-122 27462461-6 2016 Moreover, the acetylation of Cdc25A at lysine 150, which was acetylated by p300/CBP and deacetylated by HDAC3, prevented the ubiquitin-mediated degradation of Cdc25A by the proteasome. Lysine 39-45 cell division cycle 25A Homo sapiens 29-35 27462461-6 2016 Moreover, the acetylation of Cdc25A at lysine 150, which was acetylated by p300/CBP and deacetylated by HDAC3, prevented the ubiquitin-mediated degradation of Cdc25A by the proteasome. Lysine 39-45 cell division cycle 25A Homo sapiens 159-165 26967250-7 2016 We further show that DNA damage, such as exposure to methyl methanesulfonate (MMS), etoposide or arsenic, increases Cdc25A acetylation. Methyl Methanesulfonate 78-81 cell division cycle 25A Homo sapiens 116-122 26967250-7 2016 We further show that DNA damage, such as exposure to methyl methanesulfonate (MMS), etoposide or arsenic, increases Cdc25A acetylation. Etoposide 84-93 cell division cycle 25A Homo sapiens 116-122 26967250-7 2016 We further show that DNA damage, such as exposure to methyl methanesulfonate (MMS), etoposide or arsenic, increases Cdc25A acetylation. Arsenic 97-104 cell division cycle 25A Homo sapiens 116-122 24882577-5 2015 FYN knockdown in TamR cells led to reduced phosphorylation of 14-3-3 and Cdc25A, suggesting that FYN, by activation of important cell cycle-associated proteins, may overcome the anti-proliferative effects of tamoxifen. Tamoxifen 208-217 cell division cycle 25A Homo sapiens 73-79 26846469-7 2016 The results indicated that Dp treatment significantly inhibited cell proliferation in a dose- and time-dependent manner, and blocked cell cycle progression at the G1/S phase in the U87MG and T98G cells via the upregulation of p53 and p21 protein expression, and simultaneous downregulation of Cdc25A, Cdc2 and P-Cdc2 protein expression. dracorhodin 27-29 cell division cycle 25A Homo sapiens 293-299 26447757-4 2015 Knockdown of AMPKalpha significantly rescued nitroxoline-induced inhibition of cyclin D1-Rb-Cdc25A axis indicating AMPK-dependent mechanism. nitroxoline 45-56 cell division cycle 25A Homo sapiens 92-98 26447757-8 2015 In conclusion, the data suggest that nitroxoline induces anticancer activity through AMPK-dependent inhibition of mTOR-p70S6K signaling pathway and cyclin D1-Rb-Cdc25A axis, leading to G1 arrest of cell cycle and apoptosis. nitroxoline 37-48 cell division cycle 25A Homo sapiens 161-167 26250568-4 2015 Magnolol also blocked cell cycle progression at G0 /G1 phase and induced mitochondrial-related apoptosis by upregulating p53 and p21 protein levels and by downregulating cyclin D1, CDC25A, and Cdk2 protein levels. magnolol 0-8 cell division cycle 25A Homo sapiens 181-187 26141948-4 2015 The action of LY2606368 is dependent upon inhibition of CHK1 and the corresponding increase in CDC25A activation of CDK2, which increases the number of replication forks while reducing their stability. prexasertib 14-23 cell division cycle 25A Homo sapiens 95-101 26148435-0 2015 Arsenic-induced S phase cell cycle lengthening is associated with ROS generation, p53 signaling and CDC25A expression. Arsenic 0-7 cell division cycle 25A Homo sapiens 100-106 26148435-7 2015 Furthermore, for the first time, we demonstrate that arsenic activates p53-dependent transcription of ROS detoxification genes, such as SESN1, and by an indirect mechanism involving ATF3, genes that could be responsible for the S phase cell cycle arrest, such as CDC25A. Arsenic 53-60 cell division cycle 25A Homo sapiens 263-269 26451628-6 2015 Our results illustrate that PCB29-pQ increases the S-phase cell population by down-regulating cyclins A/D1/E, cyclin-dependent kinases (CDK 2/4/6), and cell division cycle 25A (CDC25A) and up-regulating p21/p27 protein expressions. 2,3,5-trichloro-6-phenyl-(1,4)benzoquinone 28-36 cell division cycle 25A Homo sapiens 177-183 25936524-4 2015 Here, we demonstrate that the depletion of serine-threonine kinase 38 (STK38) prevents the DNA-damage-induced degradation of CDC25A and subsequent G2 arrest, and that STK38 directly phosphorylates CDC25A at Ser-76, resulting in CDC25A"s degradation. Serine 207-210 cell division cycle 25A Homo sapiens 125-131 25936524-4 2015 Here, we demonstrate that the depletion of serine-threonine kinase 38 (STK38) prevents the DNA-damage-induced degradation of CDC25A and subsequent G2 arrest, and that STK38 directly phosphorylates CDC25A at Ser-76, resulting in CDC25A"s degradation. Serine 207-210 cell division cycle 25A Homo sapiens 197-203 25936524-4 2015 Here, we demonstrate that the depletion of serine-threonine kinase 38 (STK38) prevents the DNA-damage-induced degradation of CDC25A and subsequent G2 arrest, and that STK38 directly phosphorylates CDC25A at Ser-76, resulting in CDC25A"s degradation. Serine 207-210 cell division cycle 25A Homo sapiens 197-203 25936524-5 2015 Taken together, these results indicate that the STK38-mediated phosphorylation of CDC25A at Ser-76 and the subsequent degradation of CDC25A are required to promote DNA damage-induced G2/M checkpoint activation. Serine 92-95 cell division cycle 25A Homo sapiens 82-88 25965299-5 2015 RESULTS: The major novel finding of this study is the demonstration of oxidative modification of phosphatases PTEN and CDC25A by E2-generated ROS along with the subsequent activation of AKT and ERK pathways that culminated in the activation of NRF-1 leading to the upregulation of cell cycle genes. Reactive Oxygen Species 142-145 cell division cycle 25A Homo sapiens 119-125 24838526-9 2014 Mechanistically, we observed CDC25A stabilization as a result of CHK1 inhibition with consequent inhibition of gemcitabine-induced S-phase arrest as well as a decrease in canonical (ERK1/2 phosphorylation) and noncanonical EGFR signaling (RAD51 degradation) as a result of EGFR inhibition. gemcitabine 111-122 cell division cycle 25A Homo sapiens 29-35 25536607-11 2014 CyclinD1 and CDC25A were downregulated by P-EGCG by 2.49 and 2.63-fold, respectively. p-egcg 42-48 cell division cycle 25A Homo sapiens 13-19 25536607-14 2014 P-EGCG mediated apoptosis might be associated with upregulation of TGF-beta2 gene and downregulation of cyclinD1 and CDC25A genes. epigallocatechin gallate 2-6 cell division cycle 25A Homo sapiens 117-123 26119958-0 2015 Anti-Colon Cancer Effects of 6-Shogaol Through G2/M Cell Cycle Arrest by p53/p21-cdc2/cdc25A Crosstalk. shogaol 29-38 cell division cycle 25A Homo sapiens 86-92 25531367-6 2014 Concurrently, maduramicin downregulated protein expression of cyclin D1, cyclin-dependent kinases (CDK4 and CDK6), and CDC25A, and upregulated expression of the CDK inhibitors (p21Cip1 and p27Kip1), resulting in decreased phosphorylation of Rb. maduramicin 14-25 cell division cycle 25A Homo sapiens 119-125 25527123-10 2014 The S arrest and the activation of ATM-Chk1/Chk2-Cdc25A-Cdk2 pathways induced by SC-III3 in HepG2 cells could be efficiently abrogated by pretreatments of either Ku55933 (an inhibitor of ATM) or UCN-01 (an inhibitor of Chk1/Chk2). 2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one 162-169 cell division cycle 25A Homo sapiens 49-55 25527123-10 2014 The S arrest and the activation of ATM-Chk1/Chk2-Cdc25A-Cdk2 pathways induced by SC-III3 in HepG2 cells could be efficiently abrogated by pretreatments of either Ku55933 (an inhibitor of ATM) or UCN-01 (an inhibitor of Chk1/Chk2). 7-hydroxystaurosporine 195-201 cell division cycle 25A Homo sapiens 49-55 24789439-6 2014 DHM increased the production of p53 and p21 proteins and downregulated the production of Cdc25A, Cdc2 and P-Cdc2 proteins, which induced cell cycle arrest. dihydromyricetin 0-3 cell division cycle 25A Homo sapiens 89-95 24150948-4 2014 In this study, we show that Rocaglamide-A (Roc-A), a natural anticancer compound isolated from the medicinal plant Aglaia, induces a rapid phosphorylation of Cdc25A and its subsequent degradation and, thereby, blocks cell cycle progression of tumor cells at the G1-S phase. rocaglamide 28-41 cell division cycle 25A Homo sapiens 158-164 23255470-3 2014 In the NuLi-1 immortalized human lung epithelial cell line with p53 and pRb deficiency, exposure to low doses of arsenic trioxide for 72 h promoted cell proliferation and upregulated the gene transcription levels of FOXM1, CDC6, CDC25A, and cyclin D1, which are both critical cell cycle regulatory genes and proto-oncogenes. Arsenic Trioxide 113-129 cell division cycle 25A Homo sapiens 229-235 24150948-4 2014 In this study, we show that Rocaglamide-A (Roc-A), a natural anticancer compound isolated from the medicinal plant Aglaia, induces a rapid phosphorylation of Cdc25A and its subsequent degradation and, thereby, blocks cell cycle progression of tumor cells at the G1-S phase. rocaglamide 43-48 cell division cycle 25A Homo sapiens 158-164 24150948-6 2014 In this study, we demonstrate that besides the translation inhibition Roc-A can induce a rapid degradation of Cdc25A by activation of the ATM/ATR-Chk1/Chk2 checkpoint pathway. rocaglamide 70-75 cell division cycle 25A Homo sapiens 110-116 24870773-17 2014 Expression of cyclin A, Cdc25A and Cdk2 protein was down-regulated following exposure to KSC and EPI alone or in combination, exposure to KSC and EPI simultaneously resulting in the lowest values. kappa-selenocarrageenan 89-92 cell division cycle 25A Homo sapiens 24-30 24475272-11 2014 In summary, the data suggest that reevesioside A inhibits c-myc expression and down-regulates the expression of CDC25A, cyclin D1 and cyclin E, leading to a profound decrease of RB phosphorylation. reevesioside A 34-48 cell division cycle 25A Homo sapiens 112-118 24870773-17 2014 Expression of cyclin A, Cdc25A and Cdk2 protein was down-regulated following exposure to KSC and EPI alone or in combination, exposure to KSC and EPI simultaneously resulting in the lowest values. kappa-selenocarrageenan 138-141 cell division cycle 25A Homo sapiens 24-30 23943154-6 2013 DIG also activated ATM and Chk2, and induced the phosphorylation and proteasomal degradation of the proto-oncogene Cdc25A, which contributed to cell cycle attenuation. digalloylresveratrol 0-3 cell division cycle 25A Homo sapiens 115-121 23752175-10 2013 Western blotting and reverse transcription-PCR confirm that c-MYC, CDC25A and BRD4 are all downregulated after treatment with KPT-276. KPT-276 126-133 cell division cycle 25A Homo sapiens 67-73 23907019-8 2013 We found that puerarin can suppress estrogen-stimulated proliferation partly through down-regulating the transcription of cyclin D1 and cdc25A by promoting the recruitment of corepressors to estrogen receptor-alpha as well as limiting that of coactivators in ESCs. puerarin 14-22 cell division cycle 25A Homo sapiens 136-142 23675485-10 2013 In-vitro demethylation experiment by 5-aza-2"-deoxycytidine (5-aza-dC) showed upregulation of SH3GL2 and CDC25A and downregulation of EGFR expression in Hep2 cell line. Decitabine 37-59 cell division cycle 25A Homo sapiens 105-111 24041220-11 2013 The hexane extract showed highest toxicity against p53-deficient HL-60 cells (IC50 1.5 mg dry roots equivalent/ml medium) after 72 h and interestingly, inhibition of cell proliferation was preceded by the upregulation of the proto-oncogenes Cdc25A and cyclin D1 within 24 h. The hexane extract induced 18% apoptosis after 48 h of treatment. Hexanes 4-10 cell division cycle 25A Homo sapiens 241-247 23686257-11 2013 In addition, genistein caused cell cycle arrest in the G2/M phase, which was accompanied by activation of ATM/p53, p21waf1/cip1 and GADD45alpha as well as downregulation of cdc2 and cdc25A demonstrated by q-PCR and immunoblotting assay. Genistein 13-22 cell division cycle 25A Homo sapiens 182-188 23429262-7 2013 We show that the miRNA-induced silencing of CDC25A increases the tyrosine phosphorylation status of CDK4/6 cyclin-dependent kinases which, in turn, abolishes CDK4/6 capacity to associate with D-type cyclins. Tyrosine 65-73 cell division cycle 25A Homo sapiens 44-50 23675485-10 2013 In-vitro demethylation experiment by 5-aza-2"-deoxycytidine (5-aza-dC) showed upregulation of SH3GL2 and CDC25A and downregulation of EGFR expression in Hep2 cell line. Decitabine 61-69 cell division cycle 25A Homo sapiens 105-111 23314229-0 2013 Triptolide induces S phase arrest via the inhibition of cyclin E and CDC25A and triggers apoptosis via caspase- and mitochondrial-dependent signaling pathways in A375.S2 human melanoma cells. triptolide 0-10 cell division cycle 25A Homo sapiens 81-87 23467652-3 2013 LC-MS analysis indicated that RE142 binds to one of the residues Cys384-Tyr386 of CDC25A, within a pocket adjacent to the catalytic site. re142 30-35 cell division cycle 25A Homo sapiens 82-88 23518499-10 2013 In addition, expression of wee1 kinase and Cdc25A/C phosphatases also coincide with CDK1 expression and its subcellular localization in response to ATRA treatment. Tretinoin 148-152 cell division cycle 25A Homo sapiens 43-49 22843495-3 2012 We show that inhibition of Hsp90 with geldanamycin (GD) destabilizes Cdc25A independent of Chk1/2, whereas the standard drug for pancreas carcinoma treatment, gemcitabine (GEM), causes Cdc25A degradation through the activation of Chk2. geldanamycin 38-50 cell division cycle 25A Homo sapiens 69-75 22843495-3 2012 We show that inhibition of Hsp90 with geldanamycin (GD) destabilizes Cdc25A independent of Chk1/2, whereas the standard drug for pancreas carcinoma treatment, gemcitabine (GEM), causes Cdc25A degradation through the activation of Chk2. geldanamycin 38-50 cell division cycle 25A Homo sapiens 185-191 22843495-3 2012 We show that inhibition of Hsp90 with geldanamycin (GD) destabilizes Cdc25A independent of Chk1/2, whereas the standard drug for pancreas carcinoma treatment, gemcitabine (GEM), causes Cdc25A degradation through the activation of Chk2. geldanamycin 52-54 cell division cycle 25A Homo sapiens 69-75 22843495-3 2012 We show that inhibition of Hsp90 with geldanamycin (GD) destabilizes Cdc25A independent of Chk1/2, whereas the standard drug for pancreas carcinoma treatment, gemcitabine (GEM), causes Cdc25A degradation through the activation of Chk2. geldanamycin 52-54 cell division cycle 25A Homo sapiens 185-191 22843495-3 2012 We show that inhibition of Hsp90 with geldanamycin (GD) destabilizes Cdc25A independent of Chk1/2, whereas the standard drug for pancreas carcinoma treatment, gemcitabine (GEM), causes Cdc25A degradation through the activation of Chk2. gemcitabine 159-170 cell division cycle 25A Homo sapiens 185-191 22843495-5 2012 The role of Hsp90 as stabilizer of Cdc25A in pancreas carcinoma cells is further supported by two novel synthetic inhibitors 4-tosylcyclonovobiocic acid and 7-tosylcyclonovobiocic acid and specific Hsp90AB1 (Hsp90beta) shRNA. 4-tosylcyclonovobiocic acid 125-152 cell division cycle 25A Homo sapiens 35-41 22843495-5 2012 The role of Hsp90 as stabilizer of Cdc25A in pancreas carcinoma cells is further supported by two novel synthetic inhibitors 4-tosylcyclonovobiocic acid and 7-tosylcyclonovobiocic acid and specific Hsp90AB1 (Hsp90beta) shRNA. 7-tosylcyclonovobiocic acid 157-184 cell division cycle 25A Homo sapiens 35-41 21738216-8 2012 In contrast, TNF-alpha stimulation of VSMCs enhanced the association of E2F1 with proliferative promoters like thymidylate synthase and cdc25A, while Rb was dissociated. vsmcs 38-43 cell division cycle 25A Homo sapiens 136-142 22683347-5 2012 We demonstrate that non cytotoxic concentrations of sodium arsenite (As(III), 0.25-2muM) significantly reduce T cell proliferation by increasing the percentage of non dividing cells blocked in G1 phase and by preventing cyclin D3 and CDC25A expression. sodium arsenite 52-67 cell division cycle 25A Homo sapiens 234-240 22705189-0 2012 Arylstibonic acids are potent and isoform-selective inhibitors of Cdc25a and Cdc25b phosphatases. arylstibonic acids 0-18 cell division cycle 25A Homo sapiens 66-72 22417828-2 2012 Here we report that Cdc25A inhibits cisplatin-induced apoptotic cell death by stimulating nuclear factor-kappa B (NF-kappaB) activity. Cisplatin 36-45 cell division cycle 25A Homo sapiens 20-26 22417828-3 2012 In HEK-293 cells, Cdc25A decreased protein level of inhibitor subunit kappa B alpha (Ikappa-Balpha) in association with increased serine 32-phosphorylation, followed by stimulation of transcriptional activity of NF-kappaB. Serine 130-136 cell division cycle 25A Homo sapiens 18-24 22211565-4 2012 CR2408 leads to fragmentation of cells and induces an accumulation in the subG1 phase accompanied with moderately decreased levels of cyclin D1 and cdk4 and strongly decreased levels of cdc25a, pRb and p53. CR2408 0-6 cell division cycle 25A Homo sapiens 186-192 22159450-5 2012 In particular SAHA downregulates cell cycle-associated genes that modulate the G1/S transition (including cyclin D1 and cdc25a) and the G2/M transition [cyclin B1, Plk1, Stk6 (serine-threonine kinase 6, Aurora kinase A) and Kntc2] more significantly than CG-1521. Vorinostat 14-18 cell division cycle 25A Homo sapiens 144-150 22417828-4 2012 Inhibition of NF-kappaB activity by chemical inhibitor or overexpression of Ikappa-Balpha in Cdc25A-elevated cancer cells resistant to cisplatin improved their sensitivity to cisplatin-induced apoptosis. Cisplatin 135-144 cell division cycle 25A Homo sapiens 93-99 22417828-4 2012 Inhibition of NF-kappaB activity by chemical inhibitor or overexpression of Ikappa-Balpha in Cdc25A-elevated cancer cells resistant to cisplatin improved their sensitivity to cisplatin-induced apoptosis. Cisplatin 175-184 cell division cycle 25A Homo sapiens 93-99 22160829-0 2012 Widdrol activates DNA damage checkpoint through the signaling Chk2-p53-Cdc25A-p21-MCM4 pathway in HT29 cells. widdrol 0-7 cell division cycle 25A Homo sapiens 71-77 22160829-7 2012 Based on this result, the change of proteins related in checkpoint pathway was examined over a time course of 0.5-24 h. Treatment of HT29 cells with widdrol elicits the following: (1) phosphorylation of Chk2 and p53, (2) reduction of cell division cycle 25A (Cdc25A) expression, (3) increase of Cdk inhibitor p21 expression, and (4) decrease of the levels of Cdk2 and cyclin E expression in a time-dependent manner. widdrol 149-156 cell division cycle 25A Homo sapiens 259-265 22583615-5 2012 Ataxia telangiectasia mutated protein kinase (ATM) was activated by GL331 through its autophosphorylation at Ser1981, which led to the activation of DNA damage signaling pathways including p53/p21 and Chk2/Cdc25A cascades. GL 331 68-73 cell division cycle 25A Homo sapiens 206-212 22012316-4 2012 Our results also reveal that reactive oxygen species (ROS)-mediated degradation of Cdc25C rather than Cdc25A or Cdc25B is responsible for vanadate-induced G(2)/M cell cycle arrest. Vanadates 138-146 cell division cycle 25A Homo sapiens 102-108 23071577-5 2012 METHODOLOGY/PRINCIPAL FINDINGS: Here we report a novel CDC25A transcript variant with codon 110 (Glutamine) deletion, that we termed CDC25A(Q110del) in NSCLC cells. Glutamine 97-106 cell division cycle 25A Homo sapiens 55-61 23240008-9 2012 We demonstrate that the phosphorylation of Thr 600 and Thr 611 residues of FOXM1 enhanced this interaction, and that the interaction is dependent upon CDC25A phosphatase activity. Threonine 43-46 cell division cycle 25A Homo sapiens 151-157 23240008-9 2012 We demonstrate that the phosphorylation of Thr 600 and Thr 611 residues of FOXM1 enhanced this interaction, and that the interaction is dependent upon CDC25A phosphatase activity. Threonine 55-58 cell division cycle 25A Homo sapiens 151-157 23071577-5 2012 METHODOLOGY/PRINCIPAL FINDINGS: Here we report a novel CDC25A transcript variant with codon 110 (Glutamine) deletion, that we termed CDC25A(Q110del) in NSCLC cells. Glutamine 97-106 cell division cycle 25A Homo sapiens 133-139 23071577-7 2012 Biological effects of CDC25A(Q110del) were investigated in H1299 and HEK-293F cells using UV radiation, flowcytometry, cyclohexamide treatment, and confocal microscopy. 4-[2-(3,5-dimethyl-2-oxocyclohexyl)-2-hydroxyethyl]piperidine-2,6-dione 119-132 cell division cycle 25A Homo sapiens 22-28 21958871-0 2011 Involvement of Chk1-Cdc25A-cyclin A/CDK2 pathway in simvastatin induced S-phase cell cycle arrest and apoptosis in multiple myeloma cells. Simvastatin 52-63 cell division cycle 25A Homo sapiens 20-26 21761201-0 2011 3,3"-Diindolylmethane inhibits breast cancer cell growth via miR-21-mediated Cdc25A degradation. 3,3'-diindolylmethane 0-21 cell division cycle 25A Homo sapiens 77-83 21761201-4 2011 Meanwhile, it was revealed that Ser(124) phosphorylation of Cdc25A is primarily responsible for the DIM-induced Cdc25A degradation. Serine 32-35 cell division cycle 25A Homo sapiens 60-66 21761201-4 2011 Meanwhile, it was revealed that Ser(124) phosphorylation of Cdc25A is primarily responsible for the DIM-induced Cdc25A degradation. Serine 32-35 cell division cycle 25A Homo sapiens 112-118 21958871-5 2011 The results of western blot showed that simvastatin-induced S-phase cell cycle arrest was associated with activation of Chk1, downregulation of Cdc25A, cyclin A and CDK2 expression. Simvastatin 40-51 cell division cycle 25A Homo sapiens 144-150 21958871-7 2011 Further investigation revealed that silence of Chk1 expression by Chk1 specific siRNA inhibited simvastatin-induced activation of Chk1, downregulation of Cdc25A, cyclin A and CDK2 expression, and diminished S phase cell cycle arrest. Simvastatin 96-107 cell division cycle 25A Homo sapiens 154-160 21958871-9 2011 These results suggested that the Chk1-Cdc25A-cyclin A/CDk2 pathway was involved in simvastatin-induced S-phase cell cycle arrest and apoptosis in multiple myeloma cell lines. Simvastatin 83-94 cell division cycle 25A Homo sapiens 38-44 21990039-4 2011 One of the compounds obtained shows general activity similar to that of imatinib; in particular, it was observed to be more effective in decreasing the fundamental function of cdc25A phosphatases in the K-562 cell line. Imatinib Mesylate 72-80 cell division cycle 25A Homo sapiens 176-182 21310058-3 2011 This complex binds to the Cdc25A DSG motif which contains serine residues at positions 82 and 88. Serine 58-64 cell division cycle 25A Homo sapiens 26-32 22131880-7 2011 We found that daurinol is a catalytic inhibitor of human topoisomerase IIa, and it induces S-phase arrest through the enhanced expression of cyclins E and A and by activation of the ATM/Chk/Cdc25A pathway in HCT116 cells. daurinol 14-22 cell division cycle 25A Homo sapiens 190-196 22242452-4 2011 The compounds 3e, 3h, 3j and 31 showed Cdc25A phosphatase inhibitory activity of 60.6%, 58.6%, 51.4% and 98.4% respectively at the test concentration of 20 microg x mL(-1), and among them 31 had inhibition rate of 86.97% even at the concentration as low as 5 microg x mL(-1), indicating worthy to be future studied. Tritium 18-20 cell division cycle 25A Homo sapiens 39-45 21282984-0 2011 3,3"-Diindolylmethane negatively regulates Cdc25A and induces a G2/M arrest by modulation of microRNA 21 in human breast cancer cells: retraction. 3,3'-diindolylmethane 0-21 cell division cycle 25A Homo sapiens 43-49 21291864-6 2011 AZD7762 increased ATR/ATM-mediated Chk1 phosphorylation and stabilized Cdc25A, suppressed cyclin A expression in lung cancer cell lines. 3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide 0-7 cell division cycle 25A Homo sapiens 71-77 21220732-6 2011 We identified CCNE1 and cdc25A as direct miR-503 targets which are downregulated by high glucose/low growth factors in ECs. Glucose 89-96 cell division cycle 25A Homo sapiens 24-30 20800482-3 2010 Herein we report new coumarin-based scaffolds endowed with a selective inhibition against Cdc25A and Cdc25C, being 6a and 6d the most efficient inhibitors and worthy of further investigation as anticancer agents. coumarin 21-29 cell division cycle 25A Homo sapiens 90-96 20849828-8 2011 The combined disregulation of Cdc25A and Cdc25B was the most likely cause for ABNM-13 induced S-phase arrest. ABNM-13 78-85 cell division cycle 25A Homo sapiens 30-36 21035837-9 2011 Exposure to thioridazine induced G(0)/G(1) arrest and down-regulated the cell cycle regulator, Cyclin D1 and CDK4, and up-regulated p21, p16, and p-CDC25A. Thioridazine 12-24 cell division cycle 25A Homo sapiens 148-154 20587702-0 2010 A novel mechanism of indole-3-carbinol effects on breast carcinogenesis involves induction of Cdc25A degradation. indole-3-carbinol 21-38 cell division cycle 25A Homo sapiens 94-100 20724916-0 2010 3,3"-Diindolylmethane negatively regulates Cdc25A and induces a G2/M arrest by modulation of microRNA 21 in human breast cancer cells. 3,3'-diindolylmethane 0-21 cell division cycle 25A Homo sapiens 43-49 20700484-6 2010 Activated Chk1 and Chk2 increase the expression of cell cycle checkpoint proteins, including Cdc25A and Cdc25C, leading to higher levels of G2/M arrest in tumor cells treated with NPRL2 and cisplatin than in tumor cells treated with cisplatin only. Cisplatin 233-242 cell division cycle 25A Homo sapiens 93-99 20700484-6 2010 Activated Chk1 and Chk2 increase the expression of cell cycle checkpoint proteins, including Cdc25A and Cdc25C, leading to higher levels of G2/M arrest in tumor cells treated with NPRL2 and cisplatin than in tumor cells treated with cisplatin only. Cisplatin 190-199 cell division cycle 25A Homo sapiens 93-99 20354770-7 2010 RESULTS: We found that genistein inhibited cell growth accompanied by induction of apoptosis with concomitant attenuation of FoxM1 and its downstream genes, such as survivin, cdc25a, MMP-9, and VEGF, resulting in the inhibition of pancreatic cancer cell invasion. Genistein 23-32 cell division cycle 25A Homo sapiens 175-181 20368335-1 2010 Cdc25A is a dual specificity protein phosphatase that activates cyclin/cyclin-dependent protein kinase (Cdk) complexes by removing inhibitory phosphates from conserved threonine and tyrosine in Cdks. Phosphates 142-152 cell division cycle 25A Homo sapiens 0-6 20368335-1 2010 Cdc25A is a dual specificity protein phosphatase that activates cyclin/cyclin-dependent protein kinase (Cdk) complexes by removing inhibitory phosphates from conserved threonine and tyrosine in Cdks. Threonine 168-177 cell division cycle 25A Homo sapiens 0-6 20368335-1 2010 Cdc25A is a dual specificity protein phosphatase that activates cyclin/cyclin-dependent protein kinase (Cdk) complexes by removing inhibitory phosphates from conserved threonine and tyrosine in Cdks. Tyrosine 182-190 cell division cycle 25A Homo sapiens 0-6 20368335-2 2010 To address how Cdc25A promotes apoptosis, Jurkat cells were treated with staurosporine, an apoptosis inducer. Staurosporine 73-86 cell division cycle 25A Homo sapiens 15-21 20368335-3 2010 Upon staurosporine treatment, a Cdc25A C-terminal 37-kDa fragment, designated C37, was generated by caspase cleavage at Asp-223. Staurosporine 5-18 cell division cycle 25A Homo sapiens 32-38 20368335-3 2010 Upon staurosporine treatment, a Cdc25A C-terminal 37-kDa fragment, designated C37, was generated by caspase cleavage at Asp-223. Aspartic Acid 120-123 cell division cycle 25A Homo sapiens 32-38 20501833-4 2010 AZD7762 inhibited Chk1 autophosphorylation (S296 Chk1), stabilized Cdc25A, and increased ATR/ATM-mediated Chk1 phosphorylation (S345 Chk1). 3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide 0-7 cell division cycle 25A Homo sapiens 67-73 20368335-9 2010 Thus, this study reveals that Cdc25A is a pro-apoptotic protein that amplifies staurosporine-induced apoptosis through the activation of cyclin B1/Cdc2 by its C-terminal domain. Staurosporine 79-92 cell division cycle 25A Homo sapiens 30-36 19948152-7 2010 Further research on the mechanism demonstrated that inhibition of miR-125b-induced U251 glioma stem cell proliferation was due to cell cycle arrest at the G1/S transition and involved the cell cycle regulated proteins CDK6 and CDC25A; miR-125b overexpression decreased CDK6 and CDC25A expression. mir-125b 66-74 cell division cycle 25A Homo sapiens 227-233 20360007-5 2010 In Cdc25A-overexpressing cells, Cdk1 exhibits high kinase activity despite being phosphorylated on Tyr(15). Tyrosine 99-102 cell division cycle 25A Homo sapiens 3-9 20360007-6 2010 In addition, Tyr(15)-phosphorylated Cdk1 binds more cyclin B in Cdc25A-overexpressing cells compared with control cells. Tyrosine 13-16 cell division cycle 25A Homo sapiens 64-70 20360007-9 2010 Importantly, we find that Cdc25A overexpression leads to an activation of Cdk7 and increase in Thr(161) phosphorylation of Cdk1. Threonine 95-98 cell division cycle 25A Homo sapiens 26-32 20421925-9 2010 We found that the anti-proliferative activity of capsaicin is correlated with a decrease in the expression of E2F-responsive proliferative genes like cyclin E, thymidylate synthase, cdc25A and cdc6, both at mRNA and protein levels. Capsaicin 49-58 cell division cycle 25A Homo sapiens 182-188 20025242-5 2010 The sequences for the catalytic domains of Cdc25A, -B, and -C were cloned individually into a prokaryotic expression vector, and their gene products were purified from a bacterial host using nickel affinity chromatography. Nickel 191-197 cell division cycle 25A Homo sapiens 43-49 19948152-7 2010 Further research on the mechanism demonstrated that inhibition of miR-125b-induced U251 glioma stem cell proliferation was due to cell cycle arrest at the G1/S transition and involved the cell cycle regulated proteins CDK6 and CDC25A; miR-125b overexpression decreased CDK6 and CDC25A expression. mir-125b 66-74 cell division cycle 25A Homo sapiens 278-284 19948152-8 2010 These findings underscore the potential of miR-125b to regulate the proliferation of U251 glioma stem cells through the cell cycle regulated proteins CDK6 and CDC25A. mir-125b 43-51 cell division cycle 25A Homo sapiens 159-165 19909759-0 2010 Berberine and a Berberis lycium extract inactivate Cdc25A and induce alpha-tubulin acetylation that correlate with HL-60 cell cycle inhibition and apoptosis. Berberine 0-9 cell division cycle 25A Homo sapiens 51-57 19621387-7 2010 Furthermore, mithramycin, which blocks Sp1 binding sites, decreased proliferation, inhibited CDC25A and FAS expression and reduced binding of Sp1 to the promoters of these genes as assessed by ChIP assays. Plicamycin 13-24 cell division cycle 25A Homo sapiens 93-99 19621387-8 2010 Conversely, 17beta-estradiol (E(2)) increased proliferation and CDC25A and FAS expression along with increased binding of Sp1 to the promoters of the 2 genes. Estradiol 12-28 cell division cycle 25A Homo sapiens 64-70 19732843-6 2009 It is also shown that genistein increases the phosphorylation and activation of Chk1 and Chk2, which results in the phosphorylation and inactivation of phosphatases Cdc25C and Cdc25A, and thereby the phosphorylation and inactivation of Cdc2 which arrests cells in G2/M phase. Genistein 22-31 cell division cycle 25A Homo sapiens 176-182 20606298-6 2010 When serine residues in the DSG motif, which is the critical sequences for the degradation of Cdc25A induced by DNA damage, is mutated to alanine (Cdc25A(DSG2X)), both stimulatory and protective effects of TRB3 on the Cdc25A degradation is disappeared. Serine 5-11 cell division cycle 25A Homo sapiens 94-100 20606298-6 2010 When serine residues in the DSG motif, which is the critical sequences for the degradation of Cdc25A induced by DNA damage, is mutated to alanine (Cdc25A(DSG2X)), both stimulatory and protective effects of TRB3 on the Cdc25A degradation is disappeared. Serine 5-11 cell division cycle 25A Homo sapiens 147-153 20606298-6 2010 When serine residues in the DSG motif, which is the critical sequences for the degradation of Cdc25A induced by DNA damage, is mutated to alanine (Cdc25A(DSG2X)), both stimulatory and protective effects of TRB3 on the Cdc25A degradation is disappeared. Serine 5-11 cell division cycle 25A Homo sapiens 147-153 20606298-6 2010 When serine residues in the DSG motif, which is the critical sequences for the degradation of Cdc25A induced by DNA damage, is mutated to alanine (Cdc25A(DSG2X)), both stimulatory and protective effects of TRB3 on the Cdc25A degradation is disappeared. Alanine 138-145 cell division cycle 25A Homo sapiens 94-100 20606298-6 2010 When serine residues in the DSG motif, which is the critical sequences for the degradation of Cdc25A induced by DNA damage, is mutated to alanine (Cdc25A(DSG2X)), both stimulatory and protective effects of TRB3 on the Cdc25A degradation is disappeared. Alanine 138-145 cell division cycle 25A Homo sapiens 147-153 20606298-6 2010 When serine residues in the DSG motif, which is the critical sequences for the degradation of Cdc25A induced by DNA damage, is mutated to alanine (Cdc25A(DSG2X)), both stimulatory and protective effects of TRB3 on the Cdc25A degradation is disappeared. Alanine 138-145 cell division cycle 25A Homo sapiens 147-153 19734889-7 2009 Furthermore, we demonstrate that CHK1 (checkpoint kinase 1) directly activates NEK11 by phosphorylating it on Ser 273, indicating that CHK1 and NEK11 operate in a single pathway that controls proteolysis of CDC25A. Serine 110-113 cell division cycle 25A Homo sapiens 207-213 19808979-9 2009 We thus conclude that triptolide is an original pharmacologic inhibitor of RNA polymerase activity, affecting indirectly the transcription machinery, leading to a rapid depletion of short-lived mRNA, including transcription factors, cell cycle regulators such as CDC25A, and the oncogenes MYC and Src. triptolide 22-32 cell division cycle 25A Homo sapiens 263-269 19634013-4 2009 In A549(p53(wt)), MNU induced G2/M arrest, accompanied by cdc25A degradation, hnRNP B1 induction, hnRNP C1/C2 downregulation. Methylnitrosourea 18-21 cell division cycle 25A Homo sapiens 58-64 19059218-5 2009 Inhibition of CHK1 kinase by Go6976, an inhibitor of CHK1 activity, can promote DNA damage and lead to the activation of CHK2, converting G2/M checkpoint into intra-S-phase checkpoint in which two parallel branches, the ATM-CHK2-CDC25A-CDK2 and the ATM-NBS1/SMC1 cascades, are involved. Go 6976 29-35 cell division cycle 25A Homo sapiens 229-235 19638579-5 2009 Nongenotoxic stress induced by anisomycin caused rapid degradation of Cdc25B as well as Cdc25A. Anisomycin 31-41 cell division cycle 25A Homo sapiens 88-94 19289404-7 2009 On the other hand, Cdc25A was protected by Hsp90 in HEK293 cells because the specific inhibition of Hsp90 with Geldanamycin caused Cdc25A degradation in HEK293 implicating that Cdc25A is an Hsp90 client. geldanamycin 111-123 cell division cycle 25A Homo sapiens 19-25 19289404-7 2009 On the other hand, Cdc25A was protected by Hsp90 in HEK293 cells because the specific inhibition of Hsp90 with Geldanamycin caused Cdc25A degradation in HEK293 implicating that Cdc25A is an Hsp90 client. geldanamycin 111-123 cell division cycle 25A Homo sapiens 131-137 19289404-7 2009 On the other hand, Cdc25A was protected by Hsp90 in HEK293 cells because the specific inhibition of Hsp90 with Geldanamycin caused Cdc25A degradation in HEK293 implicating that Cdc25A is an Hsp90 client. geldanamycin 111-123 cell division cycle 25A Homo sapiens 131-137 19383849-3 2009 DHE suppresses the expression of cyclin D, cyclin A, cyclin-dependent kinase 2, and cdc25A and increases the amount of p53 and p21, resulting in G(0)/G(1)-S phase arrest in MCF-7 cells. dehydrocostus lactone 0-3 cell division cycle 25A Homo sapiens 84-90 19383849-4 2009 In contrast, DHE caused S-G(2)/M arrest by increasing p21 expression and chk1 activation and inhibiting cyclin A, cyclin B, cdc25A, and cdc25C expression in MDA-MB-231 cells. dehydrocostus lactone 13-16 cell division cycle 25A Homo sapiens 124-130 19318573-4 2009 In our current study, we found that TW-37 induces cell growth inhibition and S-phase cell cycle arrest, with regulation of several important cell cycle-related genes like p27, p57, E2F-1, cdc25A, CDK4, cyclin A, cyclin D1, and cyclin E. The cell growth inhibition was accompanied by increased apoptosis with concomitant attenuation of Notch-1, Jagged-1, and its downstream genes such as Hes-1 in vitro and in vivo. TW-37 36-41 cell division cycle 25A Homo sapiens 188-194 19081252-2 2009 Using DAz-1, we detect sulfenic acid modifications in the cell-cycle regulatory phosphatase Cdc25A. Sulfenic Acids 23-36 cell division cycle 25A Homo sapiens 92-98 19223497-7 2009 Gemcitabine blocked replication of all viruses despite the enhanced cell killing activity due to gemcitabine-induced delay in G1/S-cell cycle progression, with repression of cyclin E and cdc25A, which was not abrogated by viral E1A-expression. gemcitabine 0-11 cell division cycle 25A Homo sapiens 187-193 19223497-7 2009 Gemcitabine blocked replication of all viruses despite the enhanced cell killing activity due to gemcitabine-induced delay in G1/S-cell cycle progression, with repression of cyclin E and cdc25A, which was not abrogated by viral E1A-expression. gemcitabine 97-108 cell division cycle 25A Homo sapiens 187-193 19060337-6 2009 In cells deficient in both Chk1 and p53, Cdc25A down-regulation upon camptothecin-induced DNA damage is completely abolished, leading to severe defects in cell cycle checkpoints and remarkable cell death in mitosis. Camptothecin 69-81 cell division cycle 25A Homo sapiens 41-47 19075567-1 2008 The Cdc25 phosphatases (Cdc25A, Cdc25B, and Cdc25C in humans), which are responsible for dephosphorylating specific tyrosine/threonine residues on cyclin dependent kinases (CDKs), function as essential regulators of cell cycle control during normal eukaryotic cell division and as mediators of the checkpoint response in cells with DNA damage. Tyrosine 116-124 cell division cycle 25A Homo sapiens 24-30 19158509-3 2009 Herein we report that nitrosative stress catalyzed by inducible nitric oxide (*NO) synthase (iNOS) or the chemical nitrosant S-nitrosocysteine ethyl ester (SNCEE) rapidly inhibited DNA synthesis concomitant with Cdc25A loss. Nitric Oxide 64-76 cell division cycle 25A Homo sapiens 212-218 19158509-3 2009 Herein we report that nitrosative stress catalyzed by inducible nitric oxide (*NO) synthase (iNOS) or the chemical nitrosant S-nitrosocysteine ethyl ester (SNCEE) rapidly inhibited DNA synthesis concomitant with Cdc25A loss. S-nitrosocysteine ethyl ester 125-154 cell division cycle 25A Homo sapiens 212-218 19139112-4 2009 PD-321852 inhibited Chk1 in all cell lines as evidenced by stabilization of Cdc25A; in combination with gemcitabine, a synergistic loss of Chk1 protein was observed in the more sensitized cell lines. 4-(2,6-dichlorophenyl)-9-hydroxy-6-(3-methylaminopropyl)-6H-pyrrolo(3,4-c)carbazole-1,3-dione 0-9 cell division cycle 25A Homo sapiens 76-82 19075567-1 2008 The Cdc25 phosphatases (Cdc25A, Cdc25B, and Cdc25C in humans), which are responsible for dephosphorylating specific tyrosine/threonine residues on cyclin dependent kinases (CDKs), function as essential regulators of cell cycle control during normal eukaryotic cell division and as mediators of the checkpoint response in cells with DNA damage. Threonine 125-134 cell division cycle 25A Homo sapiens 24-30 18442908-0 2008 Design and synthesis of N-alkyl oxindolylidene acetic acids as a new class of potent Cdc25A inhibitors. n-alkyl oxindolylidene acetic acids 24-59 cell division cycle 25A Homo sapiens 85-91 18504625-5 2008 A detailed binding mode analysis of the known inhibitors shows that they can be stabilized in the active site of Cdc25A through the simultaneous establishment of the multiple hydrogen bonds and the hydrophobic interactions. Hydrogen 175-183 cell division cycle 25A Homo sapiens 113-119 18495657-11 2008 Notably, mesalazine also inhibited CDC25A in human CRC explants. Mesalamine 9-19 cell division cycle 25A Homo sapiens 35-41 18495657-13 2008 Data show that mesalazine negatively regulates CDC25A protein expression, thus delaying CRC cell progression. Mesalamine 15-25 cell division cycle 25A Homo sapiens 47-53 18980975-6 2008 RESULTS: Cisplatin induced degradation of Cdc25A in nonmetastatic HCC cells but not in metastatic HCC cells. Cisplatin 9-18 cell division cycle 25A Homo sapiens 42-48 18794133-2 2008 Reactive oxygen species, such as hydrogen peroxide, regulate Cdc25A, but the physiologic and pathologic effects of nitric oxide (*NO) and *NO-derived reactive species are not well defined. Reactive Oxygen Species 0-23 cell division cycle 25A Homo sapiens 61-67 18794133-2 2008 Reactive oxygen species, such as hydrogen peroxide, regulate Cdc25A, but the physiologic and pathologic effects of nitric oxide (*NO) and *NO-derived reactive species are not well defined. Hydrogen Peroxide 33-50 cell division cycle 25A Homo sapiens 61-67 18794133-4 2008 We observed direct and rapid inhibition of Cdc25A phosphatase activity after in vitro treatment with the low molecular mass cell-permeable S-nitrosothiol S-nitrosocysteine ethyl ester (SNCEE). S-Nitrosothiols 139-153 cell division cycle 25A Homo sapiens 43-49 18794133-4 2008 We observed direct and rapid inhibition of Cdc25A phosphatase activity after in vitro treatment with the low molecular mass cell-permeable S-nitrosothiol S-nitrosocysteine ethyl ester (SNCEE). S-nitrosocysteine ethyl ester 154-183 cell division cycle 25A Homo sapiens 43-49 18794133-4 2008 We observed direct and rapid inhibition of Cdc25A phosphatase activity after in vitro treatment with the low molecular mass cell-permeable S-nitrosothiol S-nitrosocysteine ethyl ester (SNCEE). S-nitrosocysteine ethyl ester 185-190 cell division cycle 25A Homo sapiens 43-49 18794133-9 2008 Nitrosative stress decreased the Cdc25A-bound fraction of apoptosis signal-regulating kinase-1 (ASK-1) and sensitized cells to apoptosis induced by the ASK-1-activating chemotherapeutic cis-diaminedichloroplatinum (II), suggesting that nitrosative stress-induced suppression of Cdc25A primed cells for ASK-1-dependent apoptosis. cis-Diaminedichloroplatinum 186-213 cell division cycle 25A Homo sapiens 33-39 18480045-2 2008 Cdc25A degradation occurs via the SCFbeta-TRCP pathway and phosphorylation of Ser-76. Serine 78-81 cell division cycle 25A Homo sapiens 0-6 18480045-3 2008 Previous work indicates that the checkpoint kinase Checkpoint kinase 1 (Chk1) is capable of phosphorylating Ser-76 in Cdc25A, thereby promoting its degradation. Serine 108-111 cell division cycle 25A Homo sapiens 118-124 18495657-0 2008 Mesalazine negatively regulates CDC25A protein expression and promotes accumulation of colon cancer cells in S phase. Mesalamine 0-10 cell division cycle 25A Homo sapiens 32-38 18495657-7 2008 Consistently, mesalazine reduced the protein content of CDC25A, a phosphatase that regulates CDK2 phosphorylation status. Mesalamine 14-24 cell division cycle 25A Homo sapiens 56-62 18495657-8 2008 Analysis of upstream kinases that negatively control CDC25A expression showed that mesalazine enhanced the activation of CHK1 and CHK2. Mesalamine 83-93 cell division cycle 25A Homo sapiens 53-59 18495657-10 2008 In contrast, CDC25A protein ubiquitination and degradation and accumulation of cells in S phase following mesalazine exposure were reverted by proteasome inhibitors. Mesalamine 106-116 cell division cycle 25A Homo sapiens 13-19 18442908-1 2008 The oxindolylidene acetic acids having long N-alkyl chains exhibited strong inhibitory activity toward dual specificity phosphatase Cdc25A. oxindolylidene acetic acids 4-31 cell division cycle 25A Homo sapiens 132-138 18088187-9 2007 The pathway of Chk1 phosphorylation --> Cdc25A degradation --> inhibition of cyclin B1/Cdk1 activity --> G2 arrest is accordingly resistant to staurosporine and UCN-01 in p53+/+ cells. 7-hydroxystaurosporine 170-176 cell division cycle 25A Homo sapiens 43-49 18321631-5 2008 Cdc25A down-regulation by RNA interference (RNAi) prolonged the S-phase arrest induced by BaP and decreased clearly the expression levels of cyclin A and cyclin E. Therefore, our results further demonstrated that Cdc25A was an effector in Chk1-Cdc25A-cyclin A/Cdk2 pathway of S-phase checkpoint elicited by the carcinogen BaP in 16HBE cells. Benzo(a)pyrene 90-93 cell division cycle 25A Homo sapiens 0-6 18321631-5 2008 Cdc25A down-regulation by RNA interference (RNAi) prolonged the S-phase arrest induced by BaP and decreased clearly the expression levels of cyclin A and cyclin E. Therefore, our results further demonstrated that Cdc25A was an effector in Chk1-Cdc25A-cyclin A/Cdk2 pathway of S-phase checkpoint elicited by the carcinogen BaP in 16HBE cells. Benzo(a)pyrene 90-93 cell division cycle 25A Homo sapiens 213-219 18321631-5 2008 Cdc25A down-regulation by RNA interference (RNAi) prolonged the S-phase arrest induced by BaP and decreased clearly the expression levels of cyclin A and cyclin E. Therefore, our results further demonstrated that Cdc25A was an effector in Chk1-Cdc25A-cyclin A/Cdk2 pathway of S-phase checkpoint elicited by the carcinogen BaP in 16HBE cells. Benzo(a)pyrene 90-93 cell division cycle 25A Homo sapiens 213-219 18321631-5 2008 Cdc25A down-regulation by RNA interference (RNAi) prolonged the S-phase arrest induced by BaP and decreased clearly the expression levels of cyclin A and cyclin E. Therefore, our results further demonstrated that Cdc25A was an effector in Chk1-Cdc25A-cyclin A/Cdk2 pathway of S-phase checkpoint elicited by the carcinogen BaP in 16HBE cells. Benzo(a)pyrene 322-325 cell division cycle 25A Homo sapiens 0-6 18321631-5 2008 Cdc25A down-regulation by RNA interference (RNAi) prolonged the S-phase arrest induced by BaP and decreased clearly the expression levels of cyclin A and cyclin E. Therefore, our results further demonstrated that Cdc25A was an effector in Chk1-Cdc25A-cyclin A/Cdk2 pathway of S-phase checkpoint elicited by the carcinogen BaP in 16HBE cells. Benzo(a)pyrene 322-325 cell division cycle 25A Homo sapiens 213-219 18321631-5 2008 Cdc25A down-regulation by RNA interference (RNAi) prolonged the S-phase arrest induced by BaP and decreased clearly the expression levels of cyclin A and cyclin E. Therefore, our results further demonstrated that Cdc25A was an effector in Chk1-Cdc25A-cyclin A/Cdk2 pathway of S-phase checkpoint elicited by the carcinogen BaP in 16HBE cells. Benzo(a)pyrene 322-325 cell division cycle 25A Homo sapiens 213-219 18204780-4 2008 Administration of CDC25A antisense (AS) oligonucleotide resulted in 25-50% inhibition of cell growth at 48 h, G0-G1 arrest, and significant inhibition of cancer cell invasion. Oligonucleotides 40-55 cell division cycle 25A Homo sapiens 18-24 18321631-0 2008 The effects of over-expression and suppression of Cdc25A on the S-phase checkpoint induced by benzo(a)pyrene. Benzo(a)pyrene 94-108 cell division cycle 25A Homo sapiens 50-56 18321631-1 2008 Our previous results have indicated that Cdc25A is involved in benzo(a)pyrene (BaP)-induced S-phase checkpoint in 16HBE cells and A549 cells. Benzo(a)pyrene 63-77 cell division cycle 25A Homo sapiens 41-47 18321631-1 2008 Our previous results have indicated that Cdc25A is involved in benzo(a)pyrene (BaP)-induced S-phase checkpoint in 16HBE cells and A549 cells. Benzo(a)pyrene 79-82 cell division cycle 25A Homo sapiens 41-47 18321631-2 2008 In this paper, we reported the changes of the downstream molecular pathway of Cdc25A and the effects of over-expression and suppression of Cdc25A on BaP-induced S-phase checkpoint. Benzo(a)pyrene 149-152 cell division cycle 25A Homo sapiens 78-84 18321631-2 2008 In this paper, we reported the changes of the downstream molecular pathway of Cdc25A and the effects of over-expression and suppression of Cdc25A on BaP-induced S-phase checkpoint. Benzo(a)pyrene 149-152 cell division cycle 25A Homo sapiens 139-145 18321631-3 2008 In the S-phase checkpoint induced by BaP the reduction of Cdc25A contributes to cyclin A inhibition. Benzo(a)pyrene 37-40 cell division cycle 25A Homo sapiens 58-64 18321631-4 2008 Over-expression of Cdc25A abrogated BaP-induced S-phase arrest in 16HBE cells and concomitantly the expression levels of Cdk2 and cyclin A were not obviously changed by BaP when compared with the control. Benzo(a)pyrene 36-39 cell division cycle 25A Homo sapiens 19-25 17653574-0 2008 Bendamustine induces G2 cell cycle arrest and apoptosis in myeloma cells: the role of ATM-Chk2-Cdc25A and ATM-p53-p21-pathways. Bendamustine Hydrochloride 0-12 cell division cycle 25A Homo sapiens 95-101 17545210-0 2007 Arsenite slows S phase progression via inhibition of cdc25A dual specificity phosphatase gene transcription. arsenite 0-8 cell division cycle 25A Homo sapiens 53-59 17545210-4 2007 Immunoblotting reveals that a 3-h treatment of U937 cells with 5 microM sodium arsenite results in a dramatic decrease in cdc25A protein levels. sodium arsenite 72-87 cell division cycle 25A Homo sapiens 122-128 17545210-6 2007 Therefore, arsenite-dependent cdc25A depletion could contribute to S phase inhibition. arsenite 11-19 cell division cycle 25A Homo sapiens 30-36 17545210-8 2007 However, cycloheximide half-life assay reveals that cdc25A is actually stabilized in arsenite-treated cells. Cycloheximide 9-22 cell division cycle 25A Homo sapiens 52-58 17545210-8 2007 However, cycloheximide half-life assay reveals that cdc25A is actually stabilized in arsenite-treated cells. arsenite 85-93 cell division cycle 25A Homo sapiens 52-58 17545210-9 2007 Real-time RT-PCR shows that cdc25A mRNA levels are substantially decreased with arsenite treatment, and actinomycin D half-life assay reveals no change in message stability. arsenite 80-88 cell division cycle 25A Homo sapiens 28-34 17545210-10 2007 Decreased cdc25A message translation is shown by sucrose density gradient polysomal analysis to be an unlikely cause for the profound arsenite-dependent reduction in cdc25A protein levels. arsenite 134-142 cell division cycle 25A Homo sapiens 166-172 17545210-11 2007 Studies are ongoing to establish the mechanism by which 5 microM arsenite decreases cdc25A message abundance, but we surmise that, given the lack of effect on mRNA stability, an inhibition of gene transcription is likely involved. arsenite 65-73 cell division cycle 25A Homo sapiens 84-90 17283158-7 2007 We further show that nelfinavir inhibits CDK2 through proteasome-dependent degradation of Cdc25A phosphatase. Nelfinavir 21-31 cell division cycle 25A Homo sapiens 90-96 17602818-0 2007 The Cdc25A is involved in S-phase checkpoint induced by benzo(a)pyrene. Benzo(a)pyrene 56-70 cell division cycle 25A Homo sapiens 4-10 17602818-3 2007 However, the role of Cdc25A in the BaP/BPDE-induced checkpoint is not clear. Benzo(a)pyrene 35-38 cell division cycle 25A Homo sapiens 21-27 17602818-3 2007 However, the role of Cdc25A in the BaP/BPDE-induced checkpoint is not clear. 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide 39-43 cell division cycle 25A Homo sapiens 21-27 17611684-8 2007 Zoledronate also induced phosphorylation of cdc25a (Thr506) in HOS cells, which is a substrate of Chk1, and its phosphorylation is known to be critical for S phase arrest. Zoledronic Acid 0-11 cell division cycle 25A Homo sapiens 44-50 17602818-4 2007 In the present study, we investigated the change of checkpoint kinase 1 (Chk1) and Cdc25A in S-phase arrest elicited by BaP. Benzo(a)pyrene 120-123 cell division cycle 25A Homo sapiens 83-89 17602818-7 2007 The level of phorsphorylated Chk1 obviously increased and Cdc25A protein level decreased in both two cell lines after treatment with BaP. Benzo(a)pyrene 133-136 cell division cycle 25A Homo sapiens 58-64 17602818-9 2007 The treatment of the proteasome inhibitor MG132 greatly increased Cdc25A protein in abundance. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 42-47 cell division cycle 25A Homo sapiens 66-72 17602818-10 2007 Over all, our results indicated Chk1-Cdc25A checkpoint pathway is involved in BaP-induced S-phase arrest. Benzo(a)pyrene 78-81 cell division cycle 25A Homo sapiens 37-43 17431115-7 2007 Thus, Apo2L/TRAIL + CPT-11 treatment-induced apoptosis is regulated through an S-phase checkpoint controlled by the Chk2-Cdc25A and Chk1-Cdc25A pathways and inhibition of Cdk2-associated kinase activity. Irinotecan 20-26 cell division cycle 25A Homo sapiens 121-127 17431115-7 2007 Thus, Apo2L/TRAIL + CPT-11 treatment-induced apoptosis is regulated through an S-phase checkpoint controlled by the Chk2-Cdc25A and Chk1-Cdc25A pathways and inhibition of Cdk2-associated kinase activity. Irinotecan 20-26 cell division cycle 25A Homo sapiens 137-143 16413407-7 2006 Induction of phosphatase activity may represent one mechanism of RNS-induced arrest, for the PP1/PP2A phosphatase inhibitor okadaic acid inhibited dephosphorylation of pRB; prevented decreases in the levels of RF-C, cyclin D1, Cdc6, and Cdc25A; and bypassed arrest by SIN-1 or NO(2), but not cisplatin or adozelesin. Reactive Nitrogen Species 65-68 cell division cycle 25A Homo sapiens 237-243 17018577-5 2007 Caulibugulone A also caused the selective degradation of Cdc25A protein by a process that was independent of reactive oxygen species production, proteasome activity, and the Chk1 signaling pathway. caulibugulone A 0-15 cell division cycle 25A Homo sapiens 57-63 16930563-10 2006 It preferentially inhibited the activities of the cell cycle controlling phosphatases Cdc25A and Cdc25B, by binding to their catalytic cysteines. Cysteine 135-144 cell division cycle 25A Homo sapiens 86-92 16928871-0 2006 The Chk1/Cdc25A pathway as activators of the cell cycle in neuronal death induced by camptothecin. Camptothecin 85-97 cell division cycle 25A Homo sapiens 9-15 16928871-11 2006 During camptothecin treatment of neurons, this activity is rapidly downregulated with a concomitant increase in Cdc25A activity. Camptothecin 7-19 cell division cycle 25A Homo sapiens 112-118 16928871-12 2006 Importantly, expression of wild-type Chk1, but not kinase-dead Chk1, inhibits the camptothecin-induced increase in Cdc25A activity. Camptothecin 82-94 cell division cycle 25A Homo sapiens 115-121 17018577-5 2007 Caulibugulone A also caused the selective degradation of Cdc25A protein by a process that was independent of reactive oxygen species production, proteasome activity, and the Chk1 signaling pathway. Reactive Oxygen Species 109-132 cell division cycle 25A Homo sapiens 57-63 17018577-6 2007 Instead, caulibugulone A stimulated the phosphorylation and subsequent activation of p38 stress kinase, leading to Cdc25A degradation. caulibugulone A 9-24 cell division cycle 25A Homo sapiens 115-121 17018577-7 2007 Thus, caulibugulone inhibition of cellular Cdc25A and B phosphatases occurred through at least two different mechanisms, leading to pronounced cell cycle arrest. caulibugulone 6-19 cell division cycle 25A Homo sapiens 43-49 17172867-0 2006 Human Cdc14A reverses CDK1 phosphorylation of Cdc25A on serines 115 and 320. Serine 56-63 cell division cycle 25A Homo sapiens 46-52 17172867-5 2006 Specifically, the Cdk1/Cyclin-B1-dependent phosphate groups on Ser115 and Ser320 of Cdc25A were found to be removed by Cdc14A. Phosphates 43-52 cell division cycle 25A Homo sapiens 84-90 17172433-0 2006 Gallic acid causes inactivating phosphorylation of cdc25A/cdc25C-cdc2 via ATM-Chk2 activation, leading to cell cycle arrest, and induces apoptosis in human prostate carcinoma DU145 cells. Gallic Acid 0-11 cell division cycle 25A Homo sapiens 51-57 17172433-5 2006 Further upstream, gallic acid also induced phosphorylation of both cdc25A and cdc25C via ataxia telangiectasia mutated (ATM)-checkpoint kinase 2 (Chk2) activation as a DNA damage response evidenced by increased phospho-histone 2AX (H2A.X) that is phosphorylated by ATM in response to DNA damage. Gallic Acid 18-29 cell division cycle 25A Homo sapiens 67-73 17172433-6 2006 Time kinetics of ATM phosphorylation, together with those of H2A.X and Chk2, was in accordance with an inactivating phosphorylation of cdc25A and cdc25C phosphatases and cdc2 kinase, suggesting that gallic acid increases cdc25A/C-cdc2 phosphorylation and thereby inactivation via ATM-Chk2 pathway following DNA damage that induces cell cycle arrest. Gallic Acid 199-210 cell division cycle 25A Homo sapiens 135-141 17055492-2 2006 We show that a metabolically stable analogue of anandamide, Met-F-AEA, induces an S phase growth arrest correlated with Chk1 activation, Cdc25A degradation and suppression of Cdk2 activity. anandamide 48-58 cell division cycle 25A Homo sapiens 137-143 16969075-7 2006 H32 preferentially inhibited the activities of the cell cycle controlling Cdc25A phosphatase likely by binding to its catalytic cysteine. Cysteine 128-136 cell division cycle 25A Homo sapiens 74-80 16931916-5 2006 Furthermore, enhanced cytotoxicity by Chk1 depletion was accompanied by inhibition of FdUrd- or gemcitabine-induced Cdc25A degradation and induction of premature mitotic entry in drug-treated cells. gemcitabine 96-107 cell division cycle 25A Homo sapiens 116-122 16598773-0 2006 17beta-estradiol (E2) induces cdc25A gene expression in breast cancer cells by genomic and non-genomic pathways. Estradiol 0-16 cell division cycle 25A Homo sapiens 30-36 16598773-0 2006 17beta-estradiol (E2) induces cdc25A gene expression in breast cancer cells by genomic and non-genomic pathways. Estradiol 18-20 cell division cycle 25A Homo sapiens 30-36 16598773-2 2006 Cdc25A mRNA levels are induced by 17beta-estradiol (E2) in ZR-75 breast cancer cells, and deletion analysis of the cdc25A promoter identified the -151 to -12 region as the minimal E2-responsive sequence. Estradiol 34-50 cell division cycle 25A Homo sapiens 0-6 16598773-4 2006 Studies with inhibitors and dominant negative expression plasmids show that E2 activates cdc25A expression through activation of genomic ERalpha/Sp1 and E2F1 and cAMP-dependent activation of NF-YA. Cyclic AMP 162-166 cell division cycle 25A Homo sapiens 89-95 16818510-0 2006 PM-20, a novel inhibitor of Cdc25A, induces extracellular signal-regulated kinase 1/2 phosphorylation and inhibits hepatocellular carcinoma growth in vitro and in vivo. maleimide analog 0-5 cell division cycle 25A Homo sapiens 28-34 16818510-5 2006 PM-20 affected two cellular signaling pathways in Hep3B cells: Cdc25 phosphatase and extracellular signal-regulated kinase (ERK) 1/2. maleimide analog 0-5 cell division cycle 25A Homo sapiens 63-68 16818510-6 2006 It competitively inhibited the activity of Cdc25 (preferentially Cdc25A) by binding to the active site, likely through the catalytic cysteine, but did not inhibit PTP1B, CD45, or MKP-1 phosphatases. Cysteine 133-141 cell division cycle 25A Homo sapiens 43-48 16818510-6 2006 It competitively inhibited the activity of Cdc25 (preferentially Cdc25A) by binding to the active site, likely through the catalytic cysteine, but did not inhibit PTP1B, CD45, or MKP-1 phosphatases. Cysteine 133-141 cell division cycle 25A Homo sapiens 65-71 16818510-7 2006 As a result of its action, tyrosine phosphorylation of the cellular Cdc25A substrates Cdk2 and Cdk4 was induced. Tyrosine 27-35 cell division cycle 25A Homo sapiens 68-74 16818510-13 2006 The mechanism(s) of growth inhibition of Hep3B hepatoma cells by the phenyl maleimide PM-20 involves prolonged ERK1/2 phosphorylation, likely resulting from inhibition of the ERK phosphatase Cdc25A. phenyl maleimide pm-20 69-91 cell division cycle 25A Homo sapiens 191-197 16651453-8 2006 We have tested our hypothesis using multiple molecular approaches and found that 3,3"-diindolylmethane inhibited cell growth and induced apoptosis in MDA-MB-231 breast cancer cells by down-regulating survivin, Bcl-2, and cdc25A expression and also caused up-regulation of p21(WAF1) expression, which could be responsible for cell cycle arrest. 3,3'-diindolylmethane 81-102 cell division cycle 25A Homo sapiens 221-227 16337966-5 2006 Only a low dose of bile acid induced the expression of cyclin D1 and CDC25A and showed high Rb phosphorylation and high CDK2 kinase activity. Bile Acids and Salts 19-28 cell division cycle 25A Homo sapiens 69-75 16413407-4 2006 As for the positive controls adozelesin and cisplatin, arrest was accompanied by phosphorylation of ATM kinase; dephosphorylation of pRB; decreases in RF-C, cyclin D1, Cdc25A, and Cdc6; and increases in p21. Cisplatin 44-53 cell division cycle 25A Homo sapiens 168-174 16413407-7 2006 Induction of phosphatase activity may represent one mechanism of RNS-induced arrest, for the PP1/PP2A phosphatase inhibitor okadaic acid inhibited dephosphorylation of pRB; prevented decreases in the levels of RF-C, cyclin D1, Cdc6, and Cdc25A; and bypassed arrest by SIN-1 or NO(2), but not cisplatin or adozelesin. Okadaic Acid 124-136 cell division cycle 25A Homo sapiens 237-243 16170030-3 2005 BN82685 inhibits recombinant CDC25A, B, and C phosphatases in vitro. BN 82685 0-7 cell division cycle 25A Homo sapiens 29-35 16061666-5 2005 We found that radiosensitizing concentrations of gemcitabine induced accumulation of phosphorylated Chk1 and Chk2 and down-regulation of Cdc25A in BxPC-3 (10 nmol/L), Panc-1 (100 nmol/L), A549 (30 nmol/L), RKO (30 nmol/L), and SW620 (30 nmol/L) cells. gemcitabine 49-60 cell division cycle 25A Homo sapiens 137-143 16061666-6 2005 Depletion of Chk1 from Panc-1 cells prevented the down-regulation of Cdc25A in response to gemcitabine. gemcitabine 91-102 cell division cycle 25A Homo sapiens 69-75 15672448-2 2005 We previously found that 2-(2-mercaptoethanol)-3-methyl-1,4-napthoquinone or Compound 5 (Cpd 5), is a Cdc25A protein phosphatase inhibitor and causes prolonged, strong ERK phosphorylation which is triggered by epidermal growth factor receptor (EGFR) activation. 2-(2-mercaptoethanol 25-45 cell division cycle 25A Homo sapiens 102-108 15672448-2 2005 We previously found that 2-(2-mercaptoethanol)-3-methyl-1,4-napthoquinone or Compound 5 (Cpd 5), is a Cdc25A protein phosphatase inhibitor and causes prolonged, strong ERK phosphorylation which is triggered by epidermal growth factor receptor (EGFR) activation. 3-methyl-1,4-napthoquinone 47-73 cell division cycle 25A Homo sapiens 102-108 15784732-4 2005 Cytarabine, at concentrations as low as 30 nM, caused activating phosphorylation of Chk1, loss of the phosphatase Cdc25A, and S-phase slowing. Cytarabine 0-10 cell division cycle 25A Homo sapiens 114-120 15937284-11 2005 From the screen, we successfully identified a positive synergistic interaction between nondetergent sulfobetaine 201 (NDSB 201) and BMC on Cdc25A refolding. sulfobetaine 100-112 cell division cycle 25A Homo sapiens 139-145 15937284-11 2005 From the screen, we successfully identified a positive synergistic interaction between nondetergent sulfobetaine 201 (NDSB 201) and BMC on Cdc25A refolding. bmc 132-135 cell division cycle 25A Homo sapiens 139-145 15677471-9 2005 Following hydrogen peroxide stimulation, STAT3 forms a repressor complex with the retinoblastoma (Rb) tumor suppressor to occupy the Cdc25A promoter and block its induction. Hydrogen Peroxide 10-27 cell division cycle 25A Homo sapiens 133-139 15845771-6 2005 When analyzed by using Xenopus eggs, the binding of beta-TrCP to the DDG motif is essential for the Chk1-induced ubiquitination and degradation of Xenopus Cdc25A and also plays a role in the degradation of human Cdc25A. ddg 69-72 cell division cycle 25A Homo sapiens 212-218 15652497-0 2005 Quinone-induced Cdc25A inhibition causes ERK-dependent connexin phosphorylation. quinone 0-7 cell division cycle 25A Homo sapiens 16-22 15608676-7 2005 5-FU confers S-phase arrest through Chk1-mediated Cdc25A proteolysis leading to inhibition of Cdk2. Fluorouracil 0-4 cell division cycle 25A Homo sapiens 50-56 15561098-3 2005 Whereas exposure of human cells to topoisomerase inhibitors camptothecin, etoposide, or adriamycin resulted in rapid (within 1 h) activation of the pathway including degradation of the Cdc25A phosphatase and inhibition of cyclin E/CDK2 kinase activity, taxol failed to activate this checkpoint even after a prolonged treatment. Camptothecin 60-72 cell division cycle 25A Homo sapiens 185-191 15561098-3 2005 Whereas exposure of human cells to topoisomerase inhibitors camptothecin, etoposide, or adriamycin resulted in rapid (within 1 h) activation of the pathway including degradation of the Cdc25A phosphatase and inhibition of cyclin E/CDK2 kinase activity, taxol failed to activate this checkpoint even after a prolonged treatment. Etoposide 74-83 cell division cycle 25A Homo sapiens 185-191 15561098-3 2005 Whereas exposure of human cells to topoisomerase inhibitors camptothecin, etoposide, or adriamycin resulted in rapid (within 1 h) activation of the pathway including degradation of the Cdc25A phosphatase and inhibition of cyclin E/CDK2 kinase activity, taxol failed to activate this checkpoint even after a prolonged treatment. Doxorubicin 88-98 cell division cycle 25A Homo sapiens 185-191 15028555-11 2004 The mTOR inhibitor rapamycin had similar inhibitory effects on G(1) cell cycle progression and on the expression of cyclin D1, CDK4, CDC25A, and retinoblastoma phosphorylation. Sirolimus 19-28 cell division cycle 25A Homo sapiens 133-139 15582411-0 2005 Synthesis of the naphthalene-derived inhibitors against Cdc25A dual-specificity protein phosphatase and their biological activity. naphthalene 17-28 cell division cycle 25A Homo sapiens 56-62 15548605-5 2004 A 147-member compound collection derived from the naturally occurring Cdc25A inhibitor dysidiolide yielded potent and selective inhibitors of the other members of the similarity cluster with a hit rate of 2-3%. dysidiolide 87-98 cell division cycle 25A Homo sapiens 70-76 15374972-0 2004 5-fluoro-2"-deoxyuridine-induced cdc25A accumulation correlates with premature mitotic entry and clonogenic death in human colon cancer cells. 5-fluoro-2'-deoxyuridine 0-24 cell division cycle 25A Homo sapiens 33-39 15547708-5 2004 Following a 24-h exposure, NaBu-induced cell growth arrest in G2/M phase in a dose-dependent fashion in association with stable expression of CDC25A, a G1-specific regulator of the cell cycle. sethoxydim 27-31 cell division cycle 25A Homo sapiens 142-148 15736430-3 2004 Furthermore, Chk1 also phosphorylates Cdc25A on serine 123 which accelerates its degradation through the ubiquitin-proteasome pathway and arrests cells in late G2-phase after DNA damage. Serine 48-54 cell division cycle 25A Homo sapiens 38-44 15261298-0 2004 Design and synthesis of novel Cdc25A-inhibitors having phosphate group as a hydrophilic residue. Phosphates 55-64 cell division cycle 25A Homo sapiens 30-36 15261298-1 2004 Compounds (6a-e) were synthesized by phosphorylation of hydrophobic perhydroindan derivatives derived from vitamin D(3), and were found to show strong inhibitory activity towards dual-specificity phosphatase Cdc25A (IC(50)=0.7-24.5 microM). perhydroindan 68-81 cell division cycle 25A Homo sapiens 208-214 15261298-1 2004 Compounds (6a-e) were synthesized by phosphorylation of hydrophobic perhydroindan derivatives derived from vitamin D(3), and were found to show strong inhibitory activity towards dual-specificity phosphatase Cdc25A (IC(50)=0.7-24.5 microM). Vitamin D 107-116 cell division cycle 25A Homo sapiens 208-214 15213307-10 2004 The observed down-regulation of DNA replication proteins cdc6, MCM2, and cdc25A after exposure to SN-38 with MSC further indicates a relationship between drug response and DNA damage. Irinotecan 98-103 cell division cycle 25A Homo sapiens 73-79 14727060-6 2004 We then describe a simple assay in which we demonstrate that growth of the humanised CDC25A strain is strongly repressed in a CDC25-dependent manner by BN2003, a potent chemical inhibitor of CDC25 belonging to the benzothiazoledione family. bn2003 152-158 cell division cycle 25A Homo sapiens 85-91 15209522-0 2004 Mechanistic studies of protein tyrosine phosphatases YopH and Cdc25A with m-nitrobenzyl phosphate. m-nitrobenzyl phosphate 74-97 cell division cycle 25A Homo sapiens 62-68 15149692-0 2004 Design and synthesis of dysidiolide analogs from vitamin D3: novel class of Cdc25A inhibitors. dysidiolide 24-35 cell division cycle 25A Homo sapiens 76-82 15149692-0 2004 Design and synthesis of dysidiolide analogs from vitamin D3: novel class of Cdc25A inhibitors. Cholecalciferol 49-59 cell division cycle 25A Homo sapiens 76-82 14727060-6 2004 We then describe a simple assay in which we demonstrate that growth of the humanised CDC25A strain is strongly repressed in a CDC25-dependent manner by BN2003, a potent chemical inhibitor of CDC25 belonging to the benzothiazoledione family. benzothiazoledione 214-232 cell division cycle 25A Homo sapiens 85-91 14734566-5 2004 We also found suramin to be a potent inhibitor (IC(50) = 1.5 microm) of Cdc25A, a phosphatase that mediates cell cycle progression and a potential target for cancer therapy. Suramin 14-21 cell division cycle 25A Homo sapiens 72-78 14988409-6 2004 Each of these agents also triggered S-phase checkpoint activation in parental ES cells, as indicated by a caffeine-inhibitable decrease in [3H]thymidine incorporation into DNA and Cdc25A down-regulation. Caffeine 106-114 cell division cycle 25A Homo sapiens 180-186 14752276-2 2004 Based on sequence homology of known betaTrCP substrates, we found that Cdc25A contains a conserved motif (DSG), phosphorylation of which is required for interaction with betaTrCP.1 Here, we show that phosphorylation at Ser 82 within the DSG motif anchors Cdc25A to betaTrCP and that Chk1-dependent phosphorylation at Ser 76 affects this interaction as well as betaTrCP-dependent degradation. Serine 219-222 cell division cycle 25A Homo sapiens 71-77 14752276-2 2004 Based on sequence homology of known betaTrCP substrates, we found that Cdc25A contains a conserved motif (DSG), phosphorylation of which is required for interaction with betaTrCP.1 Here, we show that phosphorylation at Ser 82 within the DSG motif anchors Cdc25A to betaTrCP and that Chk1-dependent phosphorylation at Ser 76 affects this interaction as well as betaTrCP-dependent degradation. Serine 219-222 cell division cycle 25A Homo sapiens 255-261 14752276-4 2004 According to our model, phosphorylation at Ser 76 is a "priming" step required for Ser 82 phosphorylation, which in turn allows recruitment of Cdc25A by betaTrCP and subsequent betaTrCP-dependent degradation. Serine 83-86 cell division cycle 25A Homo sapiens 143-149 14752276-2 2004 Based on sequence homology of known betaTrCP substrates, we found that Cdc25A contains a conserved motif (DSG), phosphorylation of which is required for interaction with betaTrCP.1 Here, we show that phosphorylation at Ser 82 within the DSG motif anchors Cdc25A to betaTrCP and that Chk1-dependent phosphorylation at Ser 76 affects this interaction as well as betaTrCP-dependent degradation. Serine 317-320 cell division cycle 25A Homo sapiens 71-77 14752276-4 2004 According to our model, phosphorylation at Ser 76 is a "priming" step required for Ser 82 phosphorylation, which in turn allows recruitment of Cdc25A by betaTrCP and subsequent betaTrCP-dependent degradation. Serine 43-46 cell division cycle 25A Homo sapiens 143-149 14980448-10 2004 The curcuminoid 004 showed an inhibitory effect on the binding of myc-max protein to the E-box element in SNU16 cells, and suppressed the expression of myc target genes including ornithine decarboxylase (ODC), cdc25a and c-myc in myc over-expressed human stomach cancer cell line SNU16. curcuminoid 4-15 cell division cycle 25A Homo sapiens 210-216 14673957-3 2004 METHODS: We used a novel and potent Cdc25A inhibitor, 2,3-bis-[2-hydroxyethylsulfonyl]-[1,4] naphthoquinone (NSC 95397), and its congener (2-mercaptoethanol)-3-methyl-1, 4-naphthoquinone (NSC 672121) to study the role of Cdc25A on the MAPK pathway in human prostate cancer cells. 2,3-bis-[2-hydroxyethylsulfonyl]-[1,4] naphthoquinone 54-107 cell division cycle 25A Homo sapiens 36-42 15048068-3 2004 Here, we demonstrated that STI571 also induces growth arrest by activating the Chk2-Cdc25A-Cdk2 axis, a pathway complementary to p53 in the activation of G(1)/S cell cycle checkpoint. Imatinib Mesylate 27-33 cell division cycle 25A Homo sapiens 84-90 14673957-3 2004 METHODS: We used a novel and potent Cdc25A inhibitor, 2,3-bis-[2-hydroxyethylsulfonyl]-[1,4] naphthoquinone (NSC 95397), and its congener (2-mercaptoethanol)-3-methyl-1, 4-naphthoquinone (NSC 672121) to study the role of Cdc25A on the MAPK pathway in human prostate cancer cells. 2-mercaptoethanol)-3-methyl-1, 4-naphthoquinone 139-186 cell division cycle 25A Homo sapiens 36-42 14673957-4 2004 RESULTS: We found Raf-1 physically interacted with Cdc25A in PC-3 and LNCap cells and inhibitors of Cdc25A induced both extracellular signal-regulated kinase (Erk) activation and Raf-1 tyrosine phosphorylation. Tyrosine 185-193 cell division cycle 25A Homo sapiens 51-57 14673957-4 2004 RESULTS: We found Raf-1 physically interacted with Cdc25A in PC-3 and LNCap cells and inhibitors of Cdc25A induced both extracellular signal-regulated kinase (Erk) activation and Raf-1 tyrosine phosphorylation. Tyrosine 185-193 cell division cycle 25A Homo sapiens 100-106 14681206-3 2003 Cdc25A is required for S-phase entry and dephosphorylates tyrosine-15 phosphorylated Cdk1 (Cdc2) and Cdk2, positive regulators of cell division. Tyrosine 58-66 cell division cycle 25A Homo sapiens 0-6 15344887-1 2004 Cdc25A phosphatase regulates cell cycle progression by removing the inhibitory phosphates from cyclin-dependent kinases. Phosphates 79-89 cell division cycle 25A Homo sapiens 0-6 14570880-4 2003 17-AAG-mediated Chk1 loss blocked the ability of Chk1 to target Cdc25A for proteolytic destruction, demonstrating that the Chk1 signaling pathway was disrupted in the 17-AAG-treated cells. tanespimycin 0-6 cell division cycle 25A Homo sapiens 64-70 14570880-4 2003 17-AAG-mediated Chk1 loss blocked the ability of Chk1 to target Cdc25A for proteolytic destruction, demonstrating that the Chk1 signaling pathway was disrupted in the 17-AAG-treated cells. tanespimycin 167-173 cell division cycle 25A Homo sapiens 64-70 14681206-9 2003 However, recognition of Cdc25A by beta-TRCP occurs via a noncanonical phosphodegron in Cdc25A containing phosphoserine 79 and phosphoserine 82, sites that are not targeted by Chk1. Phosphoserine 105-118 cell division cycle 25A Homo sapiens 24-30 14681206-9 2003 However, recognition of Cdc25A by beta-TRCP occurs via a noncanonical phosphodegron in Cdc25A containing phosphoserine 79 and phosphoserine 82, sites that are not targeted by Chk1. Phosphoserine 105-118 cell division cycle 25A Homo sapiens 87-93 14681206-9 2003 However, recognition of Cdc25A by beta-TRCP occurs via a noncanonical phosphodegron in Cdc25A containing phosphoserine 79 and phosphoserine 82, sites that are not targeted by Chk1. Phosphoserine 126-139 cell division cycle 25A Homo sapiens 24-30 12801928-4 2003 Here we report that treatment of HeLa cells with the cyclin-dependent kinase inhibitor roscovitine caused a concentration- and time-dependent increase in Cdc25A protein levels. Roscovitine 87-98 cell division cycle 25A Homo sapiens 154-160 14559997-3 2003 Phosphorylation of Cdc25A on serine 178 and threonine 507 facilitates 14-3-3 binding, and Chk1 phosphorylates both residues in vitro. Serine 29-35 cell division cycle 25A Homo sapiens 19-25 13679850-8 2003 Chk1 phosphorylation, decrease of Cdc25 A levels and S-phase arrest were abolished by caffeine, demonstrating that active checkpoint signaling rather than passive mechanical blockage by ICLs causes the PUVA-induced replication arrest. Caffeine 86-94 cell division cycle 25A Homo sapiens 34-41 12963847-0 2003 Regulation of human Cdc25A stability by Serine 75 phosphorylation is not sufficient to activate a S phase checkpoint. Serine 40-46 cell division cycle 25A Homo sapiens 20-26 12963847-3 2003 Using a panel of doxycycline-inducible phosphorylation mutants we show that the stability of human Cdc25A protein is dependent upon phosphorylation at S75. Doxycycline 17-28 cell division cycle 25A Homo sapiens 99-105 14644418-0 2003 Involvement of Akt in mitochondria-dependent apoptosis induced by a cdc25 phosphatase inhibitor naphthoquinone analog. Naphthoquinones 96-110 cell division cycle 25A Homo sapiens 68-73 14644418-1 2003 Vitamin K-related analogs induce growth inhibition via a cell cycle arrest through cdc25A phosphatase inhibition in various cancer cell lines. Vitamin K 0-9 cell division cycle 25A Homo sapiens 83-89 12676925-4 2003 The degradation of Cdc25A is abrogated by caffeine, which implicates Chk1 as the potential mediator (Mailand, N., Falck, J., Lukas, C., Syljuasen, R. G., Welcker, M., Bartek, J., and Lukas, J. Caffeine 42-50 cell division cycle 25A Homo sapiens 19-25 12759351-0 2003 Phosphorylation at serine 75 is required for UV-mediated degradation of human Cdc25A phosphatase at the S-phase checkpoint. Serine 19-25 cell division cycle 25A Homo sapiens 78-84 12759351-2 2003 In response to ionizing radiation, Cdc25A is phosphorylated by both Chk1 and Chk2 on Ser-123. Serine 85-88 cell division cycle 25A Homo sapiens 35-41 12759351-4 2003 We found that in response to UV irradiation, Cdc25A is phosphorylated at a different serine residue, Ser-75. Serine 85-91 cell division cycle 25A Homo sapiens 45-51 12759351-4 2003 We found that in response to UV irradiation, Cdc25A is phosphorylated at a different serine residue, Ser-75. Serine 101-104 cell division cycle 25A Homo sapiens 45-51 12759351-5 2003 Significantly, Cdc25A mutants carrying alanine instead of either Ser-75 or Ser-123 demonstrate that only Ser-75 mediates protein stabilization in response to UV-induced DNA damage. Alanine 39-46 cell division cycle 25A Homo sapiens 15-21 12759351-7 2003 Furthermore, we find that Cdc25A was phosphorylated by Chk1 on Ser-75 in vitro and that the same site was also phosphorylated in vivo. Serine 63-66 cell division cycle 25A Homo sapiens 26-32 12759351-8 2003 Taken together, these data strongly suggest that phosphorylation of Cdc25A on Ser-75 by Chk1 and its subsequent degradation is required to delay cell cycle progression in response to UV-induced DNA lesions. Serine 78-81 cell division cycle 25A Homo sapiens 68-74 12869643-9 2003 The conditional expression of the CDC25A gene using a tetracycline repressor expression vector increased sensitivity toward ART. Tetracycline 54-66 cell division cycle 25A Homo sapiens 34-40 12676925-8 2003 Herein, we show that camptothecin and doxorubicin, two widely used topoisomerase inhibitors conferring S and G2 arrest, respectively, cause the degradation of Cdc25A. Camptothecin 21-33 cell division cycle 25A Homo sapiens 159-165 12676925-8 2003 Herein, we show that camptothecin and doxorubicin, two widely used topoisomerase inhibitors conferring S and G2 arrest, respectively, cause the degradation of Cdc25A. Doxorubicin 38-49 cell division cycle 25A Homo sapiens 159-165 12676925-10 2003 Moreover, Cdc25A overexpression abrogates the Chk1-mediated degradation and overcomes the doxorubicin-induced G2 arrest through dephosphorylation and activation of Cdc2/Cdk1 in a dose-dependent manner. Doxorubicin 90-101 cell division cycle 25A Homo sapiens 10-16 12085185-1 2002 Cdc25B and cdc25A phosphates are prominent stimulators of cell cycle progression and recent studies have also suggested their oncogenic roles. Phosphates 18-28 cell division cycle 25A Homo sapiens 11-17 12612058-3 2003 Remarkably, tamoxifen induces transcription factors and genes involved in promoting cell cycle progression including fos, myc, myb, cdc25a, cyclins E and A2, and stk15 with kinetics that paralleled that of cells cycling in response to estrogen, even though tamoxifen-treated cells are not transiting through the cell cycle. Tamoxifen 12-21 cell division cycle 25A Homo sapiens 132-138 12356752-4 2002 Using the natural Cdc25A substrate, Tyr(15)-phosphorylated Cdk2/cyclin A, we demonstrated that NSC 663284 blocked reactivation of Cdk2/cyclin A kinase by Cdc25A catalytic domain in vitro. Tyrosine 36-39 cell division cycle 25A Homo sapiens 18-24 12356752-5 2002 In-gel trypsin digestion followed by capillary liquid chromatography-electrospray ionization mass spectrometry and tandem mass spectrometry revealed the direct binding of NSC 663284 to one of the two serine residues in the active site loop HCEFSSER of the Cdc25A catalytic domain. Serine 200-206 cell division cycle 25A Homo sapiens 256-262 12399544-6 2002 Finally, Cdc25A was phosphorylated by Chk1 in vitro on similar sites phosphorylated in vivo, including serine-123. Serine 103-109 cell division cycle 25A Homo sapiens 9-15 12181445-0 2002 Inhibition of cyclin-dependent kinase 2 by the Chk1-Cdc25A pathway during the S-phase checkpoint activated by fludarabine: dysregulation by 7-hydroxystaurosporine. fludarabine 110-121 cell division cycle 25A Homo sapiens 52-58 12181445-0 2002 Inhibition of cyclin-dependent kinase 2 by the Chk1-Cdc25A pathway during the S-phase checkpoint activated by fludarabine: dysregulation by 7-hydroxystaurosporine. 7-hydroxystaurosporine 140-162 cell division cycle 25A Homo sapiens 52-58 12181445-10 2002 Thus, the DNA damage induced by F-ara-A initiated a hierarchical regulatory cascade through Chk1 and Cdc25A that resulted in Cdk2 inhibition, affecting an S-phase checkpoint that was dysregulated by UCN-01. fludarabine 32-39 cell division cycle 25A Homo sapiens 101-107 12711320-4 2003 Mutational analyses using GST-linked Cdc25A containing serine 123 revealed that residues at positions -5 and -3 are critical determinants for the recognition of the Chk2 substrate. Serine 55-61 cell division cycle 25A Homo sapiens 37-43 12540838-1 2003 Compound 5 (Cpd 5) or 2-(2-mercaptoethanol)-3-methyl-1,4-naphthoquinone, is an inhibitor of protein phosphatase Cdc25A and causes persistent activation of extracellular signal-regulated kinase (ERK) and cell growth inhibition. 2-(2-mercaptoethanol)-3-methyl-1,4-naphthoquinone 22-71 cell division cycle 25A Homo sapiens 112-118 12676583-3 2003 The basal turnover of Cdc25A operating in unperturbed S phase required Chk1-dependent phosphorylation of serines 123, 178, 278, and 292. Serine 105-112 cell division cycle 25A Homo sapiens 22-28 12406560-4 2002 Unsaturated fatty acids also showed cytotoxicity against a SNU16 human stomach cancer cell line and conjugated linoleic acid suppressed mRNA expression of several myc-target genes; ornithine decarboxylase, p53, cdc25a in the SNU16 cells. Fatty Acids, Unsaturated 0-23 cell division cycle 25A Homo sapiens 211-217 12406560-4 2002 Unsaturated fatty acids also showed cytotoxicity against a SNU16 human stomach cancer cell line and conjugated linoleic acid suppressed mRNA expression of several myc-target genes; ornithine decarboxylase, p53, cdc25a in the SNU16 cells. Linoleic Acid 111-124 cell division cycle 25A Homo sapiens 211-217 12203101-9 2002 Cl-F-araA induced a dose- and time-dependent downregulation of the Cdc25A protein whereas the Cdc25C protein remained unchanged. Clofarabine 0-9 cell division cycle 25A Homo sapiens 67-73 11805096-5 2002 Interestingly, our Bronsted analysis and pH dependence studies reveal that Cdc25A employs a different mechanism for the hydrolysis of substrates with high leaving group pK(a) values (8.68-9.99) that appears to require the protonation of glutamic acid 431. Glutamic Acid 237-250 cell division cycle 25A Homo sapiens 75-81 11912208-4 2002 Cdc25A inhibitor Cpd 5, a vitamin K analog, inhibited Cdc25A activity in the Cdc25A-EGFR immunocomplex and consequently caused prolonged EGFR tyrosine phosphorylation. Vitamin K 26-35 cell division cycle 25A Homo sapiens 0-6 11912208-4 2002 Cdc25A inhibitor Cpd 5, a vitamin K analog, inhibited Cdc25A activity in the Cdc25A-EGFR immunocomplex and consequently caused prolonged EGFR tyrosine phosphorylation. Vitamin K 26-35 cell division cycle 25A Homo sapiens 54-60 11912208-4 2002 Cdc25A inhibitor Cpd 5, a vitamin K analog, inhibited Cdc25A activity in the Cdc25A-EGFR immunocomplex and consequently caused prolonged EGFR tyrosine phosphorylation. Vitamin K 26-35 cell division cycle 25A Homo sapiens 54-60 11912208-4 2002 Cdc25A inhibitor Cpd 5, a vitamin K analog, inhibited Cdc25A activity in the Cdc25A-EGFR immunocomplex and consequently caused prolonged EGFR tyrosine phosphorylation. Tyrosine 142-150 cell division cycle 25A Homo sapiens 0-6 11912208-5 2002 Both purified GST-Cdc25A protein and endogenous Hep3B cellular Cdc25A dephosphorylated tyrosine-phosphorylated EGFR, and Cpd 5 antagonized the phosphatase activity of Cdc25A. Tyrosine 87-95 cell division cycle 25A Homo sapiens 18-24 11912208-5 2002 Both purified GST-Cdc25A protein and endogenous Hep3B cellular Cdc25A dephosphorylated tyrosine-phosphorylated EGFR, and Cpd 5 antagonized the phosphatase activity of Cdc25A. Tyrosine 87-95 cell division cycle 25A Homo sapiens 63-69 11912208-5 2002 Both purified GST-Cdc25A protein and endogenous Hep3B cellular Cdc25A dephosphorylated tyrosine-phosphorylated EGFR, and Cpd 5 antagonized the phosphatase activity of Cdc25A. Tyrosine 87-95 cell division cycle 25A Homo sapiens 63-69 12054599-6 2002 Furthermore, SA also reduced the expressions of Cdc25A and cyclin B, blocked cell cycle progression at G2/M phase, and induced apoptosis in SiHa cells. sodium arsenite 13-15 cell division cycle 25A Homo sapiens 48-54 11805096-4 2002 Our kinetic isotope effect results, Bronsted analysis, and pH dependence studies employing a range of aryl phosphates clearly indicate a dissociative transition state for the Cdc25A reaction that does not involve a general acid for the hydrolysis of substrates with low leaving group pK(a) values (5.45-8.05). Phosphates 107-117 cell division cycle 25A Homo sapiens 175-181 11901209-5 2002 Most notable was NSC 95397 (2,3-bis-[2-hydroxyethylsulfanyl]-[1,4]naphthoquinone), which displayed mixed inhibition kinetics with in vitro K(i) values for Cdc25A, -B, and -C of 32, 96, and 40 nM, respectively. 2,3-bis(2-hydroxyethylsulfanyl)-(1,4)naphthoquinone 28-80 cell division cycle 25A Homo sapiens 155-161 11805096-8 2002 Since the activity of Cdc25A toward small molecule substrates is several orders of magnitude lower than toward the physiological substrate, cyclin-CDK, we suggest that the cyclin-CDK is able to preferentially induce this more catalytically active form of Cdc25A for efficient phosphothreonine and phosphotyrosine dephosphorylation. Phosphothreonine 276-292 cell division cycle 25A Homo sapiens 22-28 11805096-8 2002 Since the activity of Cdc25A toward small molecule substrates is several orders of magnitude lower than toward the physiological substrate, cyclin-CDK, we suggest that the cyclin-CDK is able to preferentially induce this more catalytically active form of Cdc25A for efficient phosphothreonine and phosphotyrosine dephosphorylation. Phosphothreonine 276-292 cell division cycle 25A Homo sapiens 255-261 11805096-8 2002 Since the activity of Cdc25A toward small molecule substrates is several orders of magnitude lower than toward the physiological substrate, cyclin-CDK, we suggest that the cyclin-CDK is able to preferentially induce this more catalytically active form of Cdc25A for efficient phosphothreonine and phosphotyrosine dephosphorylation. Phosphotyrosine 297-312 cell division cycle 25A Homo sapiens 22-28 11805096-8 2002 Since the activity of Cdc25A toward small molecule substrates is several orders of magnitude lower than toward the physiological substrate, cyclin-CDK, we suggest that the cyclin-CDK is able to preferentially induce this more catalytically active form of Cdc25A for efficient phosphothreonine and phosphotyrosine dephosphorylation. Phosphotyrosine 297-312 cell division cycle 25A Homo sapiens 255-261 11752153-15 2002 Finally, by using the cdk inhibitor roscovitine, we reveal that E7 activates the cdc25A promoter independently of cell cycle progression and cdk activity. Roscovitine 36-47 cell division cycle 25A Homo sapiens 81-87 11106571-7 2000 After immunoprecipitation from control and AD tissue, we found that the tyrosine dephosphorylating activity of Cdc25A against exogenous Cdc2 substrate was elevated in AD. Tyrosine 72-80 cell division cycle 25A Homo sapiens 111-117 11745413-5 2001 Expression of cdc25A, a phosphatase that activates cdk2, was reduced during 24-hr exposure to gnidimacrin. gnidimacrin 94-105 cell division cycle 25A Homo sapiens 14-20 11745413-8 2001 These results suggest that gnidimacrin exerts antitumor activity through suppression of cdc25A and inhibition of cdk2 activity. gnidimacrin 27-38 cell division cycle 25A Homo sapiens 88-94 11262093-1 2001 Silica gel supported pyrolysis of an azido-homo-oxa steroid led to rearrangement, presumably by a mechanism similar to that of solution phase Schmidt fragmentation, to produce a group of novel inhibitors for the oncogenic cell cycle regulator Cdc25A phosphatase. Silica Gel 0-10 cell division cycle 25A Homo sapiens 243-249 11262093-1 2001 Silica gel supported pyrolysis of an azido-homo-oxa steroid led to rearrangement, presumably by a mechanism similar to that of solution phase Schmidt fragmentation, to produce a group of novel inhibitors for the oncogenic cell cycle regulator Cdc25A phosphatase. azido-homo-oxa steroid 37-59 cell division cycle 25A Homo sapiens 243-249 11262093-2 2001 Cyano-containing acid 17, one of the best inhibitors in this group, inhibited the activity of Cdc25A protein phosphatase reversibly and noncompetitively with an IC(50) value of 2.2 microM. cyano-containing acid 17 0-24 cell division cycle 25A Homo sapiens 94-100 11262093-4 2001 Without the cyano group, acid 26 and xanthate 27 were found to be more selective over Cdc25A (IC(50) = 5.1 microM and 1.1 microM, respectively) than toward CD45 (IC(50) > 100 microM, in each case), a receptor protein tyrosine phosphatase. ethylxanthate 37-45 cell division cycle 25A Homo sapiens 86-92 11161293-3 2001 Cdc25A and its catalytic domain (dN25A) demonstrate very similar kinetics toward the artificial substrates p-nitrophenyl phosphate (k(cat)/K(m) = 15-25 M(-1) s(-1)) and 3-O-methylfluorescein phosphate (k(cat)/K(m) = 1.1-1.3 x 10(4) M(-1) s(-1)). nitrophenylphosphate 107-130 cell division cycle 25A Homo sapiens 0-6 11161293-3 2001 Cdc25A and its catalytic domain (dN25A) demonstrate very similar kinetics toward the artificial substrates p-nitrophenyl phosphate (k(cat)/K(m) = 15-25 M(-1) s(-1)) and 3-O-methylfluorescein phosphate (k(cat)/K(m) = 1.1-1.3 x 10(4) M(-1) s(-1)). 3-O-methylfluorescein phosphate 169-200 cell division cycle 25A Homo sapiens 0-6 11585757-4 2001 Cyclin-dependent kinase (Cdk) 4, an important regulator for G(1) progression, was found to be tyrosine-phosphorylated by the arylating analogues, and this phosphorylation was correlated with the inhibitory effects of the analogues on Cdc25A activity. Tyrosine 94-102 cell division cycle 25A Homo sapiens 234-240 11585757-5 2001 Furthermore, Cdk4 dephosphorylation experiments showed that Compound (Cpd) 5, a prototype arylating analogue, inhibited Cdc25A-mediated Cdk4 dephosphorylation, whereas Cpd 26, a nonarylating vitamin K analogue, had no effect on this event. Vitamin K 191-200 cell division cycle 25A Homo sapiens 120-126 11298456-5 2001 We show that IR-induced destruction of Cdc25A requires both ATM and the Chk2-mediated phosphorylation of Cdc25A on serine 123. Serine 115-121 cell division cycle 25A Homo sapiens 39-45 11298456-5 2001 We show that IR-induced destruction of Cdc25A requires both ATM and the Chk2-mediated phosphorylation of Cdc25A on serine 123. Serine 115-121 cell division cycle 25A Homo sapiens 105-111 11154267-8 2001 Transfection of MCF-7 cells with a dominant-negative Cdk2 construct inhibited the E(2)-dependent activation of ectopic Cdc25A. Estradiol 82-86 cell division cycle 25A Homo sapiens 119-125 11154267-9 2001 Supporting a role for Cdc25A in estrogen action, antisense CDC25A oligonucleotides inhibited estrogen-induced Cdk2 activation and DNA synthesis. Oligonucleotides 66-82 cell division cycle 25A Homo sapiens 22-28 11154267-9 2001 Supporting a role for Cdc25A in estrogen action, antisense CDC25A oligonucleotides inhibited estrogen-induced Cdk2 activation and DNA synthesis. Oligonucleotides 66-82 cell division cycle 25A Homo sapiens 59-65 11086732-1 2000 The novel analogues of natural cdc25A inhibitor dysidiolide were synthesized. dysidiolide 48-59 cell division cycle 25A Homo sapiens 31-37 11191620-7 2000 Like TNFalpha or benzamide riboside, which are also inducers of apoptosis of N.1 cells, trimidox also down-regulates the G1 cell cycle phosphatase cdc25A, whereas cyclin D1 becomes up-regulated. 3,4,5-trihydroxybenzamidoxime 88-96 cell division cycle 25A Homo sapiens 147-153 11002421-6 2000 A loss of Cdc25A expression was associated with an increased inhibitory phosphotyrosine content of cyclin E- and cyclin A-associated cdk2 and may also contribute to G1 arrest following UVB irradiation. Phosphotyrosine 72-87 cell division cycle 25A Homo sapiens 10-16 10956527-1 2000 A formal total synthesis of the sesterterpenoid (+/-)-dysidiolide (1), a structurally novel sponge metabolite that inhibits the cdc25A protein phosphatase, and approaches to the syntheses of (+/-)-15-epi- (34), (+/-)-6-epi- (36), and (+/-)-6, 15-bisepidysidiolide (39) are described. dysidiolide 48-65 cell division cycle 25A Homo sapiens 128-134 10854062-0 2000 Cdk7- and Cdc25A-independent dephosphorylation of Cdk2 during phorbol ester-mediated cell cycle arrest in U937 cells. Phorbol Esters 62-75 cell division cycle 25A Homo sapiens 10-16 11256629-3 2000 By treating cells with the DNA synthesis inhibitor hydroxyurea, Cdc25 A rapidly decreased in abundance, and this was accompanied by an increase in Cdk2 phosphotyrosine content and a decrease in Cdk2 kinase activity. Hydroxyurea 51-62 cell division cycle 25A Homo sapiens 64-71 11256629-3 2000 By treating cells with the DNA synthesis inhibitor hydroxyurea, Cdc25 A rapidly decreased in abundance, and this was accompanied by an increase in Cdk2 phosphotyrosine content and a decrease in Cdk2 kinase activity. Phosphotyrosine 152-167 cell division cycle 25A Homo sapiens 64-71 11256629-4 2000 Cdc25 A overexpression altered the ability of cells to arrest in the presence of hydroxyurea, and caused them to undergo premature chromosome condensation. Hydroxyurea 81-92 cell division cycle 25A Homo sapiens 0-7 10373531-0 1999 Tyrosine phosphorylation of the proto-oncoprotein Raf-1 is regulated by Raf-1 itself and the phosphatase Cdc25A. Tyrosine 0-8 cell division cycle 25A Homo sapiens 105-111 10762037-0 2000 Synthesis of a novel class of cdc25A inhibitors from vitamin D3. Cholecalciferol 53-63 cell division cycle 25A Homo sapiens 30-36 10762037-1 2000 We have developed a novel class of cdc25A inhibitors by drastic modification of the hydrophobic and hydrophilic substructures of dysidiolide. dysidiolide 129-140 cell division cycle 25A Homo sapiens 35-41 10543950-7 1999 In Cdc25B, both sulfate and tungstate anions are shown to bind in the catalytic site containing the signature motif (HCxxxxxR) in a conformation similar to that of other protein tyrosine phosphatases and dual specificity phosphatases, with the exception of the Cdc25A. Sulfates 16-23 cell division cycle 25A Homo sapiens 261-267 10543950-7 1999 In Cdc25B, both sulfate and tungstate anions are shown to bind in the catalytic site containing the signature motif (HCxxxxxR) in a conformation similar to that of other protein tyrosine phosphatases and dual specificity phosphatases, with the exception of the Cdc25A. tungstate anions 28-44 cell division cycle 25A Homo sapiens 261-267 10722152-0 2000 Steroidal derived acids as inhibitors of human Cdc25A protein phosphatase. steroidal 0-9 cell division cycle 25A Homo sapiens 47-53 10722152-0 2000 Steroidal derived acids as inhibitors of human Cdc25A protein phosphatase. derived acids 10-23 cell division cycle 25A Homo sapiens 47-53 10573135-5 1999 These results suggest that hypophosphorylation of pRB and repression of cyclin D3 and cdc25A are induced synergistically by treatment with ATRA plus GM-CSF in ML-1 cells. Tretinoin 139-143 cell division cycle 25A Homo sapiens 86-92 10641570-3 1999 Removal of inhibitory phosphates on these amino acid residues is required for G1 CDK activation, and is mediated by the Cdc25A phosphatase. Phosphates 22-32 cell division cycle 25A Homo sapiens 120-126 10454565-12 1999 Furthermore, Cdc25A overexpression induces a tyrosine dephosphorylation of Cdk2. Tyrosine 45-53 cell division cycle 25A Homo sapiens 13-19 10373531-6 1999 Cdc25A was found to dephosphorylate Raf-1 on tyrosines that resulted in a significant decrease in Raf-1 kinase activity. Tyrosine 45-54 cell division cycle 25A Homo sapiens 0-6 10373531-8 1999 These data suggest that the tyrosine phosphorylation of Raf-1 is regulated not only by itself but also by Cdc25A. Tyrosine 28-36 cell division cycle 25A Homo sapiens 106-112 9873570-2 1998 In this study, naphthoquinone analogs as cdc25A phosphatase inactivators were investigated. Naphthoquinones 15-29 cell division cycle 25A Homo sapiens 41-47 9989807-0 1999 A rate limiting function of cdc25A for S phase entry inversely correlates with tyrosine dephosphorylation of Cdk2. Tyrosine 79-87 cell division cycle 25A Homo sapiens 28-34 9989807-1 1999 The cdc25A phosphatase removes inhibitory phosphates from threonine-14 and tyrosine-15 of cyclin dependent kinase-2 (cdk2) in vitro, and it is therefore widely assumed that cdc25A positively regulates cyclin E- and A-associated cdk2 activity at the G1 to S phase transition of the mammalian cell division cycle. Phosphates 42-52 cell division cycle 25A Homo sapiens 4-10 9989807-1 1999 The cdc25A phosphatase removes inhibitory phosphates from threonine-14 and tyrosine-15 of cyclin dependent kinase-2 (cdk2) in vitro, and it is therefore widely assumed that cdc25A positively regulates cyclin E- and A-associated cdk2 activity at the G1 to S phase transition of the mammalian cell division cycle. Phosphates 42-52 cell division cycle 25A Homo sapiens 173-179 9989807-1 1999 The cdc25A phosphatase removes inhibitory phosphates from threonine-14 and tyrosine-15 of cyclin dependent kinase-2 (cdk2) in vitro, and it is therefore widely assumed that cdc25A positively regulates cyclin E- and A-associated cdk2 activity at the G1 to S phase transition of the mammalian cell division cycle. Threonine 58-67 cell division cycle 25A Homo sapiens 4-10 9989807-1 1999 The cdc25A phosphatase removes inhibitory phosphates from threonine-14 and tyrosine-15 of cyclin dependent kinase-2 (cdk2) in vitro, and it is therefore widely assumed that cdc25A positively regulates cyclin E- and A-associated cdk2 activity at the G1 to S phase transition of the mammalian cell division cycle. Threonine 58-67 cell division cycle 25A Homo sapiens 173-179 9989807-1 1999 The cdc25A phosphatase removes inhibitory phosphates from threonine-14 and tyrosine-15 of cyclin dependent kinase-2 (cdk2) in vitro, and it is therefore widely assumed that cdc25A positively regulates cyclin E- and A-associated cdk2 activity at the G1 to S phase transition of the mammalian cell division cycle. Tyrosine 75-83 cell division cycle 25A Homo sapiens 4-10 9989807-1 1999 The cdc25A phosphatase removes inhibitory phosphates from threonine-14 and tyrosine-15 of cyclin dependent kinase-2 (cdk2) in vitro, and it is therefore widely assumed that cdc25A positively regulates cyclin E- and A-associated cdk2 activity at the G1 to S phase transition of the mammalian cell division cycle. Tyrosine 75-83 cell division cycle 25A Homo sapiens 173-179 9398331-8 1997 Compound AC-alphaalpha69 had a Ki of approximately 10 microM for recombinant human Cdc25A, -B, and -C, and a Ki of 0.85 microM for the PTP1B. AC-alphaalpha69 9-24 cell division cycle 25A Homo sapiens 83-89 9063568-5 1997 The data showed that aloesin increased the levels of cyclin E, CDK2, and CDC25A in SK-HEP-1 cells. aloesin 21-28 cell division cycle 25A Homo sapiens 73-79 9230211-5 1997 Furthermore, subsequent apoptotic DNA fragmentation induced by GL331 could be interrupted by treatment of the cells with the cyclin B1-specific antisense oligonucleotides, suggesting that abnormal activation of cyclin B1-associated CDC 2 kinase and CDC 25A phosphatase was involved in GL331-induced apoptosis. GL 331 63-68 cell division cycle 25A Homo sapiens 249-256 9230211-5 1997 Furthermore, subsequent apoptotic DNA fragmentation induced by GL331 could be interrupted by treatment of the cells with the cyclin B1-specific antisense oligonucleotides, suggesting that abnormal activation of cyclin B1-associated CDC 2 kinase and CDC 25A phosphatase was involved in GL331-induced apoptosis. Oligonucleotides 154-170 cell division cycle 25A Homo sapiens 249-256 9230211-7 1997 Our results revealed that GL331 could facilitate the association of CDC 25A with Raf-1, resulting in the cascade of CDC 25A phosphatase activation and CDC 2 kinase activation, as well as related signaling pathways, and ultimately causing apoptosis in cancer cells. GL 331 26-31 cell division cycle 25A Homo sapiens 68-75 9230211-7 1997 Our results revealed that GL331 could facilitate the association of CDC 25A with Raf-1, resulting in the cascade of CDC 25A phosphatase activation and CDC 2 kinase activation, as well as related signaling pathways, and ultimately causing apoptosis in cancer cells. GL 331 26-31 cell division cycle 25A Homo sapiens 116-123 9230211-4 1997 GL331 treatment also induced a concomitant increase in CDC 25A phosphatase activity and a reduced level of Tyr-15-phosphorylated CDC 2 in NPC-TW01 cells. GL 331 0-5 cell division cycle 25A Homo sapiens 55-62 9163429-6 1997 Tyrosine phosphorylation and inactivation of Cdk4/6 in a human mammary epithelial cell line are shown to result from the ability of TGF-beta to repress expression of the CDK tyrosine phosphatase Cdc25A. Tyrosine 0-8 cell division cycle 25A Homo sapiens 195-201 9063568-7 1997 Collectively, these results suggest that aloesin stimulates the proliferation of SK-HEP-1 cells by inducing the intracellular levels of cyclin E/CDK2 kinase complex and CDC25A, which, together, result in the up-regulation of cyclin E-dependent kinase activity. aloesin 41-48 cell division cycle 25A Homo sapiens 169-175 8668211-4 1996 The latter resulted from the rapid alpha-interferon-mediated elimination of cdc25A, a phosphatase that is required for antagonism of negative tyrosine phosphorylation of cdk2 in cyclin-cdk complexes. Tyrosine 142-150 cell division cycle 25A Homo sapiens 76-82 9018101-6 1996 In addition, our data show that G-Rh2 reduced the protein levels of cdc25A at doses higher than 10 microM. -rh2 33-37 cell division cycle 25A Homo sapiens 68-74 8617791-4 1996 However, the cysteine mutation in both Cdc25A and -B created enzymes that still retain the ability to bind their substrates. Cysteine 13-21 cell division cycle 25A Homo sapiens 39-52 8617791-6 1996 While Cdc25A Cys --> Ser could interact with cyclin A-Cdk2, cyclin B-Cdc2, and cyclin E-Cdk2 strongly, Cdc25B mutant was only found to bind to cyclin A-Cdk2 at significant levels. Cysteine 13-16 cell division cycle 25A Homo sapiens 6-12 8617791-6 1996 While Cdc25A Cys --> Ser could interact with cyclin A-Cdk2, cyclin B-Cdc2, and cyclin E-Cdk2 strongly, Cdc25B mutant was only found to bind to cyclin A-Cdk2 at significant levels. Serine 24-27 cell division cycle 25A Homo sapiens 6-12 8771191-3 1996 Herein we identify aspartic acid 383 as a potential candidate for the catalytic acid in human Cdc25A protein phosphatase, using sequence alignment, structural information, and site-directed mutagenesis. Aspartic Acid 19-32 cell division cycle 25A Homo sapiens 94-100 34954029-0 2022 FDI-6 and Olaparib Synergistically Inhibit the Growth of Pancreatic Cancer by Repressing BUB1, BRCA1 and CDC25A Signaling Pathways. olaparib 10-18 cell division cycle 25A Homo sapiens 105-111 7635051-5 1995 A glutathione-S-transferase-cdc25a fusion protein can hydrolyze para-nitro-phenylphosphate confirming that cdc25a is a phosphatase. para-nitro-phenylphosphate 64-90 cell division cycle 25A Homo sapiens 28-34 34363019-3 2022 Here we describe a novel ubiquitin/proteasome-mediated pathway negatively regulating CDC25A stability, dependent on its phosphorylation by the serine/threonine kinase DYRK2. Serine 143-149 cell division cycle 25A Homo sapiens 85-91 34954029-5 2022 Olaparib induced the feedback overexpression of PARP1, FOXM1, CDC25A, CCND1, CDK1, CCNA2, CCNB1, CDC25B, BRCA1/2 and Rad51 to promote the acceleration of cell mitosis and recovery of DNA repair, which caused the generation of adaptive resistance. olaparib 0-8 cell division cycle 25A Homo sapiens 62-68 34954029-6 2022 FDI-6 reversed Olaparib-induced adaptive resistance and inhibited cell cycle progression and DNA damage repair by repressing the expression of FOXM1, PARP1/2, BUB1, CDC25A, BRCA1 and other genes-involved in cell cycle control and DNA damage repair. olaparib 15-23 cell division cycle 25A Homo sapiens 165-171 34800881-15 2021 According to further verification of related genes, the mRNA and protein levels of KIF11, CCNA2 and CDC25A decrease significantly after treatment with dehydroabietic acid. dehydroabietic acid 151-170 cell division cycle 25A Homo sapiens 100-106 34761581-7 2021 Co-transfection assays showed that overexpression of CDC25A reversed the inhibition of miR-34a-5p on CC growth and migration. mir-34a-5p 87-97 cell division cycle 25A Homo sapiens 53-59 34314996-0 2021 miR-199a-5p inhibits the proliferation of hepatocellular carcinoma cells by regulating CDC25A to induce cell cycle arrest. mir-199a-5p 0-11 cell division cycle 25A Homo sapiens 87-93 34743185-13 2021 Cdc25A was elevated in human cervical cancer tissues but was reduced during sorafenib-induced ferroptosis of cervical cancer cells. Sorafenib 76-85 cell division cycle 25A Homo sapiens 0-6 34743185-14 2021 Overexpression of Cdc25A inhibited sorafenib-induced ferroptosis by dephosphorylating nuclear PKM2 and suppressing autophagy. Sorafenib 35-44 cell division cycle 25A Homo sapiens 18-24 34743185-16 2021 Cdc25A increased the resistance of cervical cancer to sorafenib, while knockdown of ErbB2 blocked these effects. Sorafenib 54-63 cell division cycle 25A Homo sapiens 0-6 34479917-9 2021 Paclitaxel induced cell cycle arrest at the G1 phase in response to DNA damage, in association with the suppression of CDC25A, Cdk2 and Cyclin E1 protein expression. Paclitaxel 0-10 cell division cycle 25A Homo sapiens 119-125 34761581-8 2021 CONCLUSION: miR-34a-5p mediates growth, migration and other malignant behaviors in CC by regulating CDC25A. mir-34a-5p 12-22 cell division cycle 25A Homo sapiens 100-106 35532870-0 2022 MiR-99a-5p Constrains Epithelial-Mesenchymal Transition of Cervical Squamous Cell Carcinoma Via Targeting CDC25A/IL6. mir-99a-5p 0-10 cell division cycle 25A Homo sapiens 106-112 34156324-3 2021 Activation of CDK2 requires dephosphorylation of tyrosine-15 by CDC25A. Tyrosine 49-57 cell division cycle 25A Homo sapiens 64-70 35532870-6 2022 Also, enforced CDC25A level rescued the impact of miR-99a-5p on CSCC progression. mir-99a-5p 50-60 cell division cycle 25A Homo sapiens 15-21 35532870-8 2022 CDC25A overexpression or IL-6 treatment could attenuate inhibiting impact of miR-99a-5p overexpression on epithelial-mesenchymal transition (EMT). mir-99a 77-84 cell division cycle 25A Homo sapiens 0-6 35532870-9 2022 These findings suggested that miR-99a-5p may play an anti-tumor role in tumor metastasis by targeting CDC25A/IL6 to hamper EMT process, which revealed a novel molecular mechanism in CSCC. mir-99a-5p 30-40 cell division cycle 25A Homo sapiens 102-108 32048780-15 2020 CONCLUSIONS: WARS1 and CDC25A might be potential biomarkers for side effects of dexamethasone in lymphoma, and HELZ2 in prostate cancer. Dexamethasone 80-93 cell division cycle 25A Homo sapiens 23-29 33048473-11 2020 Pharmacological analysis showed that the administration of two cell cycle inhibitors for inactivating CDC25A phosphatase (NSC95397) and the cyclin E2/cyclin-dependent kinase 2 (CDK2) complex (purvalanol A) increased the dome number independently of MTA. purvalanol B 192-202 cell division cycle 25A Homo sapiens 102-108 33101488-0 2020 Small molecule 2,3-DCPE induces S phase arrest by activating the ATM/ATR-Chk1-Cdc25A signaling pathway in DLD-1 colon cancer cells. 2-((3-(2,3-dichlorophenoxy)propyl)amino)ethanol 15-23 cell division cycle 25A Homo sapiens 78-84 33101488-7 2020 Furthermore, wortmannin and caffeine inhibited the 2,3-DCPE-mediated phosphorylation of Chk1 and the degradation of Cdc25A. Wortmannin 13-23 cell division cycle 25A Homo sapiens 116-122 33101488-7 2020 Furthermore, wortmannin and caffeine inhibited the 2,3-DCPE-mediated phosphorylation of Chk1 and the degradation of Cdc25A. Caffeine 28-36 cell division cycle 25A Homo sapiens 116-122 33101488-7 2020 Furthermore, wortmannin and caffeine inhibited the 2,3-DCPE-mediated phosphorylation of Chk1 and the degradation of Cdc25A. 2-((3-(2,3-dichlorophenoxy)propyl)amino)ethanol 51-59 cell division cycle 25A Homo sapiens 116-122 33101488-9 2020 Taken together, the data of the current study indicated that 2,3-DCPE caused DNA damage in colon cancer cells and that 2,3-DCPE-induced S phase arrest was associated with the activation of the ATM/ATR-Chk1-Cdc25A pathway. 2-((3-(2,3-dichlorophenoxy)propyl)amino)ethanol 119-127 cell division cycle 25A Homo sapiens 206-212 33000276-5 2020 The results demonstrated that EGCG can inhibit the proliferation of HepG2 and Huh7 cells, reduce the expression of CDC25A and increase the expression of p21waf1/Cip1 in HepG2. epigallocatechin gallate 30-34 cell division cycle 25A Homo sapiens 115-121 32934772-6 2020 To target the interaction of 14-3-3epsilon with CDC25A for cancer therapy, we developed two novel phospho-peptides, pS and pT, corresponding to each of the 14-3-3 binding sites of CDC25A, to specifically interfere with 14-3-3epsilon binding to CDC25A. Phosphorus 116-118 cell division cycle 25A Homo sapiens 180-186 32934772-6 2020 To target the interaction of 14-3-3epsilon with CDC25A for cancer therapy, we developed two novel phospho-peptides, pS and pT, corresponding to each of the 14-3-3 binding sites of CDC25A, to specifically interfere with 14-3-3epsilon binding to CDC25A. Phosphorus 116-118 cell division cycle 25A Homo sapiens 180-186 32934772-6 2020 To target the interaction of 14-3-3epsilon with CDC25A for cancer therapy, we developed two novel phospho-peptides, pS and pT, corresponding to each of the 14-3-3 binding sites of CDC25A, to specifically interfere with 14-3-3epsilon binding to CDC25A. Platinum 123-125 cell division cycle 25A Homo sapiens 180-186 32934772-6 2020 To target the interaction of 14-3-3epsilon with CDC25A for cancer therapy, we developed two novel phospho-peptides, pS and pT, corresponding to each of the 14-3-3 binding sites of CDC25A, to specifically interfere with 14-3-3epsilon binding to CDC25A. Platinum 123-125 cell division cycle 25A Homo sapiens 180-186 32934772-7 2020 Peptides pT (IC50 = 22.1 muM), and pS (IC50 = 29 muM) induced SCC cell death and blocked 14-3-3epsilon binding to CDC25A. Platinum 9-11 cell division cycle 25A Homo sapiens 114-120 32934772-7 2020 Peptides pT (IC50 = 22.1 muM), and pS (IC50 = 29 muM) induced SCC cell death and blocked 14-3-3epsilon binding to CDC25A. Phosphorus 35-37 cell division cycle 25A Homo sapiens 114-120 32041019-11 2020 By contrast, Cdc25A, a downstream target of Chk2, was reduced in 1-NP-exposed trophoblasts. 1-nitropyrene 65-69 cell division cycle 25A Homo sapiens 13-19 31922225-5 2020 In the present study, the effects of CDC25A on cell proliferation and migration were analyzed using cell cycle, MTT and Transwell assays. thiazolyl blue 112-115 cell division cycle 25A Homo sapiens 37-43 32127943-6 2020 We found that B7-H3 could effectively enhance the resistance to a chemotherapeutic drug (oxaliplatin or 5-fluorouracil) via CDC25A. Oxaliplatin 89-100 cell division cycle 25A Homo sapiens 124-130 32127943-6 2020 We found that B7-H3 could effectively enhance the resistance to a chemotherapeutic drug (oxaliplatin or 5-fluorouracil) via CDC25A. Fluorouracil 104-118 cell division cycle 25A Homo sapiens 124-130 31886487-14 2019 We demonstrated that SB promotes proliferation in testicular tissue by regulating the cyclin-dependent kinase (CDK) inhibitors 4Ebp1 and P57 (proliferation inhibitor genes) and up-regulating Cdc25a and Cdk4 (cell cycle promoting genes). Antimony 21-23 cell division cycle 25A Homo sapiens 191-197 32907364-6 2020 Accompanied with cell cycle disruption, cucurbitacin B altered the expression of proteins involved in the G2/M phase transition including downregulation of cyclin A, cyclin D1, and cdc25A, and upregulation of p21. cucurbitacin B 40-54 cell division cycle 25A Homo sapiens 181-187 31563013-4 2019 Although plumbagin had a lower binding affinity for MKK7, this compound and sulfur-containing derivatives 4 and 6-8 were potent inhibitors of Cdc25A and Cdc25B. plumbagin 9-18 cell division cycle 25A Homo sapiens 142-148 31563013-4 2019 Although plumbagin had a lower binding affinity for MKK7, this compound and sulfur-containing derivatives 4 and 6-8 were potent inhibitors of Cdc25A and Cdc25B. Sulfur 76-82 cell division cycle 25A Homo sapiens 142-148 31799646-0 2019 MiRNA-98-5p inhibits the progression of osteosarcoma by regulating cell cycle via targeting CDC25A expression. mirna-98-5p 0-11 cell division cycle 25A Homo sapiens 92-98 31799646-12 2019 Subsequent experiments revealed that miRNA-98-5p significantly inhibited cell cycle progression and migratory potential, whereas induced the apoptosis of osteosarcoma cells by down-regulating CDC25A. mirna-98-5p 37-48 cell division cycle 25A Homo sapiens 192-198 30548945-9 2019 MiR-16-5p overexpression reduced expression of important cell cycle and apoptosis regulators in glioma cells, including CDK6, CDC25A, CCND3, CCNE1, WEE1, CHEK1, BCL2 and MCL1. mir-16-5p 0-9 cell division cycle 25A Homo sapiens 126-132 31601054-5 2019 For this situation, actinomycin V decreased the M-phase related proteins (Cdc2, Cdc25A and Cyclin B1) expression, arrested cells in G2/M phase and subsequently triggered apoptosis by mediating the Bcl-2 family proteins" expression (Bax and Bcl-2). Dactinomycin 20-31 cell division cycle 25A Homo sapiens 80-86 31409007-9 2019 Moreover, Western blotting revealed Cdc25A and Cyclin B1 were upregulated in Ivalin-meditated cell cycle arrest. ivalin 77-83 cell division cycle 25A Homo sapiens 36-42 31184118-4 2019 The ROS levels increased significantly after exposure to juglone, which paralleled increases in the mRNA and protein expression of p21 and decreases in the levels of CDK2, cdc25A, CHK1, and cyclin A. ros 4-7 cell division cycle 25A Homo sapiens 172-178 31184118-4 2019 The ROS levels increased significantly after exposure to juglone, which paralleled increases in the mRNA and protein expression of p21 and decreases in the levels of CDK2, cdc25A, CHK1, and cyclin A. juglone 57-64 cell division cycle 25A Homo sapiens 172-178 30214601-13 2018 These results elucidated the role of chaetominine in in the regulation of ATR/cdc25A/Chk1 expression in K562 cells. chaetominine 37-49 cell division cycle 25A Homo sapiens 78-84 30947332-6 2019 The in vitro studies revealed that DCZ0801 could inhibit cell proliferation and induce apoptosis by regulating both caspase-dependent and mitogen-activated protein kinase signaling pathways, inducing S-phase arrest of the cell cycle related to downregulation of CDK2, cyclin-A2, and CDC25A protein expression. dcz0801 35-42 cell division cycle 25A Homo sapiens 283-289 30902389-0 2019 MiR-365 enhances the radiosensitivity of non-small cell lung cancer cells through targeting CDC25A. mir-365 0-7 cell division cycle 25A Homo sapiens 92-98 30902389-10 2019 And we confirmed that miR-365 could increase the radiosensitivity of NSCLC cells by targeting CDC25A using in vitro and in vivo assays. mir-365 22-29 cell division cycle 25A Homo sapiens 94-100 30583070-6 2019 Rafoxanide also inhibited DNA synthesis and caused cell cycle arrest by regulating the cdc25A-degradation pathway. Rafoxanide 0-10 cell division cycle 25A Homo sapiens 87-93 31281464-6 2019 Loss-of-function studies showed that CDC25A promoted cisplatin-resistance and paclitaxel-resistance and inhibited the drug-induced apoptosis in ovarian cancer MCS. Cisplatin 53-62 cell division cycle 25A Homo sapiens 37-43 31281464-6 2019 Loss-of-function studies showed that CDC25A promoted cisplatin-resistance and paclitaxel-resistance and inhibited the drug-induced apoptosis in ovarian cancer MCS. Paclitaxel 78-88 cell division cycle 25A Homo sapiens 37-43 30858545-0 2019 Exosome-derived miR-339-5p mediates radiosensitivity by targeting Cdc25A in locally advanced esophageal squamous cell carcinoma. mir-339-5p 16-26 cell division cycle 25A Homo sapiens 66-72 30858545-7 2019 Mechanistically, miR-339-5p enhances radiosensitivity by targeting Cdc25A, and is transcriptionally regulated by Runx3. mir-339-5p 17-27 cell division cycle 25A Homo sapiens 67-73 30858545-8 2019 Correlations were observed between miR-339-5p levels and Cdc25A/Runx3 levels in tissue samples. mir-339-5p 35-45 cell division cycle 25A Homo sapiens 57-63 30166399-7 2018 VX-970 preferentially inhibited ATR-Chk1-CDC25a signaling, abrogated the radiotherapy-induced G2-M checkpoint, delayed resolution of DNA double-strand breaks, and reduced colony formation after radiotherapy in TNBC cells relative to normal-like breast epithelial cells. berzosertib 0-6 cell division cycle 25A Homo sapiens 41-47 30180991-8 2018 Furthermore, pre-treatment of cells with MG-132 also abolished PDGF-induced beta-TrCP reduction, Cdc25A elevation and cell proliferation. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 41-47 cell division cycle 25A Homo sapiens 97-103 30180991-9 2018 In addition, pre-depletion of Cdc25A by siRNA transfection suppressed PDGF-induced PASMCs proliferation. pasmcs 83-89 cell division cycle 25A Homo sapiens 30-36 30180991-10 2018 Taken together, our study indicates that up-regulation of CSN6 by PDGFR/PI3K/Akt signaling pathway decreases beta-TrCP by increasing its ubiquitinated degradation, and thereby increases the expression of Cdc25A, which promotes PDGF-induced PASMCs proliferation. pasmcs 240-246 cell division cycle 25A Homo sapiens 204-210 28431339-2 2017 Here, we describe the development of two novel quinone-polycycle series of CDC25A and C inhibitors on the one hand 1a-k, coumarin-based, and on the other 2a-g, quinolinone-based, which inhibit either enzymes up to a sub-micro molar level and at single-digit micro molar concentrations, respectively. quinone 47-54 cell division cycle 25A Homo sapiens 75-81 29725502-0 2018 Ciclopirox activates ATR-Chk1 signaling pathway leading to Cdc25A protein degradation. Ciclopirox 0-10 cell division cycle 25A Homo sapiens 59-65 29725502-1 2018 Ciclopirox olamine (CPX), an off-patent anti-fungal drug, has been found to inhibit the G1-cyclin dependent kinases partly by increasing the phosphorylation and degradation of Cdc25A. Ciclopirox 0-18 cell division cycle 25A Homo sapiens 176-182 29725502-1 2018 Ciclopirox olamine (CPX), an off-patent anti-fungal drug, has been found to inhibit the G1-cyclin dependent kinases partly by increasing the phosphorylation and degradation of Cdc25A. Ciclopirox 20-23 cell division cycle 25A Homo sapiens 176-182 29725502-2 2018 However, little is known about the molecular target(s) of CPX responsible for Cdc25A degradation. Ciclopirox 58-61 cell division cycle 25A Homo sapiens 78-84 29725502-3 2018 Here, we show that CPX induced the degradation of Cdc25A neither by increasing CK1alpha or decreasing DUB3 expression, nor via activating GSK3beta, but through activating Chk1 in rhabdomyosarcoma (Rh30) and breast carcinoma (MDA-MB-231) cells. Ciclopirox 19-22 cell division cycle 25A Homo sapiens 50-56 29725502-4 2018 This is strongly supported by the findings that inhibition of Chk1 with TCS2312 or knockdown of Chk1 profoundly attenuated CPX-induced Cdc25A degradation in the cells. tcs2312 72-79 cell division cycle 25A Homo sapiens 135-141 29725502-4 2018 This is strongly supported by the findings that inhibition of Chk1 with TCS2312 or knockdown of Chk1 profoundly attenuated CPX-induced Cdc25A degradation in the cells. Ciclopirox 123-126 cell division cycle 25A Homo sapiens 135-141 29725502-8 2018 In contrast, knockdown of ATR conferred high resistance to CPX-induced Chk1 phosphorylation and Cdc25A degradation. Ciclopirox 59-62 cell division cycle 25A Homo sapiens 96-102 29725502-9 2018 Therefore, the results suggest that CPX-induced degradation of Cdc25A is attributed to the activation of ATR-Chk1 signaling pathway, a consequence of iron chelation-induced DNA damage. Ciclopirox 36-39 cell division cycle 25A Homo sapiens 63-69 29725502-9 2018 Therefore, the results suggest that CPX-induced degradation of Cdc25A is attributed to the activation of ATR-Chk1 signaling pathway, a consequence of iron chelation-induced DNA damage. Iron 150-154 cell division cycle 25A Homo sapiens 63-69 28803043-0 2017 Structure-based development of novel triazoles and related thiazolotriazoles as anticancer agents and Cdc25A/B phosphatase inhibitors. Triazoles 37-46 cell division cycle 25A Homo sapiens 102-108 28803043-2 2017 Synthesis of twenty nine new 1,2,4-triazoles and some derived thiazolothiadiazoles (structurally-relevant to some reported triazoles with anticancer and/or Cdc25A/B inhibitory activities) is described in this study. 1,2,4-triazole 29-44 cell division cycle 25A Homo sapiens 156-162 28803043-2 2017 Synthesis of twenty nine new 1,2,4-triazoles and some derived thiazolothiadiazoles (structurally-relevant to some reported triazoles with anticancer and/or Cdc25A/B inhibitory activities) is described in this study. thiazolothiadiazoles 62-82 cell division cycle 25A Homo sapiens 156-162 28803043-2 2017 Synthesis of twenty nine new 1,2,4-triazoles and some derived thiazolothiadiazoles (structurally-relevant to some reported triazoles with anticancer and/or Cdc25A/B inhibitory activities) is described in this study. Triazoles 35-44 cell division cycle 25A Homo sapiens 156-162 28291626-7 2017 Mus81 knockdown also induced S phase arrest and elevated apoptosis in CDDP treated HCT116 cells through activating CHK1/CDC25A/CDK2 and CHK1/p53/Bax pathways, while these effects could be counteracted by CHK1 inhibition. Cisplatin 70-74 cell division cycle 25A Homo sapiens 120-126 29751524-8 2018 Additionally, beta-asarone modulated the cell cycle-related proteins p21, p27, Cdc25A, cyclin D, cyclin E, and CDK2. asarone 14-26 cell division cycle 25A Homo sapiens 79-85 29484412-10 2018 We found that melatonin induced cell cycle arrest and the downregulation of CDC25A, phospho-CDC25A (at Ser75), p21 (p21Cip1/p21Waf1) and phospho-p21 (at Thr145). Melatonin 14-23 cell division cycle 25A Homo sapiens 76-82 29484412-10 2018 We found that melatonin induced cell cycle arrest and the downregulation of CDC25A, phospho-CDC25A (at Ser75), p21 (p21Cip1/p21Waf1) and phospho-p21 (at Thr145). Melatonin 14-23 cell division cycle 25A Homo sapiens 92-98 28951130-7 2017 Additionally, the CDC25A inhibitors Vitamin K3 or NSC663284 were more toxic to SCC than normal keratinocytes, and CDC25A inhibition effectively suppressed skin cancer growth by increasing apoptosis without affecting normal skin biology. Vitamin K 3 36-46 cell division cycle 25A Homo sapiens 18-24 28951130-7 2017 Additionally, the CDC25A inhibitors Vitamin K3 or NSC663284 were more toxic to SCC than normal keratinocytes, and CDC25A inhibition effectively suppressed skin cancer growth by increasing apoptosis without affecting normal skin biology. NSC 663284 50-59 cell division cycle 25A Homo sapiens 18-24 29544887-9 2017 Artesunate can inhibit the growth of gastric adenocarcinoma cells SGC-7901 and induce the cell apoptosis, the mechanism may be related to the regulation of CDC25A, Bcl-2, Bax, Caspase-3 and mitochondrial membrane potential in SGC-7901 cells. Artesunate 0-10 cell division cycle 25A Homo sapiens 156-162 28431339-2 2017 Here, we describe the development of two novel quinone-polycycle series of CDC25A and C inhibitors on the one hand 1a-k, coumarin-based, and on the other 2a-g, quinolinone-based, which inhibit either enzymes up to a sub-micro molar level and at single-digit micro molar concentrations, respectively. coumarin 121-129 cell division cycle 25A Homo sapiens 75-81 28431339-2 2017 Here, we describe the development of two novel quinone-polycycle series of CDC25A and C inhibitors on the one hand 1a-k, coumarin-based, and on the other 2a-g, quinolinone-based, which inhibit either enzymes up to a sub-micro molar level and at single-digit micro molar concentrations, respectively. Quinolones 160-171 cell division cycle 25A Homo sapiens 75-81 26370218-10 2016 Western blotting results showed that BDMC inhibited Cdc25A, cyclin A and E for causing S phase arrest, furthermore, promoted the expression of AIF, Endo G and PARP and the levels of Fas ligand (Fas L) and Fas were also up-regulated. bisdemethoxycurcumin 37-41 cell division cycle 25A Homo sapiens 52-58 28680535-0 2017 Ciclopirox inhibits cancer cell proliferation by suppression of Cdc25A. Ciclopirox 0-10 cell division cycle 25A Homo sapiens 64-70 28680535-3 2017 Here we show that CPX inhibits cell proliferation in part by downregulating the protein level of Cdc25A in tumor cells. Ciclopirox 18-21 cell division cycle 25A Homo sapiens 97-103 28680535-6 2017 Since Cdc25A degradation is tightly related to its phosphorylation status, we further examined whether CPX alters Cdc25A phosphorylation. Ciclopirox 103-106 cell division cycle 25A Homo sapiens 114-120 28680535-7 2017 The results showed that CPX treatment increased the phosphorylation of Cdc25A (S76 and S82), but only Cdc25A-S82A mutant was resistant to CPX-induced degradation. Ciclopirox 24-27 cell division cycle 25A Homo sapiens 71-77 28680535-8 2017 Furthermore, ectopic expression of Cdc25A-S82A partially conferred resistance to CPX inhibition of cell proliferation. Ciclopirox 81-84 cell division cycle 25A Homo sapiens 35-41 28680535-9 2017 Therefore, our findings indicate that CPX inhibits cell proliferation at least in part by promoting Cdc25A degradation. Ciclopirox 38-41 cell division cycle 25A Homo sapiens 100-106 28101580-14 2017 MeOH fraction treatment also arrested HepG2 cells in the S phase, with decreased expression of cyclin A, CDK2, and CDC25A. Methanol 0-4 cell division cycle 25A Homo sapiens 115-121 28785594-8 2017 Moreover, pterostilbene treatment markedly induced S-phase cell cycle arrest, which was accompanied by downregulation of cdc25A, cyclin A2, and CDK2. pterostilbene 10-23 cell division cycle 25A Homo sapiens 121-127 27580187-4 2016 Here, we identify by mass spectrometry analysis a new phosphorylation event of Cdc25A on Serine283. serine283 89-98 cell division cycle 25A Homo sapiens 79-85 27626431-9 2016 Therefore, R-PE induced apoptosis by arresting the SGC-7901 cell at S phase was successful, which was achieved by the expression of the CDC25A protein, which reduced the CDK2 protein actived and the formation of Cyclin-CDK complex. r-pe 11-15 cell division cycle 25A Homo sapiens 136-142 27178385-6 2016 The binding of thiazolidinone derivative 6 onto CDC25A protein was reversible. thiazolidinone 15-29 cell division cycle 25A Homo sapiens 48-54