PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
27210748-2	2016	Using a high-throughput chemical screen, we discovered that PD407824, a checkpoint kinase 1 (CHK1) inhibitor, increases the sensitivity of cells to sub-threshold amounts of BMP4.	PD 407824	60-68	checkpoint kinase 1	Homo sapiens	72-91
27210748-2	2016	Using a high-throughput chemical screen, we discovered that PD407824, a checkpoint kinase 1 (CHK1) inhibitor, increases the sensitivity of cells to sub-threshold amounts of BMP4.	PD 407824	60-68	checkpoint kinase 1	Homo sapiens	93-97
27044938-0	2016	Phase I Study of LY2606368, a Checkpoint Kinase 1 Inhibitor, in Patients With Advanced Cancer.	prexasertib	17-26	checkpoint kinase 1	Homo sapiens	30-49
27044938-1	2016	PURPOSE: The primary objective was to determine safety, toxicity, and a recommended phase II dose regimen of LY2606368, an inhibitor of checkpoint kinase 1, as monotherapy.	prexasertib	109-118	checkpoint kinase 1	Homo sapiens	136-155
26851293-7	2016	Whereas belinostat abrogated the MLN4924-activated intra-S checkpoint through Chk1 and Wee1 inhibition/downregulation, cotreatment downregulated multiple homologous recombination and nonhomologous end-joining repair proteins, triggering robust double-stranded breaks, chromatin pulverization, and apoptosis.	belinostat	8-18	checkpoint kinase 1	Homo sapiens	78-82
27164065-0	2016	In Silico Exploration of 1,7-Diazacarbazole Analogs as Checkpoint Kinase 1 Inhibitors by Using 3D QSAR, Molecular Docking Study, and Molecular Dynamics Simulations.	9h-pyrrolo[2,3-b:5,4-c']dipyridine	25-43	checkpoint kinase 1	Homo sapiens	55-74
27164065-3	2016	In this work, a set of 1,7-diazacarbazole analogs were identified as potent Chk1 inhibitors through a series of computer-aided drug design processes, including three-dimensional quantitative structure-activity relationship (3D-QSAR) modeling, molecular docking, and molecular dynamics simulations.	9h-pyrrolo[2,3-b:5,4-c']dipyridine	23-41	checkpoint kinase 1	Homo sapiens	76-80
27035420-3	2016	In the present study, it was observed that its genotoxic metabolite, anti-benzopyrene-7,8-diol-9,10-epoxide (BPDE), triggered cell cycle arrest in S-phase in 16HBE cells by activating ataxia-telangiectasia (ATM)/checkpoint kinase (Chk)2 and ATM and Rad3 related (ATR)/Chk1 signaling pathways.	benzopyrene-7,8-diol-9,10-epoxide	74-107	checkpoint kinase 1	Homo sapiens	268-272
27035420-3	2016	In the present study, it was observed that its genotoxic metabolite, anti-benzopyrene-7,8-diol-9,10-epoxide (BPDE), triggered cell cycle arrest in S-phase in 16HBE cells by activating ataxia-telangiectasia (ATM)/checkpoint kinase (Chk)2 and ATM and Rad3 related (ATR)/Chk1 signaling pathways.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	109-113	checkpoint kinase 1	Homo sapiens	268-272
27123146-7	2016	Furthermore, triptolide enhanced gemcitabine-induced S phase arrest and DNA double-strand breaks, possibly through checkpoint kinase 1 suppression.	triptolide	13-23	checkpoint kinase 1	Homo sapiens	115-134
27123146-7	2016	Furthermore, triptolide enhanced gemcitabine-induced S phase arrest and DNA double-strand breaks, possibly through checkpoint kinase 1 suppression.	gemcitabine	33-44	checkpoint kinase 1	Homo sapiens	115-134
26960975-0	2016	The Error-Prone DNA Polymerase kappa Promotes Temozolomide Resistance in Glioblastoma through Rad17-Dependent Activation of ATR-Chk1 Signaling.	Temozolomide	46-58	checkpoint kinase 1	Homo sapiens	128-132
26960975-6	2016	Further investigation of the relationship between Pol kappa and temozolomide revealed that Pol kappa inactivation facilitated temozolomide-induced Rad17 ubiquitination and proteasomal degradation, subsequently silencing ATR-Chk1 signaling and leading to defective HR repair and the reversal of temozolomide resistance.	Temozolomide	64-76	checkpoint kinase 1	Homo sapiens	224-228
26960975-6	2016	Further investigation of the relationship between Pol kappa and temozolomide revealed that Pol kappa inactivation facilitated temozolomide-induced Rad17 ubiquitination and proteasomal degradation, subsequently silencing ATR-Chk1 signaling and leading to defective HR repair and the reversal of temozolomide resistance.	Temozolomide	126-138	checkpoint kinase 1	Homo sapiens	224-228
26960975-6	2016	Further investigation of the relationship between Pol kappa and temozolomide revealed that Pol kappa inactivation facilitated temozolomide-induced Rad17 ubiquitination and proteasomal degradation, subsequently silencing ATR-Chk1 signaling and leading to defective HR repair and the reversal of temozolomide resistance.	Temozolomide	126-138	checkpoint kinase 1	Homo sapiens	224-228
26921248-3	2016	Here, we present data that define the first endogenous activation of the CS-pathway whereby, upon DNA damage, wild type p53 acts as an endogenous regulator of CHK1 levels that modulates caspase-2 activation.	Cesium	73-75	checkpoint kinase 1	Homo sapiens	159-163
26850987-0	2016	Chk1 inhibitor synergizes quinacrine mediated apoptosis in breast cancer cells by compromising the base excision repair cascade.	Quinacrine	26-36	checkpoint kinase 1	Homo sapiens	0-4
26850987-5	2016	A CHK1 inhibitor, SB218078, was also tested alone and in combination with QC.	SB 218078	18-26	checkpoint kinase 1	Homo sapiens	2-6
26295308-0	2016	The clinical development candidate CCT245737 is an orally active CHK1 inhibitor with preclinical activity in RAS mutant NSCLC and Emicro-MYC driven B-cell lymphoma.	CCT245737	35-44	checkpoint kinase 1	Homo sapiens	65-69
27044842-7	2016	In addition, IMP1338 markedly induced the phosphorylation of histone H2AX and Chk1 in both cell lines while the combination of 5-fluorouracil (5-FU) and radiation inhibited the viability of HCT116, HCT116 p53(-/-), and HT29 cells compared to 5-FU or radiation alone.	IMP1338	13-20	checkpoint kinase 1	Homo sapiens	78-82
27087371-5	2016	The expressions of ATM, Chk1, Chk2, phosphorylated Cdc2 and CDK2 were up-regulated in the MGC-803 cells after Jaridonin treatment, while the levels of Cdc2 and CDK2 were decreased.	jaridonin	110-119	checkpoint kinase 1	Homo sapiens	24-28
26775629-8	2016	In BCC/KMC1 cells, the induction of p53 by IMQ was achieved through increased ROS production to stimulate the ATM/ATR-Chk1/Chk2 axis but was not mediated by inducing DNA damage.	Imiquimod	43-46	checkpoint kinase 1	Homo sapiens	118-122
26775629-8	2016	In BCC/KMC1 cells, the induction of p53 by IMQ was achieved through increased ROS production to stimulate the ATM/ATR-Chk1/Chk2 axis but was not mediated by inducing DNA damage.	ros	78-81	checkpoint kinase 1	Homo sapiens	118-122
26867682-5	2016	Accordingly, abrogation of Chk1 activity with UCN-01 and its expression with shChk1 increased sensitivity to bleomycin and radiation.	Bleomycin	109-118	checkpoint kinase 1	Homo sapiens	27-31
26699757-3	2016	Exposure of J/Neo cells to kaempeferol caused cytotoxicity and activation of the ATM/ATR-Chk1/Chk2 pathway, activating the phosphorylation of p53 (Ser-15), inhibitory phosphorylation of Cdc25C (Ser-216), and inactivation of cyclin-dependent kinase 1 (Cdk1), with resultant G2- arrest of the cell cycle.	kaempeferol	27-38	checkpoint kinase 1	Homo sapiens	89-93
26824362-10	2016	Consistent with the potential inhibition of ATM by squalene, IR-induced phosphorylation of ATM effectors such as p53 (Ser15) and Chk1 (Ser317) was inhibited by cell treatment with squalene.	Squalene	51-59	checkpoint kinase 1	Homo sapiens	129-133
26824362-10	2016	Consistent with the potential inhibition of ATM by squalene, IR-induced phosphorylation of ATM effectors such as p53 (Ser15) and Chk1 (Ser317) was inhibited by cell treatment with squalene.	Squalene	180-188	checkpoint kinase 1	Homo sapiens	129-133
26683224-3	2016	GL did not induce double strand DNA break but activated the ATR and ATM-mediated DNA damage response (DDR) inducing CHK1, H2AX phosphorylation (fH2AX) and CDC25C downregulation.	galiellalactone	0-2	checkpoint kinase 1	Homo sapiens	116-120
26683224-5	2016	In contrast, UCN-01, a CHK1 inhibitor, prevented GL-induced cell cycle arrest but enhanced apoptosis in DU145 cells.	7-hydroxystaurosporine	13-19	checkpoint kinase 1	Homo sapiens	23-27
26683224-5	2016	In contrast, UCN-01, a CHK1 inhibitor, prevented GL-induced cell cycle arrest but enhanced apoptosis in DU145 cells.	galiellalactone	49-51	checkpoint kinase 1	Homo sapiens	23-27
26595527-0	2016	A subset of cancer cell lines is acutely sensitive to the Chk1 inhibitor MK-8776 as monotherapy due to CDK2 activation in S phase.	MK-8776	73-80	checkpoint kinase 1	Homo sapiens	58-62
26595527-3	2016	From analysis of a large panel of cell lines, we demonstrate that 15% are very sensitive to the Chk1 inhibitor MK-8776.	MK-8776	111-118	checkpoint kinase 1	Homo sapiens	96-100
26657501-0	2016	ATR-Chk1 signaling inhibition as a therapeutic strategy to enhance cisplatin chemosensitivity in urothelial bladder cancer.	Cisplatin	67-76	checkpoint kinase 1	Homo sapiens	4-8
26872382-3	2016	We found that adenovirus prevents Chk1-mediated checkpoint activation through inactivation of Mre11 and downregulation of the pChk1 adaptor-protein, Claspin, in cells with high levels of DNA-damage induced by the cytotoxic drugs gemcitabine and irinotecan.	gemcitabine	229-240	checkpoint kinase 1	Homo sapiens	34-38
26872382-3	2016	We found that adenovirus prevents Chk1-mediated checkpoint activation through inactivation of Mre11 and downregulation of the pChk1 adaptor-protein, Claspin, in cells with high levels of DNA-damage induced by the cytotoxic drugs gemcitabine and irinotecan.	Irinotecan	245-255	checkpoint kinase 1	Homo sapiens	34-38
27001483-3	2016	In addition to gamma-H2AX, SFOM-0046 activates preferentially ATR-Chk1 in M21 and HT29 cells while both ATR-Chk1 and ATM-Chk2 pathways are activated in HCT116 cells.	sfom-0046	27-36	checkpoint kinase 1	Homo sapiens	66-70
26969379-12	2016	Western blots indicate that homochelidonine and chelidonine exposure activates Chk1 and Chk2.	homochelidonine	28-43	checkpoint kinase 1	Homo sapiens	79-83
26969379-12	2016	Western blots indicate that homochelidonine and chelidonine exposure activates Chk1 and Chk2.	chelidonine	32-43	checkpoint kinase 1	Homo sapiens	79-83
26612134-0	2016	LY2603618, a selective CHK1 inhibitor, enhances the anti-tumor effect of gemcitabine in xenograft tumor models.	LY2603618	0-9	checkpoint kinase 1	Homo sapiens	23-27
26612134-0	2016	LY2603618, a selective CHK1 inhibitor, enhances the anti-tumor effect of gemcitabine in xenograft tumor models.	gemcitabine	73-84	checkpoint kinase 1	Homo sapiens	23-27
26612134-2	2016	We report the preclinical therapeutic activity of LY2603618 (CHK1 inhibitor) at inhibiting CHK1 activation by gemcitabine and enhancing in vivo efficacy.	LY2603618	50-59	checkpoint kinase 1	Homo sapiens	61-65
26612134-2	2016	We report the preclinical therapeutic activity of LY2603618 (CHK1 inhibitor) at inhibiting CHK1 activation by gemcitabine and enhancing in vivo efficacy.	LY2603618	50-59	checkpoint kinase 1	Homo sapiens	91-95
26612134-2	2016	We report the preclinical therapeutic activity of LY2603618 (CHK1 inhibitor) at inhibiting CHK1 activation by gemcitabine and enhancing in vivo efficacy.	gemcitabine	110-121	checkpoint kinase 1	Homo sapiens	61-65
26612134-2	2016	We report the preclinical therapeutic activity of LY2603618 (CHK1 inhibitor) at inhibiting CHK1 activation by gemcitabine and enhancing in vivo efficacy.	gemcitabine	110-121	checkpoint kinase 1	Homo sapiens	91-95
26612134-6	2016	Co-administration of LY2603618 with gemcitabine showed a clear inhibition of CHK1 autophosphorylation for at least 24 h. Combining LY2603618 with gemcitabine resulted in an increase in H2AX serine 139 phosphorylation, indicating a corresponding increase in damaged DNA in the tumors.	LY2603618	21-30	checkpoint kinase 1	Homo sapiens	77-81
26612134-6	2016	Co-administration of LY2603618 with gemcitabine showed a clear inhibition of CHK1 autophosphorylation for at least 24 h. Combining LY2603618 with gemcitabine resulted in an increase in H2AX serine 139 phosphorylation, indicating a corresponding increase in damaged DNA in the tumors.	gemcitabine	36-47	checkpoint kinase 1	Homo sapiens	77-81
26612134-6	2016	Co-administration of LY2603618 with gemcitabine showed a clear inhibition of CHK1 autophosphorylation for at least 24 h. Combining LY2603618 with gemcitabine resulted in an increase in H2AX serine 139 phosphorylation, indicating a corresponding increase in damaged DNA in the tumors.	LY2603618	131-140	checkpoint kinase 1	Homo sapiens	77-81
26612134-6	2016	Co-administration of LY2603618 with gemcitabine showed a clear inhibition of CHK1 autophosphorylation for at least 24 h. Combining LY2603618 with gemcitabine resulted in an increase in H2AX serine 139 phosphorylation, indicating a corresponding increase in damaged DNA in the tumors.	gemcitabine	146-157	checkpoint kinase 1	Homo sapiens	77-81
26459098-0	2016	Chk1 phosphorylated at serine345 is a predictor of early local recurrence and radio-resistance in breast cancer.	serine345	23-32	checkpoint kinase 1	Homo sapiens	0-4
26295308-1	2016	CCT245737 is the first orally active, clinical development candidate CHK1 inhibitor to be described.	CCT245737	0-9	checkpoint kinase 1	Homo sapiens	69-73
26295308-3	2016	CCT245737 potently inhibited cellular CHK1 activity (IC50 30-220 nM) and enhanced gemcitabine and SN38 cytotoxicity in multiple human tumor cell lines and human tumor xenograft models.	CCT245737	0-9	checkpoint kinase 1	Homo sapiens	38-42
26295308-9	2016	In conclusion, CCT245737 is a new CHK1 inhibitor clinical development candidate scheduled for a first in man Phase I clinical trial, that will use the novel pS296 CHK1 ELISA to monitor target inhibition.	CCT245737	15-24	checkpoint kinase 1	Homo sapiens	34-38
26295308-9	2016	In conclusion, CCT245737 is a new CHK1 inhibitor clinical development candidate scheduled for a first in man Phase I clinical trial, that will use the novel pS296 CHK1 ELISA to monitor target inhibition.	CCT245737	15-24	checkpoint kinase 1	Homo sapiens	163-167
26623721-8	2016	Moreover, dasatinib-induced senescence was dependent on Chk1 and p21, proteins known to mediate DNA damage-induced senescence.	Dasatinib	10-19	checkpoint kinase 1	Homo sapiens	56-60
26727128-6	2016	Caffeine, which is an inhibitor of ataxia telangiectasia mutated protein (ATM) and ataxia telangiectasia mutated and Rad3-related protein (ATR), and the Chk1 inhibitor inhibited the TER increases induced by daunorubicin and rebeccamycin, whereas a Chk2 inhibitor did not.	Daunorubicin	207-219	checkpoint kinase 1	Homo sapiens	153-157
26727128-6	2016	Caffeine, which is an inhibitor of ataxia telangiectasia mutated protein (ATM) and ataxia telangiectasia mutated and Rad3-related protein (ATR), and the Chk1 inhibitor inhibited the TER increases induced by daunorubicin and rebeccamycin, whereas a Chk2 inhibitor did not.	rebeccamycin	224-236	checkpoint kinase 1	Homo sapiens	153-157
26727128-9	2016	Our results suggest that Chk1 activation by daunorubicin and rebeccamycin induced claudin-5 expression and enhanced TJ barrier function in Caco-2 cell monolayer, which suggests a link between DNA damage and TJ integrity in the human intestine.	Daunorubicin	44-56	checkpoint kinase 1	Homo sapiens	25-29
26727128-9	2016	Our results suggest that Chk1 activation by daunorubicin and rebeccamycin induced claudin-5 expression and enhanced TJ barrier function in Caco-2 cell monolayer, which suggests a link between DNA damage and TJ integrity in the human intestine.	rebeccamycin	61-73	checkpoint kinase 1	Homo sapiens	25-29
26890478-0	2016	Dissociation of gemcitabine chemosensitization by CHK1 inhibition from cell cycle checkpoint abrogation and aberrant mitotic entry.	gemcitabine	16-27	checkpoint kinase 1	Homo sapiens	50-54
26890478-1	2016	In order to determine the relative contribution of checkpoint abrogation and subsequent aberrant mitotic entry to gemcitabine chemosensitization by CHK1 inhibition, we established a model utilizing the CDK inhibitors roscovitine or purvalanol A to re-establish cell cycle arrest and prevent aberrant mitotic entry in pancreatic cancer cells treated with gemcitabine and the CHK inhibitor AZD7762.	gemcitabine	114-125	checkpoint kinase 1	Homo sapiens	148-152
26890478-4	2016	Furthermore, we found that AZD7762 augmented high-intensity gammaH2AX signaling in gemcitabine-treated cells, suggesting the presence of replication stress when CHK1 is inhibited.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	27-34	checkpoint kinase 1	Homo sapiens	161-165
26890478-4	2016	Furthermore, we found that AZD7762 augmented high-intensity gammaH2AX signaling in gemcitabine-treated cells, suggesting the presence of replication stress when CHK1 is inhibited.	gemcitabine	83-94	checkpoint kinase 1	Homo sapiens	161-165
27585602-2	2016	OBJECTIVE: Herein, we have performed three-dimensional quantitative structure-activity relationship (3D-QSAR) and molecular docking analyses on a series of diazacarbazoles to design potent Chk1 inhibitors.	diazacarbazoles	156-171	checkpoint kinase 1	Homo sapiens	189-193
26657501-2	2016	Here, we demonstrate that inhibition of ATR-Chk1 pathway with the potent inhibitor WYC0209 sensitizes bladder cancer cells to cisplatin.	Cisplatin	126-135	checkpoint kinase 1	Homo sapiens	44-48
26657501-8	2016	These results indicate that inhibiting ATR-Chk1 activation with WYC0209 suppresses p-glycoprotein expression and increases cisplatin activity in bladder cancer.	Cisplatin	123-132	checkpoint kinase 1	Homo sapiens	43-47
26657501-9	2016	Our findings collectively suggest that ATR-Chk1 is a target for improving the efficacy of cisplatin in bladder cancer.	Cisplatin	90-99	checkpoint kinase 1	Homo sapiens	43-47
27585602-9	2016	Molecular docking revealed that hydrogen bond interactions with Lys38, Glu85 and Cys87 are essential for Chk1 inhibitory activity.	Hydrogen	32-40	checkpoint kinase 1	Homo sapiens	105-109
26471831-3	2016	METHODS: Potentiation of mTOR inhibitor cytotoxicity by the Chk1 inhibitor V158411 was determined in p53 mutant colon cancer cells.	V158411	75-82	checkpoint kinase 1	Homo sapiens	60-64
27643582-2	2016	We demonstrated that DNA-PK inhibitor NU7441 enhanced phosphorylation of Chk1 and Chk2 kinases 2 h after irradiation of HeLa cells at a dose of 8 Gy in contrast to ATM kinase inhibitor KU55933, which completely blocked the Chk2 kinase phosphorylation on threonine 68, and ATR kinase inhibitor VE-821, which blocked the Chk1 kinase phosphorylation on serine 345.	8-dibenzothiophen-4-yl-2-morpholin-4-yl-chromen-4-one	38-44	checkpoint kinase 1	Homo sapiens	73-77
27643582-2	2016	We demonstrated that DNA-PK inhibitor NU7441 enhanced phosphorylation of Chk1 and Chk2 kinases 2 h after irradiation of HeLa cells at a dose of 8 Gy in contrast to ATM kinase inhibitor KU55933, which completely blocked the Chk2 kinase phosphorylation on threonine 68, and ATR kinase inhibitor VE-821, which blocked the Chk1 kinase phosphorylation on serine 345.	8-dibenzothiophen-4-yl-2-morpholin-4-yl-chromen-4-one	38-44	checkpoint kinase 1	Homo sapiens	319-323
27643582-2	2016	We demonstrated that DNA-PK inhibitor NU7441 enhanced phosphorylation of Chk1 and Chk2 kinases 2 h after irradiation of HeLa cells at a dose of 8 Gy in contrast to ATM kinase inhibitor KU55933, which completely blocked the Chk2 kinase phosphorylation on threonine 68, and ATR kinase inhibitor VE-821, which blocked the Chk1 kinase phosphorylation on serine 345.	Threonine	254-263	checkpoint kinase 1	Homo sapiens	73-77
27643582-2	2016	We demonstrated that DNA-PK inhibitor NU7441 enhanced phosphorylation of Chk1 and Chk2 kinases 2 h after irradiation of HeLa cells at a dose of 8 Gy in contrast to ATM kinase inhibitor KU55933, which completely blocked the Chk2 kinase phosphorylation on threonine 68, and ATR kinase inhibitor VE-821, which blocked the Chk1 kinase phosphorylation on serine 345.	Serine	350-356	checkpoint kinase 1	Homo sapiens	73-77
26471831-5	2016	RESULTS: mTOR inhibitors AZD8055, RAD-001, rapamycin and BEZ235 induced synergistic cytotoxicity with the Chk1 inhibitor V158411 in p53 mutant colon cancer cells.	(5-(2,4-bis((3S)-3-methylmorpholin-4-yl)pyrido(2,3-d)pyrimidin-7-yl)-2-methoxyphenyl)methanol	25-32	checkpoint kinase 1	Homo sapiens	106-110
26471831-5	2016	RESULTS: mTOR inhibitors AZD8055, RAD-001, rapamycin and BEZ235 induced synergistic cytotoxicity with the Chk1 inhibitor V158411 in p53 mutant colon cancer cells.	Sirolimus	43-52	checkpoint kinase 1	Homo sapiens	106-110
26471831-5	2016	RESULTS: mTOR inhibitors AZD8055, RAD-001, rapamycin and BEZ235 induced synergistic cytotoxicity with the Chk1 inhibitor V158411 in p53 mutant colon cancer cells.	dactolisib	57-63	checkpoint kinase 1	Homo sapiens	106-110
26471831-5	2016	RESULTS: mTOR inhibitors AZD8055, RAD-001, rapamycin and BEZ235 induced synergistic cytotoxicity with the Chk1 inhibitor V158411 in p53 mutant colon cancer cells.	V158411	121-128	checkpoint kinase 1	Homo sapiens	106-110
27598338-0	2016	Phase I Study of CHK1 Inhibitor LY2603618 in Combination with Gemcitabine in Patients with Solid Tumors.	LY2603618	32-41	checkpoint kinase 1	Homo sapiens	17-21
27598338-1	2016	OBJECTIVE: LY2603618, a selective inhibitor of checkpoint kinase 1 (CHK1) and key regulator of the DNA damage checkpoint, may enhance the effects of antimetabolites.	LY2603618	11-20	checkpoint kinase 1	Homo sapiens	47-66
27598338-1	2016	OBJECTIVE: LY2603618, a selective inhibitor of checkpoint kinase 1 (CHK1) and key regulator of the DNA damage checkpoint, may enhance the effects of antimetabolites.	LY2603618	11-20	checkpoint kinase 1	Homo sapiens	68-72
26675484-10	2015	PS alone induced differentiation and expression of p21WAF1/CIP1 and p53 and decreased CHK1 in all three cell lines, with almost no further effect when combined with erlotinib.	Phosphorus	0-2	checkpoint kinase 1	Homo sapiens	86-90
26208482-6	2015	As expected, BO-1055 induces ATM and ATR-mediated DNA damage response cascades, including downstream Chk1/Chk2 phosphorylation, S/G2 cell-cycle arrest, and cell death.	1-(3-((2-(dimethylamino)ethyl)carbamoyl)phenyl)-3-(4-(bis(2-chloroethyl)amino)phenyl)urea	13-20	checkpoint kinase 1	Homo sapiens	101-105
26516160-6	2015	Mechanistically, silibinin inhibited IR-induced DNA repair (ATM and Chk1/2) and EGFR signaling and attenuated the levels of antiapoptotic proteins.	Silybin	17-26	checkpoint kinase 1	Homo sapiens	68-74
26439697-4	2015	The JEKO-1 R cell line was cross resistant to another Chk1 inhibitor (AZD-7762) and to the Wee1 inhibitor MK-1775.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	70-78	checkpoint kinase 1	Homo sapiens	54-58
26474283-2	2015	However, no evidence are presently available on a direct cytotoxic anti-tumor activity of axitinib in RCC.Herein we reported by western blot analysis that axitinib treatment induces a DNA damage response (DDR) initially characterized by gamma-H2AX phosphorylation and Chk1 kinase activation and at later time points by p21 overexpression in A-498 and Caki-2 RCC cells although with a different potency.	Axitinib	155-163	checkpoint kinase 1	Homo sapiens	268-272
26288133-0	2015	Phase I study of LY2603618, a CHK1 inhibitor, in combination with gemcitabine in Japanese patients with solid tumors.	LY2603618	17-26	checkpoint kinase 1	Homo sapiens	30-34
26288133-1	2015	This phase I trial evaluated LY2603618, a selective inhibitor of the DNA damage checkpoint kinase 1, in combination with gemcitabine.	LY2603618	29-38	checkpoint kinase 1	Homo sapiens	80-99
26462050-4	2015	In a screen against compounds that are classified as inhibitors of DNA repair or synthesis, the reporter generation was exquisitely sensitive to ribonucleotide reductase (RNR) inhibitors such as gemcitabine and clofarabine, but not to inhibitors of PARP, ATR, ATM, Chk1, and others.	gemcitabine	195-206	checkpoint kinase 1	Homo sapiens	265-269
26462050-4	2015	In a screen against compounds that are classified as inhibitors of DNA repair or synthesis, the reporter generation was exquisitely sensitive to ribonucleotide reductase (RNR) inhibitors such as gemcitabine and clofarabine, but not to inhibitors of PARP, ATR, ATM, Chk1, and others.	Clofarabine	211-222	checkpoint kinase 1	Homo sapiens	265-269
26421495-6	2015	We also showed that TDP1 depleted cells accumulate increased gammaH2AX and pS296Chk1 signals following treatment with ETO.	Etoposide	118-121	checkpoint kinase 1	Homo sapiens	80-84
26313152-8	2015	Expression of anti-apoptotic proteins Bcl-2 and Mcl-1 and DNA repair associated molecules ATM, CHK1, TP73, p53, and ERCC1 were significantly up regulated in cisplatin-treated A549sc and H157sc cells, but no increase was detected in A549IL-6si and H157IL-6si cells.	Cisplatin	157-166	checkpoint kinase 1	Homo sapiens	95-99
26748709-3	2016	Indeed, we observe that replication stress induced by the CHK1 inhibitor AZD7762 results in replication catastrophe and apoptosis, when combined with the ATR inhibitor VE-821 specifically in cancer cells.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	73-80	checkpoint kinase 1	Homo sapiens	58-62
26061604-0	2015	Mangrove dolabrane-type of diterpenes tagalsins suppresses tumor growth via ROS-mediated apoptosis and ATM/ATR-Chk1/Chk2-regulated cell cycle arrest.	dolabrane	9-18	checkpoint kinase 1	Homo sapiens	111-115
26061604-0	2015	Mangrove dolabrane-type of diterpenes tagalsins suppresses tumor growth via ROS-mediated apoptosis and ATM/ATR-Chk1/Chk2-regulated cell cycle arrest.	Diterpenes	27-37	checkpoint kinase 1	Homo sapiens	111-115
26061604-0	2015	Mangrove dolabrane-type of diterpenes tagalsins suppresses tumor growth via ROS-mediated apoptosis and ATM/ATR-Chk1/Chk2-regulated cell cycle arrest.	tagalsin S	38-47	checkpoint kinase 1	Homo sapiens	111-115
26615020-7	2016	In comparing DNA damage signaling after dosing with veliparib/TMZ or TMZ alone, increased phosphorylation of damage-responsive proteins (KAP1, Chk1, Chk2, and H2AX) was observed only in MGMT promoter-hypermethylated lines.	veliparib	52-61	checkpoint kinase 1	Homo sapiens	143-147
26615020-7	2016	In comparing DNA damage signaling after dosing with veliparib/TMZ or TMZ alone, increased phosphorylation of damage-responsive proteins (KAP1, Chk1, Chk2, and H2AX) was observed only in MGMT promoter-hypermethylated lines.	Temozolomide	62-65	checkpoint kinase 1	Homo sapiens	143-147
26615020-7	2016	In comparing DNA damage signaling after dosing with veliparib/TMZ or TMZ alone, increased phosphorylation of damage-responsive proteins (KAP1, Chk1, Chk2, and H2AX) was observed only in MGMT promoter-hypermethylated lines.	Temozolomide	69-72	checkpoint kinase 1	Homo sapiens	143-147
26451628-8	2015	Moreover, p53 plays a pivotal role in PCB29-pQ-induced cell cycle arrest and apoptosis via the activation of ATM/Chk2 and ATR/Chk1 checkpoints.	2,3,5-trichloro-6-phenyl-(1,4)benzoquinone	38-46	checkpoint kinase 1	Homo sapiens	126-130
26439697-7	2015	Gene expression profiling showed an enrichment in gene sets involved in pro-survival pathways in JEKO-1 R. Dasatinib treatment partly restored PF-00477736 sensitivity in resistant cells suggesting that the pharmacological interference of pro-survival pathways can overcome the resistance to Chk1 inhibitors.	Dasatinib	107-116	checkpoint kinase 1	Homo sapiens	291-295
26542114-6	2015	RESULTS: Chk1 and Chk2 are overexpressed concomitant with the presence of genetic damage as suggested by the nuclear labeling for gamma-H2A.X (Ser139) in 68 % of ALL patients.	gamma-h2a	130-139	checkpoint kinase 1	Homo sapiens	9-13
26437226-2	2015	Fragment elaboration by structure guided design was utilized to identify and develop a novel series of Chk1 inhibitors culminating in the identification of V158411, a potent ATP-competitive inhibitor of the Chk1 and Chk2 kinases.	V158411	156-163	checkpoint kinase 1	Homo sapiens	103-107
26437226-2	2015	Fragment elaboration by structure guided design was utilized to identify and develop a novel series of Chk1 inhibitors culminating in the identification of V158411, a potent ATP-competitive inhibitor of the Chk1 and Chk2 kinases.	V158411	156-163	checkpoint kinase 1	Homo sapiens	207-211
26437226-2	2015	Fragment elaboration by structure guided design was utilized to identify and develop a novel series of Chk1 inhibitors culminating in the identification of V158411, a potent ATP-competitive inhibitor of the Chk1 and Chk2 kinases.	Adenosine Triphosphate	174-177	checkpoint kinase 1	Homo sapiens	103-107
26437226-2	2015	Fragment elaboration by structure guided design was utilized to identify and develop a novel series of Chk1 inhibitors culminating in the identification of V158411, a potent ATP-competitive inhibitor of the Chk1 and Chk2 kinases.	Adenosine Triphosphate	174-177	checkpoint kinase 1	Homo sapiens	207-211
26438152-13	2015	Different sensitization profiles between gemcitabine and carboplatin and ATR kinase inhibitor ETP-46464 and Chk1 kinase inhibitor UCN-01 were observed and this should be considered in the rationale for Phase I clinical trial design with ATR kinase inhibitors.	7-hydroxystaurosporine	130-136	checkpoint kinase 1	Homo sapiens	108-112
26216057-3	2015	Chk1 blocks mitosis by maintaining high levels of inhibitory tyrosine phosphorylation of the mitotic cyclin-dependent kinase 1; however, the mechanisms that underlie replication fork stabilization and suppression of origin firing are less well defined.	Tyrosine	61-69	checkpoint kinase 1	Homo sapiens	0-4
26365377-5	2015	In other S-phase cells, however, ATRi induces moderate ssDNA and triggers a DNA-PK and Chk1-mediated backup pathway to suppress origin firing.	A-tri	33-37	checkpoint kinase 1	Homo sapiens	87-91
26141863-0	2015	CHK1 Inhibition Synergizes with Gemcitabine Initially by Destabilizing the DNA Replication Apparatus.	gemcitabine	32-43	checkpoint kinase 1	Homo sapiens	0-4
26055626-8	2015	Inhibition of Chk1 in cells treated with fluoromevalonate resulted in premature entry into mitosis and massive cell death, indicating that the inhibition of mevalonate diphosphate decarboxylase triggered a DNA damage response.	6-fluoromevalonolactone	41-57	checkpoint kinase 1	Homo sapiens	14-18
26025928-7	2015	In the absence of prior irradiation, however, mitotic catastrophe could be induced with inhibitors against CHK1 (AZD7762) or WEE1 (MK-1775).	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	113-120	checkpoint kinase 1	Homo sapiens	107-111
26141948-0	2015	LY2606368 Causes Replication Catastrophe and Antitumor Effects through CHK1-Dependent Mechanisms.	prexasertib	0-9	checkpoint kinase 1	Homo sapiens	71-75
26141948-3	2015	Here, we describe the characterization of a novel CHK1 inhibitor, LY2606368, which as a single agent causes double-stranded DNA breakage while simultaneously removing the protection of the DNA damage checkpoints.	prexasertib	66-75	checkpoint kinase 1	Homo sapiens	50-54
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	checkpoint kinase 1	Homo sapiens	56-60
25790472-8	2015	Consistently, imatinib induced a persistent activation of ATR-Chk1 signaling.	Imatinib Mesylate	14-22	checkpoint kinase 1	Homo sapiens	62-66
25952464-3	2015	Gemcitabine, which has modest activity in pancreas cancer, activates Chk1, a client protein of HSP90.	gemcitabine	0-11	checkpoint kinase 1	Homo sapiens	69-73
25952464-4	2015	This phase II trial was designed to determine whether 17AAG could enhance the clinical activity of gemcitabine through degradation of Chk1 in patients with stage IV pancreatic cancer.	tanespimycin	54-59	checkpoint kinase 1	Homo sapiens	134-138
25952464-4	2015	This phase II trial was designed to determine whether 17AAG could enhance the clinical activity of gemcitabine through degradation of Chk1 in patients with stage IV pancreatic cancer.	gemcitabine	99-110	checkpoint kinase 1	Homo sapiens	134-138
26055704-5	2015	In addition, CPT-treated hMSH5-deficient cells exhibit aberrant activation of Chk1 and Chk2 kinases and therefore abnormal cell cycle progression.	Camptothecin	13-16	checkpoint kinase 1	Homo sapiens	78-82
25972552-6	2015	Regulation of gammaH2AX occurred before the onset of caspase activation without modulation of other DNA damage signaling mediators, including ATM, Chk1, or Chk2, and additionally was suppressed by inducers of DNA single-strand breaks (SSBs) and replication stress.	gammah2ax	14-23	checkpoint kinase 1	Homo sapiens	147-151
26068472-4	2015	In response to camptothecin-mediated DNA DSBs, CHK1 and RPA2 phosphorylation, which are hallmarks of HR activation, was abrogated in SERBP1-depleted cells.	Camptothecin	15-27	checkpoint kinase 1	Homo sapiens	47-51
26161259-11	2015	In addition, the results of our protein phosphorylation studies indicated that the presence of low-levels triptolide caused a decrease for cisplatin-induced CHK1 phosphorylation at Ser(317/345) but an increase for cisplatin-induced ATM phosphorylation at Ser(1981) in both HTB182 and A549 cells.	triptolide	106-116	checkpoint kinase 1	Homo sapiens	157-161
26161259-11	2015	In addition, the results of our protein phosphorylation studies indicated that the presence of low-levels triptolide caused a decrease for cisplatin-induced CHK1 phosphorylation at Ser(317/345) but an increase for cisplatin-induced ATM phosphorylation at Ser(1981) in both HTB182 and A549 cells.	Cisplatin	139-148	checkpoint kinase 1	Homo sapiens	157-161
26161259-11	2015	In addition, the results of our protein phosphorylation studies indicated that the presence of low-levels triptolide caused a decrease for cisplatin-induced CHK1 phosphorylation at Ser(317/345) but an increase for cisplatin-induced ATM phosphorylation at Ser(1981) in both HTB182 and A549 cells.	Serine	181-184	checkpoint kinase 1	Homo sapiens	157-161
26161259-11	2015	In addition, the results of our protein phosphorylation studies indicated that the presence of low-levels triptolide caused a decrease for cisplatin-induced CHK1 phosphorylation at Ser(317/345) but an increase for cisplatin-induced ATM phosphorylation at Ser(1981) in both HTB182 and A549 cells.	Serine	255-258	checkpoint kinase 1	Homo sapiens	157-161
26199910-12	2015	DNA damage was significantly increased when GBM cells treated with TPT ceased at S phase due to the inhibition of topoisomerase enzyme and phosphorylation of Chk1 enzyme.	Topotecan	67-70	checkpoint kinase 1	Homo sapiens	158-162
25521189-4	2015	Dexrazoxane induced DNA damage responses, shown by enhanced levels of gamma-H2AX/53BP1 foci, ATM (ataxia telangiectasia mutated), ATR (ATM and Rad3-related), Chk1 and Chk2 phosphorylation, and by p53 accumulation.	Dexrazoxane	0-11	checkpoint kinase 1	Homo sapiens	158-162
26054341-4	2015	METHODS: In the present study we combined a Wee1 inhibitor (MK1775) with Chk1/2 inhibitor (AZD7762) in malignant melanoma cell lines grown in vitro (2D and 3D cultures) and in xenografts models.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	91-98	checkpoint kinase 1	Homo sapiens	73-79
25956379-4	2015	In this presented work we implemented a novel combination of k-nearest neighbor/genetic function algorithm modeling coupled with dbCICA to select critical ligand-Chk1 contacts capable of explaining anti-Chk1 bioactivity among a long list of inhibitors.	dbcica	129-135	checkpoint kinase 1	Homo sapiens	162-166
25956379-4	2015	In this presented work we implemented a novel combination of k-nearest neighbor/genetic function algorithm modeling coupled with dbCICA to select critical ligand-Chk1 contacts capable of explaining anti-Chk1 bioactivity among a long list of inhibitors.	dbcica	129-135	checkpoint kinase 1	Homo sapiens	203-207
25965828-1	2015	The therapeutic efficacy of nucleoside analogues, e.g. gemcitabine, against cancer cells can be augmented by inhibitors of checkpoint kinases, including Wee1, ATR, and Chk1.	Nucleosides	28-38	checkpoint kinase 1	Homo sapiens	168-172
25965828-1	2015	The therapeutic efficacy of nucleoside analogues, e.g. gemcitabine, against cancer cells can be augmented by inhibitors of checkpoint kinases, including Wee1, ATR, and Chk1.	gemcitabine	55-66	checkpoint kinase 1	Homo sapiens	168-172
25965828-4	2015	Investigating the reasons for this potent sensitizing effect, we found that Wee1 inhibition or knockdown not only blocked Wee1 activity, but also reduced the activation of ATR/Chk1 in gemcitabine-treated cells.	gemcitabine	184-195	checkpoint kinase 1	Homo sapiens	176-180
25965828-7	2015	Taken together, these results confer a consistent signaling pathway reaching from Wee1 inhibition to impaired Chk1 activity, mechanistically dissecting how Wee1 inhibitors not only dysregulate cell cycle progression, but also enhance replicative stress and chemosensitivity towards nucleoside analogues.	Nucleosides	282-292	checkpoint kinase 1	Homo sapiens	110-114
25994202-4	2015	RESULTS: TH-302 cytotoxicity is greatly enhanced by Chk1 inhibition in p53-deficient but not in p53-proficient human cancer cell lines.	Thorium	9-11	checkpoint kinase 1	Homo sapiens	52-56
25994202-5	2015	Chk1 inhibitors reduced TH-302-induced cell cycle arrest via blocking TH-302-induced decrease of phosphorylation of histone H3 and increasing Cdc2-Y15 phosphorylation.	TH 302	24-30	checkpoint kinase 1	Homo sapiens	0-4
25994202-5	2015	Chk1 inhibitors reduced TH-302-induced cell cycle arrest via blocking TH-302-induced decrease of phosphorylation of histone H3 and increasing Cdc2-Y15 phosphorylation.	TH 302	70-76	checkpoint kinase 1	Homo sapiens	0-4
25994202-7	2015	TH-302 induced gammaH2AX and apoptosis were also increased upon the addition of Chk1 inhibitor.	TH 302	0-6	checkpoint kinase 1	Homo sapiens	80-84
25994202-7	2015	TH-302 induced gammaH2AX and apoptosis were also increased upon the addition of Chk1 inhibitor.	gammah2ax	15-24	checkpoint kinase 1	Homo sapiens	80-84
25994202-8	2015	Potentiation of TH-302 cytotoxicity by Chk1 inhibitor was only observed in cell lines proficient in, but not deficient in homology-directed DNA repair.	Thorium	16-18	checkpoint kinase 1	Homo sapiens	39-43
25994202-11	2015	CONCLUSIONS: TH-302-mediated in vitro and in vivo anti-tumor activities were greatly enhanced by the addition of Chk1 inhibitors.	TH 302	13-19	checkpoint kinase 1	Homo sapiens	113-117
25966274-0	2015	Mangiferin induces cell cycle arrest at G2/M phase through ATR-Chk1 pathway in HL-60 leukemia cells.	mangiferin	0-10	checkpoint kinase 1	Homo sapiens	63-67
25809478-4	2015	Here we report that Chk1 phosphorylates the MCM3 subunit of the MCM complex at Ser-205 under normal growth conditions.	Serine	79-82	checkpoint kinase 1	Homo sapiens	20-24
25653093-5	2015	Importantly, CHK1 downregulation sensitizes prostate tumor cells to etoposide but not to docetaxel treatment.	Etoposide	68-77	checkpoint kinase 1	Homo sapiens	13-17
25983087-13	2015	CONCLUSIONS: Cell division cycle 6, CHEK1, E2F1, EGFR, and PIK3R1 of the module and their relative pathways, cell cycle, and focal adhesion might play important roles of suppression of vemurafenib on melanoma progression.	Vemurafenib	185-196	checkpoint kinase 1	Homo sapiens	36-41
26114388-6	2015	Atrazine also sequentially elevated DNA damage checkpoint proteins of ATM- and RAD3-related (ATR), ATRIP and phospho-Chk1, suggesting that atrazine could induce DNA double-strand breaks and trigger the DNA damage response ATR-Chk1 pathway in MCF-10A cells.	Atrazine	0-8	checkpoint kinase 1	Homo sapiens	117-121
26114388-6	2015	Atrazine also sequentially elevated DNA damage checkpoint proteins of ATM- and RAD3-related (ATR), ATRIP and phospho-Chk1, suggesting that atrazine could induce DNA double-strand breaks and trigger the DNA damage response ATR-Chk1 pathway in MCF-10A cells.	Atrazine	0-8	checkpoint kinase 1	Homo sapiens	226-230
26114388-6	2015	Atrazine also sequentially elevated DNA damage checkpoint proteins of ATM- and RAD3-related (ATR), ATRIP and phospho-Chk1, suggesting that atrazine could induce DNA double-strand breaks and trigger the DNA damage response ATR-Chk1 pathway in MCF-10A cells.	Atrazine	139-147	checkpoint kinase 1	Homo sapiens	117-121
26114388-6	2015	Atrazine also sequentially elevated DNA damage checkpoint proteins of ATM- and RAD3-related (ATR), ATRIP and phospho-Chk1, suggesting that atrazine could induce DNA double-strand breaks and trigger the DNA damage response ATR-Chk1 pathway in MCF-10A cells.	Atrazine	139-147	checkpoint kinase 1	Homo sapiens	226-230
26039276-1	2015	The Chk1 protein kinase is activated in response to DNA damage through ATR-mediated phosphorylation at multiple serine-glutamine (SQ) residues within the C-terminal regulatory domain, however the molecular mechanism is not understood.	Serine	112-118	checkpoint kinase 1	Homo sapiens	4-8
26039276-1	2015	The Chk1 protein kinase is activated in response to DNA damage through ATR-mediated phosphorylation at multiple serine-glutamine (SQ) residues within the C-terminal regulatory domain, however the molecular mechanism is not understood.	Glutamine	119-128	checkpoint kinase 1	Homo sapiens	4-8
26039276-5	2015	Cell cycle arrest induced by selected Chk1-CA mutants depends on kinase catalytic activity, which is increased several-fold compared to wild-type, however phosphorylation of the key ATR regulatory site serine 345 (S345) is not required.	Serine	202-208	checkpoint kinase 1	Homo sapiens	38-42
25683911-4	2015	Inhibition of upstream kinase Chk1 under doxorubicin treatment almost completely abolishes stress-induced G2-M arrest and induces enhanced apoptosis.	Doxorubicin	41-52	checkpoint kinase 1	Homo sapiens	30-34
25683911-7	2015	Moreover, Chk1 inhibition alone induces only a slight p53/p21 induction, while a strong induction of both proteins is observed by the combination with doxorubicin.	Doxorubicin	151-162	checkpoint kinase 1	Homo sapiens	10-14
25605849-0	2015	Phase I dose-escalation trial of checkpoint kinase 1 inhibitor MK-8776 as monotherapy and in combination with gemcitabine in patients with advanced solid tumors.	MK-8776	63-70	checkpoint kinase 1	Homo sapiens	33-52
25812484-4	2015	In addition, we observed that 8-ADEQ causes phosphorylation of the cell division cycle 25C (Cdc25C) protein through the activation of checkpoint kinases 1 (Chk1) and Chk2, which in turn were activated via ataxia telangiectasia mutated (ATM)/ataxia telangiectasia-Rad3-related (ATR) kinases in response to the DNA damage.	(E)-8-acetoxy-2-(2-(3,4-diacetoxyphenyl)ethenyl)quinazoline	30-36	checkpoint kinase 1	Homo sapiens	134-154
25812484-4	2015	In addition, we observed that 8-ADEQ causes phosphorylation of the cell division cycle 25C (Cdc25C) protein through the activation of checkpoint kinases 1 (Chk1) and Chk2, which in turn were activated via ataxia telangiectasia mutated (ATM)/ataxia telangiectasia-Rad3-related (ATR) kinases in response to the DNA damage.	(E)-8-acetoxy-2-(2-(3,4-diacetoxyphenyl)ethenyl)quinazoline	30-36	checkpoint kinase 1	Homo sapiens	156-160
25812484-7	2015	8-ADEQ-induced G2/M arrest is mediated by the activation of both Chk1/2-Cdc25 and p53-p21CIP1/WAF1 via ATM/ATR pathway, and indicates that 8-ADEQ appears to have potential in the treatment of cervical cancer.	(E)-8-acetoxy-2-(2-(3,4-diacetoxyphenyl)ethenyl)quinazoline	0-6	checkpoint kinase 1	Homo sapiens	65-69
25812484-7	2015	8-ADEQ-induced G2/M arrest is mediated by the activation of both Chk1/2-Cdc25 and p53-p21CIP1/WAF1 via ATM/ATR pathway, and indicates that 8-ADEQ appears to have potential in the treatment of cervical cancer.	(E)-8-acetoxy-2-(2-(3,4-diacetoxyphenyl)ethenyl)quinazoline	139-145	checkpoint kinase 1	Homo sapiens	65-69
25880358-8	2015	Finally, we observed Chk1 inhibitor AZD7762 enhanced the effect of doxorubicin on inhibiting growth of HCC cells in vitro and in vivo.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	36-43	checkpoint kinase 1	Homo sapiens	21-25
25880358-8	2015	Finally, we observed Chk1 inhibitor AZD7762 enhanced the effect of doxorubicin on inhibiting growth of HCC cells in vitro and in vivo.	Doxorubicin	67-78	checkpoint kinase 1	Homo sapiens	21-25
25735892-2	2015	Granulatimide and isogranulatimide are marine alkaloids that have been shown to inhibit checkpoint kinase 1 (Chk1), a key protein in the DNA damage response and an emerging target for anticancer therapeutics.	granulatimide	0-13	checkpoint kinase 1	Homo sapiens	88-107
25735892-2	2015	Granulatimide and isogranulatimide are marine alkaloids that have been shown to inhibit checkpoint kinase 1 (Chk1), a key protein in the DNA damage response and an emerging target for anticancer therapeutics.	granulatimide	0-13	checkpoint kinase 1	Homo sapiens	109-113
25735892-2	2015	Granulatimide and isogranulatimide are marine alkaloids that have been shown to inhibit checkpoint kinase 1 (Chk1), a key protein in the DNA damage response and an emerging target for anticancer therapeutics.	isogranulatimide	18-34	checkpoint kinase 1	Homo sapiens	88-107
25735892-2	2015	Granulatimide and isogranulatimide are marine alkaloids that have been shown to inhibit checkpoint kinase 1 (Chk1), a key protein in the DNA damage response and an emerging target for anticancer therapeutics.	isogranulatimide	18-34	checkpoint kinase 1	Homo sapiens	109-113
25735892-2	2015	Granulatimide and isogranulatimide are marine alkaloids that have been shown to inhibit checkpoint kinase 1 (Chk1), a key protein in the DNA damage response and an emerging target for anticancer therapeutics.	Alkaloids	46-55	checkpoint kinase 1	Homo sapiens	88-107
25735892-2	2015	Granulatimide and isogranulatimide are marine alkaloids that have been shown to inhibit checkpoint kinase 1 (Chk1), a key protein in the DNA damage response and an emerging target for anticancer therapeutics.	Alkaloids	46-55	checkpoint kinase 1	Homo sapiens	109-113
25283841-4	2015	Although AZD1775 induced Chk1 activation, reflected by markedly increased Chk1 S296/S317/S345 phosphorylation leading to inhibitory T14 phosphorylation of cdc2/Cdk1, these compensatory responses were sharply abrogated by HDACIs.	adavosertib	9-16	checkpoint kinase 1	Homo sapiens	25-29
25283841-4	2015	Although AZD1775 induced Chk1 activation, reflected by markedly increased Chk1 S296/S317/S345 phosphorylation leading to inhibitory T14 phosphorylation of cdc2/Cdk1, these compensatory responses were sharply abrogated by HDACIs.	adavosertib	9-16	checkpoint kinase 1	Homo sapiens	74-78
25884494-0	2015	Topotecan synergizes with CHEK1 (CHK1) inhibitor to induce apoptosis in ovarian cancer cells.	Topotecan	0-9	checkpoint kinase 1	Homo sapiens	26-31
25884494-0	2015	Topotecan synergizes with CHEK1 (CHK1) inhibitor to induce apoptosis in ovarian cancer cells.	Topotecan	0-9	checkpoint kinase 1	Homo sapiens	33-37
25884494-11	2015	When combined with CHEK1 inhibitor, TPT potently and synergistically inhibited the proliferation of HGS ovarian cancer cells.	Topotecan	36-39	checkpoint kinase 1	Homo sapiens	19-24
25884494-13	2015	CONCLUSIONS: Our findings suggest that the addition of CHEK1 inhibitor increases the response of ovarian cancer cells to TPT.	Topotecan	121-124	checkpoint kinase 1	Homo sapiens	55-60
25605849-1	2015	PURPOSE: We determined the safety, pharmacokinetics, pharmacodynamics, and recommended phase II dose of MK-8776 (SCH 900776), a potent, selective checkpoint kinase 1 (Chk1) inhibitor, as monotherapy and in combination with gemcitabine in a first-in-human phase I clinical trial in patients with advanced solid tumor malignancies.	MK-8776	104-111	checkpoint kinase 1	Homo sapiens	146-165
25605849-1	2015	PURPOSE: We determined the safety, pharmacokinetics, pharmacodynamics, and recommended phase II dose of MK-8776 (SCH 900776), a potent, selective checkpoint kinase 1 (Chk1) inhibitor, as monotherapy and in combination with gemcitabine in a first-in-human phase I clinical trial in patients with advanced solid tumor malignancies.	MK-8776	104-111	checkpoint kinase 1	Homo sapiens	167-171
25605849-1	2015	PURPOSE: We determined the safety, pharmacokinetics, pharmacodynamics, and recommended phase II dose of MK-8776 (SCH 900776), a potent, selective checkpoint kinase 1 (Chk1) inhibitor, as monotherapy and in combination with gemcitabine in a first-in-human phase I clinical trial in patients with advanced solid tumor malignancies.	MK-8776	113-123	checkpoint kinase 1	Homo sapiens	167-171
25690891-0	2015	CHK1-driven histone H3.3 serine 31 phosphorylation is important for chromatin maintenance and cell survival in human ALT cancer cells.	Serine	25-31	checkpoint kinase 1	Homo sapiens	0-4
25594740-0	2015	Identification of novel aminothiazole and aminothiadiazole conjugated cyanopyridines as selective CHK1 inhibitors.	2-aminothiazole	24-37	checkpoint kinase 1	Homo sapiens	98-102
25594740-0	2015	Identification of novel aminothiazole and aminothiadiazole conjugated cyanopyridines as selective CHK1 inhibitors.	2-amino-1,3,4-thiadiazole	42-58	checkpoint kinase 1	Homo sapiens	98-102
25594740-0	2015	Identification of novel aminothiazole and aminothiadiazole conjugated cyanopyridines as selective CHK1 inhibitors.	cyanopyridines	70-84	checkpoint kinase 1	Homo sapiens	98-102
25594740-3	2015	The tested compounds exhibited a potent and selective CHK1 inhibitory activity at nanomolar levels that reflected their ability to abrogate cell cycle arrest and potentiate the cytotoxic effect of the genotoxic drug gemcitabine in colon cancer cells.	gemcitabine	216-227	checkpoint kinase 1	Homo sapiens	54-58
25304378-10	2015	Clonogenic survival assays showed moderate radiosensitisation of directly irradiated cells by the Chk1 inhibitor UCN-01 but increased radioresistance of bystander cells.	7-hydroxystaurosporine	113-119	checkpoint kinase 1	Homo sapiens	98-102
25749046-6	2015	The underlying mechanism is complex, but increased DNA damage upon arginine deprivation due to decreased DNA repair proteins, FANCD2, ATM, and CHK1/2 most likely leads to increased apoptosis.	Arginine	67-75	checkpoint kinase 1	Homo sapiens	143-149
25594541-10	2015	The increase in radiosensitivity induced by the miR-15 family was associated with persistent unrepaired DNA damage, abrogation of radiation-induced G2 arrest and suppressed cell proliferation, and appear to involve both the checkpoint kinase 1 (Chk1) and Wee1.	mir-15	48-54	checkpoint kinase 1	Homo sapiens	224-243
25594541-10	2015	The increase in radiosensitivity induced by the miR-15 family was associated with persistent unrepaired DNA damage, abrogation of radiation-induced G2 arrest and suppressed cell proliferation, and appear to involve both the checkpoint kinase 1 (Chk1) and Wee1.	mir-15	48-54	checkpoint kinase 1	Homo sapiens	245-249
25697484-8	2015	Both Aa and Ap attenuated daunorubicin-stimulated activation of the DNA damage response (DDR) as reflected on the levels of gammaH2AX, p-Kap-1 and p-Chk-1.	Daunorubicin	26-38	checkpoint kinase 1	Homo sapiens	149-154
25468710-10	2015	Pre-clinically, CHEK1 phosphorylation at serine(345) following replication stress was impaired in ATR knock down and in VE-821 treated breast cancer cells.	Serine	41-47	checkpoint kinase 1	Homo sapiens	16-21
25769181-0	2015	Benzo[a]pyrene-induced cell cycle progression occurs via ERK-induced Chk1 pathway activation in human lung cancer cells.	Benzo(a)pyrene	0-14	checkpoint kinase 1	Homo sapiens	69-73
25774168-6	2015	Synergistic effects have also been reported between inhibitors of ATR/Chk1/Wee1 and conventional lung cancer treatments, such as gemcitabine, cisplatin, or radiation.	gemcitabine	129-140	checkpoint kinase 1	Homo sapiens	70-74
25774168-6	2015	Synergistic effects have also been reported between inhibitors of ATR/Chk1/Wee1 and conventional lung cancer treatments, such as gemcitabine, cisplatin, or radiation.	Cisplatin	142-151	checkpoint kinase 1	Homo sapiens	70-74
25459351-5	2015	RESULTS: Hydroxyurea, UV and 4NQO induced Chk1 and H2AX phosphorylation in MCF7 and K562 cells.	Hydroxyurea	9-20	checkpoint kinase 1	Homo sapiens	42-46
25459351-5	2015	RESULTS: Hydroxyurea, UV and 4NQO induced Chk1 and H2AX phosphorylation in MCF7 and K562 cells.	4-Nitroquinoline-1-oxide	29-33	checkpoint kinase 1	Homo sapiens	42-46
25458954-2	2015	The selective Wee1 inhibitor MK-1775 has demonstrated promising results when combined with DNA damaging agents, and more recently with CHK1 inhibitors in various malignancies.	adavosertib	29-36	checkpoint kinase 1	Homo sapiens	135-139
25458954-3	2015	We have previously demonstrated that treatment with the pan-histone deacetylase inhibitor panobinostat (LBH589) can cause down-regulation of CHK1.	Panobinostat	90-102	checkpoint kinase 1	Homo sapiens	141-145
25458954-3	2015	We have previously demonstrated that treatment with the pan-histone deacetylase inhibitor panobinostat (LBH589) can cause down-regulation of CHK1.	Panobinostat	104-110	checkpoint kinase 1	Homo sapiens	141-145
25458954-5	2015	We demonstrate that MK-1775 treatment results in increased H2AX phosphorylation, indicating increased DNA double-strand breaks, and activation of CHK1, which are both dependent on CDK activity.	adavosertib	20-27	checkpoint kinase 1	Homo sapiens	146-150
25609078-7	2015	On the contrary, treatment of MM cells with nitric oxide donors correlated with the activation of a DNA damage response pathway and inhibition of the ATM /ATR/Chk1/2 kinase activities by specific inhibitors significantly abrogates up-regulation.	Nitric Oxide	44-56	checkpoint kinase 1	Homo sapiens	159-165
25593194-7	2015	G2E3 depletion led to decreased gammaH2AX levels and decreased phosphorylation of the checkpoint kinase 1 (Chk1) upon cisplatin.	Cisplatin	118-127	checkpoint kinase 1	Homo sapiens	86-105
25593194-7	2015	G2E3 depletion led to decreased gammaH2AX levels and decreased phosphorylation of the checkpoint kinase 1 (Chk1) upon cisplatin.	Cisplatin	118-127	checkpoint kinase 1	Homo sapiens	107-111
25448276-7	2015	Furthermore, specific inhibition of CHK1 increased SM toxicity in multiple human cell lines, with concomitant increases in markers of apoptosis, DNA damage and mitosis.	Mustard Gas	51-53	checkpoint kinase 1	Homo sapiens	36-40
25448276-8	2015	Finally, the effect of CHK1 inhibition on SM toxicity was much more marked in cells with non-functional p53.	Mustard Gas	42-44	checkpoint kinase 1	Homo sapiens	23-27
25450480-0	2015	Jaridonin-induced G2/M phase arrest in human esophageal cancer cells is caused by reactive oxygen species-dependent Cdc2-tyr15 phosphorylation via ATM-Chk1/2-Cdc25C pathway.	Reactive Oxygen Species	82-105	checkpoint kinase 1	Homo sapiens	151-155
25450480-0	2015	Jaridonin-induced G2/M phase arrest in human esophageal cancer cells is caused by reactive oxygen species-dependent Cdc2-tyr15 phosphorylation via ATM-Chk1/2-Cdc25C pathway.	jaridonin	0-9	checkpoint kinase 1	Homo sapiens	151-155
25450480-4	2015	Jaridonin also resulted in enhanced phosphorylation of Cdc25C via the activation of checkpoint kinases Chk1 and Chk2, as well as in increased phospho-H2A.X (Ser139), which is known to be phosphorylated by ATM in response to DNA damage.	jaridonin	0-9	checkpoint kinase 1	Homo sapiens	103-107
25450480-6	2015	On the other hand, addition of ATM inhibitors reversed Jaridonin-related activation of ATM and Chk1/2 as well as phosphorylation of Cdc25C, Cdc2 and H2A.X and G2/M phase arrest.	jaridonin	55-64	checkpoint kinase 1	Homo sapiens	95-101
25450480-7	2015	In conclusion, these findings identified that Jaridonin-induced cell cycle arrest in human esophageal cancer cells is associated with ROS-mediated activation of ATM-Chk1/2-Cdc25C pathway.	jaridonin	46-55	checkpoint kinase 1	Homo sapiens	165-169
25450480-7	2015	In conclusion, these findings identified that Jaridonin-induced cell cycle arrest in human esophageal cancer cells is associated with ROS-mediated activation of ATM-Chk1/2-Cdc25C pathway.	Reactive Oxygen Species	134-137	checkpoint kinase 1	Homo sapiens	165-169
25296725-0	2015	Evaluation of the likelihood of a selective CHK1 inhibitor (LY2603618) to inhibit CYP2D6 with desipramine as a probe substrate in cancer patients.	LY2603618	60-69	checkpoint kinase 1	Homo sapiens	44-48
25296725-0	2015	Evaluation of the likelihood of a selective CHK1 inhibitor (LY2603618) to inhibit CYP2D6 with desipramine as a probe substrate in cancer patients.	Desipramine	94-105	checkpoint kinase 1	Homo sapiens	44-48
25296725-1	2015	LY2603618 is a selective inhibitor of deoxyribonucleic acid damage checkpoint kinase 1 (CHK1) and has been in development for the enhancement of chemotherapeutic agents.	LY2603618	0-9	checkpoint kinase 1	Homo sapiens	67-86
25296725-1	2015	LY2603618 is a selective inhibitor of deoxyribonucleic acid damage checkpoint kinase 1 (CHK1) and has been in development for the enhancement of chemotherapeutic agents.	LY2603618	0-9	checkpoint kinase 1	Homo sapiens	88-92
26529495-1	2015	MK-1775 is the first-in-class selective Wee1 inhibitor which has been demonstrated to synergize with CHK1 inhibitors in various malignancies.	adavosertib	0-7	checkpoint kinase 1	Homo sapiens	101-105
26529495-5	2015	Interestingly, treatment with panobinostat alone or in combination with MK-1775 resulted in decreased Wee1 protein levels as well as downregulation of the CHK1 pathway.	adavosertib	72-79	checkpoint kinase 1	Homo sapiens	155-159
26529495-6	2015	shRNA knockdown of CHK1 significantly sensitized AML cells to MK-1775 treatment, while knockdown of Wee1 significantly enhanced both MK-1775- and panobinostat-induced cell death.	adavosertib	62-69	checkpoint kinase 1	Homo sapiens	19-23
26529495-7	2015	Our results demonstrate that panobinostat synergizes with MK-1775 in AML cells, at least in part through downregulation of CHK1 and/or Wee1, providing compelling evidence for the clinical development of the combination treatment in AML.	adavosertib	58-65	checkpoint kinase 1	Homo sapiens	123-127
25643258-1	2015	Activation of checkpoint kinase 1 (Chk1) is essential in chemoresistance of hepatocarcinoma (HCC) to 5-fluorouracil (5-FU) and other antimetabolite family of drugs.	Fluorouracil	101-115	checkpoint kinase 1	Homo sapiens	14-33
25565400-4	2015	The p53-independent DMC cytotoxicity associates with the activation, and subsequent depletion, of Chk1.	10-decarbamoylmitomycin C	20-23	checkpoint kinase 1	Homo sapiens	98-102
25565400-10	2015	Our results suggest that DMC induces a p53-independent disassociation of ATR from chromatin that facilitates Chk1 checkpoint activation and Rad51 chromatin recruitment.	10-decarbamoylmitomycin C	25-28	checkpoint kinase 1	Homo sapiens	109-113
25643258-1	2015	Activation of checkpoint kinase 1 (Chk1) is essential in chemoresistance of hepatocarcinoma (HCC) to 5-fluorouracil (5-FU) and other antimetabolite family of drugs.	Fluorouracil	101-115	checkpoint kinase 1	Homo sapiens	35-39
25643258-1	2015	Activation of checkpoint kinase 1 (Chk1) is essential in chemoresistance of hepatocarcinoma (HCC) to 5-fluorouracil (5-FU) and other antimetabolite family of drugs.	Fluorouracil	117-121	checkpoint kinase 1	Homo sapiens	14-33
25643258-1	2015	Activation of checkpoint kinase 1 (Chk1) is essential in chemoresistance of hepatocarcinoma (HCC) to 5-fluorouracil (5-FU) and other antimetabolite family of drugs.	Fluorouracil	117-121	checkpoint kinase 1	Homo sapiens	35-39
25643258-4	2015	PHA-767491 directly counteracted the 5-FU-induced phosphorylation of Chk1, a substrate of Cdc7; and decreased the expression of the anti-apoptotic protein myeloid leukemia cell 1, a downstream target of Cdk9.	Fluorouracil	37-41	checkpoint kinase 1	Homo sapiens	69-73
25643258-6	2015	Our study suggests that PHA- 767491 could enhance the efficacy of 5-FU by inhibiting Chk1 phosphorylation and down-regulating Mcl1 expression through inhibition of Cdc7 and Cdk9, thus combinational administration of PHA-767491 with 5-FU could be potentially beneficial to patients with advanced and resistant HCC.	Fluorouracil	66-70	checkpoint kinase 1	Homo sapiens	85-89
26441204-7	2015	The application of benfluron led to phosphorylation of Chk1 on serine 345 and phosphorylation of Chk2 on threonine 68 in the treated cells.	Serine	63-69	checkpoint kinase 1	Homo sapiens	55-59
25310623-5	2015	5-FU treatment induced DNA damage and activation of ataxia telangiectasia mutated (ATM) and Chk1, leading to S-phase arrest, and Chk1 inhibition using SB218078 reduced S-phase arrest and increased apoptosis in the presence of 5-FU.	Fluorouracil	0-4	checkpoint kinase 1	Homo sapiens	92-96
25310623-0	2015	5-FU resistance abrogates the amplified cytotoxic effects induced by inhibiting checkpoint kinase 1 in p53-mutated colon cancer cells.	Fluorouracil	0-4	checkpoint kinase 1	Homo sapiens	80-99
25372494-0	2015	Computational studies on the binding mechanism between triazolone inhibitors and Chk1 by molecular docking and molecular dynamics.	5-((3-(((3,5-bis(trifluoromethyl)phenyl)methyl)oxy)-2-phenylpiperidino)methyl)-3-oxo-1,2,4-triazolone	55-65	checkpoint kinase 1	Homo sapiens	81-85
25372494-2	2015	As a novel Chk1 inhibitor, the triazolone"s bioactivity mechanism is not clear.	5-((3-(((3,5-bis(trifluoromethyl)phenyl)methyl)oxy)-2-phenylpiperidino)methyl)-3-oxo-1,2,4-triazolone	31-41	checkpoint kinase 1	Homo sapiens	11-15
25372494-4	2015	With the aim of discerning the structural features that affect the inhibitory activity of triazolones, MK-8776, a Chk1 inhibitor that reached the clinical stage, was also used as a reference for simulations.	MK-8776	103-110	checkpoint kinase 1	Homo sapiens	114-118
25372494-7	2015	Moreover, introducing hydrophobic groups into triazolone inhibitors is favorable for binding to Chk1, which is corroborated by residue Leu136 with a relatively large difference in the contribution between MK-8776 and five triazolones to the total binding free energies.	5-((3-(((3,5-bis(trifluoromethyl)phenyl)methyl)oxy)-2-phenylpiperidino)methyl)-3-oxo-1,2,4-triazolone	46-56	checkpoint kinase 1	Homo sapiens	96-100
25372494-7	2015	Moreover, introducing hydrophobic groups into triazolone inhibitors is favorable for binding to Chk1, which is corroborated by residue Leu136 with a relatively large difference in the contribution between MK-8776 and five triazolones to the total binding free energies.	MK-8776	205-212	checkpoint kinase 1	Homo sapiens	96-100
25372494-7	2015	Moreover, introducing hydrophobic groups into triazolone inhibitors is favorable for binding to Chk1, which is corroborated by residue Leu136 with a relatively large difference in the contribution between MK-8776 and five triazolones to the total binding free energies.	triazolones	222-233	checkpoint kinase 1	Homo sapiens	96-100
25372494-8	2015	A hydrogen bond between the polar hydrogen atoms at R1 and Cys86 can facilitate proper placement of the inhibitor in the binding pocket of Chk1 that favors binding.	Hydrogen	2-10	checkpoint kinase 1	Homo sapiens	139-143
25372494-8	2015	A hydrogen bond between the polar hydrogen atoms at R1 and Cys86 can facilitate proper placement of the inhibitor in the binding pocket of Chk1 that favors binding.	Hydrogen	34-42	checkpoint kinase 1	Homo sapiens	139-143
25465126-0	2015	Synergism between bosutinib (SKI-606) and the Chk1 inhibitor (PF-00477736) in highly imatinib-resistant BCR/ABL+ leukemia cells.	Imatinib Mesylate	85-93	checkpoint kinase 1	Homo sapiens	46-50
25349305-5	2015	Here, we show that TP53-CDKN1A double-mutant bladder cancer cell lines, 647V and RT-112, have a remarkable increase in p-Chk1 levels and G2-M arrest in response to gemcitabine treatment, with a heightened sensitivity to combination treatment with gemcitabine and either Chk1 inhibitor PF477736 or AZD7762, in comparison with other bladder cancer cell lines (either TP53 or p21 deficient).	gemcitabine	164-175	checkpoint kinase 1	Homo sapiens	121-125
25349305-5	2015	Here, we show that TP53-CDKN1A double-mutant bladder cancer cell lines, 647V and RT-112, have a remarkable increase in p-Chk1 levels and G2-M arrest in response to gemcitabine treatment, with a heightened sensitivity to combination treatment with gemcitabine and either Chk1 inhibitor PF477736 or AZD7762, in comparison with other bladder cancer cell lines (either TP53 or p21 deficient).	gemcitabine	164-175	checkpoint kinase 1	Homo sapiens	270-274
25310623-5	2015	5-FU treatment induced DNA damage and activation of ataxia telangiectasia mutated (ATM) and Chk1, leading to S-phase arrest, and Chk1 inhibition using SB218078 reduced S-phase arrest and increased apoptosis in the presence of 5-FU.	Fluorouracil	0-4	checkpoint kinase 1	Homo sapiens	129-133
25310623-5	2015	5-FU treatment induced DNA damage and activation of ataxia telangiectasia mutated (ATM) and Chk1, leading to S-phase arrest, and Chk1 inhibition using SB218078 reduced S-phase arrest and increased apoptosis in the presence of 5-FU.	SB 218078	151-159	checkpoint kinase 1	Homo sapiens	129-133
25310623-8	2015	These results indicate that 5-FU-resistance abrogated the anticancer effect amplified by Chk1 inhibition, even in p53-deficient cancer cells.	Fluorouracil	28-32	checkpoint kinase 1	Homo sapiens	89-93
25269479-6	2014	As expected, the combination of Top1 inhibitors with VE-821 inhibited the phosphorylation of ATR and Chk1; however, it strongly induced gammaH2AX.	3-amino-6-(4-(methylsulfonyl)phenyl)-N-phenylpyrazine-2-carboxamide	53-59	checkpoint kinase 1	Homo sapiens	101-105
25866222-4	2015	Deltonin treatment selectively prevents proliferation of FaDu cells by cell-cycle arrest and induction of apoptosis, via activating checkpoint kinase Chk1and Chk2 as well as caspases 8, 9 and 3.	deltonin	0-8	checkpoint kinase 1	Homo sapiens	150-154
25308916-9	2015	MK-1775 treatment in SK-N-BE(2) cells induced increased levels of p-CHK1(S345) , which could be decreased by the addition of panobinostat.	adavosertib	0-7	checkpoint kinase 1	Homo sapiens	68-72
25308916-9	2015	MK-1775 treatment in SK-N-BE(2) cells induced increased levels of p-CHK1(S345) , which could be decreased by the addition of panobinostat.	sk-n-be	21-28	checkpoint kinase 1	Homo sapiens	68-72
25308916-9	2015	MK-1775 treatment in SK-N-BE(2) cells induced increased levels of p-CHK1(S345) , which could be decreased by the addition of panobinostat.	Panobinostat	125-137	checkpoint kinase 1	Homo sapiens	68-72
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	checkpoint kinase 1	Homo sapiens	39-43
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	checkpoint kinase 1	Homo sapiens	219-223
25520248-8	2014	Deregulated expression of Rad9 accompanied by down expression of chk1 enhanced the sensitivity of human breast cancer cells to doxorubicin.	Doxorubicin	127-138	checkpoint kinase 1	Homo sapiens	65-69
25336189-3	2014	Thus, a logical rationale to sensitize p53-deficient cancers to DNA-damaging chemotherapy is through the use of ATP-competitive inhibitors of ATR or Chk1.	Adenosine Triphosphate	112-115	checkpoint kinase 1	Homo sapiens	149-153
25435354-8	2014	After 24h, Cd treatment downregulated the expression of CHEK1, CHEK2 and CDK2 genes and upregulated the expression of CCNE1 gene.	Cadmium	11-13	checkpoint kinase 1	Homo sapiens	56-61
25351918-7	2015	Consistent with this biologic response, DP68 induces a strong DNA damage response, including phosphorylation of ATM, Chk1 and Chk2 kinases, KAP1, and histone variant H2AX.	dp68	40-44	checkpoint kinase 1	Homo sapiens	117-121
25312395-14	2014	This study also highlights the role of conserved water molecules in the active site of Chk1 for the successful identification of novel inhibitors.	Water	49-54	checkpoint kinase 1	Homo sapiens	87-91
25249630-7	2014	This suggests that polyamides induce replication stress that ATR can counteract independently of Chk1 and that the FA/BRCA pathway may also be involved in the response to polyamides.	Nylons	19-29	checkpoint kinase 1	Homo sapiens	97-101
25302047-8	2014	We further demonstrated that the induction of MN-gamma-H2AX (+) by replication stress can also be attenuated by NAC, and that H2O2 also leads to increased phosphorylation of Chk1 and Rad17 that mimics replication stress, suggesting that replication stress and oxidative stress are intertwined and may reinforce each other in driving genomic instability.	Hydrogen Peroxide	126-130	checkpoint kinase 1	Homo sapiens	174-178
25301733-6	2014	Small-molecule inhibitors of CHK1 (AZD7762) or WEE1 (MK-1775) induced mitotic catastrophe, as characterized by dephosphorylation of CDK1(Tyr15), phosphorylation of histone H39(Ser10), and apoptosis.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	35-42	checkpoint kinase 1	Homo sapiens	29-33
25301733-6	2014	Small-molecule inhibitors of CHK1 (AZD7762) or WEE1 (MK-1775) induced mitotic catastrophe, as characterized by dephosphorylation of CDK1(Tyr15), phosphorylation of histone H39(Ser10), and apoptosis.	adavosertib	53-60	checkpoint kinase 1	Homo sapiens	29-33
25253693-3	2014	Inhibition of Gli1 in tumor cells induced replication stress-mediated DNA damage response, attenuated their clonogenic potential, abrogated camptothecin (CPT)-induced Chk1 phosphorylation, and potentiated its cytotoxicity.	Camptothecin	140-152	checkpoint kinase 1	Homo sapiens	167-171
25253693-3	2014	Inhibition of Gli1 in tumor cells induced replication stress-mediated DNA damage response, attenuated their clonogenic potential, abrogated camptothecin (CPT)-induced Chk1 phosphorylation, and potentiated its cytotoxicity.	Camptothecin	154-157	checkpoint kinase 1	Homo sapiens	167-171
25281057-5	2014	Accordingly, lentiviral-mediated CHK1 overexpression increased the proliferation rate of FLT3-ITD expressing cells, as judged by cell viability and [3H] thymidine incorporation experiments.	Tritium	149-151	checkpoint kinase 1	Homo sapiens	33-37
25281057-5	2014	Accordingly, lentiviral-mediated CHK1 overexpression increased the proliferation rate of FLT3-ITD expressing cells, as judged by cell viability and [3H] thymidine incorporation experiments.	Thymidine	153-162	checkpoint kinase 1	Homo sapiens	33-37
25453805-0	2014	Discovery of the 1,7-diazacarbazole class of inhibitors of checkpoint kinase 1.	9h-pyrrolo[2,3-b:5,4-c']dipyridine	17-35	checkpoint kinase 1	Homo sapiens	59-78
25453805-6	2014	Here we present the genesis of this novel series and the identification of GNE-783, a potent, selective and orally bioavailable inhibitor of ChK1.	gne	75-78	checkpoint kinase 1	Homo sapiens	141-145
25438756-7	2014	In cells, T2Pt persistently induced cell cycle arrest, activated ATR-Chk1 signaling and modestly induced DNA strand breaks, features typical of cellular replication stress.	t2pt	10-14	checkpoint kinase 1	Homo sapiens	69-73
25375241-3	2014	Combinatorial ablation of RRM1 or RRM2 and Chk1 causes a dramatic accumulation of gamma-H2AX, a marker of double-strand DNA breaks, suggesting that activation of Chk1 in this context is essential for suppression of DNA damage.	gamma-h2ax	82-92	checkpoint kinase 1	Homo sapiens	43-47
25375241-3	2014	Combinatorial ablation of RRM1 or RRM2 and Chk1 causes a dramatic accumulation of gamma-H2AX, a marker of double-strand DNA breaks, suggesting that activation of Chk1 in this context is essential for suppression of DNA damage.	gamma-h2ax	82-92	checkpoint kinase 1	Homo sapiens	162-166
25176258-2	2014	Due to the importance of cell cycle redistribution in DADS-mediated anticarcinogenic effects, we investigated the role of checkpoint kinases (Chk1 and Chk2) during DADS-induced cell cycle arrest.	diallyl disulfide	164-168	checkpoint kinase 1	Homo sapiens	142-146
25176258-4	2014	Notably, DADS induced the accumulation of phosphorylated Chk1, but not of Chk2, activated phospho-ATR (ATM-RAD3-related gene), and dowregulated CDC25C and cyclin B1 expression.	diallyl disulfide	9-13	checkpoint kinase 1	Homo sapiens	57-61
25176258-6	2014	Results of the overexpression and knockdown studies, showed that Chk1 but not Chk2 regulated the DADS-induced G2/M arrest of MGC803 cells.	diallyl disulfide	97-101	checkpoint kinase 1	Homo sapiens	65-69
25176258-7	2014	The overexpression of Chk1 resulted in significantly increased DADS-induced G2/M arrest, increased DADS-induced Chk1 phosphorylation and inhibited CDC25C expression.	diallyl disulfide	63-67	checkpoint kinase 1	Homo sapiens	22-26
25176258-7	2014	The overexpression of Chk1 resulted in significantly increased DADS-induced G2/M arrest, increased DADS-induced Chk1 phosphorylation and inhibited CDC25C expression.	diallyl disulfide	99-103	checkpoint kinase 1	Homo sapiens	22-26
25176258-7	2014	The overexpression of Chk1 resulted in significantly increased DADS-induced G2/M arrest, increased DADS-induced Chk1 phosphorylation and inhibited CDC25C expression.	diallyl disulfide	99-103	checkpoint kinase 1	Homo sapiens	112-116
25176258-8	2014	Knockdown of Chk1 reduced DADS-induced G2/M arrest and blocked the DADS-induced inhibition of CDC25C and cyclin B1 expression.	diallyl disulfide	26-30	checkpoint kinase 1	Homo sapiens	13-17
25176258-8	2014	Knockdown of Chk1 reduced DADS-induced G2/M arrest and blocked the DADS-induced inhibition of CDC25C and cyclin B1 expression.	diallyl disulfide	67-71	checkpoint kinase 1	Homo sapiens	13-17
25176258-9	2014	These results suggested that Chk1 is important in DADS-induced cell cycle G2/M arrest in the human MGC803 gastric cancer cell line.	diallyl disulfide	50-54	checkpoint kinase 1	Homo sapiens	29-33
25176258-10	2014	Furthermore, the DADS-induced G2/M checkpoint response is mediated by Chk1 signaling through ATR/Chk1/CDC25C/cyclin B1.	diallyl disulfide	17-21	checkpoint kinase 1	Homo sapiens	70-74
25176258-10	2014	Furthermore, the DADS-induced G2/M checkpoint response is mediated by Chk1 signaling through ATR/Chk1/CDC25C/cyclin B1.	diallyl disulfide	17-21	checkpoint kinase 1	Homo sapiens	97-101
25301724-0	2014	Targeting the DNA replication checkpoint by pharmacologic inhibition of Chk1 kinase: a strategy to sensitize APC mutant colon cancer cells to 5-fluorouracil chemotherapy.	Fluorouracil	142-156	checkpoint kinase 1	Homo sapiens	72-76
25301724-6	2014	Furthermore, we could increase sensitivity of APC truncated cells to 5-FU by inactivating the Chk1 kinase using drug treatment or siRNA-mediated knockdown.	Fluorouracil	69-73	checkpoint kinase 1	Homo sapiens	94-98
25301724-7	2014	Our findings identify mutant APC as a potential tumor biomarker of resistance to 5-FU, and importantly we show that APC-mutant CRC cells can be made more sensitive to 5-FU by use of Chk1 inhibitors.	Fluorouracil	167-171	checkpoint kinase 1	Homo sapiens	182-186
24942404-1	2014	LY2603618 is an inhibitor of checkpoint kinase 1 (CHK1), an important regulator of the DNA damage checkpoints.	LY2603618	0-9	checkpoint kinase 1	Homo sapiens	50-54
25249323-4	2014	DNA damage caused by ultraviolet light or the alkylating agent methyl methanesulphonate strongly activates Chk1, leading to phosphorylation of Smurf1 that enhances its self-degradation, hence resulting in a RhoB accumulation to promote apoptosis.	Methyl Methanesulfonate	63-87	checkpoint kinase 1	Homo sapiens	107-111
25070753-5	2014	In support of this idea, we have identified a small molecule termed HAMNO ((1Z)-1-[(2-hydroxyanilino)methylidene]naphthalen-2-one), a novel protein interaction inhibitor of replication protein A (RPA), a protein involved in the ATR/Chk1 pathway.	hamno ((1z)-1-[(2-hydroxyanilino)methylidene]naphthalen-2-one	68-129	checkpoint kinase 1	Homo sapiens	232-236
25015292-0	2014	Chk1 protects against chromatin bridges by constitutively phosphorylating BLM serine 502 to inhibit BLM degradation.	Serine	78-84	checkpoint kinase 1	Homo sapiens	0-4
25015292-5	2014	Furthermore, Chk1 constitutively phosphorylates human BLM at serine 502 (S502) and phosphorylated BLM localises to chromatin bridges.	Serine	61-67	checkpoint kinase 1	Homo sapiens	13-17
25232489-5	2014	UCN-01, a Chk1 inhibitor, reversed MJ-66-induced activation of Cdc25C and caspase 3.	7-hydroxystaurosporine	0-6	checkpoint kinase 1	Homo sapiens	10-14
25232489-5	2014	UCN-01, a Chk1 inhibitor, reversed MJ-66-induced activation of Cdc25C and caspase 3.	mj-66	35-40	checkpoint kinase 1	Homo sapiens	10-14
24928205-3	2014	In this study, we investigated the molecular mechanisms underlying the antitumor activity of LY2603618, a potent and selective small molecule inhibitor of Chk1 protein kinase, in human lung cancer cells.	LY2603618	93-102	checkpoint kinase 1	Homo sapiens	155-159
24928205-6	2014	LY2603618 inhibited Chk1 autophosphorylation (S296 Chk1) and increased DNA damage-mediated Chk1 phosphorylation (S345 Chk1).	LY2603618	0-9	checkpoint kinase 1	Homo sapiens	20-24
24928205-6	2014	LY2603618 inhibited Chk1 autophosphorylation (S296 Chk1) and increased DNA damage-mediated Chk1 phosphorylation (S345 Chk1).	LY2603618	0-9	checkpoint kinase 1	Homo sapiens	51-55
24928205-6	2014	LY2603618 inhibited Chk1 autophosphorylation (S296 Chk1) and increased DNA damage-mediated Chk1 phosphorylation (S345 Chk1).	LY2603618	0-9	checkpoint kinase 1	Homo sapiens	51-55
24928205-6	2014	LY2603618 inhibited Chk1 autophosphorylation (S296 Chk1) and increased DNA damage-mediated Chk1 phosphorylation (S345 Chk1).	LY2603618	0-9	checkpoint kinase 1	Homo sapiens	51-55
24928205-11	2014	These results suggest the following: (i) the biological consequences of LY2603618 in lung cancer cells is associated with both inhibition of Chk1 phosphorylation on S296 and activation of the DNA damage response network; and (ii) the anticancer property of LY2603618 might be increased by inhibiting autophagy.	LY2603618	72-81	checkpoint kinase 1	Homo sapiens	141-145
25042558-0	2014	Design, synthesis and biological evaluation of thienopyridinones as Chk1 inhibitors.	thienopyridinones	47-64	checkpoint kinase 1	Homo sapiens	68-72
25042558-1	2014	A series of thienopyridinone derivatives was designed and synthesized as inhibitors of checkpoint kinase 1 (Chk1).	thienopyridinone	12-28	checkpoint kinase 1	Homo sapiens	87-106
25042558-1	2014	A series of thienopyridinone derivatives was designed and synthesized as inhibitors of checkpoint kinase 1 (Chk1).	thienopyridinone	12-28	checkpoint kinase 1	Homo sapiens	108-112
25042558-3	2014	Among them, compounds 8q, 8t, and 8w with excellent Chk1 inhibitory activities (IC50 values of 4.05, 6.23, and 2.33nM, respectively) displayed strong synergistic effects with melphalan, a DNA-damaging agent in the cell-based assay.	Melphalan	175-184	checkpoint kinase 1	Homo sapiens	52-56
25047935-0	2014	Design of granulatimide and isogranulatimide analogues as potential Chk1 inhibitors: Study of amino-platforms for their synthesis.	granulatimide	10-23	checkpoint kinase 1	Homo sapiens	68-72
25047935-0	2014	Design of granulatimide and isogranulatimide analogues as potential Chk1 inhibitors: Study of amino-platforms for their synthesis.	isogranulatimide	28-44	checkpoint kinase 1	Homo sapiens	68-72
25047935-1	2014	The two marine alkaloids granulatimide and isogranulatimide have been shown to inhibit the checkpoint kinase 1 (Chk1), a promising target for cancer treatment.	Alkaloids	15-24	checkpoint kinase 1	Homo sapiens	91-110
25047935-1	2014	The two marine alkaloids granulatimide and isogranulatimide have been shown to inhibit the checkpoint kinase 1 (Chk1), a promising target for cancer treatment.	Alkaloids	15-24	checkpoint kinase 1	Homo sapiens	112-116
25047935-1	2014	The two marine alkaloids granulatimide and isogranulatimide have been shown to inhibit the checkpoint kinase 1 (Chk1), a promising target for cancer treatment.	granulatimide	25-38	checkpoint kinase 1	Homo sapiens	91-110
25047935-1	2014	The two marine alkaloids granulatimide and isogranulatimide have been shown to inhibit the checkpoint kinase 1 (Chk1), a promising target for cancer treatment.	granulatimide	25-38	checkpoint kinase 1	Homo sapiens	112-116
25047935-1	2014	The two marine alkaloids granulatimide and isogranulatimide have been shown to inhibit the checkpoint kinase 1 (Chk1), a promising target for cancer treatment.	isogranulatimide	43-59	checkpoint kinase 1	Homo sapiens	91-110
25047935-1	2014	The two marine alkaloids granulatimide and isogranulatimide have been shown to inhibit the checkpoint kinase 1 (Chk1), a promising target for cancer treatment.	isogranulatimide	43-59	checkpoint kinase 1	Homo sapiens	112-116
24934408-4	2014	Whole-genome sequencing revealed a clonal hemizygous mutation in the Mre11 complex gene RAD50 that attenuated ATM signaling which in the context of CHK1 inhibition contributed, via synthetic lethality, to extreme sensitivity to irinotecan.	Irinotecan	228-238	checkpoint kinase 1	Homo sapiens	148-152
24913641-3	2014	METHODS: Growth inhibition induced by the small molecule Chk1 inhibitor V158411 was assessed in a panel of human leukemia and lymphoma cell lines and compared to cancer cell lines derived from solid tumors.	V158411	72-79	checkpoint kinase 1	Homo sapiens	57-61
24823293-4	2014	Both CHK1 and CHK2 were phosphorylated in response to BO-1012 treatment, but only depletion of CHK1, but not CHK2, impaired BO-1012-induced S phase arrest and facilitated the entry of gammaH2AX-positive cells into G2 phase.	BO-1012	54-61	checkpoint kinase 1	Homo sapiens	5-9
24823293-4	2014	Both CHK1 and CHK2 were phosphorylated in response to BO-1012 treatment, but only depletion of CHK1, but not CHK2, impaired BO-1012-induced S phase arrest and facilitated the entry of gammaH2AX-positive cells into G2 phase.	gammah2ax	184-193	checkpoint kinase 1	Homo sapiens	5-9
24823293-5	2014	CHK1 depletion also significantly enhanced BO-1012-induced cell death and apoptosis.	BO-1012	43-50	checkpoint kinase 1	Homo sapiens	0-4
24996846-0	2014	gammaH2AX and Chk1 phosphorylation as predictive pharmacodynamic biomarkers of Chk1 inhibitor-chemotherapy combination treatments.	gammah2ax	0-9	checkpoint kinase 1	Homo sapiens	79-83
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	checkpoint kinase 1	Homo sapiens	65-69
24942404-1	2014	LY2603618 is an inhibitor of checkpoint kinase 1 (CHK1), an important regulator of the DNA damage checkpoints.	LY2603618	0-9	checkpoint kinase 1	Homo sapiens	29-48
24965470-16	2014	In addition, upon establishment of full viral replication, MVM infection prevented activation of Chk1 in response to hydroxyurea and various other drug treatments.	Hydroxyurea	117-128	checkpoint kinase 1	Homo sapiens	97-101
24666335-0	2014	Disposition and metabolism of LY2603618, a Chk-1 inhibitor following intravenous administration in patients with advanced and/or metastatic solid tumors.	LY2603618	30-39	checkpoint kinase 1	Homo sapiens	43-48
24666335-1	2014	The disposition and metabolism of a Chk-1 inhibitor (LY2603618) was characterized following a 1-h intravenous administration of a single 250-mg dose of [14C]LY2603618 (50 microCi) to patients with advanced or metastatic solid tumors.	LY2603618	53-62	checkpoint kinase 1	Homo sapiens	36-41
24666335-1	2014	The disposition and metabolism of a Chk-1 inhibitor (LY2603618) was characterized following a 1-h intravenous administration of a single 250-mg dose of [14C]LY2603618 (50 microCi) to patients with advanced or metastatic solid tumors.	LY2603618	157-166	checkpoint kinase 1	Homo sapiens	36-41
25104095-3	2014	METHODS: Here we describe the cellular effects of the pharmacological inhibition of the checkpoint kinase Chk1 by the novel inhibitor V158411 in triple-negative breast cancer and ovarian cancer.	V158411	134-141	checkpoint kinase 1	Homo sapiens	106-110
25104095-6	2014	RESULTS: The Chk1 inhibitors V158411, PF-477736 and AZD7762 potently inhibited the proliferation of triple-negative breast cancer cells as well as ovarian cancer cells, and these cell lines were sensitive compared to ER positive breast and other solid cancer cells lines.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	52-59	checkpoint kinase 1	Homo sapiens	13-17
24915421-9	2014	WJ35435 was less effective than camptothecin and etoposide in inducing the phosphorylation and activation of Chk1, Chk2 and RPA32 which were crucial coordinators in DNA repair pathway, indicating a low DNA repair activity to WJ35435 action.	N-hydroxy-6-(4-carbamoylacridinyl)hexanamide	0-7	checkpoint kinase 1	Homo sapiens	109-113
24915421-9	2014	WJ35435 was less effective than camptothecin and etoposide in inducing the phosphorylation and activation of Chk1, Chk2 and RPA32 which were crucial coordinators in DNA repair pathway, indicating a low DNA repair activity to WJ35435 action.	Camptothecin	32-44	checkpoint kinase 1	Homo sapiens	109-113
24915421-9	2014	WJ35435 was less effective than camptothecin and etoposide in inducing the phosphorylation and activation of Chk1, Chk2 and RPA32 which were crucial coordinators in DNA repair pathway, indicating a low DNA repair activity to WJ35435 action.	Etoposide	49-58	checkpoint kinase 1	Homo sapiens	109-113
25084614-0	2014	CHK1 plays a critical role in the anti-leukemic activity of the wee1 inhibitor MK-1775 in acute myeloid leukemia cells.	adavosertib	79-86	checkpoint kinase 1	Homo sapiens	0-4
25084614-10	2014	Time-course experiments, using AML cell lines, revealed a time-dependent increase in DNA DSBs, activation of CHK1 and subsequent apoptosis following MK-1775 treatment, which could be attenuated by a CDK1/2 inhibitor, Roscovitine.	adavosertib	149-156	checkpoint kinase 1	Homo sapiens	109-113
25084614-10	2014	Time-course experiments, using AML cell lines, revealed a time-dependent increase in DNA DSBs, activation of CHK1 and subsequent apoptosis following MK-1775 treatment, which could be attenuated by a CDK1/2 inhibitor, Roscovitine.	Roscovitine	217-228	checkpoint kinase 1	Homo sapiens	109-113
25084614-12	2014	CONCLUSIONS: Our study provides compelling evidence that CHK1 plays a critical role in the anti-leukemic activity of MK-1775 and highlights a possible mechanism of resistance to MK-1775.	adavosertib	117-124	checkpoint kinase 1	Homo sapiens	57-61
24823293-6	2014	These results indicate that BO-1012-induced S phase arrest is a CHK1-dependent pro-survival response.	BO-1012	28-35	checkpoint kinase 1	Homo sapiens	64-68
24823293-8	2014	Depletion of ATG7 or co-treatment of cells with BO-1012 and either 3-methyladenine or bafilomycin A1, two inhibitors of autophagy, not only reduced CHK1 phosphorylation and disrupted S phase arrest, but also increased cleavage of caspase-9 and PARP, and cell death.	BO-1012	48-55	checkpoint kinase 1	Homo sapiens	148-152
24823293-8	2014	Depletion of ATG7 or co-treatment of cells with BO-1012 and either 3-methyladenine or bafilomycin A1, two inhibitors of autophagy, not only reduced CHK1 phosphorylation and disrupted S phase arrest, but also increased cleavage of caspase-9 and PARP, and cell death.	3-methyladenine	67-82	checkpoint kinase 1	Homo sapiens	148-152
24823293-9	2014	These results suggest that cells initiate S phase arrest and autophagy as pro-survival responses to BO-1012-induced DNA damage, and that suppression of autophagy enhances BO-1012-induced apoptosis via disruption of CHK1-dependent S phase arrest.	BO-1012	171-178	checkpoint kinase 1	Homo sapiens	215-219
25010037-6	2014	VX-970 markedly sensitized a large proportion of a lung cancer cell line and primary tumor panel in vitro to multiple DNA damaging drugs with clear differences to Chk1 inhibition observed.	berzosertib	0-6	checkpoint kinase 1	Homo sapiens	163-167
24971543-5	2014	We show that v-Src suppresses thymidine-induced Chk1 phosphorylation and induces replication fork collapse.	Thymidine	30-39	checkpoint kinase 1	Homo sapiens	48-52
24913980-3	2014	Our findings indicate that sublethal doses of doxorubicin and melphalan initiate a DNA damage response (DDR) controlling ligand upregulation on MM cell lines and patient-derived malignant plasma cells in Chk1/2-dependent and p53-independent manner.	Doxorubicin	46-57	checkpoint kinase 1	Homo sapiens	204-208
24913980-3	2014	Our findings indicate that sublethal doses of doxorubicin and melphalan initiate a DNA damage response (DDR) controlling ligand upregulation on MM cell lines and patient-derived malignant plasma cells in Chk1/2-dependent and p53-independent manner.	Melphalan	62-71	checkpoint kinase 1	Homo sapiens	204-208
24913641-5	2014	RESULTS: Leukemia and lymphoma cell lines were identified as particularly sensitive to the Chk1 inhibitor V158411 (mean GI50 0.17 muM) compared to colon (2.8 muM) or lung (6.9 muM) cancer cell lines.	V158411	106-113	checkpoint kinase 1	Homo sapiens	91-95
24650757-0	2014	Chk1, but not Chk2, is responsible for G2/M phase arrest induced by diallyl disulfide in human gastric cancer BGC823 cells.	diallyl disulfide	68-85	checkpoint kinase 1	Homo sapiens	0-4
24650757-2	2014	Here we demonstrate a mechanism by which DADS induces G2/M phase arrest in BGC823 human gastric cancer cells via Chk1.	diallyl disulfide	41-45	checkpoint kinase 1	Homo sapiens	113-117
24650757-5	2014	Moreover, overexpression of Chk1 promoted the effect of DADS-induced G2/M arrest.	diallyl disulfide	56-60	checkpoint kinase 1	Homo sapiens	28-32
24650757-6	2014	Augmented phosphorylation of Chk1 by DADS was observed in Chk1-transfected cells, followed by downregulation of Cdc25C and cyclin B1 proteins.	diallyl disulfide	37-41	checkpoint kinase 1	Homo sapiens	29-33
24650757-6	2014	Augmented phosphorylation of Chk1 by DADS was observed in Chk1-transfected cells, followed by downregulation of Cdc25C and cyclin B1 proteins.	diallyl disulfide	37-41	checkpoint kinase 1	Homo sapiens	58-62
24650757-8	2014	Furthermore, knockdown of Chk1 by siRNA partially abrogated DADS-induced downregulation of Cdc25C and cyclin B1 proteins and G2/M arrest.	diallyl disulfide	60-64	checkpoint kinase 1	Homo sapiens	26-30
24650757-10	2014	Therefore, these data indicate that DADS may specifically modulate Chk1 phosphorylation, and DADS-induced G2/M phase arrest in BGC823 cells could result in part from Chk1-mediated inhibition of the Cdc25C/cyclin B1 pathway.	diallyl disulfide	36-40	checkpoint kinase 1	Homo sapiens	67-71
24650757-10	2014	Therefore, these data indicate that DADS may specifically modulate Chk1 phosphorylation, and DADS-induced G2/M phase arrest in BGC823 cells could result in part from Chk1-mediated inhibition of the Cdc25C/cyclin B1 pathway.	diallyl disulfide	36-40	checkpoint kinase 1	Homo sapiens	166-170
24650757-10	2014	Therefore, these data indicate that DADS may specifically modulate Chk1 phosphorylation, and DADS-induced G2/M phase arrest in BGC823 cells could result in part from Chk1-mediated inhibition of the Cdc25C/cyclin B1 pathway.	diallyl disulfide	93-97	checkpoint kinase 1	Homo sapiens	166-170
24728469-6	2014	This may indicate that the alteration of p21 and CHK1 following zebularine administration was not due to inhibition of methylation of their promoter.	pyrimidin-2-one beta-ribofuranoside	64-74	checkpoint kinase 1	Homo sapiens	49-53
24804869-9	2014	HNF-1beta (+) cells were treated with a CHK1 inhibitor after bleomycin treatment.	Bleomycin	61-70	checkpoint kinase 1	Homo sapiens	40-44
24804719-0	2014	Piperine causes G1 phase cell cycle arrest and apoptosis in melanoma cells through checkpoint kinase-1 activation.	piperine	0-8	checkpoint kinase 1	Homo sapiens	83-102
24996846-9	2014	CONCLUSIONS: Our results suggest that Chk1 phosphorylation could be a useful biomarker for monitoring inhibition of Chk1 activity in clinical trials involving a range of V158411-chemotherapy combinations and gammaH2AX induction as a predictor of potentiation in combinations containing gemcitabine or camptothecin.	gemcitabine	286-297	checkpoint kinase 1	Homo sapiens	38-42
24996846-9	2014	CONCLUSIONS: Our results suggest that Chk1 phosphorylation could be a useful biomarker for monitoring inhibition of Chk1 activity in clinical trials involving a range of V158411-chemotherapy combinations and gammaH2AX induction as a predictor of potentiation in combinations containing gemcitabine or camptothecin.	gemcitabine	286-297	checkpoint kinase 1	Homo sapiens	116-120
24996846-9	2014	CONCLUSIONS: Our results suggest that Chk1 phosphorylation could be a useful biomarker for monitoring inhibition of Chk1 activity in clinical trials involving a range of V158411-chemotherapy combinations and gammaH2AX induction as a predictor of potentiation in combinations containing gemcitabine or camptothecin.	Camptothecin	301-313	checkpoint kinase 1	Homo sapiens	38-42
24996846-9	2014	CONCLUSIONS: Our results suggest that Chk1 phosphorylation could be a useful biomarker for monitoring inhibition of Chk1 activity in clinical trials involving a range of V158411-chemotherapy combinations and gammaH2AX induction as a predictor of potentiation in combinations containing gemcitabine or camptothecin.	Camptothecin	301-313	checkpoint kinase 1	Homo sapiens	116-120
24694947-10	2014	Importantly, we also demonstrate that olaparib, but not veliparib, induced a robust phosphorylation of Chk1, a crucial component of the replicative stress response pathway.	olaparib	38-46	checkpoint kinase 1	Homo sapiens	103-107
24804719-5	2014	Furthermore, this growth arrest by piperine treatment was associated with DNA damage as indicated by phosphorylation of H2AX at Ser139, activation of ataxia telangiectasia and rad3-related protein (ATR) and checkpoint kinase 1 (Chk1).	piperine	35-43	checkpoint kinase 1	Homo sapiens	207-226
24804719-5	2014	Furthermore, this growth arrest by piperine treatment was associated with DNA damage as indicated by phosphorylation of H2AX at Ser139, activation of ataxia telangiectasia and rad3-related protein (ATR) and checkpoint kinase 1 (Chk1).	piperine	35-43	checkpoint kinase 1	Homo sapiens	228-232
24804719-6	2014	Pretreatment with AZD 7762, a Chk1 inhibitor not only abrogated the activation of Chk1 but also piperine mediated G1 arrest.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	18-26	checkpoint kinase 1	Homo sapiens	30-34
24804719-6	2014	Pretreatment with AZD 7762, a Chk1 inhibitor not only abrogated the activation of Chk1 but also piperine mediated G1 arrest.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	18-26	checkpoint kinase 1	Homo sapiens	82-86
24804719-6	2014	Pretreatment with AZD 7762, a Chk1 inhibitor not only abrogated the activation of Chk1 but also piperine mediated G1 arrest.	piperine	96-104	checkpoint kinase 1	Homo sapiens	30-34
24804719-7	2014	Similarly, transfection of cells with Chk1 siRNA completely protected the cells from G1 arrest induced by piperine.	piperine	106-114	checkpoint kinase 1	Homo sapiens	38-42
24804719-12	2014	These results suggest that piperine mediated ROS played a critical role in inducing DNA damage and activation of Chk1 leading to G1 cell cycle arrest and apoptosis.	piperine	27-35	checkpoint kinase 1	Homo sapiens	113-117
24804719-12	2014	These results suggest that piperine mediated ROS played a critical role in inducing DNA damage and activation of Chk1 leading to G1 cell cycle arrest and apoptosis.	ros	45-48	checkpoint kinase 1	Homo sapiens	113-117
24634213-6	2014	Src-dependent nuclear protein tyrosine phosphorylation and v-Src expression suppress the ATR-mediated Chk1 and Rad17 phosphorylation induced by DNA double strand breaks or DNA replication stress.	Tyrosine	30-38	checkpoint kinase 1	Homo sapiens	102-106
24316097-5	2014	Further examination showed that moniliformediquinone induced a DNA damage response associated with Chk1, Chk2, c-Jun and JNK activation.	2,6-dimethoxy-1,4,5,8-phenanthrenetetrone	32-52	checkpoint kinase 1	Homo sapiens	99-103
24434653-4	2014	In response to hydroxyurea, CHK1 was delocalized from the centrosome by RRM1 depletion.	Hydroxyurea	15-26	checkpoint kinase 1	Homo sapiens	28-32
24853623-0	2014	Co-abrogation of Chk1 and Chk2 by potent oncolytic adenovirus potentiates the antitumor efficacy of cisplatin or irradiation.	Cisplatin	100-109	checkpoint kinase 1	Homo sapiens	17-21
24464582-7	2014	Pu-27 down-regulates telomeric shelterin proteins, DNA damage response mediators (RAD17 and RAD50), double-stranded break repair molecule 53BP1, G2 checkpoint regulators (CHK1 and CHK2), and anti-apoptosis gene survivin.	pu-27	0-5	checkpoint kinase 1	Homo sapiens	171-175
24676336-12	2014	For the TSA+DAC group, higher levels of p53, p21, cyclin B1 and Chk1 were detected, concomitant with lower levels of CDK1, when compared to the control group.	trichostatin A	8-11	checkpoint kinase 1	Homo sapiens	64-68
24676336-12	2014	For the TSA+DAC group, higher levels of p53, p21, cyclin B1 and Chk1 were detected, concomitant with lower levels of CDK1, when compared to the control group.	Decitabine	12-15	checkpoint kinase 1	Homo sapiens	64-68
24150948-0	2014	The natural anticancer compound rocaglamide selectively inhibits the G1-S-phase transition in cancer cells through the ATM/ATR-mediated Chk1/2 cell cycle checkpoints.	rocaglamide	32-43	checkpoint kinase 1	Homo sapiens	136-140
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	checkpoint kinase 1	Homo sapiens	146-150
24412704-8	2014	These two thiol compounds also partially suppressed oxidative frameshift mutations in the coding microsatellites of the hMSH6 and CHK1 genes based on a fluoresceinated PCR-based assay.	Sulfhydryl Compounds	10-15	checkpoint kinase 1	Homo sapiens	130-134
24114124-11	2014	Treatment of Calu-6 human mutant TP53 lung cancer cell xenografts with gemcitabine resulted in a stimulation of Chk1 kinase activity that was inhibited by co-administration of LY2603618.	gemcitabine	71-82	checkpoint kinase 1	Homo sapiens	112-116
24114124-11	2014	Treatment of Calu-6 human mutant TP53 lung cancer cell xenografts with gemcitabine resulted in a stimulation of Chk1 kinase activity that was inhibited by co-administration of LY2603618.	LY2603618	176-185	checkpoint kinase 1	Homo sapiens	112-116
24114124-12	2014	By all criteria, LY2603618 is a highly effective inhibitor of multiple aspects of Chk1 biology.	LY2603618	17-26	checkpoint kinase 1	Homo sapiens	82-86
24179152-6	2014	The CHK1 inhibitor MK8776 sensitized acute myeloid leukemia cell lines and primary leukemia specimens to MK1775 ex vivo, whereas smaller effects were observed with the MK1775/MK8776 combination in normal myeloid progenitors.	MK-8776	19-25	checkpoint kinase 1	Homo sapiens	4-8
24179152-6	2014	The CHK1 inhibitor MK8776 sensitized acute myeloid leukemia cell lines and primary leukemia specimens to MK1775 ex vivo, whereas smaller effects were observed with the MK1775/MK8776 combination in normal myeloid progenitors.	MK-8776	175-181	checkpoint kinase 1	Homo sapiens	4-8
24179152-8	2014	Further studies showed that MK8776 enhanced MK1775-mediated activation of the ATR/CHK1 pathway in acute leukemia cell lines and ex vivo.	MK-8776	28-34	checkpoint kinase 1	Homo sapiens	82-86
24179152-8	2014	Further studies showed that MK8776 enhanced MK1775-mediated activation of the ATR/CHK1 pathway in acute leukemia cell lines and ex vivo.	adavosertib	44-50	checkpoint kinase 1	Homo sapiens	82-86
24114124-0	2014	Characterization and preclinical development of LY2603618: a selective and potent Chk1 inhibitor.	LY2603618	48-57	checkpoint kinase 1	Homo sapiens	82-86
24114124-6	2014	LY2603618 is a potent and selective small molecule inhibitor of Chk1 protein kinase activity in vitro (IC(50) = 7 nM) and the first selective Chk1 inhibitor to enter clinical cancer trials.	LY2603618	0-9	checkpoint kinase 1	Homo sapiens	64-68
24114124-6	2014	LY2603618 is a potent and selective small molecule inhibitor of Chk1 protein kinase activity in vitro (IC(50) = 7 nM) and the first selective Chk1 inhibitor to enter clinical cancer trials.	LY2603618	0-9	checkpoint kinase 1	Homo sapiens	142-146
24114124-7	2014	Treatment of cells with LY2603618 produced a cellular phenotype similar to that reported for depletion of Chk1 by RNAi.	LY2603618	24-33	checkpoint kinase 1	Homo sapiens	106-110
24114124-8	2014	Inhibition of intracellular Chk1 by LY2603618 results in impaired DNA synthesis, elevated H2A.X phosphorylation indicative of DNA damage and premature entry into mitosis.	LY2603618	36-45	checkpoint kinase 1	Homo sapiens	28-32
24182986-10	2014	Both Amaryllidaceae alkaloids accumulate cells preferentially at G1 and G2 stages of the cell cycle with increased p16 expression and Chk1 Ser345 phosphorylation.	Amaryllidaceae Alkaloids	5-29	checkpoint kinase 1	Homo sapiens	134-138
24448638-1	2014	PURPOSE: AZD7762 is a Chk1 kinase inhibitor which increases sensitivity to DNA-damaging agents, including gemcitabine.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	9-16	checkpoint kinase 1	Homo sapiens	22-26
24448638-1	2014	PURPOSE: AZD7762 is a Chk1 kinase inhibitor which increases sensitivity to DNA-damaging agents, including gemcitabine.	gemcitabine	106-117	checkpoint kinase 1	Homo sapiens	22-26
24349411-5	2013	The two most potent radiosensitizers were the Chk1/2 inhibitor AZD7762 and the PI3K/mTOR inhibitor BEZ235.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	63-70	checkpoint kinase 1	Homo sapiens	46-52
23748345-1	2014	Phosphorylation by Akt on Ser 280 was reported to induce cytoplasmic retention and inactivation of CHK1 with consequent genetic instability in PTEN-/- cells.	Serine	26-29	checkpoint kinase 1	Homo sapiens	99-103
24388752-6	2014	These lesions are converted to DSBs in the subsequent G2 phase, which subsequently activate Chk1, delay G2 progression, and lead to chromosome instability.	1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione	31-35	checkpoint kinase 1	Homo sapiens	92-96
25483185-7	2014	Moreover, Chk1 was phosphorylated, accompanied with the persistent increase of cyclin B1 expression in HMG-treated ST8814 cells.	hmg	103-106	checkpoint kinase 1	Homo sapiens	10-14
25483185-8	2014	The knockdown of Chk1 by the siRNA prevented the Nf1-deficient cells from undergoing HMG-mediated mitotic arrest as well as mitotic catastrophe.	hmg	85-88	checkpoint kinase 1	Homo sapiens	17-21
24247149-3	2014	Within 4-8 h of Chk1 inhibition following gemcitabine induced DNA damage, cells with both sub-4N and 4N DNA content prematurely enter mitosis.	gemcitabine	42-53	checkpoint kinase 1	Homo sapiens	16-20
24158981-6	2014	Both ischemic and oxidant stress resulted in a dramatic increase in reactive oxygen species that phosphorylated and activated Chk1, which subsequently bound to STAT3, phosphorylating it at S727.	Reactive Oxygen Species	68-91	checkpoint kinase 1	Homo sapiens	126-130
24197116-4	2014	Using tandem mass spectrometry and biochemical analysis, it was determined that CHK1 phosphorylates RASSF1A on Serine 184, which has been shown to be mutated in a subset of human primary nasopharyngeal carcinomas.	Serine	111-117	checkpoint kinase 1	Homo sapiens	80-84
24197116-5	2014	Furthermore, Serine 184 phosphorylation of RASSF1A was significantly diminished by a CHK1-specific kinase inhibitor.	Serine	13-19	checkpoint kinase 1	Homo sapiens	85-89
24197116-9	2014	IMPLICATIONS: This study reveals that CHK1-mediated phosphorylation of RASSF1A, at Serine 184, plays an important role in cell-cycle regulation and highlights that mutation of this CHK1 phosphorylation site in nasopharyngeal carcinoma has disease relevance.	Serine	83-89	checkpoint kinase 1	Homo sapiens	38-42
24197116-9	2014	IMPLICATIONS: This study reveals that CHK1-mediated phosphorylation of RASSF1A, at Serine 184, plays an important role in cell-cycle regulation and highlights that mutation of this CHK1 phosphorylation site in nasopharyngeal carcinoma has disease relevance.	Serine	83-89	checkpoint kinase 1	Homo sapiens	181-185
24218165-7	2014	The presence of gammaH2AX foci and phosphorylation of TP53(ser15) and CHK1(ser317) were shown in U343 cells, compatible with cisplatin-induced DNA damage.	Cisplatin	125-134	checkpoint kinase 1	Homo sapiens	70-74
24048439-8	2014	Terfenadine also induced an indirect-but not direct-DNA damage response through the cleavage and activation of caspase-2, phosphorylation and activation of Chk1 and Chk2 kinases, phosphorylation of RPA32 and acetylation of Histone H3; these processes were highly correlated to severe mitochondrial dysfunction and the activation of caspase cascades.	Terfenadine	0-11	checkpoint kinase 1	Homo sapiens	156-160
24911214-0	2014	Docking-based 3D-QSAR study of pyridyl aminothiazole derivatives as checkpoint kinase 1 inhibitors.	pyridyl aminothiazole	31-52	checkpoint kinase 1	Homo sapiens	68-87
24911214-2	2014	In the present work, molecular docking simulations and three-dimensional quantitative structure-activity relationship (3D-QSAR) studies were performed on pyridyl aminothiazole derivatives as Chk1 inhibitors.	pyridyl aminothiazole	154-175	checkpoint kinase 1	Homo sapiens	191-195
24359526-0	2013	Sensitization of human cancer cells to gemcitabine by the Chk1 inhibitor MK-8776: cell cycle perturbation and impact of administration schedule in vitro and in vivo.	gemcitabine	39-50	checkpoint kinase 1	Homo sapiens	58-62
24359526-0	2013	Sensitization of human cancer cells to gemcitabine by the Chk1 inhibitor MK-8776: cell cycle perturbation and impact of administration schedule in vitro and in vivo.	MK-8776	73-80	checkpoint kinase 1	Homo sapiens	58-62
24359526-1	2013	BACKGROUND: Chk1 inhibitors have emerged as promising anticancer therapeutic agents particularly when combined with antimetabolites such as gemcitabine, cytarabine or hydroxyurea.	gemcitabine	140-151	checkpoint kinase 1	Homo sapiens	12-16
24359526-1	2013	BACKGROUND: Chk1 inhibitors have emerged as promising anticancer therapeutic agents particularly when combined with antimetabolites such as gemcitabine, cytarabine or hydroxyurea.	Cytarabine	153-163	checkpoint kinase 1	Homo sapiens	12-16
24359526-1	2013	BACKGROUND: Chk1 inhibitors have emerged as promising anticancer therapeutic agents particularly when combined with antimetabolites such as gemcitabine, cytarabine or hydroxyurea.	Hydroxyurea	167-178	checkpoint kinase 1	Homo sapiens	12-16
24359526-2	2013	Here, we address the importance of appropriate drug scheduling when gemcitabine is combined with the Chk1 inhibitor MK-8776, and the mechanisms involved in the schedule dependence.	MK-8776	116-123	checkpoint kinase 1	Homo sapiens	101-105
24359526-14	2013	CONCLUSIONS: There are two reasons why delayed addition of MK-8776 enhances sensitivity to gemcitabine: first, there is an increased number of cells arrested in S phase; and second, the arrested cells have adequate time to initiate recombination and thereby become Chk1 dependent.	MK-8776	59-66	checkpoint kinase 1	Homo sapiens	265-269
24359526-14	2013	CONCLUSIONS: There are two reasons why delayed addition of MK-8776 enhances sensitivity to gemcitabine: first, there is an increased number of cells arrested in S phase; and second, the arrested cells have adequate time to initiate recombination and thereby become Chk1 dependent.	gemcitabine	91-102	checkpoint kinase 1	Homo sapiens	265-269
24418519-6	2014	We analyzed CHK1 signaling by Western blotting to confirm that AZD7762 inhibits CHK1.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	63-70	checkpoint kinase 1	Homo sapiens	12-16
24418519-6	2014	We analyzed CHK1 signaling by Western blotting to confirm that AZD7762 inhibits CHK1.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	63-70	checkpoint kinase 1	Homo sapiens	80-84
24418519-12	2014	CONCLUSIONS: CHK1 inhibition by AZD7762 preferentially sensitizes high CHK1 expressing cells, H1299, to anti-metabolite chemotherapy as compared with low CHK1 expressing H1993 cells.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	32-39	checkpoint kinase 1	Homo sapiens	13-17
24418519-12	2014	CONCLUSIONS: CHK1 inhibition by AZD7762 preferentially sensitizes high CHK1 expressing cells, H1299, to anti-metabolite chemotherapy as compared with low CHK1 expressing H1993 cells.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	32-39	checkpoint kinase 1	Homo sapiens	71-75
24418519-12	2014	CONCLUSIONS: CHK1 inhibition by AZD7762 preferentially sensitizes high CHK1 expressing cells, H1299, to anti-metabolite chemotherapy as compared with low CHK1 expressing H1993 cells.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	32-39	checkpoint kinase 1	Homo sapiens	71-75
24413181-6	2014	Mechanistic studies within reveal that triapine inhibits cyclin-dependent kinase (CDK) activity and blocks olaparib-induced CtIP phosphorylation through Chk1 activation.	3-aminopyridine-2-carboxaldehyde thiosemicarbazone	39-47	checkpoint kinase 1	Homo sapiens	153-157
24413181-6	2014	Mechanistic studies within reveal that triapine inhibits cyclin-dependent kinase (CDK) activity and blocks olaparib-induced CtIP phosphorylation through Chk1 activation.	olaparib	107-115	checkpoint kinase 1	Homo sapiens	153-157
24525428-0	2014	Targeting CDC25C, PLK1 and CHEK1 to overcome Docetaxel resistance induced by loss of LZTS1 in prostate cancer.	Docetaxel	45-54	checkpoint kinase 1	Homo sapiens	27-32
24505404-9	2014	Taken together, these results suggested that Cuc B induces DNA damage in A549 cells mediated by increasing intracellular ROS formation, which lead to G2/M cell phase arrest through ATM-activated Chk1-Cdc25C-Cdk1 and p53-14-3-3-sigma parallel branches.	cucurbitacin B	45-50	checkpoint kinase 1	Homo sapiens	195-199
24505404-9	2014	Taken together, these results suggested that Cuc B induces DNA damage in A549 cells mediated by increasing intracellular ROS formation, which lead to G2/M cell phase arrest through ATM-activated Chk1-Cdc25C-Cdk1 and p53-14-3-3-sigma parallel branches.	Reactive Oxygen Species	121-124	checkpoint kinase 1	Homo sapiens	195-199
24380689-6	2014	ATR knock down by siRNA or caffeine addition provoked increased cell death in both XP-V and XP-C cells exposed to low-dose of UVC, underscoring the involvement of ATR/Chk1 pathway in both DNA damage tolerance mechanisms.	Caffeine	27-35	checkpoint kinase 1	Homo sapiens	167-171
23748345-2	2014	In acute myeloid leukemia cells carrying the FLT3-internal tandem duplication (ITD) mutation, we observed high rates of FLT3-ITD-dependent CHK1 Ser 280 phosphorylation.	Serine	144-147	checkpoint kinase 1	Homo sapiens	139-143
23748345-7	2014	Consistently, etoposide-induced CHK1-dependent phosphorylations of CDC25C on Ser 216 and histone H3 on Thr11 were decreased upon FLT3 inhibition.	Etoposide	14-23	checkpoint kinase 1	Homo sapiens	32-36
23748345-7	2014	Consistently, etoposide-induced CHK1-dependent phosphorylations of CDC25C on Ser 216 and histone H3 on Thr11 were decreased upon FLT3 inhibition.	Serine	77-80	checkpoint kinase 1	Homo sapiens	32-36
23748345-9	2014	Finally, FLT3- and Pim-dependent phosphorylation of CHK1 on Ser 280 was confirmed in primary blasts from patients.	Serine	60-63	checkpoint kinase 1	Homo sapiens	52-56
23748345-10	2014	These results identify a new pathway involved in the resistance of FLT3-ITD leukemic cells to genotoxic agents, and they constitute the first report of CHK1 Ser 280 regulation in myeloid malignancies.	Serine	157-160	checkpoint kinase 1	Homo sapiens	152-156
24583858-0	2014	Glionitrin A, a new diketopiperazine disulfide, activates ATM-ATR-Chk1/2 via 53BP1 phosphorylation in DU145 cells and shows antitumor effect in xenograft model.	glionitrin A	0-12	checkpoint kinase 1	Homo sapiens	66-72
24583858-4	2014	Glionitrin A-treated cells exhibited elevated levels of phospho-histone 2AX (Ser139), a marker of DNA damage, and accumulated in both S phase and G2/M phase due to the activation of checkpoints associated with the ataxia-telangiectasia-mutated and ataxia-telangiectasia-mutated-Rad3-related Chk1/2 pathway downstream of p53-binding protein 1 phosphorylation at Ser1778.	glionitrin A	0-12	checkpoint kinase 1	Homo sapiens	291-297
24955955-6	2014	In vitro and cell-based assays showed that both the authentic bosutinib and Bos-I inhibited DNA damage checkpoint kinases Chk1 and Wee1, with Bos-I showing greater potency.	bosutinib	62-71	checkpoint kinase 1	Homo sapiens	122-126
24955955-6	2014	In vitro and cell-based assays showed that both the authentic bosutinib and Bos-I inhibited DNA damage checkpoint kinases Chk1 and Wee1, with Bos-I showing greater potency.	bos-i	76-81	checkpoint kinase 1	Homo sapiens	122-126
25485589-5	2014	LARG-deficient cells exhibit replication stress signaling defects as evidenced by; supernumerary centrosomes, reduced replication stress-induced gammaH2AX and RPA nuclear foci formation, and reduced activation of the replication stress signaling effector kinase Chk1 in response to hydroxyurea.	Hydroxyurea	282-293	checkpoint kinase 1	Homo sapiens	262-266
24556918-10	2014	Importantly, in BxPC-3 and MIA PaCa-2 cells, inhibition of MK2 also rescued increased H2AX phosphorylation caused by inhibition of the checkpoint kinase Chk1 in the presence of gemcitabine.	gemcitabine	177-188	checkpoint kinase 1	Homo sapiens	153-157
25382189-4	2014	JM118 increased the phosphorylation of the cell cycle proteins CDK2 and CHK1 after 24 hr exposure.	amminedichloro(cyclohexylamine)platinum(II)	0-5	checkpoint kinase 1	Homo sapiens	72-76
24362713-2	2014	The present study was aimed to assess the potential to use the Chk1 and Chk2 inhibitor, AZD7762, with other anticancer agents in chemotherapy to treat ovarian clear cell carcinoma.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	88-95	checkpoint kinase 1	Homo sapiens	63-67
24362713-9	2014	Combinations of small interfering RNA against Chk 1 and small interfering RNA against Chk2 enhanced the cytotoxic effect of cisplatin in both RMG-I and KK cells.	Cisplatin	124-133	checkpoint kinase 1	Homo sapiens	46-51
24324060-7	2013	Upstream of Chk-1 signal transduction depended on both ATM and ATR for all drugs except methotrexate.	Methotrexate	88-100	checkpoint kinase 1	Homo sapiens	12-17
24113549-0	2013	CHK1 levels correlate with sensitization to pemetrexed by CHK1 inhibitors in non-small cell lung cancer cells.	Pemetrexed	44-54	checkpoint kinase 1	Homo sapiens	0-4
25431671-11	2014	Phosphorylation of p53 and Chk1 and expression of ATF4 and CHOP genes were detected in IS-, PCS-, and PhS-treated cells, but not in IAA-treated cells.	phenylsulfate	102-105	checkpoint kinase 1	Homo sapiens	27-31
24113549-0	2013	CHK1 levels correlate with sensitization to pemetrexed by CHK1 inhibitors in non-small cell lung cancer cells.	Pemetrexed	44-54	checkpoint kinase 1	Homo sapiens	58-62
24113549-3	2013	In this study, we evaluated the effects of a novel CHK1 inhibitor, MK-8776, in combination with pemetrexed (PMX) on cell proliferation and survival in a panel of p53 mutant non-small cell lung cancer (NSCLC) cell lines.	MK-8776	67-74	checkpoint kinase 1	Homo sapiens	51-55
24113549-8	2013	We examined cell line sensitization to PMX in response to CHK1 inhibition with MK-8776 using WST-1 and clonogenic survival assays.	Pemetrexed	39-42	checkpoint kinase 1	Homo sapiens	58-62
24113549-8	2013	We examined cell line sensitization to PMX in response to CHK1 inhibition with MK-8776 using WST-1 and clonogenic survival assays.	MK-8776	79-86	checkpoint kinase 1	Homo sapiens	58-62
24113549-11	2013	CHK1 inhibition by MK-8776 enhances sensitivity of NSCLC cell lines to PMX.	MK-8776	19-26	checkpoint kinase 1	Homo sapiens	0-4
24113549-11	2013	CHK1 inhibition by MK-8776 enhances sensitivity of NSCLC cell lines to PMX.	Pemetrexed	71-74	checkpoint kinase 1	Homo sapiens	0-4
24038068-1	2013	Here we report that GNE-783, a novel checkpoint kinase-1 (CHK1) inhibitor, enhances the activity of gemcitabine by disabling the S- and G2 cell-cycle checkpoints following DNA damage.	gemcitabine	100-111	checkpoint kinase 1	Homo sapiens	37-56
24081328-8	2013	Hyperactivation of Akt inhibits Chk1 phosphorylation after hydroxyurea treatment, and this effect is dependent on TopBP1 phosphorylation at Ser-1159.	Hydroxyurea	59-70	checkpoint kinase 1	Homo sapiens	32-36
24081328-8	2013	Hyperactivation of Akt inhibits Chk1 phosphorylation after hydroxyurea treatment, and this effect is dependent on TopBP1 phosphorylation at Ser-1159.	Serine	140-143	checkpoint kinase 1	Homo sapiens	32-36
24260231-4	2013	In cells expressing BCR/ABL, FLT3-ITD, or Jak2-V617F, etoposide induced a sustained activation of Chk1, thus leading to the G2/M arrest of cells.	Etoposide	54-63	checkpoint kinase 1	Homo sapiens	98-102
24260231-5	2013	Inhibition of these kinases by their inhibitors, imatinib, sorafenib, or JakI-1, significantly abbreviated Chk1 activation, and drastically enhanced apoptosis induced by etoposide.	Imatinib Mesylate	49-57	checkpoint kinase 1	Homo sapiens	107-111
24260231-5	2013	Inhibition of these kinases by their inhibitors, imatinib, sorafenib, or JakI-1, significantly abbreviated Chk1 activation, and drastically enhanced apoptosis induced by etoposide.	Sorafenib	59-68	checkpoint kinase 1	Homo sapiens	107-111
24260231-7	2013	GSK3 inhibitors, including LiCl and SB216763, restored the sustained Chk1 activation and mitigated apoptosis in cells treated with etoposide and the inhibitors for aberrant kinases, PI3K, or Akt.	Lithium Chloride	27-31	checkpoint kinase 1	Homo sapiens	69-73
24260231-7	2013	GSK3 inhibitors, including LiCl and SB216763, restored the sustained Chk1 activation and mitigated apoptosis in cells treated with etoposide and the inhibitors for aberrant kinases, PI3K, or Akt.	SB 216763	36-44	checkpoint kinase 1	Homo sapiens	69-73
24260231-7	2013	GSK3 inhibitors, including LiCl and SB216763, restored the sustained Chk1 activation and mitigated apoptosis in cells treated with etoposide and the inhibitors for aberrant kinases, PI3K, or Akt.	Etoposide	131-140	checkpoint kinase 1	Homo sapiens	69-73
24072747-3	2013	Inhibiting chronic Chk1 activity in cancer cells induced the tumor suppressor activity of protein phosphatase protein phosphatase 2A (PP2A), which by dephosphorylating MYC serine 62, inhibited MYC activity and impaired cancer cell survival.	Serine	172-178	checkpoint kinase 1	Homo sapiens	19-23
24038068-1	2013	Here we report that GNE-783, a novel checkpoint kinase-1 (CHK1) inhibitor, enhances the activity of gemcitabine by disabling the S- and G2 cell-cycle checkpoints following DNA damage.	gemcitabine	100-111	checkpoint kinase 1	Homo sapiens	58-62
24038068-7	2013	We finally compared the ability of a structurally related CHK1 inhibitor, GNE-900, to enhance the in vivo activity of gemcitabine, CPT-11, and temozolomide in xenograft models.	gemcitabine	118-129	checkpoint kinase 1	Homo sapiens	58-62
24038068-7	2013	We finally compared the ability of a structurally related CHK1 inhibitor, GNE-900, to enhance the in vivo activity of gemcitabine, CPT-11, and temozolomide in xenograft models.	Irinotecan	131-137	checkpoint kinase 1	Homo sapiens	58-62
24038068-7	2013	We finally compared the ability of a structurally related CHK1 inhibitor, GNE-900, to enhance the in vivo activity of gemcitabine, CPT-11, and temozolomide in xenograft models.	Temozolomide	143-155	checkpoint kinase 1	Homo sapiens	58-62
23722650-0	2013	Staurosporine is chemoprotective by inducing G1 arrest in a Chk1- and pRb-dependent manner.	Staurosporine	0-13	checkpoint kinase 1	Homo sapiens	60-64
24002546-0	2013	Dihydromyricetin suppresses the proliferation of hepatocellular carcinoma cells by inducing G2/M arrest through the Chk1/Chk2/Cdc25C pathway.	dihydromyricetin	0-16	checkpoint kinase 1	Homo sapiens	116-120
24002546-3	2013	DHM induced G2/M cell-cycle arrest in HepG2 and Hep3B cells by altering the expression of cell cycle proteins such as cyclin A, cyclin B1, Cdk1, p53, Cdc25c, p-Cdc25c Chk1 and Chk, which are critical for G2/M transition.	dihydromyricetin	0-3	checkpoint kinase 1	Homo sapiens	167-171
24002546-6	2013	These findings indicate that DHM inhibits the growth of hepatocellular carcinoma (HCC) cells via G2/M phase cell cycle arrest through Chk1/Chk2/Cdc25C pathway.	dihydromyricetin	29-32	checkpoint kinase 1	Homo sapiens	134-138
23873850-0	2013	Combination drug scheduling defines a "window of opportunity" for chemopotentiation of gemcitabine by an orally bioavailable, selective ChK1 inhibitor, GNE-900.	gemcitabine	87-98	checkpoint kinase 1	Homo sapiens	136-140
23722650-9	2013	Further assessment of this pathway revealed that Chk1 expression and activity were required for the Rb-dependent arrest.	Rubidium	100-102	checkpoint kinase 1	Homo sapiens	49-53
24204313-3	2013	Here, we show that MUS81-induced DSBs are specifically triggered by CHK1 inhibition in a manner that is unrelated to the loss of RAD51, and does not involve formation of a RAD51 substrate.	dsbs	33-37	checkpoint kinase 1	Homo sapiens	68-72
24098799-9	2013	Furthermore, panobinostat treatment resulted in substantial down-regulation of CHK1 and its downstream pathway and abrogation of the G2 cell cycle checkpoint.	Panobinostat	13-25	checkpoint kinase 1	Homo sapiens	79-83
24098799-10	2013	Synergistic antitumor interactions were also observed when the DNA damaging agents were combined with a CHK1-specific inhibitor, LY2603618.	LY2603618	129-138	checkpoint kinase 1	Homo sapiens	104-108
23593991-5	2013	Current clinical trials with Chk1 inhibitors are primarily focusing on their combination with gemcitabine.	gemcitabine	94-105	checkpoint kinase 1	Homo sapiens	29-33
23593991-10	2013	We emphasize the need to assess cell cycle perturbation and Chk1 dependence of tumours in patients administered gemcitabine.	gemcitabine	112-123	checkpoint kinase 1	Homo sapiens	60-64
23852422-9	2013	Finally, increased hydrogen peroxide was found to mediate Chk1 phosphorylation at Ser345, p53 protein induction, cell apoptotic induction, and transformation inhibition following Chel A treatment.	Hydrogen Peroxide	19-36	checkpoint kinase 1	Homo sapiens	58-62
23852422-9	2013	Finally, increased hydrogen peroxide was found to mediate Chk1 phosphorylation at Ser345, p53 protein induction, cell apoptotic induction, and transformation inhibition following Chel A treatment.	chel	179-183	checkpoint kinase 1	Homo sapiens	58-62
23873850-4	2013	Here, we describe the characterization of GNE-900, an ATP-competitive, selective, and orally bioavailable ChK1 inhibitor.	Adenosine Triphosphate	54-57	checkpoint kinase 1	Homo sapiens	106-110
23873850-8	2013	In vivo scheduling studies show that optimal administration of the ChK1 inhibitor requires a defined lag between gemcitabine and GNE-900 administration.	gemcitabine	113-124	checkpoint kinase 1	Homo sapiens	67-71
23873850-10	2013	In summary, we show that in vivo potentiation of gemcitabine activity is mechanism based, with optimal efficacy observed when S-phase arrest and release is followed by checkpoint abrogation with a ChK1 inhibitor.	gemcitabine	49-60	checkpoint kinase 1	Homo sapiens	197-201
23892959-1	2013	PURPOSE: AZD7762, a potent Chk1/Chk2 inhibitor, has shown chemosensitizing activity with gemcitabine in xenograft models.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	9-16	checkpoint kinase 1	Homo sapiens	27-31
23892959-1	2013	PURPOSE: AZD7762, a potent Chk1/Chk2 inhibitor, has shown chemosensitizing activity with gemcitabine in xenograft models.	gemcitabine	89-100	checkpoint kinase 1	Homo sapiens	27-31
23932155-5	2013	Chk1 was inhibited by the selective inhibitor PF-00477736.	pyrazofurin	46-48	checkpoint kinase 1	Homo sapiens	0-4
23693077-3	2013	Activation of ATM and ATR sequentially led to induction of phospho-Chk1/2 and phospho-Cdc25 in response to RB.	retigeric acid B	107-109	checkpoint kinase 1	Homo sapiens	67-73
23530568-6	2013	We report a staged study to address the effects of various aspects of protein flexibility and inclusion of active site water molecules on docking effectiveness to retrieve (and to be able to predict) correct ligand poses and to rank docked ligands in relation to their biological activity for CHK1, ERK2, LpxC, and UPA.	Water	119-124	checkpoint kinase 1	Homo sapiens	293-297
23804422-0	2013	Sensitization of pancreatic cancer to chemoradiation by the Chk1 inhibitor MK8776.	MK-8776	75-81	checkpoint kinase 1	Homo sapiens	60-64
23804422-2	2013	To improve upon this regimen, we combined the selective Checkpoint kinase 1 (Chk1) inhibitor MK8776 with gemcitabine-based chemoradiation in preclinical pancreatic cancer models.	MK-8776	93-99	checkpoint kinase 1	Homo sapiens	56-75
23804422-2	2013	To improve upon this regimen, we combined the selective Checkpoint kinase 1 (Chk1) inhibitor MK8776 with gemcitabine-based chemoradiation in preclinical pancreatic cancer models.	MK-8776	93-99	checkpoint kinase 1	Homo sapiens	77-81
23804422-7	2013	We also assessed pChk1 (S345), a pharmacodynamic biomarker of DNA damage in response to Chk1 inhibition in both tumor and small intestine and found that MK8776 combined with gemcitabine or gemcitabine-radiation produced a significantly greater increase in pChk1 (S345) in tumor relative to small intestine, suggesting greater DNA damage in tumor than in normal tissue.	MK-8776	153-159	checkpoint kinase 1	Homo sapiens	18-22
23687379-9	2013	Our data suggest RAD17 as a novel target protein for gemcitabine combination therapy supplementing or complementing inhibition of CHK1.	gemcitabine	53-64	checkpoint kinase 1	Homo sapiens	130-134
23733185-0	2013	4-Hydroxynonenal induces G2/M phase cell cycle arrest by activation of the ataxia telangiectasia mutated and Rad3-related protein (ATR)/checkpoint kinase 1 (Chk1) signaling pathway.	4-hydroxy-2-nonenal	0-16	checkpoint kinase 1	Homo sapiens	136-155
23733185-0	2013	4-Hydroxynonenal induces G2/M phase cell cycle arrest by activation of the ataxia telangiectasia mutated and Rad3-related protein (ATR)/checkpoint kinase 1 (Chk1) signaling pathway.	4-hydroxy-2-nonenal	0-16	checkpoint kinase 1	Homo sapiens	157-161
23733185-8	2013	HNE-mediated ATR/Chk1 signaling was inhibited by ATR kinase inhibitor (caffeine).	Caffeine	71-79	checkpoint kinase 1	Homo sapiens	17-21
23550703-6	2013	These systematic analyses identified a total of 27 Ser/Thr residues as Chk1- or Chk2- target sites.	Serine	51-54	checkpoint kinase 1	Homo sapiens	71-75
23839309-0	2013	Chk1/2 inhibition overcomes the cisplatin resistance of head and neck cancer cells secondary to the loss of functional p53.	Cisplatin	32-41	checkpoint kinase 1	Homo sapiens	0-4
23861943-5	2013	Here we show that Chk1 phosphorylates rat CK1delta at serine residues 328, 331, 370, and threonine residue 397 as well as the human CK1delta transcription variants 1 and 2.	Serine	54-60	checkpoint kinase 1	Homo sapiens	18-22
23861943-5	2013	Here we show that Chk1 phosphorylates rat CK1delta at serine residues 328, 331, 370, and threonine residue 397 as well as the human CK1delta transcription variants 1 and 2.	Threonine	89-98	checkpoint kinase 1	Homo sapiens	18-22
23849174-2	2013	We have now evaluated NIS-expressing oncolytic measles virus (MV-NIS) combined with NIS-guided radioiodide, EBRT and specific checkpoint kinase 1 (Chk1) inhibition in head and neck and colorectal models.	Nickel	22-25	checkpoint kinase 1	Homo sapiens	147-151
23548269-4	2013	In contrast, while cisplatin, topotecan, and gemcitabine each activated Chk1, RNAi-mediated depletion or inhibition of this kinase in cells sensitized them only to gemcitabine.	Cisplatin	19-28	checkpoint kinase 1	Homo sapiens	72-76
23548269-4	2013	In contrast, while cisplatin, topotecan, and gemcitabine each activated Chk1, RNAi-mediated depletion or inhibition of this kinase in cells sensitized them only to gemcitabine.	Topotecan	30-39	checkpoint kinase 1	Homo sapiens	72-76
23548269-4	2013	In contrast, while cisplatin, topotecan, and gemcitabine each activated Chk1, RNAi-mediated depletion or inhibition of this kinase in cells sensitized them only to gemcitabine.	gemcitabine	45-56	checkpoint kinase 1	Homo sapiens	72-76
23550703-6	2013	These systematic analyses identified a total of 27 Ser/Thr residues as Chk1- or Chk2- target sites.	Threonine	55-58	checkpoint kinase 1	Homo sapiens	71-75
23667469-0	2013	Early Chk1 phosphorylation is driven by temozolomide-induced, DNA double strand break- and mismatch repair-independent DNA damage.	Temozolomide	40-52	checkpoint kinase 1	Homo sapiens	6-10
23536721-0	2013	The novel Chk1 inhibitor MK-8776 sensitizes human leukemia cells to HDAC inhibitors by targeting the intra-S checkpoint and DNA replication and repair.	MK-8776	25-32	checkpoint kinase 1	Homo sapiens	10-14
23536721-1	2013	Interactions between the novel Chk1 inhibitor MK-8776 and the histone deacetylase (HDAC) inhibitor (HDACI) vorinostat were examined in human leukemia cells harboring wild-type (wt) or deficient p53.	MK-8776	46-53	checkpoint kinase 1	Homo sapiens	31-35
23536721-8	2013	Together, these findings indicate that the novel Chk1 inhibitor MK-8776 markedly potentiates HDACI lethality in leukemia cells displaying various genetic backgrounds through mechanisms involving disruption of the intra-S checkpoint, DNA replication, and DNA repair.	MK-8776	64-71	checkpoint kinase 1	Homo sapiens	49-53
23587425-0	2013	Potency switch between CHK1 and MK2: discovery of imidazo[1,2-a]pyrazine- and imidazo[1,2-c]pyrimidine-based kinase inhibitors.	imidazo(1,2-a)pyrazine	50-72	checkpoint kinase 1	Homo sapiens	23-27
23587425-0	2013	Potency switch between CHK1 and MK2: discovery of imidazo[1,2-a]pyrazine- and imidazo[1,2-c]pyrimidine-based kinase inhibitors.	imidazo(1,2-c)pyrimidine	78-102	checkpoint kinase 1	Homo sapiens	23-27
23667469-5	2013	Furthermore, TMZ-induced early phosphorylation of Chk1 was noted in glioma cells regardless of whether they were MGMT-proficient or MGMT-deficient, and regardless of their MMR status.	Temozolomide	13-16	checkpoint kinase 1	Homo sapiens	50-54
23535330-0	2013	Structure-based design and optimization of 2-aminothiazole-4-carboxamide as a new class of CHK1 inhibitors.	2-aminothiazole-4-carboxamide	43-72	checkpoint kinase 1	Homo sapiens	91-95
23535330-1	2013	Drug design efforts in the emerging 2-aminothiazole-4-carboxamide class of CHK1 inhibitors have uncovered specific combinations of key substructures within the molecule; resulting in significant improvements in cell-based activity while retaining a greater than one hundred-fold selectivity against CDK2.	2-aminothiazole-4-carboxamide	36-65	checkpoint kinase 1	Homo sapiens	75-79
23535330-2	2013	The X-ray crystal structure of a complex between compound 39 and the CHK1 protein detailing a "U-shaped" topology and key interactions with the protein surface at the ATP site is also reported.	Adenosine Triphosphate	167-170	checkpoint kinase 1	Homo sapiens	69-73
23917378-2	2013	PARP1 inhibitors [AZD2281 ; ABT888 ; NU1025 ; AG014699] interacted with CHK1 inhibitors [UCN-01 ; AZD7762 ; LY2603618] to kill mammary carcinoma cells.	olaparib	18-25	checkpoint kinase 1	Homo sapiens	72-76
23917378-2	2013	PARP1 inhibitors [AZD2281 ; ABT888 ; NU1025 ; AG014699] interacted with CHK1 inhibitors [UCN-01 ; AZD7762 ; LY2603618] to kill mammary carcinoma cells.	veliparib	28-34	checkpoint kinase 1	Homo sapiens	72-76
23917378-2	2013	PARP1 inhibitors [AZD2281 ; ABT888 ; NU1025 ; AG014699] interacted with CHK1 inhibitors [UCN-01 ; AZD7762 ; LY2603618] to kill mammary carcinoma cells.	NU 1025	37-43	checkpoint kinase 1	Homo sapiens	72-76
23917378-2	2013	PARP1 inhibitors [AZD2281 ; ABT888 ; NU1025 ; AG014699] interacted with CHK1 inhibitors [UCN-01 ; AZD7762 ; LY2603618] to kill mammary carcinoma cells.	rucaparib	46-54	checkpoint kinase 1	Homo sapiens	72-76
23917378-2	2013	PARP1 inhibitors [AZD2281 ; ABT888 ; NU1025 ; AG014699] interacted with CHK1 inhibitors [UCN-01 ; AZD7762 ; LY2603618] to kill mammary carcinoma cells.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	98-105	checkpoint kinase 1	Homo sapiens	72-76
23917378-2	2013	PARP1 inhibitors [AZD2281 ; ABT888 ; NU1025 ; AG014699] interacted with CHK1 inhibitors [UCN-01 ; AZD7762 ; LY2603618] to kill mammary carcinoma cells.	LY2603618	108-117	checkpoint kinase 1	Homo sapiens	72-76
23635654-6	2013	Treatment with CHK1 inhibitors during acute or prolonged hypoxia (< 0.03%, 0.2%, and 1% O2; 3 h or 20-24 h) gave similar effects on cell survival as treatment with these inhibitors during normoxia.	Oxygen	91-93	checkpoint kinase 1	Homo sapiens	15-19
23478633-9	2013	NAP photosensitization with UVA led to protein S-glutathionylation, oxidation of the proliferating cell nuclear antigen (PCNA), oxidation of cellular tryptophan, phosphorylation of Chk1 and inhibition of DNA replication.	Naproxen	0-3	checkpoint kinase 1	Homo sapiens	181-185
23478633-11	2013	Nevertheless, inhibition of Chk1, but not of p38, sensitized the cells to the phototoxic effects of NAP.	Naproxen	100-103	checkpoint kinase 1	Homo sapiens	28-32
23667469-6	2013	Early Chk1 phosphorylation was not associated with TMZ-induced reactive oxygen species, but was temporally associated with TMZ-induced alkalai-labile DNA damage produced by the non-O6-methylguanine DNA adducts and which, like Chk1 phosphorylation, was transient in MGMT-proficient cells but persistent in MGMT-deficient cells.	Temozolomide	123-126	checkpoint kinase 1	Homo sapiens	6-10
23667469-6	2013	Early Chk1 phosphorylation was not associated with TMZ-induced reactive oxygen species, but was temporally associated with TMZ-induced alkalai-labile DNA damage produced by the non-O6-methylguanine DNA adducts and which, like Chk1 phosphorylation, was transient in MGMT-proficient cells but persistent in MGMT-deficient cells.	Temozolomide	123-126	checkpoint kinase 1	Homo sapiens	226-230
23667469-6	2013	Early Chk1 phosphorylation was not associated with TMZ-induced reactive oxygen species, but was temporally associated with TMZ-induced alkalai-labile DNA damage produced by the non-O6-methylguanine DNA adducts and which, like Chk1 phosphorylation, was transient in MGMT-proficient cells but persistent in MGMT-deficient cells.	O-(6)-methylguanine	181-197	checkpoint kinase 1	Homo sapiens	6-10
23667469-7	2013	These results re-define the TMZ-induced DNA damage response, and show that Chk1 phosphorylation is driven by TMZ-induced mismatch repair-independent DNA damage independently of DNA double strand breaks, Chk2 activation, and cell cycle arrest, and as such is a suboptimal biomarker of TMZ-induced drug action.	Temozolomide	28-31	checkpoint kinase 1	Homo sapiens	75-79
23620807-0	2013	Toxic effect of silica nanoparticles on endothelial cells through DNA damage response via Chk1-dependent G2/M checkpoint.	Silicon Dioxide	16-22	checkpoint kinase 1	Homo sapiens	90-94
23620807-9	2013	Silica nanoparticles also induced G2/M arrest through the upregulation of Chk1 and the downregulation of Cdc25C, cyclin B1/Cdc2.	Silicon Dioxide	0-6	checkpoint kinase 1	Homo sapiens	74-78
23620807-10	2013	In summary, our data indicated that the toxic effect mechanisms of silica nanoparticles on endothelial cells was through DNA damage response (DDR) via Chk1-dependent G2/M checkpoint signaling pathway, suggesting that exposure to silica nanoparticles could be a potential hazards for the development of cardiovascular diseases.	Silicon Dioxide	67-73	checkpoint kinase 1	Homo sapiens	151-155
23620807-10	2013	In summary, our data indicated that the toxic effect mechanisms of silica nanoparticles on endothelial cells was through DNA damage response (DDR) via Chk1-dependent G2/M checkpoint signaling pathway, suggesting that exposure to silica nanoparticles could be a potential hazards for the development of cardiovascular diseases.	Silicon Dioxide	229-235	checkpoint kinase 1	Homo sapiens	151-155
23533280-1	2013	B-cell translocation gene 3 (BTG3) is a member of the antiproliferative BTG/ Transducer of ErbB2 gene family and is induced by genotoxic stress in a p53- and Checkpoint kinase 1 (CHK1)-dependent manner.	beta-2'-deoxythioguanosine	29-32	checkpoint kinase 1	Homo sapiens	158-177
23533280-1	2013	B-cell translocation gene 3 (BTG3) is a member of the antiproliferative BTG/ Transducer of ErbB2 gene family and is induced by genotoxic stress in a p53- and Checkpoint kinase 1 (CHK1)-dependent manner.	beta-2'-deoxythioguanosine	29-32	checkpoint kinase 1	Homo sapiens	179-183
23337567-8	2013	Additionally, these effects of ATO on gamma-H2AX, Chk1, Chk2, p53, and p21(waf1/cip1) were reduced by an ATM inhibitor.	Arsenic Trioxide	31-34	checkpoint kinase 1	Homo sapiens	50-54
23275151-7	2013	Furthermore, mechanistic studies indicated that combined PARP inhibitor and cisplatin could lead to sustained DNA double-strand breaks, prolonged G2/M cell cycle arrest with distinct activation of checkpoint kinase 1 signaling and more pronounced apoptosis preferentially in lung cancer cells with low ERCC1 expression.	Cisplatin	76-85	checkpoint kinase 1	Homo sapiens	197-216
23544166-3	2013	EXPERIMENTAL DESIGN: We evaluated a specific small molecule inhibitor of Chk1/2, AZD7762, in combination with radiation using in vitro human cell lines and in vivo using a genetically engineered GBM mouse model.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	81-88	checkpoint kinase 1	Homo sapiens	73-77
23200172-4	2013	(212)Pb-TCMC-trastuzumab after gemcitabine pretreatment abrogated G2/M arrest at the same time points, which may be associated with the inhibition of Chk1 phosphorylation and, in turn, cell cycle perturbation, resulting in apoptosis.	(212)pb-tcmc	0-12	checkpoint kinase 1	Homo sapiens	150-154
23200172-4	2013	(212)Pb-TCMC-trastuzumab after gemcitabine pretreatment abrogated G2/M arrest at the same time points, which may be associated with the inhibition of Chk1 phosphorylation and, in turn, cell cycle perturbation, resulting in apoptosis.	gemcitabine	31-42	checkpoint kinase 1	Homo sapiens	150-154
23321637-4	2013	Phosphorylation of Aurora-B at serine 331 (Ser331) by Chk1 is high in prometaphase and decreases significantly in metaphase cells.	Serine	31-37	checkpoint kinase 1	Homo sapiens	54-58
23739596-5	2013	At the same time, GN, but not gamma-Sch, inhibited the phosphorylation of checkpoint proteins such as p53, structural maintenance of chromosomes 1, and checkpoint kinase 1 in UV-irradiated cells.	schizandrin B	18-20	checkpoint kinase 1	Homo sapiens	152-171
23541946-6	2013	Chidamide enhanced gemcitabine-induced DNA double-strand breaks and S phase arrest, and abrogated the G2/M cell cycle checkpoint, potentially through suppression of CHK1 expression.	N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide	0-9	checkpoint kinase 1	Homo sapiens	165-169
23253900-10	2013	We observed that 5-FU treatment induced an enhanced S-phase arrest and CHK1 activation plus an increase in the formation of strand breaks and alkali-labile sites in all sublines.	Fluorouracil	17-21	checkpoint kinase 1	Homo sapiens	71-75
23667469-7	2013	These results re-define the TMZ-induced DNA damage response, and show that Chk1 phosphorylation is driven by TMZ-induced mismatch repair-independent DNA damage independently of DNA double strand breaks, Chk2 activation, and cell cycle arrest, and as such is a suboptimal biomarker of TMZ-induced drug action.	Temozolomide	109-112	checkpoint kinase 1	Homo sapiens	75-79
23667469-7	2013	These results re-define the TMZ-induced DNA damage response, and show that Chk1 phosphorylation is driven by TMZ-induced mismatch repair-independent DNA damage independently of DNA double strand breaks, Chk2 activation, and cell cycle arrest, and as such is a suboptimal biomarker of TMZ-induced drug action.	Temozolomide	109-112	checkpoint kinase 1	Homo sapiens	75-79
22086611-7	2013	However, quercetin-3-methyl ether caused a pronounced G(2)/M block mainly through the Chk1-Cdc25c-cyclin B1/Cdk1 pathway in lapatinib-sensitive and -resistant cells.	quercetin 3-O-methyl ether	9-33	checkpoint kinase 1	Homo sapiens	86-90
22086611-7	2013	However, quercetin-3-methyl ether caused a pronounced G(2)/M block mainly through the Chk1-Cdc25c-cyclin B1/Cdk1 pathway in lapatinib-sensitive and -resistant cells.	Lapatinib	124-133	checkpoint kinase 1	Homo sapiens	86-90
23220466-5	2013	Persistent activation of checkpoint kinase 1 (Chk1) was observed at significantly lower BP equivalent concentrations in air PM extracts than BP alone.	Benzo(a)pyrene	88-90	checkpoint kinase 1	Homo sapiens	25-44
23220466-5	2013	Persistent activation of checkpoint kinase 1 (Chk1) was observed at significantly lower BP equivalent concentrations in air PM extracts than BP alone.	Benzo(a)pyrene	88-90	checkpoint kinase 1	Homo sapiens	46-50
23220466-5	2013	Persistent activation of checkpoint kinase 1 (Chk1) was observed at significantly lower BP equivalent concentrations in air PM extracts than BP alone.	Benzo(a)pyrene	141-143	checkpoint kinase 1	Homo sapiens	25-44
23220466-5	2013	Persistent activation of checkpoint kinase 1 (Chk1) was observed at significantly lower BP equivalent concentrations in air PM extracts than BP alone.	Benzo(a)pyrene	141-143	checkpoint kinase 1	Homo sapiens	46-50
23220710-6	2013	The reduction in expression of cyclin B1 protein and the increased activity of reactive oxygen species were observed in BGC823 cells treated with 12-deoxyphorbol 13-palmitate for 24 h. In addition, we found down-regulation of cdc2/cyclin B, cyclin A and p-chk1 in tumor cells.	Reactive Oxygen Species	79-102	checkpoint kinase 1	Homo sapiens	256-260
23220710-6	2013	The reduction in expression of cyclin B1 protein and the increased activity of reactive oxygen species were observed in BGC823 cells treated with 12-deoxyphorbol 13-palmitate for 24 h. In addition, we found down-regulation of cdc2/cyclin B, cyclin A and p-chk1 in tumor cells.	12-deoxyphorbol 13-palmitate	146-174	checkpoint kinase 1	Homo sapiens	256-260
23390564-11	2013	Either cladribine or bendamustine led to a remarkable increase of the phosphorylated H2A.X, CHK1 and CHK2 in both MM1.S and MM1.R cells, suggesting an induction of DNA damage response.	Cladribine	7-17	checkpoint kinase 1	Homo sapiens	92-96
23390564-11	2013	Either cladribine or bendamustine led to a remarkable increase of the phosphorylated H2A.X, CHK1 and CHK2 in both MM1.S and MM1.R cells, suggesting an induction of DNA damage response.	Bendamustine Hydrochloride	21-33	checkpoint kinase 1	Homo sapiens	92-96
23242585-4	2013	UCN-01, a non-selective Chk1 inhibitor, combined with irinotecan demonstrated activity in advanced TNBC in our Phase I study.	7-hydroxystaurosporine	0-6	checkpoint kinase 1	Homo sapiens	24-28
23242585-13	2013	Immunostains of gammaH2AX and pChk1(S296) on serial tumor biopsies from four patients demonstrated an induction of DNA damage and Chk1 activation following irinotecan.	Irinotecan	156-166	checkpoint kinase 1	Homo sapiens	31-35
24356582-0	2013	Poly(ADP-ribose) binding to Chk1 at stalled replication forks is required for S-phase checkpoint activation.	Poly Adenosine Diphosphate Ribose	0-16	checkpoint kinase 1	Homo sapiens	28-32
24005565-7	2013	After treatment with MMC, reduced phosphorylation of the ATR substrate CHK1 occurs in HELQ-knockout cells, and accumulation of G2/M cells is reduced.	Mitomycin	21-24	checkpoint kinase 1	Homo sapiens	71-75
23483975-0	2013	A kinome screen identifies checkpoint kinase 1 (CHK1) as a sensitizer for RRM1-dependent gemcitabine efficacy.	gemcitabine	89-100	checkpoint kinase 1	Homo sapiens	27-46
23483975-0	2013	A kinome screen identifies checkpoint kinase 1 (CHK1) as a sensitizer for RRM1-dependent gemcitabine efficacy.	gemcitabine	89-100	checkpoint kinase 1	Homo sapiens	48-52
23483975-7	2013	CHK1 was identified has the kinase with the most significant and robust interaction, and it was validated using AZD7762, a small-molecule ATP-competitive inhibitor of CHK1 activation.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	112-119	checkpoint kinase 1	Homo sapiens	0-4
23483975-7	2013	CHK1 was identified has the kinase with the most significant and robust interaction, and it was validated using AZD7762, a small-molecule ATP-competitive inhibitor of CHK1 activation.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	112-119	checkpoint kinase 1	Homo sapiens	167-171
23483975-7	2013	CHK1 was identified has the kinase with the most significant and robust interaction, and it was validated using AZD7762, a small-molecule ATP-competitive inhibitor of CHK1 activation.	Adenosine Triphosphate	138-141	checkpoint kinase 1	Homo sapiens	0-4
23483975-7	2013	CHK1 was identified has the kinase with the most significant and robust interaction, and it was validated using AZD7762, a small-molecule ATP-competitive inhibitor of CHK1 activation.	Adenosine Triphosphate	138-141	checkpoint kinase 1	Homo sapiens	167-171
23483975-8	2013	Synergism between CHK1 inhibition and RRM1-dependent gemcitabine efficacy was observed in cells with high RRM1 levels, while antagonism was observed in cells with low RRM1 levels.	gemcitabine	53-64	checkpoint kinase 1	Homo sapiens	18-22
23483975-9	2013	In addition, four cell lines with natural gemcitabine resistance demonstrated improved gemcitabine efficacy after CHK1 inhibition.	gemcitabine	42-53	checkpoint kinase 1	Homo sapiens	114-118
23483975-9	2013	In addition, four cell lines with natural gemcitabine resistance demonstrated improved gemcitabine efficacy after CHK1 inhibition.	gemcitabine	87-98	checkpoint kinase 1	Homo sapiens	114-118
23483975-11	2013	We conclude that inhibition of CHK1 may have its greatest clinical utility in malignancies where gemcitabine resistance is a result of elevated RRM1 levels.	gemcitabine	97-108	checkpoint kinase 1	Homo sapiens	31-35
23483975-12	2013	We also conclude that CHK1 inhibition in tumors with low RRM1 levels may be detrimental to gemcitabine efficacy.	gemcitabine	91-102	checkpoint kinase 1	Homo sapiens	22-26
23451128-5	2013	Cell cycle arrest induced by alpha-santalol was associated with changes in the protein levels of BRCA1, Chk1, G2/M regulatory cyclins, Cyclin dependent kinases (CDKs), Cell division cycle 25B (Cdc25B), Cdc25C and Ser-216 phosphorylation of Cdc25C.	a-santalol	29-43	checkpoint kinase 1	Homo sapiens	104-108
23359652-7	2013	SB225002-induced mitotic catastrophe appeared to be mediated by down-regulation of checkpoint kinase Chk1 and Cdk1-cyclin B activation.	SB 225002	0-8	checkpoint kinase 1	Homo sapiens	101-105
22492020-1	2013	PURPOSE: This phase I study aims at assessing the safety and tolerability of LY2603618, a selective inhibitor of Checkpoint Kinase 1, in combination with pemetrexed and determining the maximum tolerable dose and the pharmacokinetic parameters.	LY2603618	77-86	checkpoint kinase 1	Homo sapiens	113-132
23092873-1	2012	PURPOSE: Incorporation of cytarabine into DNA activates checkpoint kinase 1 (Chk1), which stabilizes stalled replication forks, induces S-phase slowing, and diminishes cytarabine cytotoxicity.	Cytarabine	26-36	checkpoint kinase 1	Homo sapiens	56-75
23092873-1	2012	PURPOSE: Incorporation of cytarabine into DNA activates checkpoint kinase 1 (Chk1), which stabilizes stalled replication forks, induces S-phase slowing, and diminishes cytarabine cytotoxicity.	Cytarabine	26-36	checkpoint kinase 1	Homo sapiens	77-81
23092873-1	2012	PURPOSE: Incorporation of cytarabine into DNA activates checkpoint kinase 1 (Chk1), which stabilizes stalled replication forks, induces S-phase slowing, and diminishes cytarabine cytotoxicity.	Cytarabine	168-178	checkpoint kinase 1	Homo sapiens	56-75
23092873-1	2012	PURPOSE: Incorporation of cytarabine into DNA activates checkpoint kinase 1 (Chk1), which stabilizes stalled replication forks, induces S-phase slowing, and diminishes cytarabine cytotoxicity.	Cytarabine	168-178	checkpoint kinase 1	Homo sapiens	77-81
23092873-2	2012	The selective Chk1 inhibitor SCH 900776 abrogates cytarabine-induced S-phase arrest and enhances cytarabine cytotoxicity in acute leukemia cell lines and leukemic blasts in vitro.	MK-8776	29-39	checkpoint kinase 1	Homo sapiens	14-18
23092873-2	2012	The selective Chk1 inhibitor SCH 900776 abrogates cytarabine-induced S-phase arrest and enhances cytarabine cytotoxicity in acute leukemia cell lines and leukemic blasts in vitro.	Cytarabine	50-60	checkpoint kinase 1	Homo sapiens	14-18
23092873-2	2012	The selective Chk1 inhibitor SCH 900776 abrogates cytarabine-induced S-phase arrest and enhances cytarabine cytotoxicity in acute leukemia cell lines and leukemic blasts in vitro.	Cytarabine	97-107	checkpoint kinase 1	Homo sapiens	14-18
23082860-0	2012	Discovery of 3-alkoxyamino-5-(pyridin-2-ylamino)pyrazine-2-carbonitriles as selective, orally bioavailable CHK1 inhibitors.	3-alkoxyamino-5-(pyridin-2-ylamino)pyrazine-2-carbonitriles	13-72	checkpoint kinase 1	Homo sapiens	107-111
23082860-2	2012	A novel series of potent and orally bioavailable 3-alkoxyamino-5-(pyridin-2-ylamino)pyrazine-2-carbonitrile CHK1 inhibitors was generated by hybridization of two lead scaffolds derived from fragment-based drug design and optimized for CHK1 potency and high selectivity using a cell-based assay cascade.	3-alkoxyamino-5-(pyridin-2-ylamino)pyrazine-2-carbonitrile	49-107	checkpoint kinase 1	Homo sapiens	108-112
23082860-2	2012	A novel series of potent and orally bioavailable 3-alkoxyamino-5-(pyridin-2-ylamino)pyrazine-2-carbonitrile CHK1 inhibitors was generated by hybridization of two lead scaffolds derived from fragment-based drug design and optimized for CHK1 potency and high selectivity using a cell-based assay cascade.	3-alkoxyamino-5-(pyridin-2-ylamino)pyrazine-2-carbonitrile	49-107	checkpoint kinase 1	Homo sapiens	235-239
23082860-4	2012	The optimized compound (CCT244747) was a potent and highly selective CHK1 inhibitor, which modulated the DNA damage response pathway in human tumor xenografts and showed antitumor activity in combination with genotoxic chemotherapies and as a single agent.	3-((1-(dimethylamino)propan-2-yl)oxy)-5-((4-methoxy-5-(1-methyl-1H-pyrazol-4-yl)pyridin-2-yl)amino)pyrazine-2-carbonitrile	24-33	checkpoint kinase 1	Homo sapiens	69-73
23359652-12	2013	The present studies demonstrate for the first time that SB225002 has dual actions in OVCA cells, inducing classic apoptosis through p53 activation and provoking mitotic catastrophe in both p53 wild-type and deficient cells by Chk1 inhibition and Cdk activation.	SB 225002	56-64	checkpoint kinase 1	Homo sapiens	226-230
22942255-0	2012	Cisplatin sensitivity mediated by WEE1 and CHK1 is mediated by miR-155 and the miR-15 family.	Cisplatin	0-9	checkpoint kinase 1	Homo sapiens	43-47
22942255-3	2012	Overexpression of the cell-cycle kinases WEE1 and CHK1 occurred commonly in cisplatin-resistant cells.	Cisplatin	76-85	checkpoint kinase 1	Homo sapiens	50-54
22942255-4	2012	miRNAs in the miR-15/16/195/424/497 family were found to sensitize cisplatin-resistant cells to apoptosis by targeting WEE1 and CHK1.	Cisplatin	67-76	checkpoint kinase 1	Homo sapiens	128-132
23148684-5	2012	METHODS: Small molecules MK-8776 and MK-1775 were used to selectively and potently inhibit CHK1 and WEE1, respectively.	MK-8776	25-32	checkpoint kinase 1	Homo sapiens	91-95
23148684-5	2012	METHODS: Small molecules MK-8776 and MK-1775 were used to selectively and potently inhibit CHK1 and WEE1, respectively.	adavosertib	37-44	checkpoint kinase 1	Homo sapiens	91-95
22743332-5	2012	Here we report that BRCA1 is critical for Chk1 phosphorylation in response to inhibition of replication by either cisplatin or hydroxyurea.	Cisplatin	114-123	checkpoint kinase 1	Homo sapiens	42-46
22743332-5	2012	Here we report that BRCA1 is critical for Chk1 phosphorylation in response to inhibition of replication by either cisplatin or hydroxyurea.	Hydroxyurea	127-138	checkpoint kinase 1	Homo sapiens	42-46
22743332-8	2012	Inhibition of Chk1 kinase by UCN-01 or expression of Chk1 phosphorylation mutants in which the serine residues were substituted with alanine residues abrogates BRCA1-dependent cell cycle arrest in response replication inhibition.	Serine	95-101	checkpoint kinase 1	Homo sapiens	14-18
22743332-8	2012	Inhibition of Chk1 kinase by UCN-01 or expression of Chk1 phosphorylation mutants in which the serine residues were substituted with alanine residues abrogates BRCA1-dependent cell cycle arrest in response replication inhibition.	Serine	95-101	checkpoint kinase 1	Homo sapiens	53-57
22743332-8	2012	Inhibition of Chk1 kinase by UCN-01 or expression of Chk1 phosphorylation mutants in which the serine residues were substituted with alanine residues abrogates BRCA1-dependent cell cycle arrest in response replication inhibition.	Alanine	133-140	checkpoint kinase 1	Homo sapiens	14-18
22743332-8	2012	Inhibition of Chk1 kinase by UCN-01 or expression of Chk1 phosphorylation mutants in which the serine residues were substituted with alanine residues abrogates BRCA1-dependent cell cycle arrest in response replication inhibition.	Alanine	133-140	checkpoint kinase 1	Homo sapiens	53-57
22417805-5	2012	We assessed the effect of garcinol on the cell cycle checkpoint after IR treatment by analyzing the phosphorylation levels of checkpoint kinases CHK1 and CHK2 and histone H3, and by cell cycle profile analysis using flow cytometry.	garcinol	26-34	checkpoint kinase 1	Homo sapiens	145-149
23076878-4	2012	Phosphorylation of H2AX, Chk1, and RPA2 was more strongly activated in K562 cells than in hMSCs, at equivalent doses of doxorubicin.	Doxorubicin	120-131	checkpoint kinase 1	Homo sapiens	25-29
22929806-0	2012	CCT244747 is a novel potent and selective CHK1 inhibitor with oral efficacy alone and in combination with genotoxic anticancer drugs.	3-((1-(dimethylamino)propan-2-yl)oxy)-5-((4-methoxy-5-(1-methyl-1H-pyrazol-4-yl)pyridin-2-yl)amino)pyrazine-2-carbonitrile	0-9	checkpoint kinase 1	Homo sapiens	42-46
22929806-3	2012	We have therefore discovered a novel potent, highly selective, orally active ATP-competitive CHK1 inhibitor, CCT244747, and present its preclinical pharmacology and therapeutic activity.	Adenosine Triphosphate	77-80	checkpoint kinase 1	Homo sapiens	93-97
22929806-3	2012	We have therefore discovered a novel potent, highly selective, orally active ATP-competitive CHK1 inhibitor, CCT244747, and present its preclinical pharmacology and therapeutic activity.	3-((1-(dimethylamino)propan-2-yl)oxy)-5-((4-methoxy-5-(1-methyl-1H-pyrazol-4-yl)pyridin-2-yl)amino)pyrazine-2-carbonitrile	109-118	checkpoint kinase 1	Homo sapiens	93-97
22929806-10	2012	The antitumor activity of both gemcitabine and irinotecan were significantly enhanced by CCT244747 in several human tumor xenografts, giving concomitant biomarker modulation indicative of CHK1 inhibition.	gemcitabine	31-42	checkpoint kinase 1	Homo sapiens	188-192
22929806-10	2012	The antitumor activity of both gemcitabine and irinotecan were significantly enhanced by CCT244747 in several human tumor xenografts, giving concomitant biomarker modulation indicative of CHK1 inhibition.	Irinotecan	47-57	checkpoint kinase 1	Homo sapiens	188-192
22869869-0	2012	Effects of selective checkpoint kinase 1 inhibition on cytarabine cytotoxicity in acute myelogenous leukemia cells in vitro.	Cytarabine	55-65	checkpoint kinase 1	Homo sapiens	21-40
22869869-1	2012	PURPOSE: Previous studies have shown that the replication checkpoint, which involves the kinases ataxia telangiectasia mutated and Rad3 related (ATR) and Chk1, contributes to cytarabine resistance in cell lines.	Cytarabine	175-185	checkpoint kinase 1	Homo sapiens	154-158
22869869-2	2012	In the present study, we examined whether this checkpoint is activated in clinical acute myelogenous leukemia (AML) during cytarabine infusion in vivo and then assessed the impact of combining cytarabine with the recently described Chk1 inhibitor SCH 900776 in vitro.	MK-8776	247-257	checkpoint kinase 1	Homo sapiens	232-236
22869869-6	2012	RESULTS: Immunoblotting revealed increased Chk1 phosphorylation, a marker of checkpoint activation, in more than half of Chk1-containing AMLs after 48 hours of cytarabine infusion.	Cytarabine	160-170	checkpoint kinase 1	Homo sapiens	43-47
22869869-6	2012	RESULTS: Immunoblotting revealed increased Chk1 phosphorylation, a marker of checkpoint activation, in more than half of Chk1-containing AMLs after 48 hours of cytarabine infusion.	Cytarabine	160-170	checkpoint kinase 1	Homo sapiens	121-125
22869869-7	2012	In human AML lines, SCH 900776 not only disrupted cytarabine-induced Chk1 activation and S-phase arrest but also markedly increased cytarabine-induced apoptosis.	Cytarabine	50-60	checkpoint kinase 1	Homo sapiens	69-73
22869869-9	2012	CONCLUSIONS: These results not only provide evidence for cytarabine-induced S-phase checkpoint activation in AML in the clinical setting, but also show that a selective Chk1 inhibitor can overcome the S-phase checkpoint and enhance the cytotoxicity of cytarabine.	Cytarabine	57-67	checkpoint kinase 1	Homo sapiens	169-173
22869869-9	2012	CONCLUSIONS: These results not only provide evidence for cytarabine-induced S-phase checkpoint activation in AML in the clinical setting, but also show that a selective Chk1 inhibitor can overcome the S-phase checkpoint and enhance the cytotoxicity of cytarabine.	Cytarabine	252-262	checkpoint kinase 1	Homo sapiens	169-173
22825736-0	2012	The Chk1 inhibitor AZD7762 sensitises p53 mutant breast cancer cells to radiation in vitro and in vivo.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	19-26	checkpoint kinase 1	Homo sapiens	4-8
22858649-7	2012	In contrast, protein expression levels of the Chk1, Wee1, LC3-II, Beclin-1, Atg 5, Atg 7 and Atg 12 were upregulated in SK-HEP-1 cells after bufalin treatment.	bufalin	141-148	checkpoint kinase 1	Homo sapiens	46-50
22825736-1	2012	AZD7762, a novel checkpoint kinase 1 (Chk 1)inhibitor, has been proven to sensitize various tumor cells to DNA damage.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	0-7	checkpoint kinase 1	Homo sapiens	17-36
22825736-1	2012	AZD7762, a novel checkpoint kinase 1 (Chk 1)inhibitor, has been proven to sensitize various tumor cells to DNA damage.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	0-7	checkpoint kinase 1	Homo sapiens	38-43
22753029-2	2012	The checkpoint kinase, CHK1 has been shown to stabilize replication forks following hydroxyurea treatment.	Hydroxyurea	84-95	checkpoint kinase 1	Homo sapiens	23-27
22825331-6	2012	VE-821 inhibited radiation- and gemcitabine-induced phosphorylation of Chk1, confirming inhibition of ATR signaling.	3-amino-6-(4-(methylsulfonyl)phenyl)-N-phenylpyrazine-2-carboxamide	0-6	checkpoint kinase 1	Homo sapiens	71-75
22825331-6	2012	VE-821 inhibited radiation- and gemcitabine-induced phosphorylation of Chk1, confirming inhibition of ATR signaling.	gemcitabine	32-43	checkpoint kinase 1	Homo sapiens	71-75
22753029-3	2012	Therefore, we wanted to test if the increased UV sensitivity caused by the unspecific kinase inhibitor caffeine--inhibiting ATM and ATR amongst other kinases--is explained by inability to activate the CHK1 kinase to stabilize replicative structures.	Caffeine	103-111	checkpoint kinase 1	Homo sapiens	201-205
22095529-5	2012	Finally, we assayed the ability of RSV in modulating the expression of target proteins involved in DNA damage signalling, namely ATR, ATM, Chk1, Chk2 and gammaH2AX.	Resveratrol	35-38	checkpoint kinase 1	Homo sapiens	139-143
22842784-5	2012	CHK1/CHK2-dependent phosphorylation of CDC25C at Ser 216 is required for CDC25C nuclear export and destruction, which in turn acts to sustain the G2/M arrest elicited by TRF2- or POT1-depleted telomeres.	Serine	49-52	checkpoint kinase 1	Homo sapiens	0-4
22855742-2	2012	Phosphorylation of Chk1 at 2 Ser/Gln (SQ) sites, Ser-317 and Ser-345, by the upstream kinase ATR is critical for checkpoint activation.	Serine	29-32	checkpoint kinase 1	Homo sapiens	19-23
22855742-2	2012	Phosphorylation of Chk1 at 2 Ser/Gln (SQ) sites, Ser-317 and Ser-345, by the upstream kinase ATR is critical for checkpoint activation.	Glutamine	33-36	checkpoint kinase 1	Homo sapiens	19-23
22855742-2	2012	Phosphorylation of Chk1 at 2 Ser/Gln (SQ) sites, Ser-317 and Ser-345, by the upstream kinase ATR is critical for checkpoint activation.	Serine	49-52	checkpoint kinase 1	Homo sapiens	19-23
22855742-2	2012	Phosphorylation of Chk1 at 2 Ser/Gln (SQ) sites, Ser-317 and Ser-345, by the upstream kinase ATR is critical for checkpoint activation.	Serine	49-52	checkpoint kinase 1	Homo sapiens	19-23
22797300-7	2012	Our identification of HCLK2 as a substrate of PHD3 reveals the mechanism through which hypoxia inhibits the DDR, suggesting hydroxylation of HCLK2 is a potential therapeutic target for regulating the ATR/CHK1/p53 pathway.	ddr	108-111	checkpoint kinase 1	Homo sapiens	204-208
22797300-5	2012	Inhibiting PHD3, either with the pan-hydroxylase inhibitor dimethyloxaloylglycine (DMOG) or through hypoxia, prevented activation of the ATR/CHK1/p53 pathway and decreased apoptosis induced by DNA damage.	dimethyloxallyl glycine	83-87	checkpoint kinase 1	Homo sapiens	141-145
22797300-7	2012	Our identification of HCLK2 as a substrate of PHD3 reveals the mechanism through which hypoxia inhibits the DDR, suggesting hydroxylation of HCLK2 is a potential therapeutic target for regulating the ATR/CHK1/p53 pathway.	hclk2	22-27	checkpoint kinase 1	Homo sapiens	204-208
22653969-3	2012	The ability of AZD7762, an ATP-competitive Chk1/2 inhibitor to increase the efficacy of the DNA-damaging agents bendamustine, melphalan, and doxorubicin was examined using four human myeloma cell lines, KMS-12-BM, KMS-12-PE, RPMI-8226, and U266B1.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	15-22	checkpoint kinase 1	Homo sapiens	43-49
22653969-5	2012	The Chk1/2 inhibitor AZD7762 potentiated the antiproliferative effects of bendamustine, melphalan, and doxorubicin but not bortezomib in multiple myeloma cell lines that were p53-deficient.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	21-28	checkpoint kinase 1	Homo sapiens	4-8
22653969-5	2012	The Chk1/2 inhibitor AZD7762 potentiated the antiproliferative effects of bendamustine, melphalan, and doxorubicin but not bortezomib in multiple myeloma cell lines that were p53-deficient.	Bendamustine Hydrochloride	74-86	checkpoint kinase 1	Homo sapiens	4-8
22653969-5	2012	The Chk1/2 inhibitor AZD7762 potentiated the antiproliferative effects of bendamustine, melphalan, and doxorubicin but not bortezomib in multiple myeloma cell lines that were p53-deficient.	Melphalan	88-97	checkpoint kinase 1	Homo sapiens	4-8
22653969-5	2012	The Chk1/2 inhibitor AZD7762 potentiated the antiproliferative effects of bendamustine, melphalan, and doxorubicin but not bortezomib in multiple myeloma cell lines that were p53-deficient.	Doxorubicin	103-114	checkpoint kinase 1	Homo sapiens	4-8
22621920-0	2012	ATP depletion triggers acute myeloid leukemia differentiation through an ATR/Chk1 protein-dependent and p53 protein-independent pathway.	Adenosine Triphosphate	0-3	checkpoint kinase 1	Homo sapiens	77-81
22621920-8	2012	Utilizing an AML differentiation agent that is in development, we found that AML differentiation can be induced through ATP depletion and the subsequent activation of DNA damage signaling through an ATR/Chk1-dependent and p53-independent pathway.	Adenosine Triphosphate	120-123	checkpoint kinase 1	Homo sapiens	203-207
22417802-1	2012	PURPOSE: 7-Hydroxystaurosporine (UCN-01), a Chk1-specific inhibitor, showed promising in vitro and in vivo chemo- or radiosensitizing activity.	7-hydroxystaurosporine	9-31	checkpoint kinase 1	Homo sapiens	44-48
22417802-1	2012	PURPOSE: 7-Hydroxystaurosporine (UCN-01), a Chk1-specific inhibitor, showed promising in vitro and in vivo chemo- or radiosensitizing activity.	7-hydroxystaurosporine	33-39	checkpoint kinase 1	Homo sapiens	44-48
22417802-4	2012	Celecoxib is a cyclooxygenase-2 (COX-2)-specific inhibitor that downregulates ataxia telangiectasia and rad3-related (ATR) protein, an upstream kinase of Chk1.	Celecoxib	0-9	checkpoint kinase 1	Homo sapiens	154-158
22246285-0	2012	Structural requirements of pyrimidine, thienopyridine and ureido thiophene carboxamide-based inhibitors of the checkpoint kinase 1: QSAR, docking, molecular dynamics analysis.	pyrimidine	27-37	checkpoint kinase 1	Homo sapiens	111-130
22246285-0	2012	Structural requirements of pyrimidine, thienopyridine and ureido thiophene carboxamide-based inhibitors of the checkpoint kinase 1: QSAR, docking, molecular dynamics analysis.	thienopyridine	39-53	checkpoint kinase 1	Homo sapiens	111-130
22246285-0	2012	Structural requirements of pyrimidine, thienopyridine and ureido thiophene carboxamide-based inhibitors of the checkpoint kinase 1: QSAR, docking, molecular dynamics analysis.	ureido thiophene carboxamide	58-86	checkpoint kinase 1	Homo sapiens	111-130
22246285-1	2012	Our focus of current research is directed toward clarification of novel inhibitors (pyrazolo[1,5-a] pyrimidine (PP), thienopyridines (TP) and 2-ureido thiophene carboxamide (UTC) derivatives) targeting Checkpoint kinase 1 (CHK(1)), which is an oncology target of significant current interest.	pyrazolo(1,5-a)pyrimidine	84-110	checkpoint kinase 1	Homo sapiens	202-221
22246285-1	2012	Our focus of current research is directed toward clarification of novel inhibitors (pyrazolo[1,5-a] pyrimidine (PP), thienopyridines (TP) and 2-ureido thiophene carboxamide (UTC) derivatives) targeting Checkpoint kinase 1 (CHK(1)), which is an oncology target of significant current interest.	2-ureido thiophene carboxamide	142-172	checkpoint kinase 1	Homo sapiens	202-221
22246285-4	2012	(ii) Molecular docking and molecular dynamics simulations experiments of the inhibitors into the binding site of CHK(1) aided the interpretation of the QSAR models and demonstrated the binding modes in the aspects of inhibitor"s conformation, subsite interaction, and hydrogen bonding interactions, which indicated that a set of critical residues (Cys87, Glu91, Glu85, Ser147, Asp148, Glu17, Leu84 and Asn135) played a key role in the drug-target interactions.	Hydrogen	268-276	checkpoint kinase 1	Homo sapiens	113-119
22551018-3	2012	Thiophenecarboxamide ureas (TCUs) were identified as inhibitors of CHK1 by high throughput screening.	thiophenecarboxamide ureas	0-26	checkpoint kinase 1	Homo sapiens	67-71
22551018-3	2012	Thiophenecarboxamide ureas (TCUs) were identified as inhibitors of CHK1 by high throughput screening.	tcus	28-32	checkpoint kinase 1	Homo sapiens	67-71
22551018-5	2012	The ribose binding pocket of CHK1 was targeted to generate inhibitors with excellent cellular potency and selectivity over CDK1and IKKbeta, key features lacking from the initial compounds.	Ribose	4-10	checkpoint kinase 1	Homo sapiens	29-33
22484375-4	2012	This report elucidates how melanoma orchestrates these mechanisms to become extremely resistant to methotrexate, where both E2F1 and checkpoint kinase 1 (Chk1), two molecules with dual roles in survival/apoptosis, play prominent roles.	Methotrexate	99-111	checkpoint kinase 1	Homo sapiens	133-152
22484375-4	2012	This report elucidates how melanoma orchestrates these mechanisms to become extremely resistant to methotrexate, where both E2F1 and checkpoint kinase 1 (Chk1), two molecules with dual roles in survival/apoptosis, play prominent roles.	Methotrexate	99-111	checkpoint kinase 1	Homo sapiens	154-158
22484375-6	2012	The elevate expression of dihydrofolate reductase and thymidylate synthase, two E2F1-target genes involved in folate metabolism and required for G(1) progression, favored dTTP accumulation, which promoted DNA single strand breaks and the subsequent activation of Chk1.	Folic Acid	33-39	checkpoint kinase 1	Homo sapiens	263-267
22496453-4	2012	Here, we show that, depending on the type of DNA damage that occurs, KAP1 Ser-473 can be phosphorylated by ATM-Chk2 or ATR-Chk1 kinases.	Serine	74-77	checkpoint kinase 1	Homo sapiens	123-127
22585575-3	2012	We further showed that the CHK1 inhibitor GO6976 was capable of sensitizing HCC cells to cisplatin, indicating that CHK1 may have oncogenic function in HCC.	Go 6976	42-48	checkpoint kinase 1	Homo sapiens	27-31
22585575-3	2012	We further showed that the CHK1 inhibitor GO6976 was capable of sensitizing HCC cells to cisplatin, indicating that CHK1 may have oncogenic function in HCC.	Go 6976	42-48	checkpoint kinase 1	Homo sapiens	116-120
22585575-3	2012	We further showed that the CHK1 inhibitor GO6976 was capable of sensitizing HCC cells to cisplatin, indicating that CHK1 may have oncogenic function in HCC.	Cisplatin	89-98	checkpoint kinase 1	Homo sapiens	27-31
22585575-3	2012	We further showed that the CHK1 inhibitor GO6976 was capable of sensitizing HCC cells to cisplatin, indicating that CHK1 may have oncogenic function in HCC.	Cisplatin	89-98	checkpoint kinase 1	Homo sapiens	116-120
22787433-0	2012	Sensitization of pancreatic cancer stem cells to gemcitabine by Chk1 inhibition.	gemcitabine	49-60	checkpoint kinase 1	Homo sapiens	64-68
22787433-1	2012	Checkpoint kinase 1 (Chk1) inhibition sensitizes pancreatic cancer cells and tumors to gemcitabine.	gemcitabine	87-98	checkpoint kinase 1	Homo sapiens	0-19
22787433-1	2012	Checkpoint kinase 1 (Chk1) inhibition sensitizes pancreatic cancer cells and tumors to gemcitabine.	gemcitabine	87-98	checkpoint kinase 1	Homo sapiens	21-25
22787433-2	2012	We hypothesized that Chk1 inhibition would sensitize pancreatic cancer stem cells to gemcitabine.	gemcitabine	85-96	checkpoint kinase 1	Homo sapiens	21-25
22787433-10	2012	Furthermore, the finding that the Chk1-mediated DNA damage response was greater in stem cells than in non-stem cells suggests that Chk1 inhibition may selectively sensitize pancreatic cancer stem cells to gemcitabine, thus making Chk1 a potential therapeutic target for improving pancreatic cancer therapy.	gemcitabine	205-216	checkpoint kinase 1	Homo sapiens	34-38
22787433-10	2012	Furthermore, the finding that the Chk1-mediated DNA damage response was greater in stem cells than in non-stem cells suggests that Chk1 inhibition may selectively sensitize pancreatic cancer stem cells to gemcitabine, thus making Chk1 a potential therapeutic target for improving pancreatic cancer therapy.	gemcitabine	205-216	checkpoint kinase 1	Homo sapiens	131-135
22787433-10	2012	Furthermore, the finding that the Chk1-mediated DNA damage response was greater in stem cells than in non-stem cells suggests that Chk1 inhibition may selectively sensitize pancreatic cancer stem cells to gemcitabine, thus making Chk1 a potential therapeutic target for improving pancreatic cancer therapy.	gemcitabine	205-216	checkpoint kinase 1	Homo sapiens	131-135
22797300-7	2012	Our identification of HCLK2 as a substrate of PHD3 reveals the mechanism through which hypoxia inhibits the DDR, suggesting hydroxylation of HCLK2 is a potential therapeutic target for regulating the ATR/CHK1/p53 pathway.	hclk2	141-146	checkpoint kinase 1	Homo sapiens	204-208
22117197-7	2012	Consistently, the co-administration of the Chk1 inhibitor AZD7762 and chemotherapy abrogated tumor growth in vivo, whereas chemotherapy alone was scarcely effective.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	58-65	checkpoint kinase 1	Homo sapiens	43-47
21927021-0	2012	The oncogenic phosphatase PPM1D confers cisplatin resistance in ovarian carcinoma cells by attenuating checkpoint kinase 1 and p53 activation.	Cisplatin	40-49	checkpoint kinase 1	Homo sapiens	103-122
22505024-6	2012	Mass spectrometric analyses suggested that Ser 251 of Mig-6 was a major phosphorylation site by Chk1 in vitro and in vivo.	Serine	43-46	checkpoint kinase 1	Homo sapiens	96-100
22505024-9	2012	Our results suggest that Chk1 phosphorylates Mig-6 on Ser 251, resulting in the inhibition of Mig-6, and that Chk1 acts as a positive regulator of EGF signalling.	Serine	54-57	checkpoint kinase 1	Homo sapiens	25-29
22023523-6	2012	We demonstrated that the [2 NAs + Bu] combination activates a DNA damage response through the ATM-CHK2 and ATM-CHK1 pathways, leading to cell cycle checkpoint activation and apoptosis.	Busulfan	34-36	checkpoint kinase 1	Homo sapiens	111-115
22552540-0	2012	Bortezomib induces G2-M arrest in human colon cancer cells through ROS-inducible             phosphorylation of ATM-CHK1.	Bortezomib	0-10	checkpoint kinase 1	Homo sapiens	116-120
22552540-0	2012	Bortezomib induces G2-M arrest in human colon cancer cells through ROS-inducible             phosphorylation of ATM-CHK1.	Reactive Oxygen Species	67-70	checkpoint kinase 1	Homo sapiens	116-120
22456510-3	2012	We show here that Ser-409 residing in the Poleta-binding motif of Rad18 is phosphorylated in a checkpoint kinase 1-dependent manner in genotoxin-treated cells.	Serine	18-21	checkpoint kinase 1	Homo sapiens	95-114
22537224-11	2012	CONCLUSION: Our findings suggest that, despite their lack of specificity, pharmaceutical inhibition of the FA pathway by bortezomib, CA-074-Me, CHK1 inhibitors or HSP90 inhibitors may be a promising strategy to sensitize cisplatin-resistant, FA pathway-proficient tumor cells to cisplatin.	Cisplatin	221-230	checkpoint kinase 1	Homo sapiens	144-148
22537224-11	2012	CONCLUSION: Our findings suggest that, despite their lack of specificity, pharmaceutical inhibition of the FA pathway by bortezomib, CA-074-Me, CHK1 inhibitors or HSP90 inhibitors may be a promising strategy to sensitize cisplatin-resistant, FA pathway-proficient tumor cells to cisplatin.	Cisplatin	279-288	checkpoint kinase 1	Homo sapiens	144-148
21927021-6	2012	Our findings establish for the first time that PPM1D confers CDDP resistance in OVCA cells through attenuating CDDP-induced, Chk1-mediated, p53-dependent apoptosis.	Cisplatin	111-115	checkpoint kinase 1	Homo sapiens	125-129
21927021-3	2012	A determinant of CDDP sensitivity in OVCA, p53, is activated by checkpoint kinase 1 (Chk1) in response to DNA damage.	Cisplatin	17-21	checkpoint kinase 1	Homo sapiens	64-83
21927021-3	2012	A determinant of CDDP sensitivity in OVCA, p53, is activated by checkpoint kinase 1 (Chk1) in response to DNA damage.	Cisplatin	17-21	checkpoint kinase 1	Homo sapiens	85-89
21927021-6	2012	Our findings establish for the first time that PPM1D confers CDDP resistance in OVCA cells through attenuating CDDP-induced, Chk1-mediated, p53-dependent apoptosis.	Cisplatin	61-65	checkpoint kinase 1	Homo sapiens	125-129
22374217-0	2012	Pyridyl aminothiazoles as potent inhibitors of Chk1 with slow dissociation rates.	pyridyl aminothiazoles	0-22	checkpoint kinase 1	Homo sapiens	47-51
22365762-0	2012	Pyridyl aminothiazoles as potent Chk1 inhibitors: optimization of cellular activity.	pyridyl aminothiazoles	0-22	checkpoint kinase 1	Homo sapiens	33-37
22365762-1	2012	Translation of significant biochemical activity of pyridyl aminothiazole class of Chk1 inhibitors into functional CEA potency required analysis and adjustment of both physical properties and kinase selectivity profile of the series.	pyridyl aminothiazole	51-72	checkpoint kinase 1	Homo sapiens	82-86
22446188-5	2012	We therefore tested whether inhibition of Chk1 could potentiate the cytotoxicity of the DNA damaging agent irinotecan in TNBC using xenotransplant tumor models.	Irinotecan	107-117	checkpoint kinase 1	Homo sapiens	42-46
22446188-7	2012	These lines were tested for their response to irinotecan and a Chk1 inhibitor (either UCN-01 or AZD7762), either as single agents or in combination.	7-hydroxystaurosporine	86-92	checkpoint kinase 1	Homo sapiens	63-67
22357623-4	2012	Here we show that Chk1 is phosphorylated predominantly at Ser-280 and translocated from cytoplasm to nucleus in response to serum stimulation.	Serine	58-61	checkpoint kinase 1	Homo sapiens	18-22
22357623-5	2012	Nonphosphorylated Chk1-Ser-280 mutation attenuates nuclear Chk1 accumulation, whereas the phosphomimic mutation has a reverse effect on the localization.	Serine	23-26	checkpoint kinase 1	Homo sapiens	18-22
22357623-5	2012	Nonphosphorylated Chk1-Ser-280 mutation attenuates nuclear Chk1 accumulation, whereas the phosphomimic mutation has a reverse effect on the localization.	Serine	23-26	checkpoint kinase 1	Homo sapiens	59-63
22357623-6	2012	Treatment with p90 RSK inhibitor impairs Chk1 phosphorylation at Ser-280 and accumulation at the nucleus after serum stimulation, whereas these two phenomena are induced by the expression of the constitutively active mutant of p90 RSK in serum-starved cells.	Serine	65-68	checkpoint kinase 1	Homo sapiens	41-45
22357623-7	2012	In vitro analyses indicate that p90 RSK stoichiometrically phosphorylates Ser-280 on Chk1.	Serine	74-77	checkpoint kinase 1	Homo sapiens	85-89
22357623-8	2012	Together with Chk1 phosphorylation at Ser-345 by ATR and its autophosphorylation at Ser-296, which are critical for checkpoint signaling, Chk1-Ser-280 phosphorylation is elevated in a p90 RSK-dependent manner after UV irradiation.	Serine	38-41	checkpoint kinase 1	Homo sapiens	14-18
22357623-8	2012	Together with Chk1 phosphorylation at Ser-345 by ATR and its autophosphorylation at Ser-296, which are critical for checkpoint signaling, Chk1-Ser-280 phosphorylation is elevated in a p90 RSK-dependent manner after UV irradiation.	Serine	38-41	checkpoint kinase 1	Homo sapiens	138-142
22357623-8	2012	Together with Chk1 phosphorylation at Ser-345 by ATR and its autophosphorylation at Ser-296, which are critical for checkpoint signaling, Chk1-Ser-280 phosphorylation is elevated in a p90 RSK-dependent manner after UV irradiation.	Serine	84-87	checkpoint kinase 1	Homo sapiens	14-18
22357623-8	2012	Together with Chk1 phosphorylation at Ser-345 by ATR and its autophosphorylation at Ser-296, which are critical for checkpoint signaling, Chk1-Ser-280 phosphorylation is elevated in a p90 RSK-dependent manner after UV irradiation.	Serine	84-87	checkpoint kinase 1	Homo sapiens	138-142
22357623-8	2012	Together with Chk1 phosphorylation at Ser-345 by ATR and its autophosphorylation at Ser-296, which are critical for checkpoint signaling, Chk1-Ser-280 phosphorylation is elevated in a p90 RSK-dependent manner after UV irradiation.	Serine	84-87	checkpoint kinase 1	Homo sapiens	14-18
22357623-8	2012	Together with Chk1 phosphorylation at Ser-345 by ATR and its autophosphorylation at Ser-296, which are critical for checkpoint signaling, Chk1-Ser-280 phosphorylation is elevated in a p90 RSK-dependent manner after UV irradiation.	Serine	84-87	checkpoint kinase 1	Homo sapiens	138-142
22357623-9	2012	In addition, Chk1 phosphorylation at Ser-345 and Ser-296 after UV irradiation is also attenuated by the treatment with p90 RSK inhibitor or by Ser-280 mutation to Ala.	Serine	37-40	checkpoint kinase 1	Homo sapiens	13-17
22357623-9	2012	In addition, Chk1 phosphorylation at Ser-345 and Ser-296 after UV irradiation is also attenuated by the treatment with p90 RSK inhibitor or by Ser-280 mutation to Ala.	Serine	49-52	checkpoint kinase 1	Homo sapiens	13-17
22357623-10	2012	These results suggest that p90 RSK facilitates nuclear Chk1 accumulation through Chk1-Ser-280 phosphorylation and that this pathway plays an important role in the preparation for monitoring genetic stability during cell proliferation.	Serine	86-89	checkpoint kinase 1	Homo sapiens	55-59
22357623-10	2012	These results suggest that p90 RSK facilitates nuclear Chk1 accumulation through Chk1-Ser-280 phosphorylation and that this pathway plays an important role in the preparation for monitoring genetic stability during cell proliferation.	Serine	86-89	checkpoint kinase 1	Homo sapiens	81-85
22401965-0	2012	Activation of the BRCA1/Chk1/p53/p21(Cip1/Waf1) pathway by nitric oxide and cell cycle arrest in human neuroblastoma NB69 cells.	Nitric Oxide	59-71	checkpoint kinase 1	Homo sapiens	24-28
22342147-0	2012	Synthesis and evaluation of triazolones as checkpoint kinase 1 inhibitors.	triazolones	28-39	checkpoint kinase 1	Homo sapiens	43-62
22342147-2	2012	Synthesis and evaluation of a previously described class of Chk1 inhibitors, triazoloquinolones/triazolones (TZs) is further described herein.	triazoloquinolones	77-95	checkpoint kinase 1	Homo sapiens	60-64
22342147-2	2012	Synthesis and evaluation of a previously described class of Chk1 inhibitors, triazoloquinolones/triazolones (TZs) is further described herein.	triazolones	96-107	checkpoint kinase 1	Homo sapiens	60-64
22342147-2	2012	Synthesis and evaluation of a previously described class of Chk1 inhibitors, triazoloquinolones/triazolones (TZs) is further described herein.	CHEMBL1783617	109-112	checkpoint kinase 1	Homo sapiens	60-64
22044003-0	2012	Synthesis of Cis-fused pyran indolocarbazole derivatives that inhibit FLT3 kinase and the DNA damage kinase, checkpoint kinase 1.	Pyrans	23-28	checkpoint kinase 1	Homo sapiens	109-128
22044003-0	2012	Synthesis of Cis-fused pyran indolocarbazole derivatives that inhibit FLT3 kinase and the DNA damage kinase, checkpoint kinase 1.	Indolocarbazole	29-44	checkpoint kinase 1	Homo sapiens	109-128
22258035-2	2012	Here, we show that checkpoint abrogation by AZD7762, a potent and selective CHK1/2 kinase inhibitor enhances genotoxic treatment efficacy in immature KG1a leukemic cell line and in AML patient samples, particularly those with a complex karyotype, which display major genomic instability and chemoresistance.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	44-51	checkpoint kinase 1	Homo sapiens	76-80
21984341-0	2012	Gossypin induces G2/M arrest in human malignant glioma U251 cells by the activation of Chk1/Cdc25C pathway.	gossypin	0-8	checkpoint kinase 1	Homo sapiens	87-91
21984341-6	2012	An analysis of cell-cycle regulatory proteins indicated that the arresting effect of gossypin on the cell cycle at G2/M phase was involved in the phosphorylation of cell division cycle 25C (Cdc25C) tyrosine phosphatase via the activation of checkpoint kinase 1 (Chk1).	gossypin	85-93	checkpoint kinase 1	Homo sapiens	241-260
21984341-6	2012	An analysis of cell-cycle regulatory proteins indicated that the arresting effect of gossypin on the cell cycle at G2/M phase was involved in the phosphorylation of cell division cycle 25C (Cdc25C) tyrosine phosphatase via the activation of checkpoint kinase 1 (Chk1).	gossypin	85-93	checkpoint kinase 1	Homo sapiens	262-266
21984341-7	2012	These findings indicate that gossypin is a potential treatment of gliomas because of gossypin"s potential to regulate the proliferation of U251 cells via the cell-cycle regulatory proteins Chk1 and Cdc25C.	gossypin	29-37	checkpoint kinase 1	Homo sapiens	189-193
22189968-0	2012	Potentiation of the novel topoisomerase I inhibitor indenoisoquinoline LMP-400 by the cell checkpoint and Chk1-Chk2 inhibitor AZD7762.	Indenoisoquinoline	52-70	checkpoint kinase 1	Homo sapiens	106-110
22189968-0	2012	Potentiation of the novel topoisomerase I inhibitor indenoisoquinoline LMP-400 by the cell checkpoint and Chk1-Chk2 inhibitor AZD7762.	NSC 724998	71-78	checkpoint kinase 1	Homo sapiens	106-110
22189968-0	2012	Potentiation of the novel topoisomerase I inhibitor indenoisoquinoline LMP-400 by the cell checkpoint and Chk1-Chk2 inhibitor AZD7762.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	126-133	checkpoint kinase 1	Homo sapiens	106-110
22189968-6	2012	AZD7762 inhibited both the activation/autophosphosphorylation of Chk1 and Chk2 at nanomolar concentrations in LMP-400-treated cells.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	0-7	checkpoint kinase 1	Homo sapiens	65-69
22189968-6	2012	AZD7762 inhibited both the activation/autophosphosphorylation of Chk1 and Chk2 at nanomolar concentrations in LMP-400-treated cells.	NSC 724998	110-117	checkpoint kinase 1	Homo sapiens	65-69
22189968-7	2012	This potent dual inhibition of Chk1 and Chk2 by AZD7762 was below the drug concentrations required to abrogate cell-cycle inhibition and produce synergism with LMP-400.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	48-55	checkpoint kinase 1	Homo sapiens	31-35
22189968-7	2012	This potent dual inhibition of Chk1 and Chk2 by AZD7762 was below the drug concentrations required to abrogate cell-cycle inhibition and produce synergism with LMP-400.	NSC 724998	160-167	checkpoint kinase 1	Homo sapiens	31-35
22203733-0	2012	Preclinical development of the novel Chk1 inhibitor SCH900776 in combination with DNA-damaging agents and antimetabolites.	MK-8776	52-61	checkpoint kinase 1	Homo sapiens	37-41
22203733-4	2012	SCH900776 is a novel and more selective Chk1 inhibitor that potently inhibits Chk1 and abrogates cell-cycle arrest induced by SN38.	MK-8776	0-9	checkpoint kinase 1	Homo sapiens	40-44
22203733-4	2012	SCH900776 is a novel and more selective Chk1 inhibitor that potently inhibits Chk1 and abrogates cell-cycle arrest induced by SN38.	MK-8776	0-9	checkpoint kinase 1	Homo sapiens	78-82
24900442-1	2012	A novel series of CHK1 inhibitors with a distinctive hinge binding mode, exemplified by 2-aryl-N-(2-(piperazin-1-yl)phenyl)thiazole-4-carboxamide, was discovered through high-throughput screening using the affinity selection-mass spectrometry (AS-MS)-based Automated Ligand Identification System (ALIS) platform.	2-aryl-n-(2-(piperazin-1-yl)phenyl)thiazole-4-carboxamide	88-145	checkpoint kinase 1	Homo sapiens	18-22
22537224-10	2012	In addition, geldanamycin (HSP90 inhibitor) and two CHK1 inhibitors (UCN-01 and SB218078) exhibited a significantly stronger synergism with cisplatin in FA-proficient cells when compared to FA-deficient cells, suggesting a contribution of their FA pathway inhibitory activity to cisplatin sensitization.	7-hydroxystaurosporine	69-75	checkpoint kinase 1	Homo sapiens	52-56
22537224-10	2012	In addition, geldanamycin (HSP90 inhibitor) and two CHK1 inhibitors (UCN-01 and SB218078) exhibited a significantly stronger synergism with cisplatin in FA-proficient cells when compared to FA-deficient cells, suggesting a contribution of their FA pathway inhibitory activity to cisplatin sensitization.	SB 218078	80-88	checkpoint kinase 1	Homo sapiens	52-56
22537224-10	2012	In addition, geldanamycin (HSP90 inhibitor) and two CHK1 inhibitors (UCN-01 and SB218078) exhibited a significantly stronger synergism with cisplatin in FA-proficient cells when compared to FA-deficient cells, suggesting a contribution of their FA pathway inhibitory activity to cisplatin sensitization.	Cisplatin	140-149	checkpoint kinase 1	Homo sapiens	52-56
22537224-10	2012	In addition, geldanamycin (HSP90 inhibitor) and two CHK1 inhibitors (UCN-01 and SB218078) exhibited a significantly stronger synergism with cisplatin in FA-proficient cells when compared to FA-deficient cells, suggesting a contribution of their FA pathway inhibitory activity to cisplatin sensitization.	Cisplatin	279-288	checkpoint kinase 1	Homo sapiens	52-56
22313687-2	2012	Multiple MEK1/2 inhibitors (CI-1040 (PD184352); AZD6244 (ARRY-142886)) interacted with multiple CHK1 inhibitors (UCN-01, AZD7762) to kill multiple primary human glioma cell isolates that have a diverse set of genetic alterations typically found in the disease.	2-(2-chloro-4-iodophenylamino)-N-cyclopropylmethoxy-3,4-difluorobenzamide	28-35	checkpoint kinase 1	Homo sapiens	96-100
22313687-2	2012	Multiple MEK1/2 inhibitors (CI-1040 (PD184352); AZD6244 (ARRY-142886)) interacted with multiple CHK1 inhibitors (UCN-01, AZD7762) to kill multiple primary human glioma cell isolates that have a diverse set of genetic alterations typically found in the disease.	2-(2-chloro-4-iodophenylamino)-N-cyclopropylmethoxy-3,4-difluorobenzamide	37-45	checkpoint kinase 1	Homo sapiens	96-100
22313687-2	2012	Multiple MEK1/2 inhibitors (CI-1040 (PD184352); AZD6244 (ARRY-142886)) interacted with multiple CHK1 inhibitors (UCN-01, AZD7762) to kill multiple primary human glioma cell isolates that have a diverse set of genetic alterations typically found in the disease.	AZD 6244	48-55	checkpoint kinase 1	Homo sapiens	96-100
22313687-2	2012	Multiple MEK1/2 inhibitors (CI-1040 (PD184352); AZD6244 (ARRY-142886)) interacted with multiple CHK1 inhibitors (UCN-01, AZD7762) to kill multiple primary human glioma cell isolates that have a diverse set of genetic alterations typically found in the disease.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	121-128	checkpoint kinase 1	Homo sapiens	96-100
22532985-3	2012	Vitamin D has also been implicated in asthma through its effects on the obesity, bacillus Calmettee Guerin (BCG) vaccination and high vitamin D level, vitamin D supplement, checkpoint protein kinase 1 (Chk1), plasminogen activator inhibitor-1 (PAI-1) and gamma delta T cells (gdT).	Vitamin D	0-9	checkpoint kinase 1	Homo sapiens	173-200
22532985-3	2012	Vitamin D has also been implicated in asthma through its effects on the obesity, bacillus Calmettee Guerin (BCG) vaccination and high vitamin D level, vitamin D supplement, checkpoint protein kinase 1 (Chk1), plasminogen activator inhibitor-1 (PAI-1) and gamma delta T cells (gdT).	Vitamin D	0-9	checkpoint kinase 1	Homo sapiens	202-206
22399496-6	2012	In FLO-1 cells, wortmannin suppressed ataxia telangiectasia and Rad3-related protein (ATR)-checkpoint kinase 1 (CHK1)-mediated checkpoint and multiple DNA repair genes, whereas RAD51 and CHK2 were not affected.	Wortmannin	16-26	checkpoint kinase 1	Homo sapiens	112-116
22021033-5	2012	MMEQ induced G2/M arrest through the             promotion of chk1, chk2 and cdc25c in TSGH8301 cells.	2-(3-methoxyphenyl)-6, 7-methylenedioxoquinolin-4-one	0-4	checkpoint kinase 1	Homo sapiens	62-66
21765472-4	2012	However, it has recently been shown that Chk1 itself is also subject to Cdk-mediated phosphorylation at serines 286 and 301 (S286 and 301).	Serine	104-111	checkpoint kinase 1	Homo sapiens	41-45
21765472-6	2012	We also find that substitution of S286 and S301 with non-phosphorylatable alanine residues strongly attenuates DNA damage-induced Chk1 activation and G2 checkpoint proficiency, but does not eliminate the underlying cell cycle dependence of Chk1 regulation.	Alanine	74-81	checkpoint kinase 1	Homo sapiens	130-134
22374217-1	2012	Pyridyl aminothiazoles comprise a novel class of ATP-competitive Chk1 inhibitors with excellent inhibitory potential.	pyridyl aminothiazoles	0-22	checkpoint kinase 1	Homo sapiens	65-69
22374217-1	2012	Pyridyl aminothiazoles comprise a novel class of ATP-competitive Chk1 inhibitors with excellent inhibitory potential.	Adenosine Triphosphate	49-52	checkpoint kinase 1	Homo sapiens	65-69
22223332-7	2012	Thus, we concluded that pycnidione abrogated bleomycin-induced G2 arrest by decreasing Chk1 and Chk2.	pycnidione	24-34	checkpoint kinase 1	Homo sapiens	87-91
22223332-7	2012	Thus, we concluded that pycnidione abrogated bleomycin-induced G2 arrest by decreasing Chk1 and Chk2.	Bleomycin	45-54	checkpoint kinase 1	Homo sapiens	87-91
21971960-9	2012	The binding of pre-S2 LHBs with             C53 causes increased Cdk1 activation and mitotic entry, and the function of Chk1             is partially inhibited by the binding of pre-S2 LHBs with C53.	Luteinizing Hormone, beta Subunit	185-189	checkpoint kinase 1	Homo sapiens	120-124
21971960-11	2012	By counteracting C53, pre-S2 LHBs             promotes Cdk1 activation and mitotic entry in unperturbed cell cycle progression             and delays the function of Chk1, which may be a novel potential mechanism for             HBV-induced hepatocellular carcinoma (HCC).	Luteinizing Hormone, beta Subunit	29-33	checkpoint kinase 1	Homo sapiens	166-170
22957056-5	2012	We suggested that depletion of HDAC6 increased cisplatin-induced cytotoxicity was due to the enhancement of apoptosis via activating ATR/Chk1 pathway.	Cisplatin	47-56	checkpoint kinase 1	Homo sapiens	137-141
22937147-6	2012	Upon incubation with the Chk1 inhibitor MK-8776, single-stranded DNA regions (ssDNA) and double-strand breaks (DSB) begin to appear within 6 h. These DSB have been attributed to the structure-specific DNA endonuclease, Mus81.	MK-8776	40-47	checkpoint kinase 1	Homo sapiens	25-29
22905093-8	2012	Proteins and genes related to DNA damage response, elongation and telomere extension and repair related directly and indirectly to platinum resistance were overexpressed, as the CHK1 protein and the genes CHEK2, LIG3, POLD1, POLA2, FANCD2, PRPF19, RECQ5 respectively, the last two not previously described in mesothelioma.	Platinum	131-139	checkpoint kinase 1	Homo sapiens	178-182
22160723-7	2011	These cells exhibited a high yield of ROS-induced DNA single- and double-strand breaks and activation of the ATR-Chk1-ATM-Chk2-p53 pathway that led to Fas and caspase-8, -3, and -7 activation, whereas macrophages and DCs derived from them were protected.	Reactive Oxygen Species	38-41	checkpoint kinase 1	Homo sapiens	113-117
22111927-1	2011	Pyrazolopyridine inhibitors with low micromolar potency for CHK1 and good selectivity against CHK2 were previously identified by fragment-based screening.	pyrazolopyridine	0-16	checkpoint kinase 1	Homo sapiens	60-64
22111927-2	2011	The optimization of the pyrazolopyridines to a series of potent and CHK1-selective isoquinolines demonstrates how fragment-growing and scaffold morphing strategies arising from a structure-based understanding of CHK1 inhibitor binding can be combined to successfully progress fragment-derived hit matter to compounds with activity in vivo.	pyrazolopyridine	24-41	checkpoint kinase 1	Homo sapiens	68-72
22111927-2	2011	The optimization of the pyrazolopyridines to a series of potent and CHK1-selective isoquinolines demonstrates how fragment-growing and scaffold morphing strategies arising from a structure-based understanding of CHK1 inhibitor binding can be combined to successfully progress fragment-derived hit matter to compounds with activity in vivo.	pyrazolopyridine	24-41	checkpoint kinase 1	Homo sapiens	212-216
22111927-2	2011	The optimization of the pyrazolopyridines to a series of potent and CHK1-selective isoquinolines demonstrates how fragment-growing and scaffold morphing strategies arising from a structure-based understanding of CHK1 inhibitor binding can be combined to successfully progress fragment-derived hit matter to compounds with activity in vivo.	Isoquinolines	83-96	checkpoint kinase 1	Homo sapiens	68-72
22111927-2	2011	The optimization of the pyrazolopyridines to a series of potent and CHK1-selective isoquinolines demonstrates how fragment-growing and scaffold morphing strategies arising from a structure-based understanding of CHK1 inhibitor binding can be combined to successfully progress fragment-derived hit matter to compounds with activity in vivo.	Isoquinolines	83-96	checkpoint kinase 1	Homo sapiens	212-216
22111927-3	2011	The challenges of improving CHK1 potency and selectivity, addressing synthetic tractability, and achieving novelty in the crowded kinase inhibitor chemical space were tackled by multiple scaffold morphing steps, which progressed through tricyclic pyrimido[2,3-b]azaindoles to N-(pyrazin-2-yl)pyrimidin-4-amines and ultimately to imidazo[4,5-c]pyridines and isoquinolines.	tricyclic pyrimido[2,3-b]azaindoles	237-272	checkpoint kinase 1	Homo sapiens	28-32
22111927-4	2011	A potent and highly selective isoquinoline CHK1 inhibitor (SAR-020106) was identified, which potentiated the efficacies of irinotecan and gemcitabine in SW620 human colon carcinoma xenografts in nude mice.	isoquinoline	30-42	checkpoint kinase 1	Homo sapiens	43-47
22111927-4	2011	A potent and highly selective isoquinoline CHK1 inhibitor (SAR-020106) was identified, which potentiated the efficacies of irinotecan and gemcitabine in SW620 human colon carcinoma xenografts in nude mice.	SAR 020106	59-69	checkpoint kinase 1	Homo sapiens	43-47
22111927-4	2011	A potent and highly selective isoquinoline CHK1 inhibitor (SAR-020106) was identified, which potentiated the efficacies of irinotecan and gemcitabine in SW620 human colon carcinoma xenografts in nude mice.	Irinotecan	123-133	checkpoint kinase 1	Homo sapiens	43-47
22111927-4	2011	A potent and highly selective isoquinoline CHK1 inhibitor (SAR-020106) was identified, which potentiated the efficacies of irinotecan and gemcitabine in SW620 human colon carcinoma xenografts in nude mice.	gemcitabine	138-149	checkpoint kinase 1	Homo sapiens	43-47
22134241-3	2011	Thus, we hypothesized that inhibition of HRR (mediated by Chk1 via AZD7762) and PARP1 [via olaparib (AZD2281)] would selectively sensitize p53 mutant pancreatic cancer cells to radiation.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	67-74	checkpoint kinase 1	Homo sapiens	58-62
22106282-5	2011	Inhibition of Chk1 activity with Chk1 inhibitor (UCN-01, AZD7762, or CHIR-124) in normal cells increases their sensitivity to HDACi (vorinostat, romidepsin, or entinostat) induced cell death, associated with extensive mitotic disruption.	7-hydroxystaurosporine	49-55	checkpoint kinase 1	Homo sapiens	14-18
22106282-5	2011	Inhibition of Chk1 activity with Chk1 inhibitor (UCN-01, AZD7762, or CHIR-124) in normal cells increases their sensitivity to HDACi (vorinostat, romidepsin, or entinostat) induced cell death, associated with extensive mitotic disruption.	7-hydroxystaurosporine	49-55	checkpoint kinase 1	Homo sapiens	33-37
22106282-5	2011	Inhibition of Chk1 activity with Chk1 inhibitor (UCN-01, AZD7762, or CHIR-124) in normal cells increases their sensitivity to HDACi (vorinostat, romidepsin, or entinostat) induced cell death, associated with extensive mitotic disruption.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	57-64	checkpoint kinase 1	Homo sapiens	14-18
22106282-5	2011	Inhibition of Chk1 activity with Chk1 inhibitor (UCN-01, AZD7762, or CHIR-124) in normal cells increases their sensitivity to HDACi (vorinostat, romidepsin, or entinostat) induced cell death, associated with extensive mitotic disruption.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	57-64	checkpoint kinase 1	Homo sapiens	33-37
22106282-5	2011	Inhibition of Chk1 activity with Chk1 inhibitor (UCN-01, AZD7762, or CHIR-124) in normal cells increases their sensitivity to HDACi (vorinostat, romidepsin, or entinostat) induced cell death, associated with extensive mitotic disruption.	Vorinostat	133-143	checkpoint kinase 1	Homo sapiens	14-18
22106282-5	2011	Inhibition of Chk1 activity with Chk1 inhibitor (UCN-01, AZD7762, or CHIR-124) in normal cells increases their sensitivity to HDACi (vorinostat, romidepsin, or entinostat) induced cell death, associated with extensive mitotic disruption.	Vorinostat	133-143	checkpoint kinase 1	Homo sapiens	33-37
22106282-5	2011	Inhibition of Chk1 activity with Chk1 inhibitor (UCN-01, AZD7762, or CHIR-124) in normal cells increases their sensitivity to HDACi (vorinostat, romidepsin, or entinostat) induced cell death, associated with extensive mitotic disruption.	romidepsin	145-155	checkpoint kinase 1	Homo sapiens	14-18
22106282-5	2011	Inhibition of Chk1 activity with Chk1 inhibitor (UCN-01, AZD7762, or CHIR-124) in normal cells increases their sensitivity to HDACi (vorinostat, romidepsin, or entinostat) induced cell death, associated with extensive mitotic disruption.	romidepsin	145-155	checkpoint kinase 1	Homo sapiens	33-37
22106282-5	2011	Inhibition of Chk1 activity with Chk1 inhibitor (UCN-01, AZD7762, or CHIR-124) in normal cells increases their sensitivity to HDACi (vorinostat, romidepsin, or entinostat) induced cell death, associated with extensive mitotic disruption.	entinostat	160-170	checkpoint kinase 1	Homo sapiens	14-18
22106282-5	2011	Inhibition of Chk1 activity with Chk1 inhibitor (UCN-01, AZD7762, or CHIR-124) in normal cells increases their sensitivity to HDACi (vorinostat, romidepsin, or entinostat) induced cell death, associated with extensive mitotic disruption.	entinostat	160-170	checkpoint kinase 1	Homo sapiens	33-37
21889927-6	2011	An M2 induced DDR in p53-defective MDA-MB-231 cells was abrogated by UCN-01, a ubiquitous inhibitor of kinases including Chk1, in a response associated with substantial mitotic catastrophe and strong synergy.	ddr	14-17	checkpoint kinase 1	Homo sapiens	121-125
21889927-6	2011	An M2 induced DDR in p53-defective MDA-MB-231 cells was abrogated by UCN-01, a ubiquitous inhibitor of kinases including Chk1, in a response associated with substantial mitotic catastrophe and strong synergy.	7-hydroxystaurosporine	69-75	checkpoint kinase 1	Homo sapiens	121-125
22159421-9	2011	Together, our results strongly suggest an essential regulatory role for WRN in controlling the ATR-CHK1-mediated S-phase checkpoint in CPT-treated cells.	cpt	135-138	checkpoint kinase 1	Homo sapiens	99-103
22905155-2	2012	This arrest can be abrogated in p53-defective cells by the Chk1 inhibitor 7-hydroxystaurosporine (UCN-01).	7-hydroxystaurosporine	74-96	checkpoint kinase 1	Homo sapiens	59-63
22905155-2	2012	This arrest can be abrogated in p53-defective cells by the Chk1 inhibitor 7-hydroxystaurosporine (UCN-01).	7-hydroxystaurosporine	98-104	checkpoint kinase 1	Homo sapiens	59-63
22768182-11	2012	TMZ induced in monocytes the DNA damage response pathways ATM-Chk2 and ATR-Chk1 resulting in p53 activation.	Temozolomide	0-3	checkpoint kinase 1	Homo sapiens	75-79
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	checkpoint kinase 1	Homo sapiens	15-19
21958871-2	2011	Recently simvastatin has been found to result in the synergistic induction of apoptosis with 7-hydroxystaurosporine (UCN-01) (a Chk1 inhibitor) in myeloma cells.	Simvastatin	9-20	checkpoint kinase 1	Homo sapiens	128-132
21958871-2	2011	Recently simvastatin has been found to result in the synergistic induction of apoptosis with 7-hydroxystaurosporine (UCN-01) (a Chk1 inhibitor) in myeloma cells.	7-hydroxystaurosporine	93-115	checkpoint kinase 1	Homo sapiens	128-132
21958871-2	2011	Recently simvastatin has been found to result in the synergistic induction of apoptosis with 7-hydroxystaurosporine (UCN-01) (a Chk1 inhibitor) in myeloma cells.	7-hydroxystaurosporine	117-123	checkpoint kinase 1	Homo sapiens	128-132
21958871-3	2011	Therefore we hypothesized that Chk1 plays a role in the anti-myeloma effect of simvastatin.	Simvastatin	79-90	checkpoint kinase 1	Homo sapiens	31-35
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	checkpoint kinase 1	Homo sapiens	120-124
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	checkpoint kinase 1	Homo sapiens	47-51
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	checkpoint kinase 1	Homo sapiens	66-70
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	checkpoint kinase 1	Homo sapiens	66-70
21958871-8	2011	Additionally, inhibition of Chk1 expression enhanced simvastatin-induced downregulation of Bcl-2, caspase 9 cleavage and subsequent apoptosis.	Simvastatin	53-64	checkpoint kinase 1	Homo sapiens	28-32
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	checkpoint kinase 1	Homo sapiens	33-37
21965652-10	2011	Other studies indicate that excess of MCM3 up-regulates the phosphorylation of CHK1 Ser-345 and CDK2 Thr-14.	Serine	84-87	checkpoint kinase 1	Homo sapiens	79-83
21911831-2	2011	Coexposure to the Chk1 and MEK1/2 inhibitors AZD7762 and selumetinib (AZD6244) robustly induced apoptosis in various MM cells and CD138(+) primary samples, but spared normal CD138(-) and CD34(+) cells.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	45-52	checkpoint kinase 1	Homo sapiens	18-22
21911831-2	2011	Coexposure to the Chk1 and MEK1/2 inhibitors AZD7762 and selumetinib (AZD6244) robustly induced apoptosis in various MM cells and CD138(+) primary samples, but spared normal CD138(-) and CD34(+) cells.	AZD 6244	57-68	checkpoint kinase 1	Homo sapiens	18-22
21911831-2	2011	Coexposure to the Chk1 and MEK1/2 inhibitors AZD7762 and selumetinib (AZD6244) robustly induced apoptosis in various MM cells and CD138(+) primary samples, but spared normal CD138(-) and CD34(+) cells.	AZD 6244	70-77	checkpoint kinase 1	Homo sapiens	18-22
21911831-8	2011	Finally, Chk1/MEK1/2 inhibition increased cell death in the Hoechst-positive (Hst(+)), low pyronin Y (PY)-staining (2N Hst(+)/PY(-)) G(0) population and in sorted small side-population (SSP) MM cells.	hoechst	60-67	checkpoint kinase 1	Homo sapiens	9-13
21911831-8	2011	Finally, Chk1/MEK1/2 inhibition increased cell death in the Hoechst-positive (Hst(+)), low pyronin Y (PY)-staining (2N Hst(+)/PY(-)) G(0) population and in sorted small side-population (SSP) MM cells.	Pyronine	91-100	checkpoint kinase 1	Homo sapiens	9-13
21892012-3	2011	In an effort to discover sensitizing mutations and novel combination strategies for Chk1 inhibition, an siRNA screen was performed in combination with the selective Chk1 inhibitor AR458323.	ar458323	180-188	checkpoint kinase 1	Homo sapiens	165-169
22037398-7	2011	gamma-Irradiation arrested hMSCs in the G 1 phase of the cell cycle, while cisplatin induced S-phase arrest, mediated in part by the ATR/Chk1 checkpoint pathway.	Cisplatin	75-84	checkpoint kinase 1	Homo sapiens	137-141
22024163-3	2011	Chk1 kinase is essential for Ser331 phosphorylation during unperturbed prometaphase or during spindle disruption by taxol but not nocodazole.	Paclitaxel	116-121	checkpoint kinase 1	Homo sapiens	0-4
21791475-1	2011	BACKGROUND: In preclinical studies the heat shock protein 90 (Hsp90) inhibitor tanespimycin induced down-regulation of checkpoint kinase 1 (Chk1) and other client proteins as well as increased sensitivity of acute leukemia cells to cytarabine.	tanespimycin	79-91	checkpoint kinase 1	Homo sapiens	119-138
21791475-1	2011	BACKGROUND: In preclinical studies the heat shock protein 90 (Hsp90) inhibitor tanespimycin induced down-regulation of checkpoint kinase 1 (Chk1) and other client proteins as well as increased sensitivity of acute leukemia cells to cytarabine.	tanespimycin	79-91	checkpoint kinase 1	Homo sapiens	140-144
21791475-1	2011	BACKGROUND: In preclinical studies the heat shock protein 90 (Hsp90) inhibitor tanespimycin induced down-regulation of checkpoint kinase 1 (Chk1) and other client proteins as well as increased sensitivity of acute leukemia cells to cytarabine.	Cytarabine	232-242	checkpoint kinase 1	Homo sapiens	140-144
21717478-3	2011	In this study, multiple docking strategies and Prime/Molecular Mechanics Generalized Born Surface Area (Prime/MM-GBSA) calculation were applied to predict the binding mode and free energy for a series of benzoisoquinolinones as Chk1 inhibitors.	benzoisoquinolinones	204-224	checkpoint kinase 1	Homo sapiens	228-232
21154747-2	2011	The in vitro and in vivo effects of the Chk1/2 inhibitor AZD7762 when combined with these agents were examined using neuroblastoma cell lines with known p53/MDM2/p14(ARF)  genomic status.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	57-64	checkpoint kinase 1	Homo sapiens	40-44
20623183-4	2011	We report that induction of ERbeta expression causes abrogation of the S-phase, and the Chk1/Cdc25C-mediated G2/M checkpoints after cisplatin and doxorubicin exposure in p53-defective breast cancer cells but not in p53 wild-type mammary cells.	Cisplatin	132-141	checkpoint kinase 1	Homo sapiens	88-92
21907702-5	2011	The mutation strongly attenuates aphidicolin induced Chk1 activation without altering the S-phase dependent Chk1 activation.	Aphidicolin	33-44	checkpoint kinase 1	Homo sapiens	53-57
21642769-2	2011	Multiple MEK1/2 inhibitors (PD184352, AZD6244 (ARRY-142886)) interacted with multiple CHK1 inhibitors (UCN-01 (7-hydroxystaurosporine), AZD7762) to kill mammary carcinoma cells and transformed fibroblasts.	2-(2-chloro-4-iodophenylamino)-N-cyclopropylmethoxy-3,4-difluorobenzamide	28-36	checkpoint kinase 1	Homo sapiens	86-90
21642769-2	2011	Multiple MEK1/2 inhibitors (PD184352, AZD6244 (ARRY-142886)) interacted with multiple CHK1 inhibitors (UCN-01 (7-hydroxystaurosporine), AZD7762) to kill mammary carcinoma cells and transformed fibroblasts.	AZD 6244	38-45	checkpoint kinase 1	Homo sapiens	86-90
21642769-2	2011	Multiple MEK1/2 inhibitors (PD184352, AZD6244 (ARRY-142886)) interacted with multiple CHK1 inhibitors (UCN-01 (7-hydroxystaurosporine), AZD7762) to kill mammary carcinoma cells and transformed fibroblasts.	AZD 6244	47-58	checkpoint kinase 1	Homo sapiens	86-90
21642769-2	2011	Multiple MEK1/2 inhibitors (PD184352, AZD6244 (ARRY-142886)) interacted with multiple CHK1 inhibitors (UCN-01 (7-hydroxystaurosporine), AZD7762) to kill mammary carcinoma cells and transformed fibroblasts.	7-hydroxystaurosporine	103-109	checkpoint kinase 1	Homo sapiens	86-90
21642769-2	2011	Multiple MEK1/2 inhibitors (PD184352, AZD6244 (ARRY-142886)) interacted with multiple CHK1 inhibitors (UCN-01 (7-hydroxystaurosporine), AZD7762) to kill mammary carcinoma cells and transformed fibroblasts.	7-hydroxystaurosporine	111-133	checkpoint kinase 1	Homo sapiens	86-90
21642769-2	2011	Multiple MEK1/2 inhibitors (PD184352, AZD6244 (ARRY-142886)) interacted with multiple CHK1 inhibitors (UCN-01 (7-hydroxystaurosporine), AZD7762) to kill mammary carcinoma cells and transformed fibroblasts.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	136-143	checkpoint kinase 1	Homo sapiens	86-90
21642769-3	2011	In transformed cells, CHK1 inhibitor -induced activation of ERK1/2 was dependent upon activation of SRC family non-receptor tyrosine kinases as judged by use of multiple SRC kinase inhibitors (PP2, Dasatinib; AZD0530), use of SRC/FYN/YES deleted transformed fibroblasts or by expression of dominant negative SRC.	Dasatinib	198-207	checkpoint kinase 1	Homo sapiens	22-26
21642769-3	2011	In transformed cells, CHK1 inhibitor -induced activation of ERK1/2 was dependent upon activation of SRC family non-receptor tyrosine kinases as judged by use of multiple SRC kinase inhibitors (PP2, Dasatinib; AZD0530), use of SRC/FYN/YES deleted transformed fibroblasts or by expression of dominant negative SRC.	saracatinib	209-216	checkpoint kinase 1	Homo sapiens	22-26
21592546-5	2011	RESULTS: Cisplatin consistently induced transient S-phase arrest by inhibiting Cdk2/cyclin A complex in S-phase at 12 h and then a durable G2/M-arrest by inhibiting Cdc2/cyclin B complex at 12-18 h. These inhibitions were associated with Chk1 and Chk2 activation and resultant increase in inhibitory tyrosine phosphorylation of Cdk2 and Cdc2.	Cisplatin	9-18	checkpoint kinase 1	Homo sapiens	238-242
21374707-3	2011	BITC and PEITC induced cell cycle arrest at G2/M phase at 48 h treatment and inhibited the levels of cell cycle regulatory proteins such as cyclin A and B1 in U-2 OS cells but promoted the level of Chk1 and p53 that led to G2/M arrest.	phenethyl isothiocyanate	9-14	checkpoint kinase 1	Homo sapiens	198-202
21654193-4	2011	Decitabine, and to a lesser degree azacitidine, induced the activation of checkpoint kinases Chk-1 and Chk-2 and the phosphorylation of the DDR-sensor H2AX.	Decitabine	0-10	checkpoint kinase 1	Homo sapiens	93-98
21654193-4	2011	Decitabine, and to a lesser degree azacitidine, induced the activation of checkpoint kinases Chk-1 and Chk-2 and the phosphorylation of the DDR-sensor H2AX.	Azacitidine	35-46	checkpoint kinase 1	Homo sapiens	93-98
21561856-5	2011	Caffeine blocked UVB-induced Chk1 phosphorylation.	Caffeine	0-8	checkpoint kinase 1	Homo sapiens	29-33
21566061-3	2011	We show that hsp90 inhibition with 17-allylamino-demehoxygeldanamycin or the novel, nongeldanamycin analogue AUY922 (resorcinylic isoxazole amide; Novartis Pharma) dose-dependently reduced the levels of ATR and CHK1 without affecting ATM levels.	17-allylamino-demehoxygeldanamycin	35-69	checkpoint kinase 1	Homo sapiens	211-215
21566061-3	2011	We show that hsp90 inhibition with 17-allylamino-demehoxygeldanamycin or the novel, nongeldanamycin analogue AUY922 (resorcinylic isoxazole amide; Novartis Pharma) dose-dependently reduced the levels of ATR and CHK1 without affecting ATM levels.	resorcinylic isoxazole amide	117-145	checkpoint kinase 1	Homo sapiens	211-215
21566061-4	2011	AUY922-mediated depletion of ATR and CHK1 was associated with an increase in their polyubiquitylation and decreased binding to hsp90.	5-(2,4-dihydroxy-5-isopropylphenyl)-4-(4-morpholin-4-ylmethylphenyl)isoxazole-3-carboxylic acid ethylamide	0-6	checkpoint kinase 1	Homo sapiens	37-41
21566061-5	2011	Cotreatment with bortezomib partially restored AUY922-mediated depletion of ATR and CHK1 levels.	Bortezomib	17-27	checkpoint kinase 1	Homo sapiens	84-88
21566061-6	2011	Additionally, treatment with AUY922 reduced the accumulation of ATR, p53BP1, and CHK1 but not gamma-H2AX to the sites of DNA damage.	5-(2,4-dihydroxy-5-isopropylphenyl)-4-(4-morpholin-4-ylmethylphenyl)isoxazole-3-carboxylic acid ethylamide	29-35	checkpoint kinase 1	Homo sapiens	81-85
21566061-7	2011	Following exposure to IR, AUY922 treatment abrogated IR-induced phospho (p)-ATR and p-CHK1 levels, but significantly enhanced gamma-H2AX levels.	5-(2,4-dihydroxy-5-isopropylphenyl)-4-(4-morpholin-4-ylmethylphenyl)isoxazole-3-carboxylic acid ethylamide	26-32	checkpoint kinase 1	Homo sapiens	86-90
21558560-6	2011	Consistently, hydroxyurea induced persistent single strand DNA lesions and sustained CHK1 activation in RNF8-depleted cells.	Hydroxyurea	14-25	checkpoint kinase 1	Homo sapiens	85-89
21998290-9	2011	Artesunate provoked a DNA damage response (DDR) with phosphorylation of ATM, ATR, Chk1, and Chk2.	Artesunate	0-10	checkpoint kinase 1	Homo sapiens	82-86
21674128-3	2011	The pattern of DNA damage checkpoint activation in bolus 5-FU-treated HT29 (TP53-deficient/MMR-proficient) cultures suggested SSB formation (CHEK1 activation) followed by DSB formation (CHEK2 activation and increased phospho-H2AX levels), but no cell death suggested that DNA repair capacity was not overwhelmed.	Fluorouracil	57-61	checkpoint kinase 1	Homo sapiens	141-146
21674128-8	2011	Overall, activation of ATM, CHEK1 and/or CHEK2 and phospho-H2AX levels reflected the nature of 5-FU-induced DNA damage and indi-cated when DNA damage was significant (5-FU-dose-dependent).	Fluorouracil	95-99	checkpoint kinase 1	Homo sapiens	28-33
21609781-8	2011	Oxygen beam irradiated cells showed phosphorylation of Chk1, Chk2 and p53.	Oxygen	0-6	checkpoint kinase 1	Homo sapiens	55-59
21609781-10	2011	The noteworthy finding of this study is the activation of the sensor proteins, ATM and ATR by oxygen irradiation and the significant activation of Chk1, Chk2 and p53 only in the oxygen beam irradiated cells.	Oxygen	178-184	checkpoint kinase 1	Homo sapiens	147-151
21736880-6	2011	One Chk1 inhibitor, the indolocarbazole S27888, was active in the checkpoint bypass assay.	Indolocarbazole	24-39	checkpoint kinase 1	Homo sapiens	4-8
21736880-6	2011	One Chk1 inhibitor, the indolocarbazole S27888, was active in the checkpoint bypass assay.	S 27888	40-46	checkpoint kinase 1	Homo sapiens	4-8
21502314-4	2011	Here, using the well defined Escherichia coli lac repressor/operator system, we have found that directly tethering the ATR activator topoisomerase IIbeta-binding protein 1 (TopBP1) to DNA is sufficient to induce ATR phosphorylation of Chk1 in an in vitro system as well as in vivo in mammalian cells.	Lactose	46-49	checkpoint kinase 1	Homo sapiens	235-239
20623183-4	2011	We report that induction of ERbeta expression causes abrogation of the S-phase, and the Chk1/Cdc25C-mediated G2/M checkpoints after cisplatin and doxorubicin exposure in p53-defective breast cancer cells but not in p53 wild-type mammary cells.	Doxorubicin	146-157	checkpoint kinase 1	Homo sapiens	88-92
20013349-0	2011	Hypoxia-targeting by tirapazamine (TPZ) induces preferential growth inhibition of nasopharyngeal carcinoma cells with Chk1/2 activation.	Tirapazamine	21-33	checkpoint kinase 1	Homo sapiens	118-122
21482692-1	2011	PURPOSE: Chk1 inhibitors, such as AZD7762, are in clinical development in combination with cytotoxic agents for the treatment of solid tumors, including pancreatic cancers.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	34-41	checkpoint kinase 1	Homo sapiens	9-13
21482692-8	2011	Of the biomarkers assessed, pS345 Chk1 was most consistently increased in response to gemcitabine and AZD7762 in tumors and normal tissues (hair follicles).	gemcitabine	86-97	checkpoint kinase 1	Homo sapiens	34-38
21482692-8	2011	Of the biomarkers assessed, pS345 Chk1 was most consistently increased in response to gemcitabine and AZD7762 in tumors and normal tissues (hair follicles).	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	102-109	checkpoint kinase 1	Homo sapiens	34-38
21482692-9	2011	pS345 Chk1 induction in response to gemcitabine and AZD7762 occurred in the presence of PP2A inhibition and in association with elevated gammaH2AX, suggesting that DNA damage is an underlying mechanism.	gemcitabine	36-47	checkpoint kinase 1	Homo sapiens	6-10
21482692-9	2011	pS345 Chk1 induction in response to gemcitabine and AZD7762 occurred in the presence of PP2A inhibition and in association with elevated gammaH2AX, suggesting that DNA damage is an underlying mechanism.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	52-59	checkpoint kinase 1	Homo sapiens	6-10
21482692-10	2011	CONCLUSIONS: AZD7762 sensitizes pancreatic cancer cells and tumors to gemcitabine in association with induction of pS345 Chk1.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	13-20	checkpoint kinase 1	Homo sapiens	121-125
20013349-0	2011	Hypoxia-targeting by tirapazamine (TPZ) induces preferential growth inhibition of nasopharyngeal carcinoma cells with Chk1/2 activation.	Tirapazamine	35-38	checkpoint kinase 1	Homo sapiens	118-122
21336968-4	2011	The Chk1-specific inhibitor, UCN-01, and the ATR inhibitor, Caffeine, cause neuronal apoptosis in differentiated neurons in the absence of additional treatment, whereas inhibition of ATM or Chk2, does not.	7-hydroxystaurosporine	29-35	checkpoint kinase 1	Homo sapiens	4-8
21344307-0	2011	2ME and 2OHE2 exhibit growth inhibitory effects and cell cycle arrest at G2/M in RL95-2 human endometrial cancer cells through activation of p53 and Chk1.	2-Methoxyestradiol	0-3	checkpoint kinase 1	Homo sapiens	149-153
21344307-0	2011	2ME and 2OHE2 exhibit growth inhibitory effects and cell cycle arrest at G2/M in RL95-2 human endometrial cancer cells through activation of p53 and Chk1.	2-hydroxyestradiol	8-13	checkpoint kinase 1	Homo sapiens	149-153
21615992-0	2011	Knock-down of human MutY homolog (hMYH) decreases phosphorylation of checkpoint kinase 1 (Chk1) induced by hydroxyurea and UV treatment.	Hydroxyurea	107-118	checkpoint kinase 1	Homo sapiens	69-88
21615992-0	2011	Knock-down of human MutY homolog (hMYH) decreases phosphorylation of checkpoint kinase 1 (Chk1) induced by hydroxyurea and UV treatment.	Hydroxyurea	107-118	checkpoint kinase 1	Homo sapiens	90-94
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	checkpoint kinase 1	Homo sapiens	35-39
21289082-7	2011	Thus, the growth-suppressive effect of CHK1 inhibition in BRCA2-mutant tumors can be opposed by concurrent KRAS activation and TP53 mutations typical of pancreatic adenocarcinoma, and CHK1i resistance in this setting can be overcome by gemcitabine.	gemcitabine	236-247	checkpoint kinase 1	Homo sapiens	39-43
21321066-0	2011	Targeting the replication checkpoint using SCH 900776, a potent and functionally selective CHK1 inhibitor identified via high content screening.	MK-8776	43-53	checkpoint kinase 1	Homo sapiens	91-95
21321066-9	2011	Using this approach, SCH 900776 was identified as a highly potent and functionally optimal CHK1 inhibitor with minimal intrinsic antagonistic properties.	MK-8776	21-31	checkpoint kinase 1	Homo sapiens	91-95
21321066-10	2011	SCH 900776 exposure phenocopies short interfering RNA-mediated CHK1 ablation and interacts synergistically with DNA antimetabolite agents in vitro and in vivo to selectively induce dsDNA breaks and cell death in tumor cell backgrounds.	MK-8776	0-10	checkpoint kinase 1	Homo sapiens	63-67
21540473-3	2011	7-Hydroxystaurosporine, or UCN-01, is a clinically relevant and well-studied kinase activity inhibitor that exerts chemosensitizing effects by inhibition of Chk1, and a multitude of Chk1 inhibitors have entered development.	7-hydroxystaurosporine	0-22	checkpoint kinase 1	Homo sapiens	157-161
21540473-3	2011	7-Hydroxystaurosporine, or UCN-01, is a clinically relevant and well-studied kinase activity inhibitor that exerts chemosensitizing effects by inhibition of Chk1, and a multitude of Chk1 inhibitors have entered development.	7-hydroxystaurosporine	0-22	checkpoint kinase 1	Homo sapiens	182-186
21540473-3	2011	7-Hydroxystaurosporine, or UCN-01, is a clinically relevant and well-studied kinase activity inhibitor that exerts chemosensitizing effects by inhibition of Chk1, and a multitude of Chk1 inhibitors have entered development.	7-hydroxystaurosporine	27-33	checkpoint kinase 1	Homo sapiens	157-161
21540473-3	2011	7-Hydroxystaurosporine, or UCN-01, is a clinically relevant and well-studied kinase activity inhibitor that exerts chemosensitizing effects by inhibition of Chk1, and a multitude of Chk1 inhibitors have entered development.	7-hydroxystaurosporine	27-33	checkpoint kinase 1	Homo sapiens	182-186
21266192-3	2011	Norcantharidin induced potent cytotoxicity and arrested cell growth through increasing phosphorylation of Chk1, Chk2 and total p21(Waf1/Cip1) and reducing cyclin B and cdc25c expression.	norcantharidin	0-14	checkpoint kinase 1	Homo sapiens	106-110
21212274-0	2011	TAp73 induction by nitric oxide: regulation by checkpoint kinase 1 (CHK1) and protection against apoptosis.	Nitric Oxide	19-31	checkpoint kinase 1	Homo sapiens	47-66
21212274-0	2011	TAp73 induction by nitric oxide: regulation by checkpoint kinase 1 (CHK1) and protection against apoptosis.	Nitric Oxide	19-31	checkpoint kinase 1	Homo sapiens	68-72
21212274-10	2011	In support of this hypothesis, DNA replication inhibitors such as hydroxyurea and aphidicolin similarly enhanced TAp73alpha expression and Chk1 phosphorylation.	Hydroxyurea	66-77	checkpoint kinase 1	Homo sapiens	139-143
21212274-10	2011	In support of this hypothesis, DNA replication inhibitors such as hydroxyurea and aphidicolin similarly enhanced TAp73alpha expression and Chk1 phosphorylation.	Aphidicolin	82-93	checkpoint kinase 1	Homo sapiens	139-143
21131555-6	2011	We used data from a study assessing the effects of radiation, gemcitabine, and a Chk1/2 inhibitor on MiaPaCa-2 xenografts.	miapaca-2	101-110	checkpoint kinase 1	Homo sapiens	81-87
21347609-0	2011	Premature chromosome condensation induced by caffeine, 2-aminopurine, staurosporine and sodium metavanadate in S-phase arrested HeLa cells is associated with a decrease in Chk1 phosphorylation, formation of phospho-H2AX and minor cytoskeletal rearrangements.	Caffeine	45-53	checkpoint kinase 1	Homo sapiens	172-176
21347609-0	2011	Premature chromosome condensation induced by caffeine, 2-aminopurine, staurosporine and sodium metavanadate in S-phase arrested HeLa cells is associated with a decrease in Chk1 phosphorylation, formation of phospho-H2AX and minor cytoskeletal rearrangements.	2-Aminopurine	55-68	checkpoint kinase 1	Homo sapiens	172-176
21347609-0	2011	Premature chromosome condensation induced by caffeine, 2-aminopurine, staurosporine and sodium metavanadate in S-phase arrested HeLa cells is associated with a decrease in Chk1 phosphorylation, formation of phospho-H2AX and minor cytoskeletal rearrangements.	Staurosporine	70-83	checkpoint kinase 1	Homo sapiens	172-176
21347609-0	2011	Premature chromosome condensation induced by caffeine, 2-aminopurine, staurosporine and sodium metavanadate in S-phase arrested HeLa cells is associated with a decrease in Chk1 phosphorylation, formation of phospho-H2AX and minor cytoskeletal rearrangements.	Vanadates	88-107	checkpoint kinase 1	Homo sapiens	172-176
21289283-7	2011	Neuroblastoma cells were sensitive to the two CHK1 inhibitors SB21807 and TCS2312, with median IC(50) values of 564 nM and 548 nM, respectively.	1-tert-Butyl 2-ethyl 4,4-difluoropyrrolidine-1,2-dicarboxylate	62-69	checkpoint kinase 1	Homo sapiens	46-50
21289283-7	2011	Neuroblastoma cells were sensitive to the two CHK1 inhibitors SB21807 and TCS2312, with median IC(50) values of 564 nM and 548 nM, respectively.	tcs2312	74-81	checkpoint kinase 1	Homo sapiens	46-50
21148814-3	2011	The dual Src/Abl inhibitors BMS354825 and SKI-606 blocked Chk1-inhibitor-induced extracellular signal-regulated kinase 1/2 (ERK1/2) activation, markedly increasing apoptosis in association with BimEL up-regulation, p34(cdc2) activation, and DNA damage in MM cell lines and primary CD138(+) MM samples.	Dasatinib	28-37	checkpoint kinase 1	Homo sapiens	58-62
21130714-1	2011	Treatment of PARP-1-expressing cells with the combination of a DNA methylating agent (MMS) and the PARP inhibitor 4-amino-1,8-naphthalimide (4-AN) leads to an ATR/Chk1-dependent S phase checkpoint and cell death by apoptosis.	Methyl Methanesulfonate	86-89	checkpoint kinase 1	Homo sapiens	163-167
21130714-1	2011	Treatment of PARP-1-expressing cells with the combination of a DNA methylating agent (MMS) and the PARP inhibitor 4-amino-1,8-naphthalimide (4-AN) leads to an ATR/Chk1-dependent S phase checkpoint and cell death by apoptosis.	4-amino-1,8-naphthalimide	114-139	checkpoint kinase 1	Homo sapiens	163-167
21130714-1	2011	Treatment of PARP-1-expressing cells with the combination of a DNA methylating agent (MMS) and the PARP inhibitor 4-amino-1,8-naphthalimide (4-AN) leads to an ATR/Chk1-dependent S phase checkpoint and cell death by apoptosis.	4-amino-1,8-naphthalimide	141-145	checkpoint kinase 1	Homo sapiens	163-167
21098122-8	2011	A Tel1-to-Chk1 checkpoint pathway acting at unresected DSBs provides a mechanism for coupling Chk1 activation to the initial detection of DSBs and suggests that ATM may activate Chk1 by both direct and indirect mechanisms in mammalian cells.	dsbs	55-59	checkpoint kinase 1	Homo sapiens	10-14
21098122-8	2011	A Tel1-to-Chk1 checkpoint pathway acting at unresected DSBs provides a mechanism for coupling Chk1 activation to the initial detection of DSBs and suggests that ATM may activate Chk1 by both direct and indirect mechanisms in mammalian cells.	dsbs	55-59	checkpoint kinase 1	Homo sapiens	94-98
21098122-8	2011	A Tel1-to-Chk1 checkpoint pathway acting at unresected DSBs provides a mechanism for coupling Chk1 activation to the initial detection of DSBs and suggests that ATM may activate Chk1 by both direct and indirect mechanisms in mammalian cells.	dsbs	55-59	checkpoint kinase 1	Homo sapiens	94-98
21186793-2	2011	Structure-activity relationships for multiple substituent positions were optimized separately and in combination leading to the 2-(quinazolin-2-yl)phenol 46 (IC(50) 3 nM) with good selectivity for CHK2 against CHK1 and a wider panel of kinases and with promising in vitro ADMET properties.	2-(quinazolin-2-yl)phenol	128-153	checkpoint kinase 1	Homo sapiens	210-214
20447761-7	2010	Furthermore, studies on DNA damage response revealed that phospho-histone H2A.X (gammaH2A.X), a hall marker of DNA double strand break, along with phosphorylated CHK1 (P-CHK1) and CHK2 (P-CHK2) was dramatically induced by SNDX-275 or melphalan.	entinostat	222-230	checkpoint kinase 1	Homo sapiens	162-166
21390062-4	2011	We show that DFO treatment induces phosphorylation of SMC1 at Ser966, NBS1 at Ser343, Chk1 at Ser317, Chk2 at Thr68, and p53 at Ser15.	Deferoxamine	13-16	checkpoint kinase 1	Homo sapiens	86-90
21390062-5	2011	Among these sites, phosphorylation of SMC1, NBS1, and Chk1 by DFO are mediated by ATR as it is greatly reduced in both ATR-deficient human fibroblasts and HCT116 human colon cancer cells in which ATR is heterozygously mutated, whereas these proteins are phosphorylated in cells deficient for ATM and DNA-PKcs.	Deferoxamine	62-65	checkpoint kinase 1	Homo sapiens	54-58
20840867-3	2011	This resulted in reduction of HU-induced phosphorylation of CHK1 S345 (serine 345), p53 S15, and H2AX S139.	Hydroxyurea	30-32	checkpoint kinase 1	Homo sapiens	60-66
20840867-3	2011	This resulted in reduction of HU-induced phosphorylation of CHK1 S345 (serine 345), p53 S15, and H2AX S139.	Serine	71-77	checkpoint kinase 1	Homo sapiens	60-66
20619533-0	2010	Chk1 inhibitor Go6976 enhances the sensitivity of nasopharyngeal carcinoma cells to radiotherapy and chemotherapy in vitro and in vivo.	Go 6976	15-21	checkpoint kinase 1	Homo sapiens	0-4
20619533-4	2010	We determined that the Chk1 inhibitor Go6976 enhanced the sensitivity of CNE1 and CNE2 cells to ionizing radiation (IR) or cisplatin by abrogating S and G(2)/M arrest and subsequently promoting apoptosis.	Go 6976	38-44	checkpoint kinase 1	Homo sapiens	23-27
20619533-4	2010	We determined that the Chk1 inhibitor Go6976 enhanced the sensitivity of CNE1 and CNE2 cells to ionizing radiation (IR) or cisplatin by abrogating S and G(2)/M arrest and subsequently promoting apoptosis.	Cisplatin	123-132	checkpoint kinase 1	Homo sapiens	23-27
20619533-6	2010	This is the first report to show that the Chk1 inhibitor Go6976 sensitizes NPC cells to treatment using in vitro and in vivo models.	Go 6976	57-63	checkpoint kinase 1	Homo sapiens	42-46
20943405-1	2010	The structure-activity relationship (SAR) of 5-substituted pyrrolo[3,4-c]carbazole-1,3(2H,6H)-dione derivatives 5 was investigated for their potential as Chk1 inhibitors for possible chemo- and radio-potentiators in anticancer chemotherapies.	5-substituted pyrrolo[3,4-c]carbazole-1,3(2h,6h)-dione	45-99	checkpoint kinase 1	Homo sapiens	154-158
20805228-5	2010	Inhibition of cancer cell growth by MitoQ was associated with G(1)/S cell cycle arrest and phosphorylation of the checkpoint kinases Chk1 and Chk2.	mitoquinone	36-41	checkpoint kinase 1	Homo sapiens	133-137
21390062-7	2011	Expression of SMC1 S966A in which Ser966 is substituted to Ala attenuates apoptosis and phosphorylation of Chk1 at Ser317 after DFO treatment, although levels of HIF1alpha are not significantly changed.	Deferoxamine	128-131	checkpoint kinase 1	Homo sapiens	107-111
21094607-0	2011	Discovery of pyrazolo[1,5-a]pyrimidine-based CHK1 inhibitors: a template-based approach--part 2.	pyrazolo(1,5-a)pyrimidine	13-38	checkpoint kinase 1	Homo sapiens	45-49
21094607-2	2011	As part of an effort to utilize the pyrazolo[1,5-a]pyrimidine core as a template for the design and synthesis of potent and selective kinase inhibitors, we focused on a key regulator in the cell cycle progression, CHK1.	pyrazolo(1,5-a)pyrimidine	36-61	checkpoint kinase 1	Homo sapiens	214-218
21094607-3	2011	Continued SAR development of the pyrazolo[1,5-a]pyrimidine core at the C5 and C6 positions, in conjunction with previously disclosed SAR at the C3 and C7 positions, led to the discovery of potent and selective CHK1 inhibitors.	pyrazolo(1,5-a)pyrimidine	33-58	checkpoint kinase 1	Homo sapiens	210-214
21094608-0	2011	Discovery of pyrazolo[1,5-a]pyrimidine-based CHK1 inhibitors: a template-based approach--part 1.	pyrazolo(1,5-a)pyrimidine	13-38	checkpoint kinase 1	Homo sapiens	45-49
21094608-1	2011	The synthesis and hit-to-lead SAR development of a pyrazolo[1,5-a]pyrimidine hit 4 is described leading to a series of potent, selective CHK1 inhibitors such as compound 17r.	pyrazolo(1,5-a)pyrimidine	51-76	checkpoint kinase 1	Homo sapiens	137-141
21512242-6	2011	PLE and PLEg reduced the phosphorylation of checkpoint proteins such as structural maintenance of chromosomes 1 (SMC1), checkpoint kinase 1 (Chk1), and p53 in DOX-treated cells.	Doxorubicin	159-162	checkpoint kinase 1	Homo sapiens	120-139
21512242-6	2011	PLE and PLEg reduced the phosphorylation of checkpoint proteins such as structural maintenance of chromosomes 1 (SMC1), checkpoint kinase 1 (Chk1), and p53 in DOX-treated cells.	Doxorubicin	159-162	checkpoint kinase 1	Homo sapiens	141-145
21870291-5	2011	Within the regulatory domain there are two residues, Serine-317 (S317) and Serine-345 (S345), which are phosphorylated in active Chk1 molecules, and subsequently dephosphorylated to inactivate Chk1 and allow mitotic entry.	Serine	53-59	checkpoint kinase 1	Homo sapiens	129-133
21870291-5	2011	Within the regulatory domain there are two residues, Serine-317 (S317) and Serine-345 (S345), which are phosphorylated in active Chk1 molecules, and subsequently dephosphorylated to inactivate Chk1 and allow mitotic entry.	Serine	53-59	checkpoint kinase 1	Homo sapiens	193-197
21870291-5	2011	Within the regulatory domain there are two residues, Serine-317 (S317) and Serine-345 (S345), which are phosphorylated in active Chk1 molecules, and subsequently dephosphorylated to inactivate Chk1 and allow mitotic entry.	Serine	75-81	checkpoint kinase 1	Homo sapiens	129-133
21870291-5	2011	Within the regulatory domain there are two residues, Serine-317 (S317) and Serine-345 (S345), which are phosphorylated in active Chk1 molecules, and subsequently dephosphorylated to inactivate Chk1 and allow mitotic entry.	Serine	75-81	checkpoint kinase 1	Homo sapiens	193-197
22329197-9	2011	We previously assessed radiation survival of lung cancer cell lines after treating them with Chk1 inhibitor, AZD7762.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	109-116	checkpoint kinase 1	Homo sapiens	93-97
21858012-12	2011	Together, our data indicate that association of RAD18 with DSBs through ubiquitylated H2A and other ubiquitylated chromatin components allows recruitment of RAD9, which may function directly in DSB repair, independent of downstream activation of the checkpoint kinases CHK1 and CHK2.	1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione	59-63	checkpoint kinase 1	Homo sapiens	269-273
21074424-0	2010	Design, synthesis and SAR of thienopyridines as potent CHK1 inhibitors.	Thienopyridines	29-44	checkpoint kinase 1	Homo sapiens	55-59
21074424-1	2010	A novel series of CHK1 inhibitors based on thienopyridine template has been designed and synthesized.	thienopyridine	43-57	checkpoint kinase 1	Homo sapiens	18-22
20447761-7	2010	Furthermore, studies on DNA damage response revealed that phospho-histone H2A.X (gammaH2A.X), a hall marker of DNA double strand break, along with phosphorylated CHK1 (P-CHK1) and CHK2 (P-CHK2) was dramatically induced by SNDX-275 or melphalan.	Melphalan	234-243	checkpoint kinase 1	Homo sapiens	162-166
20599444-8	2010	The relevance of cell cycle control was further demonstrated by experiments showing the association of Chk1 activation with greater TK/GCV cytotoxicity.	Ganciclovir	135-138	checkpoint kinase 1	Homo sapiens	103-107
20948546-1	2010	The DNA-damage-induced transcriptional suppression of cell cycle regulatory genes correlates with a reduction in histone H3-Thr 11 phosphorylation (H3-pThr 11) on their promoters that is partly mediated by the dissociation of Chk1 from chromatin.	Threonine	124-127	checkpoint kinase 1	Homo sapiens	226-230
21051833-2	2010	METHODS: Envision Tm immunohistochemistry was used to detect the expression level of CHK1 and PLK1 in conventional paraffin-embedded sections from specimens of primary foci (n=59)and metastatic foci of lymph node (n=42) of gastric cancer, peritumoral tissues (n=20), and benign lesions of the stomach (n=95).	Paraffin	115-123	checkpoint kinase 1	Homo sapiens	85-89
20413215-0	2010	Gambogic acid triggers DNA damage signaling that induces p53/p21(Waf1/CIP1) activation through the ATR-Chk1 pathway.	gambogic acid	0-13	checkpoint kinase 1	Homo sapiens	103-107
20413215-7	2010	GA induces p53 phosphorylation through activation of an ATM- and Rad3-related pathway, and GA-induced phosphorylation of Chk1 is also involved.	gambogic acid	91-93	checkpoint kinase 1	Homo sapiens	121-125
20811685-10	2010	PTX combined with radiation maintained high expressions of Chk1 and MAD2 proteins for 24 h post-radiation and, in particular, MAD2 protein was strongly induced by PTX with high-dose radiation.	Paclitaxel	0-3	checkpoint kinase 1	Homo sapiens	59-63
20811685-10	2010	PTX combined with radiation maintained high expressions of Chk1 and MAD2 proteins for 24 h post-radiation and, in particular, MAD2 protein was strongly induced by PTX with high-dose radiation.	Paclitaxel	163-166	checkpoint kinase 1	Homo sapiens	59-63
20674356-0	2010	Synthesis of selenophene derivatives as novel CHK1 inhibitors.	Selenophene	13-24	checkpoint kinase 1	Homo sapiens	46-50
20805465-6	2010	We use the Cdk inhibitor roscovitine or RNAi depletion of Cdc7 to inhibit origin firing in Chk1-inhibited or RNAi-depleted cells.	Roscovitine	25-36	checkpoint kinase 1	Homo sapiens	91-95
20643585-4	2010	The RECQL5 protein relocates specifically to stalled replication forks and suppresses thymidine-induced RPA foci, CHK1 signalling, homologous recombination and gammaH2AX activation.	Thymidine	86-95	checkpoint kinase 1	Homo sapiens	114-118
20673630-2	2010	A novel class of Chk1 inhibitors, triazoloquinolones/triazolones (TZ"s) was identified by high throughput screening.	triazoloquinolones	34-52	checkpoint kinase 1	Homo sapiens	17-21
20673630-2	2010	A novel class of Chk1 inhibitors, triazoloquinolones/triazolones (TZ"s) was identified by high throughput screening.	triazolones	53-64	checkpoint kinase 1	Homo sapiens	17-21
20673630-2	2010	A novel class of Chk1 inhibitors, triazoloquinolones/triazolones (TZ"s) was identified by high throughput screening.	tz"s	66-70	checkpoint kinase 1	Homo sapiens	17-21
20722101-7	2010	Inhibition of ATR and CHK1 resulted in the greatest modulation of cisplatin response.	Cisplatin	66-75	checkpoint kinase 1	Homo sapiens	22-26
20722101-9	2010	To show that the siRNA data could be successfully translated into potential therapeutic strategies, CHK1 was further targeted with small molecule inhibitor PD 407824 in combination with cisplatin.	Cisplatin	186-195	checkpoint kinase 1	Homo sapiens	100-104
20722101-10	2010	Results showed that treatment of SKOV3 and OVCAR3 cells with CHK1 inhibitor PD 407824 led to sensitization of ovarian cancer cells to cisplatin.	Cisplatin	134-143	checkpoint kinase 1	Homo sapiens	61-65
20719863-0	2010	Chk1-dependent constitutive phosphorylation of BLM helicase at serine 646 decreases after DNA damage.	Serine	63-69	checkpoint kinase 1	Homo sapiens	0-4
20719863-5	2010	Using in silico analysis involving the Chk1 structure and its known substrate specificity, we predicted that Chk1 should preferentially phosphorylate BLM on serine 646 (Ser(646)).	Serine	157-163	checkpoint kinase 1	Homo sapiens	39-43
20719863-5	2010	Using in silico analysis involving the Chk1 structure and its known substrate specificity, we predicted that Chk1 should preferentially phosphorylate BLM on serine 646 (Ser(646)).	Serine	157-163	checkpoint kinase 1	Homo sapiens	109-113
20719863-5	2010	Using in silico analysis involving the Chk1 structure and its known substrate specificity, we predicted that Chk1 should preferentially phosphorylate BLM on serine 646 (Ser(646)).	Serine	169-172	checkpoint kinase 1	Homo sapiens	39-43
20719863-5	2010	Using in silico analysis involving the Chk1 structure and its known substrate specificity, we predicted that Chk1 should preferentially phosphorylate BLM on serine 646 (Ser(646)).	Serine	169-172	checkpoint kinase 1	Homo sapiens	109-113
20719863-11	2010	These results indicated that Chk1-mediated phosphorylation on BLM at Ser(646) might be a determinant for regulating subnuclear localization and could act as a marker for the activation status of BLM in response to DNA damage.	Serine	69-72	checkpoint kinase 1	Homo sapiens	29-33
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	checkpoint kinase 1	Homo sapiens	10-14
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	checkpoint kinase 1	Homo sapiens	10-14
20561787-1	2010	A range of 3,6-di(hetero)arylimidazo[1,2-a]pyrazine ATP-competitive inhibitors of CHK1 were developed by scaffold hopping from a weakly active screening hit.	3,6-di(hetero)arylimidazo[1,2-a]pyrazine	11-51	checkpoint kinase 1	Homo sapiens	82-86
20561787-1	2010	A range of 3,6-di(hetero)arylimidazo[1,2-a]pyrazine ATP-competitive inhibitors of CHK1 were developed by scaffold hopping from a weakly active screening hit.	Adenosine Triphosphate	52-55	checkpoint kinase 1	Homo sapiens	82-86
20599444-9	2010	Combination treatment with Chk1 inhibitor UCN-01 induced, in sensitive cells, an antagonistic effect on TK/GCV cytotoxicity highlighting the relevance of Chk1"s activity on TK/GCV mechanism of action.	Ganciclovir	107-110	checkpoint kinase 1	Homo sapiens	27-31
20599444-9	2010	Combination treatment with Chk1 inhibitor UCN-01 induced, in sensitive cells, an antagonistic effect on TK/GCV cytotoxicity highlighting the relevance of Chk1"s activity on TK/GCV mechanism of action.	Ganciclovir	176-179	checkpoint kinase 1	Homo sapiens	27-31
20599444-9	2010	Combination treatment with Chk1 inhibitor UCN-01 induced, in sensitive cells, an antagonistic effect on TK/GCV cytotoxicity highlighting the relevance of Chk1"s activity on TK/GCV mechanism of action.	Ganciclovir	176-179	checkpoint kinase 1	Homo sapiens	154-158
20599444-11	2010	Moreover it points out, for the first time at Chk1 activation as a key factor to mediate TK/GCV cytotoxicity.	Ganciclovir	92-95	checkpoint kinase 1	Homo sapiens	46-50
20674356-1	2010	A series of selenophene derivatives 3 were synthesized as potential CHK1 inhibitors.	Selenophene	12-23	checkpoint kinase 1	Homo sapiens	68-72
20514394-5	2010	At the same time, ATR is activated, activating CHK1 that may phosphorylate P53 but also contribute to inhibition of MnSOD expression leading to accumulation of ROS (reactive oxygen species) and subsequent DNA injury, which in turn maintains ATR/CHK1 activated.	Reactive Oxygen Species	160-163	checkpoint kinase 1	Homo sapiens	47-51
20536192-6	2010	Checkpoint 1 protein (Chk1) was depleted following DMC, and the depletion of Chk1 by DMC was achieved through the ubiquitin proteasome pathway since chemical inhibition of the proteasome protected against Chk1 depletion.	10-decarbamoylmitomycin C	51-54	checkpoint kinase 1	Homo sapiens	22-26
20536192-6	2010	Checkpoint 1 protein (Chk1) was depleted following DMC, and the depletion of Chk1 by DMC was achieved through the ubiquitin proteasome pathway since chemical inhibition of the proteasome protected against Chk1 depletion.	10-decarbamoylmitomycin C	85-88	checkpoint kinase 1	Homo sapiens	77-81
20536192-6	2010	Checkpoint 1 protein (Chk1) was depleted following DMC, and the depletion of Chk1 by DMC was achieved through the ubiquitin proteasome pathway since chemical inhibition of the proteasome protected against Chk1 depletion.	10-decarbamoylmitomycin C	85-88	checkpoint kinase 1	Homo sapiens	77-81
20536192-7	2010	Gene silencing of Chk1 by siRNA increased the cytotoxicity of MC.	Mitomycin	62-64	checkpoint kinase 1	Homo sapiens	18-22
20536192-9	2010	Thus, the mitosene-1-beta stereoisomeric DNA adducts produced by the DMC signal for a p53-independent mode of cell death correlated with reduced nuclear size, persistent DNA damage, increased ubiquitin proteolysis and reduced Chk1 protein.	10-decarbamoylmitomycin C	69-72	checkpoint kinase 1	Homo sapiens	226-230
20020310-2	2010	A structure-based modeling approach complemented with shape components was pursued to develop a reliable pharmacophore model for ATP-competitive Chk1 inhibitors.	Adenosine Triphosphate	129-132	checkpoint kinase 1	Homo sapiens	145-149
20514394-5	2010	At the same time, ATR is activated, activating CHK1 that may phosphorylate P53 but also contribute to inhibition of MnSOD expression leading to accumulation of ROS (reactive oxygen species) and subsequent DNA injury, which in turn maintains ATR/CHK1 activated.	Reactive Oxygen Species	165-188	checkpoint kinase 1	Homo sapiens	47-51
20514394-5	2010	At the same time, ATR is activated, activating CHK1 that may phosphorylate P53 but also contribute to inhibition of MnSOD expression leading to accumulation of ROS (reactive oxygen species) and subsequent DNA injury, which in turn maintains ATR/CHK1 activated.	Reactive Oxygen Species	165-188	checkpoint kinase 1	Homo sapiens	245-249
20042274-9	2010	Thus, depending on the biological context, the camptothecin activated ATM-Chk2 or ATR-Chk1 pathways, both having a protective role.	Camptothecin	47-59	checkpoint kinase 1	Homo sapiens	86-90
20421415-4	2010	We show that ATM-dependent resection at a subset of DSBs leads to ATR-dependent Chk1 activation.	dsbs	52-56	checkpoint kinase 1	Homo sapiens	80-84
20440261-4	2010	We investigated the mechanisms involved and show that a reduction in MCM levels causes dose-dependent DNA damage involving activation of ATR & ATM and Chk1 & Chk2.	Adenosine Monophosphate	161-164	checkpoint kinase 1	Homo sapiens	155-159
20514472-0	2010	Pectenotoxin-2 induces G2/M phase cell cycle arrest in human breast cancer cells via ATM and Chk1/2-mediated phosphorylation of cdc25C.	pectenotoxin 2	0-14	checkpoint kinase 1	Homo sapiens	93-97
20514472-4	2010	We found increased phosphorylation of ATM and Chk1/2 in a PTX-2 dose-dependent manner.	ptx	58-61	checkpoint kinase 1	Homo sapiens	46-52
19739070-3	2010	By using hMLH1 expressing clones or cells transduced with the hMLH1-expressing adenovirus as well as siRNA technology, we show that in response to SN-38-induced DNA damage the MMR proficient (MMR(+)) cells make: (i) a stronger G2/M arrest, (ii) a subsequent longer tetraploid G1 arrest, (iii) a stronger activation of Chk1 and Chk2 kinases than the MMR deficient (MMR(-)) counterparts.	Irinotecan	147-152	checkpoint kinase 1	Homo sapiens	318-322
20501833-0	2010	Mechanism of radiosensitization by the Chk1/2 inhibitor AZD7762 involves abrogation of the G2 checkpoint and inhibition of homologous recombinational DNA repair.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	56-63	checkpoint kinase 1	Homo sapiens	39-45
20501833-2	2010	To develop improved treatment, we have combined a Chk1/2-targeted agent, AZD7762, currently in phase I clinical trials, with gemcitabine and ionizing radiation in preclinical pancreatic tumor models.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	73-80	checkpoint kinase 1	Homo sapiens	50-54
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	checkpoint kinase 1	Homo sapiens	18-22
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	checkpoint kinase 1	Homo sapiens	49-53
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	checkpoint kinase 1	Homo sapiens	49-53
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	checkpoint kinase 1	Homo sapiens	49-53
20368736-7	2010	Furthermore, suppression of Checkpoint kinase 1 (Chk1) expression with a subsequent reduction in 6-TG-induced G2/M cell cycle arrest by Chk1 siRNA promotes the extent of 6-TG-induced autophagy.	Thioguanine	97-101	checkpoint kinase 1	Homo sapiens	28-47
20368736-7	2010	Furthermore, suppression of Checkpoint kinase 1 (Chk1) expression with a subsequent reduction in 6-TG-induced G2/M cell cycle arrest by Chk1 siRNA promotes the extent of 6-TG-induced autophagy.	Thioguanine	97-101	checkpoint kinase 1	Homo sapiens	49-53
20368736-7	2010	Furthermore, suppression of Checkpoint kinase 1 (Chk1) expression with a subsequent reduction in 6-TG-induced G2/M cell cycle arrest by Chk1 siRNA promotes the extent of 6-TG-induced autophagy.	Thioguanine	97-101	checkpoint kinase 1	Homo sapiens	136-140
20368736-7	2010	Furthermore, suppression of Checkpoint kinase 1 (Chk1) expression with a subsequent reduction in 6-TG-induced G2/M cell cycle arrest by Chk1 siRNA promotes the extent of 6-TG-induced autophagy.	Thioguanine	170-174	checkpoint kinase 1	Homo sapiens	28-47
20368736-7	2010	Furthermore, suppression of Checkpoint kinase 1 (Chk1) expression with a subsequent reduction in 6-TG-induced G2/M cell cycle arrest by Chk1 siRNA promotes the extent of 6-TG-induced autophagy.	Thioguanine	170-174	checkpoint kinase 1	Homo sapiens	49-53
20368736-7	2010	Furthermore, suppression of Checkpoint kinase 1 (Chk1) expression with a subsequent reduction in 6-TG-induced G2/M cell cycle arrest by Chk1 siRNA promotes the extent of 6-TG-induced autophagy.	Thioguanine	170-174	checkpoint kinase 1	Homo sapiens	136-140
20368736-9	2010	Additionally, the duration of Chk1-activated G2/M cell cycle arrest determines the level of autophagy following MMR processing of these nucleoside analogs.	Nucleosides	136-146	checkpoint kinase 1	Homo sapiens	30-34
21034966-5	2010	In response to DSBs, ATM is required both for ATR-Chk1 activation and to initiate DNA repair via homologous recombination (HRR) by promoting formation of single-stranded DNA at sites of damage through nucleolytic resection.	dsbs	15-19	checkpoint kinase 1	Homo sapiens	50-54
20123862-6	2010	Addition of a low concentration of caffeine post-irradiation, although inefficient to restore S-phase progression, significantly decreases Chk1 activation and abrogates DNA synthesis in XP-V cells.	Caffeine	35-43	checkpoint kinase 1	Homo sapiens	139-143
20372057-5	2010	While siRNA-mediated depletion of ATR and CHEK1 increased the mitotic index in ICRF-193 treated NHDF lines, depletion of these proteins did not affect the mitotic entry rate, indicating that the decatenation G2 checkpoint was functional.	nhdf	96-100	checkpoint kinase 1	Homo sapiens	42-47
20233881-2	2010	A novel checkpoint kinase 1/2 inhibitor, AZD7762, was evaluated for potential enhancement of radiosensitivity for human tumor cells in vitro and in vivo xenografts.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	41-48	checkpoint kinase 1	Homo sapiens	8-29
20401435-0	2010	Growth inhibitory effect and Chk1-dependent signaling involved in G2/M arrest on human gastric cancer cells induced by diallyl disulfide.	diallyl disulfide	119-136	checkpoint kinase 1	Homo sapiens	29-33
20401435-4	2010	We hypothesized that DADS could mediate G2/M phase arrest through either Chk1 or Chk2 signal transduction pathways.	diallyl disulfide	21-25	checkpoint kinase 1	Homo sapiens	73-77
20401435-5	2010	We demonstrated that DADS induced the accumulation of phosphorylated Chk1, but not of Chk2, and that DADS down-regulated Cdc25C and cyclin B1.	diallyl disulfide	21-25	checkpoint kinase 1	Homo sapiens	69-73
20401435-10	2010	Furthermore, the DADS-induced G2/M checkpoint response is mediated by Chk1 signaling through ATR/Chk1/Cdc25C/cyclin B1, and is independent of Chk2.	diallyl disulfide	17-21	checkpoint kinase 1	Homo sapiens	70-74
20401435-10	2010	Furthermore, the DADS-induced G2/M checkpoint response is mediated by Chk1 signaling through ATR/Chk1/Cdc25C/cyclin B1, and is independent of Chk2.	diallyl disulfide	17-21	checkpoint kinase 1	Homo sapiens	97-101
20053681-2	2010	Here we show that gammaH2AX formation is greatly enhanced in response to replication inhibitors but not ionizing radiation in HCT116 or SW480 cells depleted of Chk1.	gammah2ax	18-27	checkpoint kinase 1	Homo sapiens	160-164
20053681-6	2010	BrdU incorporation only occurs in a minority of Chk1-depleted cells containing gammaH2AX foci after release from thymidine arrest and, in cells incorporating BrdU, DNA synthesis does not occur at sites of gammaH2AX foci.	Bromodeoxyuridine	0-4	checkpoint kinase 1	Homo sapiens	48-52
19643530-3	2010	Butein-induced G(2)/M phase arrest was associated with increased ATM, Chk1, and Chk2 phosphorylations and reduced cdc25C levels.	butein	0-6	checkpoint kinase 1	Homo sapiens	70-74
20029092-8	2010	Use of a modified chromatin immunoprecipitation assay showed that proliferating cell nuclear antigen, ATR, TopBP1, and Chk1 are recruited to chromatin in a MutLalpha- and MutSalpha-dependent fashion after N-methyl-N"-nitro-N-nitrosoguanidine treatment.	Methylnitronitrosoguanidine	205-241	checkpoint kinase 1	Homo sapiens	119-123
20128919-8	2010	Like irradiation, loratadine initially induced G2/M arrest and activation of the cell-cycle associated protein Chk1 to pChk1(ser345), however a subsequent decrease in expression of total Chk1 and Cyclin B correlated with abrogation of the G2/M checkpoint.	Loratadine	18-28	checkpoint kinase 1	Homo sapiens	111-115
20128919-8	2010	Like irradiation, loratadine initially induced G2/M arrest and activation of the cell-cycle associated protein Chk1 to pChk1(ser345), however a subsequent decrease in expression of total Chk1 and Cyclin B correlated with abrogation of the G2/M checkpoint.	Loratadine	18-28	checkpoint kinase 1	Homo sapiens	120-124
20128919-10	2010	Taken together, these data suggest that the observed effects of loratadine are multifactorial in that loratadine 1) directly damages DNA, 2) activates Chk1 thereby promoting G2/M arrest making cells more susceptible to radiation-induced DNA damage and, 3) downregulates total Chk1 and Cyclin B abrogating the radiation-induced G2/M checkpoint and allowing cells to re-enter the cell cycle despite the persistence of damaged DNA.	Loratadine	64-74	checkpoint kinase 1	Homo sapiens	151-155
20128919-10	2010	Taken together, these data suggest that the observed effects of loratadine are multifactorial in that loratadine 1) directly damages DNA, 2) activates Chk1 thereby promoting G2/M arrest making cells more susceptible to radiation-induced DNA damage and, 3) downregulates total Chk1 and Cyclin B abrogating the radiation-induced G2/M checkpoint and allowing cells to re-enter the cell cycle despite the persistence of damaged DNA.	Loratadine	64-74	checkpoint kinase 1	Homo sapiens	276-280
20128919-10	2010	Taken together, these data suggest that the observed effects of loratadine are multifactorial in that loratadine 1) directly damages DNA, 2) activates Chk1 thereby promoting G2/M arrest making cells more susceptible to radiation-induced DNA damage and, 3) downregulates total Chk1 and Cyclin B abrogating the radiation-induced G2/M checkpoint and allowing cells to re-enter the cell cycle despite the persistence of damaged DNA.	Loratadine	102-112	checkpoint kinase 1	Homo sapiens	151-155
20128919-10	2010	Taken together, these data suggest that the observed effects of loratadine are multifactorial in that loratadine 1) directly damages DNA, 2) activates Chk1 thereby promoting G2/M arrest making cells more susceptible to radiation-induced DNA damage and, 3) downregulates total Chk1 and Cyclin B abrogating the radiation-induced G2/M checkpoint and allowing cells to re-enter the cell cycle despite the persistence of damaged DNA.	Loratadine	102-112	checkpoint kinase 1	Homo sapiens	276-280
20090422-6	2010	The activity of NEK11 is in turn controlled by CHK1 that activates NEK11 via phosphorylation on serine 273.	Serine	96-102	checkpoint kinase 1	Homo sapiens	47-51
19931410-0	2010	Checkpoint kinase 1 modulates sensitivity to cisplatin after spindle checkpoint activation in SW620 cells.	Cisplatin	45-54	checkpoint kinase 1	Homo sapiens	0-19
19931410-9	2010	These studies showed that SW620 cells undergo synergistic cell death after spindle checkpoint activation followed by cisplatin treatment, suggesting a role of Chk1 in this checkpoint, very likely dependent on BubR1 protein.	Cisplatin	117-126	checkpoint kinase 1	Homo sapiens	159-163
20053762-6	2010	SAR-020106 is an ATP-competitive, potent, and selective CHK1 inhibitor with an IC(50) of 13.3 nmol/L on the isolated human enzyme.	Adenosine Triphosphate	17-20	checkpoint kinase 1	Homo sapiens	56-60
19589639-6	2009	Furthermore, gallic acid is shown to block the growth of DU145 cells at G2/M phases by activating Chk1 and Chk2 and inhibiting Cdc25C and Cdc2 activities.	Gallic Acid	13-24	checkpoint kinase 1	Homo sapiens	98-102
19732843-8	2009	These results demonstrate that genistein-activated ATM-Chk2-Cdc25 and ATR-Chk1-Cdc25 DNA damage checkpoint pathways can arrest ovarian cancer cells in G2/M phase, and induce apoptosis while the cellular DNA damage is too serious to be repaired.	Genistein	31-40	checkpoint kinase 1	Homo sapiens	74-78
19837665-3	2009	We reported recently that Chk1 is phosphorylated at Ser(286) and Ser(301) by Cdk1 during mitosis.	Serine	52-55	checkpoint kinase 1	Homo sapiens	26-30
19837665-3	2009	We reported recently that Chk1 is phosphorylated at Ser(286) and Ser(301) by Cdk1 during mitosis.	Serine	65-68	checkpoint kinase 1	Homo sapiens	26-30
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	checkpoint kinase 1	Homo sapiens	80-84
19679195-7	2009	Finally, 4,4"-dihydroxy-trans-stilbene increased p21(CDKN1A) and p53 protein levels, whereas resveratrol led to phosphorylation of the S-phase checkpoint protein Chk1.	Resveratrol	93-104	checkpoint kinase 1	Homo sapiens	162-166
19517066-1	2009	Previous studies have revealed that p38, a member of the family of stress-activated protein kinases (SAPKs), cooperates with the Chk1-pathway to bring about temozolomide (TMZ)-induced G2 arrest, and that the inhibition of either pathway alone is sufficient to sensitize U87MG glioma cells to TMZ-induced cytotoxicity.	Temozolomide	157-169	checkpoint kinase 1	Homo sapiens	129-133
19931733-6	2009	TMZ induced G2/M cell-cycle arrest at 48-72 h, coincident with phosphorylation of Chk1 and Chk2.	Temozolomide	0-3	checkpoint kinase 1	Homo sapiens	82-86
19931733-7	2009	Additive G2/M arrest and Chk1/Chk2 phosphorylation was only observed when TMZ preceded radiation by 72 h. The ataxia-telangiectasia mutated (ATM) inhibitor KU-55933 increased radiation sensitivity and delayed repair of radiation-induced DNA breaks, but did not influence TMZ effects.	Temozolomide	74-77	checkpoint kinase 1	Homo sapiens	25-29
19517066-1	2009	Previous studies have revealed that p38, a member of the family of stress-activated protein kinases (SAPKs), cooperates with the Chk1-pathway to bring about temozolomide (TMZ)-induced G2 arrest, and that the inhibition of either pathway alone is sufficient to sensitize U87MG glioma cells to TMZ-induced cytotoxicity.	Temozolomide	171-174	checkpoint kinase 1	Homo sapiens	129-133
19517066-1	2009	Previous studies have revealed that p38, a member of the family of stress-activated protein kinases (SAPKs), cooperates with the Chk1-pathway to bring about temozolomide (TMZ)-induced G2 arrest, and that the inhibition of either pathway alone is sufficient to sensitize U87MG glioma cells to TMZ-induced cytotoxicity.	Temozolomide	292-295	checkpoint kinase 1	Homo sapiens	129-133
19459175-0	2009	Diallyl trisulfide-induced apoptosis in human cancer cells is linked to checkpoint kinase 1-mediated mitotic arrest.	diallyl trisulfide	0-18	checkpoint kinase 1	Homo sapiens	72-91
20098609-1	2009	Granulatimide and isogranulatimide are alkaloids obtained from marine sources which have been shown to inhibit cell-cycle G2-checkpoint, targeting more particularly checkpoint 1 kinase (Chk1).	granulatimide	0-13	checkpoint kinase 1	Homo sapiens	165-184
20098609-1	2009	Granulatimide and isogranulatimide are alkaloids obtained from marine sources which have been shown to inhibit cell-cycle G2-checkpoint, targeting more particularly checkpoint 1 kinase (Chk1).	granulatimide	0-13	checkpoint kinase 1	Homo sapiens	186-190
20098609-1	2009	Granulatimide and isogranulatimide are alkaloids obtained from marine sources which have been shown to inhibit cell-cycle G2-checkpoint, targeting more particularly checkpoint 1 kinase (Chk1).	isogranulatimide	18-34	checkpoint kinase 1	Homo sapiens	165-184
20098609-1	2009	Granulatimide and isogranulatimide are alkaloids obtained from marine sources which have been shown to inhibit cell-cycle G2-checkpoint, targeting more particularly checkpoint 1 kinase (Chk1).	isogranulatimide	18-34	checkpoint kinase 1	Homo sapiens	186-190
20098609-1	2009	Granulatimide and isogranulatimide are alkaloids obtained from marine sources which have been shown to inhibit cell-cycle G2-checkpoint, targeting more particularly checkpoint 1 kinase (Chk1).	Alkaloids	39-48	checkpoint kinase 1	Homo sapiens	165-184
20098609-1	2009	Granulatimide and isogranulatimide are alkaloids obtained from marine sources which have been shown to inhibit cell-cycle G2-checkpoint, targeting more particularly checkpoint 1 kinase (Chk1).	Alkaloids	39-48	checkpoint kinase 1	Homo sapiens	186-190
19808933-6	2009	MEPE/OF45, interacting with CHK1, increases CHK1 half-life and decreases CHK1 degradation through the ubiquitine-mediated pathway.	ubiquitine	102-112	checkpoint kinase 1	Homo sapiens	28-32
19843865-4	2009	Moreover, we observe a beneficial effect of CHK1 inhibition in high-DNA damage level AML samples treated with 1-beta-d-arabinofuranosylcytosine.	Cytarabine	110-143	checkpoint kinase 1	Homo sapiens	44-48
19814732-0	2009	Vitamin D inhibits growth of human airway smooth muscle cells through growth factor-induced phosphorylation of retinoblastoma protein and checkpoint kinase 1.	Vitamin D	0-9	checkpoint kinase 1	Homo sapiens	138-157
19814732-9	2009	Calcitriol inhibited PDGF-induced phosphorylation of retinoblastoma protein (Rb) and Chk1, with no effects on PDGF-mediated activation of extracellular signal-regulated kinases 1/2, PI3-kinase and S6 kinase, or expression of p21(Waf/Cip-1), p27(Kip1), cyclin D and E2F-1.	Calcitriol	0-10	checkpoint kinase 1	Homo sapiens	85-89
19814732-11	2009	CONCLUSIONS AND IMPLICATIONS: Calcitriol decreased PDGF-induced ASM cell growth by inhibiting Rb and Chk1 phosphorylation.	Calcitriol	30-40	checkpoint kinase 1	Homo sapiens	101-105
19881958-1	2009	Naphthalimides, particularly amonafide and 2-(2-dimethylamino)-6-thia-2-aza-benzo[def]chrysene-1,3-diones (R16), have been identified to possess anticancer activities and to induce G(2)-M arrest through inhibiting topoisomerase II accompanied by Chk1 degradation.	Naphthalimides	0-14	checkpoint kinase 1	Homo sapiens	246-250
19881958-1	2009	Naphthalimides, particularly amonafide and 2-(2-dimethylamino)-6-thia-2-aza-benzo[def]chrysene-1,3-diones (R16), have been identified to possess anticancer activities and to induce G(2)-M arrest through inhibiting topoisomerase II accompanied by Chk1 degradation.	amonafide	29-38	checkpoint kinase 1	Homo sapiens	246-250
19881958-1	2009	Naphthalimides, particularly amonafide and 2-(2-dimethylamino)-6-thia-2-aza-benzo[def]chrysene-1,3-diones (R16), have been identified to possess anticancer activities and to induce G(2)-M arrest through inhibiting topoisomerase II accompanied by Chk1 degradation.	2-(2-dimethylamino)-6-thia-2-azabenzo(def)chrysene-1,3-dione	43-105	checkpoint kinase 1	Homo sapiens	246-250
19881958-7	2009	Moreover, the naphthalimides phosphorylated Chk2 in an ATM-dependent manner but induced Chk1 degradation.	Naphthalimides	14-28	checkpoint kinase 1	Homo sapiens	88-92
19881958-8	2009	These data indicate that R16 and amonafide preferentially used Chk2 as evidenced by the differential ATM-executed phosphorylation of Chk1 and Chk2.	amonafide	33-42	checkpoint kinase 1	Homo sapiens	133-137
19459175-1	2009	Growth suppressive effect of diallyl trisulfide (DATS), a promising cancer chemopreventive constituent of garlic, against cultured human cancer cells correlates with checkpoint kinase 1 (Chk1)-mediated mitotic arrest, but the fate of the cells arrested in mitosis remains elusive.	diallyl trisulfide	29-47	checkpoint kinase 1	Homo sapiens	166-185
19459175-1	2009	Growth suppressive effect of diallyl trisulfide (DATS), a promising cancer chemopreventive constituent of garlic, against cultured human cancer cells correlates with checkpoint kinase 1 (Chk1)-mediated mitotic arrest, but the fate of the cells arrested in mitosis remains elusive.	diallyl trisulfide	29-47	checkpoint kinase 1	Homo sapiens	187-191
19459175-1	2009	Growth suppressive effect of diallyl trisulfide (DATS), a promising cancer chemopreventive constituent of garlic, against cultured human cancer cells correlates with checkpoint kinase 1 (Chk1)-mediated mitotic arrest, but the fate of the cells arrested in mitosis remains elusive.	diallyl trisulfide	49-53	checkpoint kinase 1	Homo sapiens	166-185
19459175-1	2009	Growth suppressive effect of diallyl trisulfide (DATS), a promising cancer chemopreventive constituent of garlic, against cultured human cancer cells correlates with checkpoint kinase 1 (Chk1)-mediated mitotic arrest, but the fate of the cells arrested in mitosis remains elusive.	diallyl trisulfide	49-53	checkpoint kinase 1	Homo sapiens	187-191
19743875-3	2009	To date, most CHK1 inhibition approaches have involved targeting the ATP site of this kinase.	Adenosine Triphosphate	69-72	checkpoint kinase 1	Homo sapiens	14-18
19743875-5	2009	Analysis of kinetic and biophysical data has led to the conclusion that these small molecule allosteric site inhibitors of CHK1 are reversible and are neither ATP- nor peptide substrate-competitive.	Adenosine Triphosphate	159-162	checkpoint kinase 1	Homo sapiens	123-127
19530246-0	2009	Involvement of ATM-mediated Chk1/2 and JNK kinase signaling activation in HKH40A-induced cell growth inhibition.	RTA 502	74-80	checkpoint kinase 1	Homo sapiens	28-34
20137342-0	2009	[Silencing of cell cycle checkpoint kinase gene enhances cisplatin-induced apoptosis of lung cancer cells].	Cisplatin	57-66	checkpoint kinase 1	Homo sapiens	14-42
20137342-1	2009	OBJECTIVE: To investigate the changes in cell cycle induced by cisplatin (DDP) and the effect of antisense oligonucleotide (AsODN) targeting Chk1/2 on DDP-induced apoptosis in lung cancer cell line A549 cells.	Oligonucleotides	107-122	checkpoint kinase 1	Homo sapiens	141-147
20137342-1	2009	OBJECTIVE: To investigate the changes in cell cycle induced by cisplatin (DDP) and the effect of antisense oligonucleotide (AsODN) targeting Chk1/2 on DDP-induced apoptosis in lung cancer cell line A549 cells.	asodn	124-129	checkpoint kinase 1	Homo sapiens	141-147
20137342-6	2009	Transfection with antisense oligonucleotide targeting Chk1/2 inhibited the Chk1/2 expression at both mRNA and protein levels.	Oligonucleotides	28-43	checkpoint kinase 1	Homo sapiens	54-60
20137342-6	2009	Transfection with antisense oligonucleotide targeting Chk1/2 inhibited the Chk1/2 expression at both mRNA and protein levels.	Oligonucleotides	28-43	checkpoint kinase 1	Homo sapiens	54-58
19755861-8	2009	In contrast, a chemical inhibitor of CHK1, Chir124, sensitized cancer cells to the lethal effect of AZD1152.	2-((3-((4-((5-(2-((3-fluorophenyl)amino)-2-oxoethyl)-1H-pyrazol-3-yl)amino)quinazolin-7-yl)oxy)propyl)(ethyl)amino)ethyl dihydrogen phosphate	100-107	checkpoint kinase 1	Homo sapiens	37-41
19530246-8	2009	Our data support the hypothesis that binding of HKH40A to cellular DNA likely activates ATM kinase, which then induces parallel Chk 1/2 and JNK signaling pathways, leading to G2/M cell cycle block and apoptosis.	RTA 502	48-54	checkpoint kinase 1	Homo sapiens	128-133
19713747-7	2009	Furthermore, Chk1 inhibition sensitizes poleta-deficient cells to the cytotoxic effects of carboplatin.	Carboplatin	91-102	checkpoint kinase 1	Homo sapiens	13-17
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	checkpoint kinase 1	Homo sapiens	33-37
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	checkpoint kinase 1	Homo sapiens	135-139
19713747-4	2009	We show that both cisplatin and carboplatin induce strong S-phase arrest in poleta-deficient XP30RO cells, associated with reduced expression of cyclin E and cyclin B. PIK kinase-mediated phosphorylation of Chk1, H2AX and RPA2 was strongly activated by both cisplatin and carboplatin, but phosphorylation of these proteins was induced earlier by cisplatin than by an equitoxic dose of carboplatin.	Cisplatin	18-27	checkpoint kinase 1	Homo sapiens	207-211
19713747-4	2009	We show that both cisplatin and carboplatin induce strong S-phase arrest in poleta-deficient XP30RO cells, associated with reduced expression of cyclin E and cyclin B. PIK kinase-mediated phosphorylation of Chk1, H2AX and RPA2 was strongly activated by both cisplatin and carboplatin, but phosphorylation of these proteins was induced earlier by cisplatin than by an equitoxic dose of carboplatin.	Carboplatin	32-43	checkpoint kinase 1	Homo sapiens	207-211
19570909-7	2009	Moreover, disruption of ATR and Chk1 in MMR-deficient cells enhanced the sensitivity to treatment with the commonly used colorectal chemotherapeutic compound, 5-fluorouracil.	Fluorouracil	159-173	checkpoint kinase 1	Homo sapiens	32-36
19625493-9	2009	The extent of UV-induced phosphorylation of p53 and Chk1 was markedly reduced by SchB in ATM-deficient but not siATR-treated cells.	schizandrin B	81-85	checkpoint kinase 1	Homo sapiens	52-56
19541796-7	2009	Western blot analysis indicated that AZT caused a decrease in checkpoint kinase 1 (Chk1) and kinase 2 (Chk2) and an increase in phosphorylated Chk1 (Ser345) and Chk2 (Thr68).	Zidovudine	37-40	checkpoint kinase 1	Homo sapiens	62-81
19541796-7	2009	Western blot analysis indicated that AZT caused a decrease in checkpoint kinase 1 (Chk1) and kinase 2 (Chk2) and an increase in phosphorylated Chk1 (Ser345) and Chk2 (Thr68).	Zidovudine	37-40	checkpoint kinase 1	Homo sapiens	83-87
19541796-7	2009	Western blot analysis indicated that AZT caused a decrease in checkpoint kinase 1 (Chk1) and kinase 2 (Chk2) and an increase in phosphorylated Chk1 (Ser345) and Chk2 (Thr68).	Zidovudine	37-40	checkpoint kinase 1	Homo sapiens	143-147
19541796-10	2009	They also indicate that a combination of a delay of cell cycle progression, an induction of apoptosis, and a decrease in telomerase activity is contributing to the decrease in the number of viable cells from AZT treatment, and that checkpoint enzymes Chk1 and Chk2 may play an important role in the delay of cell cycle progression.	Zidovudine	208-211	checkpoint kinase 1	Homo sapiens	251-255
19716789-5	2009	Further, we show that low levels of Fbx6 and consequent impairment of replication stress-induced Chk1 degradation are associated with cancer cell resistance to the chemotherapeutic agent, camptothecin.	Camptothecin	188-200	checkpoint kinase 1	Homo sapiens	97-101
19572549-7	2009	One low molecular weight, weakly active purine template hit was progressed by iterative structure-based design to give submicromolar pyrazolopyridines with good ligand efficiency and appropriate CHK1-mediated cellular activity in HT29 colon cancer cells.	purine	40-46	checkpoint kinase 1	Homo sapiens	195-199
19572549-7	2009	One low molecular weight, weakly active purine template hit was progressed by iterative structure-based design to give submicromolar pyrazolopyridines with good ligand efficiency and appropriate CHK1-mediated cellular activity in HT29 colon cancer cells.	pyrazolopyridine	133-150	checkpoint kinase 1	Homo sapiens	195-199
19614620-2	2009	In addition, it is the main target for a Chk1 (checkpoint kinase 1)-dependent Cdc25/CDK2 (cyclin-dependent kinase 2)-independent DNA damage checkpoint signal transduction pathway following low doses of BPDE (benzo[a]pyrene dihydrodiol epoxide) treatment, which causes DNA damage similar to UV-induced adducts.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	202-206	checkpoint kinase 1	Homo sapiens	41-45
19614620-2	2009	In addition, it is the main target for a Chk1 (checkpoint kinase 1)-dependent Cdc25/CDK2 (cyclin-dependent kinase 2)-independent DNA damage checkpoint signal transduction pathway following low doses of BPDE (benzo[a]pyrene dihydrodiol epoxide) treatment, which causes DNA damage similar to UV-induced adducts.	pyrene dihydrodiol epoxide	216-242	checkpoint kinase 1	Homo sapiens	41-45
19502782-0	2009	Knockdown of Chk1 sensitizes human colon carcinoma HCT116 cells in a p53-dependent manner to lidamycin through abrogation of a G2/M checkpoint and induction of apoptosis.	C 1027	93-102	checkpoint kinase 1	Homo sapiens	13-17
19502782-2	2009	In this study, we investigate whether knockdowns of checkpoint kinases Chk1 and Chk2 by RNA interfering potentiate the cytotoxicity and abrogate G(2)/M checkpoint induced by DNA-damaging agent lidamycin (LDM) in HCT116 cells with different p53 status.	C 1027	193-202	checkpoint kinase 1	Homo sapiens	71-75
19778378-6	2009	In addition, Chk1-depleted U2OS cells failed to arrest in mitosis after spindle disruption by nocodazole and showed decreased protein levels of Mad2 and BubR1.	Nocodazole	94-104	checkpoint kinase 1	Homo sapiens	13-17
19453842-4	2009	METHOD: Treatment with doxorubicin involving DNA damage and gene silencing of Chk1/2 by shRNA constructs was performed in pulp, periodontal ligament, gingival tissues (HGF), and mouth epithelial carcinoma cells (KB).	Doxorubicin	23-34	checkpoint kinase 1	Homo sapiens	78-82
19584159-2	2009	We examined the preclinical use of the Chk1 inhibitor PF-00477736 as a docetaxel-sensitizing agent.	Docetaxel	71-80	checkpoint kinase 1	Homo sapiens	39-43
19584159-13	2009	Chk1 inhibitor PF-00477736 offers a therapeutic potential for the enhancement of taxane therapy.	PF 00477736	15-26	checkpoint kinase 1	Homo sapiens	0-4
19584159-6	2009	Docetaxel induced dose- and time-dependent increase in the levels of phosphorylated Chk1 (Ser(345)), phosphorylated histone H3 (Ser(10)), and gammaH2AX foci and promoted the cytoplasmic localization of phosphorylated Cdc25C (Ser(216)).	Docetaxel	0-9	checkpoint kinase 1	Homo sapiens	84-88
19584159-6	2009	Docetaxel induced dose- and time-dependent increase in the levels of phosphorylated Chk1 (Ser(345)), phosphorylated histone H3 (Ser(10)), and gammaH2AX foci and promoted the cytoplasmic localization of phosphorylated Cdc25C (Ser(216)).	Serine	90-93	checkpoint kinase 1	Homo sapiens	84-88
19584159-13	2009	Chk1 inhibitor PF-00477736 offers a therapeutic potential for the enhancement of taxane therapy.	taxane	81-87	checkpoint kinase 1	Homo sapiens	0-4
19242509-0	2009	ATR-Chk1 pathway inhibition promotes apoptosis after UV treatment in primary human keratinocytes: potential basis for the UV protective effects of caffeine.	Caffeine	147-155	checkpoint kinase 1	Homo sapiens	4-8
19242509-10	2009	These data suggest that a relevant target of caffeine is the ATR-Chk1 pathway and that inhibiting ATR or Chk1 might have promise in preventing or reversing UV damage.	Caffeine	45-53	checkpoint kinase 1	Homo sapiens	65-69
19242509-10	2009	These data suggest that a relevant target of caffeine is the ATR-Chk1 pathway and that inhibiting ATR or Chk1 might have promise in preventing or reversing UV damage.	Caffeine	45-53	checkpoint kinase 1	Homo sapiens	105-109
19403702-5	2009	However, depleting Chk1 with small interfering RNA or inhibiting Chk1 with 3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide (AZD7762) did not sensitize these cells to cisplatin, oxaliplatin, or carboplatin.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	75-151	checkpoint kinase 1	Homo sapiens	65-69
19519883-10	2009	CHK1 was further targeted with specific small molecule inhibitors SB 218078 and PD 407824 in combination with gemcitabine.	Antimony	66-68	checkpoint kinase 1	Homo sapiens	0-4
19477925-3	2009	We find that in estrogen receptor (ER)-positive breast cancer cells, UV or ionizing radiation and hydroxyurea rapidly activate ATR-dependent phosphorylation of endogenous p53 and Chk1.	Hydroxyurea	98-109	checkpoint kinase 1	Homo sapiens	179-183
19519883-10	2009	CHK1 was further targeted with specific small molecule inhibitors SB 218078 and PD 407824 in combination with gemcitabine.	gemcitabine	110-121	checkpoint kinase 1	Homo sapiens	0-4
19519883-11	2009	Results showed that treatment of MIA PaCa-2 cells with either of the CHK1 inhibitors SB 218078 or PD 407824 led to sensitization of the pancreatic cancer cells to gemcitabine.	SB 218078	85-94	checkpoint kinase 1	Homo sapiens	69-73
19519883-11	2009	Results showed that treatment of MIA PaCa-2 cells with either of the CHK1 inhibitors SB 218078 or PD 407824 led to sensitization of the pancreatic cancer cells to gemcitabine.	gemcitabine	163-174	checkpoint kinase 1	Homo sapiens	69-73
19519883-13	2009	These results also indicate that CHK1 could serve as a putative therapeutic target for sensitizing pancreatic cancer cells to gemcitabine.	gemcitabine	126-137	checkpoint kinase 1	Homo sapiens	33-37
19411857-9	2009	Incubation with the phosphatase inhibitor okadaic acid produced more phosphorylation of CHK1 in UV-treated HPV16E6-expressing cells than in p53-H179Q-expressing cells suggesting that HPV16E6 may interfere with the recovery of coupled DNA replication at replication forks that are stalled at [6-4]pyrimidine-pyrimidone photoproducts and BPDE-DNA adducts.	Okadaic Acid	42-54	checkpoint kinase 1	Homo sapiens	88-92
19411857-9	2009	Incubation with the phosphatase inhibitor okadaic acid produced more phosphorylation of CHK1 in UV-treated HPV16E6-expressing cells than in p53-H179Q-expressing cells suggesting that HPV16E6 may interfere with the recovery of coupled DNA replication at replication forks that are stalled at [6-4]pyrimidine-pyrimidone photoproducts and BPDE-DNA adducts.	[6-4]pyrimidine-pyrimidone	291-317	checkpoint kinase 1	Homo sapiens	88-92
19411857-9	2009	Incubation with the phosphatase inhibitor okadaic acid produced more phosphorylation of CHK1 in UV-treated HPV16E6-expressing cells than in p53-H179Q-expressing cells suggesting that HPV16E6 may interfere with the recovery of coupled DNA replication at replication forks that are stalled at [6-4]pyrimidine-pyrimidone photoproducts and BPDE-DNA adducts.	benzo(a)pyrene diolepoxide I	336-340	checkpoint kinase 1	Homo sapiens	88-92
19401701-4	2009	Immunoblot studies revealed increased phosphorylation of H2A.X at Ser-139 and Chk1 at Ser-280 and a decrease in DNA polymerase-beta level in curcumin-treated cells.	Serine	86-89	checkpoint kinase 1	Homo sapiens	78-82
19421147-2	2009	Here, we show that Chk1 kinase activity is rapidly stimulated in a cell-cycle phase-specific manner in response to both DNA damage and replication arrest, and that the extent and duration of activation correlates closely with regulatory phosphorylation at serines (S) S317, S345 and S366.	Serine	256-263	checkpoint kinase 1	Homo sapiens	19-23
19261750-0	2009	Bifunctional DNA alkylator 1,3-bis(2-chloroethyl)-1-nitrosourea activates the ATR-Chk1 pathway independently of the mismatch repair pathway.	Carmustine	27-63	checkpoint kinase 1	Homo sapiens	82-86
19261750-3	2009	In this study, we investigated the activation of the ATR-Chk1 pathway in response to BCNU treatment and the dependence of this response on the DNA mismatch repair (MMR) capacity.	Carmustine	85-89	checkpoint kinase 1	Homo sapiens	57-61
19261750-5	2009	In response to BCNU, Chk1 was found to be phosphorylated at serine 345 and exhibited increased kinase activity.	Serine	60-66	checkpoint kinase 1	Homo sapiens	21-25
19261750-8	2009	Small interfering RNA knockdown of ATR also reduced Chk1 phosphorylation after exposure to BCNU.	Carmustine	91-95	checkpoint kinase 1	Homo sapiens	52-56
19421147-3	2009	Despite their evident co-regulation, substitutions of individual Chk1 regulatory sites with alanine (A) residues have differential effects on checkpoint proficiency and kinase activation.	Alanine	92-99	checkpoint kinase 1	Homo sapiens	65-69
19401701-4	2009	Immunoblot studies revealed increased phosphorylation of H2A.X at Ser-139 and Chk1 at Ser-280 and a decrease in DNA polymerase-beta level in curcumin-treated cells.	Curcumin	141-149	checkpoint kinase 1	Homo sapiens	78-82
19401701-7	2009	In addition, we also observed a significant increase in the phosphorylation of Chk1 at Ser-345, Cdc25C at Ser-216 and a subtle increase in ATM phosphorylation at Ser-1981.	Serine	87-90	checkpoint kinase 1	Homo sapiens	79-83
19401701-10	2009	Silencing ATM/Chk1 expression by transfecting BxPC-3 cells with ATM or Chk1-specific SiRNA blocked the phosphorylation of ATM, Chk1 and Cdc25C and protected the cells from curcumin-mediated G2/M arrest and apoptosis.	Curcumin	172-180	checkpoint kinase 1	Homo sapiens	14-18
19401701-10	2009	Silencing ATM/Chk1 expression by transfecting BxPC-3 cells with ATM or Chk1-specific SiRNA blocked the phosphorylation of ATM, Chk1 and Cdc25C and protected the cells from curcumin-mediated G2/M arrest and apoptosis.	Curcumin	172-180	checkpoint kinase 1	Homo sapiens	71-75
19401701-10	2009	Silencing ATM/Chk1 expression by transfecting BxPC-3 cells with ATM or Chk1-specific SiRNA blocked the phosphorylation of ATM, Chk1 and Cdc25C and protected the cells from curcumin-mediated G2/M arrest and apoptosis.	Curcumin	172-180	checkpoint kinase 1	Homo sapiens	71-75
19401701-11	2009	This study reflects the critical role of ATM/Chk1 in curcumin-mediated G2/M cell cycle arrest and apoptosis in pancreatic cancer cells.	Curcumin	53-61	checkpoint kinase 1	Homo sapiens	45-49
19366835-10	2009	Cells treated with AZD6244 had an increased mitotic index and decreased Chk1 phosphorylation at 1 and 2 hours after irradiation.	AZD 6244	19-26	checkpoint kinase 1	Homo sapiens	72-76
18602198-0	2009	A three-step synthesis from rebeccamycin of an efficient checkpoint kinase 1 inhibitor.	rebeccamycin	28-40	checkpoint kinase 1	Homo sapiens	57-76
19360349-5	2009	TAS-106 potently inhibited the expression of Chk1 protein and the phosphorylation of Chk1 and Chk2.	1-(3-C-ethynylribopentofuranosyl)cytosine	0-7	checkpoint kinase 1	Homo sapiens	45-49
19360349-5	2009	TAS-106 potently inhibited the expression of Chk1 protein and the phosphorylation of Chk1 and Chk2.	1-(3-C-ethynylribopentofuranosyl)cytosine	0-7	checkpoint kinase 1	Homo sapiens	85-89
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	checkpoint kinase 1	Homo sapiens	73-77
19137017-8	2009	In the Mapo1-defective mutant cells treated with MNU, the mitochondrial membrane depolarization and caspase-3 activation were severely suppressed, although phosphorylation of p53, CHK1 and histone H2AX was observed.	Methylnitrosourea	49-52	checkpoint kinase 1	Homo sapiens	180-184
19401701-0	2009	Activation of ATM/Chk1 by curcumin causes cell cycle arrest and apoptosis in human pancreatic cancer cells.	Curcumin	26-34	checkpoint kinase 1	Homo sapiens	18-22
19139065-3	2009	We show that base adducts caused by a potent carcinogen, benzo[a]pyrene diol epoxide (BPDE), constitute a strong signal for TopBP1-dependent ATR kinase activity on Chk1 and p53.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	57-84	checkpoint kinase 1	Homo sapiens	164-168
19139065-3	2009	We show that base adducts caused by a potent carcinogen, benzo[a]pyrene diol epoxide (BPDE), constitute a strong signal for TopBP1-dependent ATR kinase activity on Chk1 and p53.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	86-90	checkpoint kinase 1	Homo sapiens	164-168
19218339-9	2009	Furthermore, Chk1 silencing sensitized p53-null MM cells to both an S phase block and apoptosis in the presence of doxorubicin.	Doxorubicin	115-126	checkpoint kinase 1	Homo sapiens	13-17
19059218-0	2009	Inhibition of CHK1 kinase by Go6976 converts 8-chloro-adenosine-induced G2/M arrest into S arrest in human myelocytic leukemia K562 cells.	Go 6976	29-35	checkpoint kinase 1	Homo sapiens	14-18
19059218-0	2009	Inhibition of CHK1 kinase by Go6976 converts 8-chloro-adenosine-induced G2/M arrest into S arrest in human myelocytic leukemia K562 cells.	8-chloroadenosine	45-63	checkpoint kinase 1	Homo sapiens	14-18
19059218-4	2009	In this study, we demonstrate that 8-Cl-Ado-induced DNA damage activates G2/M phase checkpoint, which is associated with ATM-activated CHK1-CDC25C-CDC2 pathway joined by BRCA1-CHK1 branch in apoptosis-resistant human myelocytic leukemia K562 (p53-null) cells.	8-chloroadenosine	35-43	checkpoint kinase 1	Homo sapiens	135-139
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	checkpoint kinase 1	Homo sapiens	14-18
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	checkpoint kinase 1	Homo sapiens	53-57
19615254-1	2009	OBJECTIVE: To explore the increasing effect of blocking Chk1 and /or Chk2 gene by Chk1 or Chk2-specific antisense oligodeoxynucleotides (AsODN) on apoptosis in HeLa cell line after irradiation and its mechanism of action.	Oligodeoxyribonucleotides	114-135	checkpoint kinase 1	Homo sapiens	56-60
19615254-1	2009	OBJECTIVE: To explore the increasing effect of blocking Chk1 and /or Chk2 gene by Chk1 or Chk2-specific antisense oligodeoxynucleotides (AsODN) on apoptosis in HeLa cell line after irradiation and its mechanism of action.	asodn	137-142	checkpoint kinase 1	Homo sapiens	56-60
19060337-2	2009	A systematic screening of the protein kinase small interfering RNA library reveals that Chk1 and ataxia telangiectasia-mutated (ATM) and Rad3-related (ATR) are the main kinases responsible for intra-S-phase checkpoint upon topoisomerase I inhibitor camptothecin-induced DNA damage.	Camptothecin	249-261	checkpoint kinase 1	Homo sapiens	88-92
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	checkpoint kinase 1	Homo sapiens	27-31
19111462-0	2009	Synthesis and CHK1 inhibitory potency of Hymenialdisine analogues.	hymenialdisine	41-55	checkpoint kinase 1	Homo sapiens	14-18
19111462-1	2009	A series of thieno[3,2-b]pyrroloazepinones derivatives related to Hymenialdisine were prepared and tested for CHK1 inhibitory activity.	thieno[3,2-b]pyrroloazepinones	12-42	checkpoint kinase 1	Homo sapiens	110-114
19158509-6	2009	The apparent lack of checkpoint activation was due to an active suppression because accumulation of pSer345-Chk1, pThr68-Chk2 and gammaH2AX was inhibited by nitrosative stress in cells exposed to DNA damage or replication inhibitors.	pser345	100-107	checkpoint kinase 1	Homo sapiens	108-112
18984588-7	2009	Furthermore, a single amino acid substitution at an invariant leucine in a conserved domain of the non-catalytic C terminus restored viability to cells expressing the ATR(Mec1) phosphorylation site-mutated protein and relieved the requirement of an upstream mediator for Chk1 activation.	Leucine	62-69	checkpoint kinase 1	Homo sapiens	271-275
19139112-0	2009	Gemcitabine sensitization by checkpoint kinase 1 inhibition correlates with inhibition of a Rad51 DNA damage response in pancreatic cancer cells.	gemcitabine	0-11	checkpoint kinase 1	Homo sapiens	29-48
19155174-4	2009	An X-ray crystal structure for the complex of our best inhibitor bound to Chk1 was solved, indicating that it binds to an allosteric site approximately 13A from the ATP binding site.	Adenosine Triphosphate	165-168	checkpoint kinase 1	Homo sapiens	74-78
19139112-2	2009	We have examined the ability of PD-321852, a small-molecule Chk1 inhibitor, to potentiate gemcitabine-induced clonogenic death in a panel of pancreatic cancer cell lines and evaluated the relationship between endpoints associated with Chk1 inhibition and chemosensitization.	4-(2,6-dichlorophenyl)-9-hydroxy-6-(3-methylaminopropyl)-6H-pyrrolo(3,4-c)carbazole-1,3-dione	32-41	checkpoint kinase 1	Homo sapiens	60-64
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	checkpoint kinase 1	Homo sapiens	20-24
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	checkpoint kinase 1	Homo sapiens	139-143
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.	gemcitabine	104-115	checkpoint kinase 1	Homo sapiens	139-143
19139112-7	2009	Our data suggest the inhibition of this Chk1-mediated Rad51 response to gemcitabine-induced replication stress is an important factor in determining gemcitabine chemosensitization by Chk1 inhibition in pancreatic cancer cells.	gemcitabine	72-83	checkpoint kinase 1	Homo sapiens	40-44
19139112-7	2009	Our data suggest the inhibition of this Chk1-mediated Rad51 response to gemcitabine-induced replication stress is an important factor in determining gemcitabine chemosensitization by Chk1 inhibition in pancreatic cancer cells.	gemcitabine	72-83	checkpoint kinase 1	Homo sapiens	183-187
18820127-8	2009	Knockdown of Chk1 and Wee1 by short interfering RNA each resulted in abrogation of the G(2)/M checkpoint induced by SN-38.	Irinotecan	116-121	checkpoint kinase 1	Homo sapiens	13-17
19139112-7	2009	Our data suggest the inhibition of this Chk1-mediated Rad51 response to gemcitabine-induced replication stress is an important factor in determining gemcitabine chemosensitization by Chk1 inhibition in pancreatic cancer cells.	gemcitabine	149-160	checkpoint kinase 1	Homo sapiens	40-44
19139112-7	2009	Our data suggest the inhibition of this Chk1-mediated Rad51 response to gemcitabine-induced replication stress is an important factor in determining gemcitabine chemosensitization by Chk1 inhibition in pancreatic cancer cells.	gemcitabine	149-160	checkpoint kinase 1	Homo sapiens	183-187
19177354-7	2009	However, the mode of inhibition differs from that of the previously studied structure of Chk2 in complex with debromohymenialdisine, a compound that inhibits both Chk1 and Chk2.	debromohymenialdisine	110-131	checkpoint kinase 1	Homo sapiens	163-167
18787399-4	2008	Pretreatment of HCT116 cells with the proteasome inhibitors MG132 or lactacystin prevented Chk1 decline induced by R16, accompanied by significant accumulation of ubiquitinated Chk1 protein, indicating the involvement of ubiquitin-proteasome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	60-65	checkpoint kinase 1	Homo sapiens	91-95
18768386-0	2008	Rebeccamycin derivatives as dual DNA-damaging agents and potent checkpoint kinase 1 inhibitors.	rebeccamycin	0-12	checkpoint kinase 1	Homo sapiens	64-83
18768386-3	2008	Some analogs, especially those with substitutions at the 6" position of the carbohydrate moiety, exhibit potent inhibitory activity toward checkpoint kinase 1 (Chk1), a kinase that has a major role in the G(2)/M checkpoint in response to DNA damage.	Carbohydrates	76-88	checkpoint kinase 1	Homo sapiens	139-158
18768386-3	2008	Some analogs, especially those with substitutions at the 6" position of the carbohydrate moiety, exhibit potent inhibitory activity toward checkpoint kinase 1 (Chk1), a kinase that has a major role in the G(2)/M checkpoint in response to DNA damage.	Carbohydrates	76-88	checkpoint kinase 1	Homo sapiens	160-164
18787399-4	2008	Pretreatment of HCT116 cells with the proteasome inhibitors MG132 or lactacystin prevented Chk1 decline induced by R16, accompanied by significant accumulation of ubiquitinated Chk1 protein, indicating the involvement of ubiquitin-proteasome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	60-65	checkpoint kinase 1	Homo sapiens	177-181
18787399-4	2008	Pretreatment of HCT116 cells with the proteasome inhibitors MG132 or lactacystin prevented Chk1 decline induced by R16, accompanied by significant accumulation of ubiquitinated Chk1 protein, indicating the involvement of ubiquitin-proteasome pathway.	lactacystin	69-80	checkpoint kinase 1	Homo sapiens	91-95
18787399-4	2008	Pretreatment of HCT116 cells with the proteasome inhibitors MG132 or lactacystin prevented Chk1 decline induced by R16, accompanied by significant accumulation of ubiquitinated Chk1 protein, indicating the involvement of ubiquitin-proteasome pathway.	lactacystin	69-80	checkpoint kinase 1	Homo sapiens	177-181
18773878-13	2008	RTX treatment also induced foci of RAD51, gamma-H2AX, phospho-Chk1, and phospho-NBS1, although the extent of co-localization with RPA2 foci varied.	raltitrexed	0-3	checkpoint kinase 1	Homo sapiens	62-66
18980967-4	2008	Two of the most promising targets, described in this review, for improving the efficacy of gemcitabine radiation are epidermal growth factor receptor and checkpoint kinase 1.	gemcitabine	91-102	checkpoint kinase 1	Homo sapiens	154-173
18852132-5	2008	During this interval, LAQ-824 induced early (4-8 h) increases in gamma-H2AX, which persisted (48 h) secondary to LAQ-824-mediated inhibition of DNA repair (e.g., down-regulation of Ku86 and Rad50, increased Ku70 acetylation, diminished Ku70 and Ku86 DNA-binding activity, and down-regulated DNA repair genes BRCA1, CHEK1, and RAD51).	LAQ824	22-29	checkpoint kinase 1	Homo sapiens	315-320
18927314-2	2008	We conducted a phase I study of irinotecan and the Hsp90 inhibitor 17AAG, which can also down-regulate Chk1, in patients with solid tumors.	Irinotecan	32-42	checkpoint kinase 1	Homo sapiens	103-107
18927314-2	2008	We conducted a phase I study of irinotecan and the Hsp90 inhibitor 17AAG, which can also down-regulate Chk1, in patients with solid tumors.	tanespimycin	67-72	checkpoint kinase 1	Homo sapiens	103-107
18927314-13	2008	Evidence for Hsp90 inhibition by 17AAG, resulting in phospho-Chk1 loss, abrogation of the G(2)-M cell cycle checkpoint, and cell death could be shown in tumor biopsy samples obtained at the MTD.	tanespimycin	33-38	checkpoint kinase 1	Homo sapiens	61-65
18787700-9	2008	Strikingly, CHK2 phosphorylation was undetectable in MLH1-deficient cells, and phosphorylation of CHK1 was reduced after PUVA treatment, indicating that MLH1 is involved in signaling psoralen ICL-induced checkpoint activation.	puva	121-125	checkpoint kinase 1	Homo sapiens	98-102
18813828-7	2008	These results demonstrate that gemcitabine inhibited the growth of HCC and CCC cells by cell cycle arrest without apoptosis and that the ERK/Chk1/2 signaling pathway was in part responsible for the resistance to gemcitabine.	gemcitabine	212-223	checkpoint kinase 1	Homo sapiens	141-147
18813828-8	2008	Our findings shed light on treating patients with HCC and CCC by gemcitabine, especially when combined with a MEK inhibitor and Chk1/2 inhibitors.	gemcitabine	65-76	checkpoint kinase 1	Homo sapiens	128-134
18550533-6	2008	The cleavage of Chk1 was similarly observed in human Jurkat cells treated with a non-genotoxic apoptosis inducer, staurosporine.	Staurosporine	114-127	checkpoint kinase 1	Homo sapiens	16-20
18787700-9	2008	Strikingly, CHK2 phosphorylation was undetectable in MLH1-deficient cells, and phosphorylation of CHK1 was reduced after PUVA treatment, indicating that MLH1 is involved in signaling psoralen ICL-induced checkpoint activation.	psoralen icl	183-195	checkpoint kinase 1	Homo sapiens	98-102
18492607-8	2008	Overexpression of ATR reverted the MMC induced phenotype of Chk1 and FANCD2 in HBx transformed cells.	Mitomycin	35-38	checkpoint kinase 1	Homo sapiens	60-64
18602917-1	2008	In this study, we showed that curcumin treatment resulted in activation of Chk1-mediated G2 checkpoint, which was associated with the induction of G2/M arrest and the resistance of cancer cells to curcumin-induced apoptosis.	Curcumin	30-38	checkpoint kinase 1	Homo sapiens	75-79
18602917-1	2008	In this study, we showed that curcumin treatment resulted in activation of Chk1-mediated G2 checkpoint, which was associated with the induction of G2/M arrest and the resistance of cancer cells to curcumin-induced apoptosis.	Curcumin	197-205	checkpoint kinase 1	Homo sapiens	75-79
18602917-2	2008	Further investigation revealed that inhibition of Chk1 significantly abrogated G2/M arrest and sensitized curcumin-resistant cells to apoptosis via upregulation of Bad and in turn the loss of mitochondrial membrane potential.	Curcumin	106-114	checkpoint kinase 1	Homo sapiens	50-54
18602917-3	2008	These results indicate that Chk1-mediated G2/M arrest may serve as a mechanism for curcumin resistance and Chk1 represents a potential target for the reversal of this resistance.	Curcumin	83-91	checkpoint kinase 1	Homo sapiens	28-32
18690823-4	2008	This review reports the synthesis and Chk1 inhibitory activities of pyrrolocarbazole compounds bearing four or five fused rings.	pyrrolocarbazole	68-84	checkpoint kinase 1	Homo sapiens	38-42
18495871-3	2008	We showed that after etoposide treatment, Mcl-1 could coimmunoprecipitate with the regulatory kinase, Chk1.	Etoposide	21-30	checkpoint kinase 1	Homo sapiens	102-106
18723495-3	2008	We show that phosphorylation of Chk1 at Ser(317) but not at Ser(345) is required for phosphorylation of PTEN at Thr(383) by CKII, making cell cycle reentry after HU treatment possible.	Serine	40-43	checkpoint kinase 1	Homo sapiens	32-36
18723495-3	2008	We show that phosphorylation of Chk1 at Ser(317) but not at Ser(345) is required for phosphorylation of PTEN at Thr(383) by CKII, making cell cycle reentry after HU treatment possible.	Threonine	112-115	checkpoint kinase 1	Homo sapiens	32-36
18723495-6	2008	We conclude that, in response to stalled DNA replication, Chk1 is phosphorylated at Ser(317) by ATR resulting in stabilization of CKII, which in turn leads to phosphorylation of PTEN at Thr(383).	Serine	84-87	checkpoint kinase 1	Homo sapiens	58-62
18723495-6	2008	We conclude that, in response to stalled DNA replication, Chk1 is phosphorylated at Ser(317) by ATR resulting in stabilization of CKII, which in turn leads to phosphorylation of PTEN at Thr(383).	Threonine	186-189	checkpoint kinase 1	Homo sapiens	58-62
18547806-2	2008	A novel class of 2-ureido thiophene carboxamide urea (TCU) Chk1 inhibitors is described.	2-ureido thiophene carboxamide urea	17-52	checkpoint kinase 1	Homo sapiens	59-63
18547806-2	2008	A novel class of 2-ureido thiophene carboxamide urea (TCU) Chk1 inhibitors is described.	5-Hexyl-2-(2-Methylphenoxy)phenol	54-57	checkpoint kinase 1	Homo sapiens	59-63
18632613-0	2008	Thymoquinone triggers inactivation of the stress response pathway sensor CHEK1 and contributes to apoptosis in colorectal cancer cells.	thymoquinone	0-12	checkpoint kinase 1	Homo sapiens	73-78
18632613-4	2008	A significant up-regulation of the survival gene CHEK1 was observed in p53-/- cells in response to thymoquinone due to the lack of transcriptional repression of p53.	thymoquinone	99-111	checkpoint kinase 1	Homo sapiens	49-54
18632613-7	2008	Immunofluorescence analysis revealed that the apoptosis resistance in p53-/- cells after thymoquinone treatment might be conveyed by shuttling of CHEK1 into the nucleus.	thymoquinone	89-101	checkpoint kinase 1	Homo sapiens	146-151
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	checkpoint kinase 1	Homo sapiens	72-76
18509065-5	2008	In particular, SN-38 arrested cells in S phase, enhanced the accumulation of gemcitabine metabolites, and diminished checkpoint kinase 1, thereby sensitizing cells in the SN-38 --> gemcitabine sequence.	Irinotecan	15-20	checkpoint kinase 1	Homo sapiens	117-136
18698031-5	2008	RESULTS: Transient Chk1 down-regulation sensitized HCT-116 cells, p53-/- more than the p53 wild-type counterpart, to DNA-damaging agents 5-fluorouracil (5-FU), doxorubicin, and etoposide treatments, with no modification of Taxol and PS341 cytotoxic activities.	Fluorouracil	137-151	checkpoint kinase 1	Homo sapiens	19-23
18698031-5	2008	RESULTS: Transient Chk1 down-regulation sensitized HCT-116 cells, p53-/- more than the p53 wild-type counterpart, to DNA-damaging agents 5-fluorouracil (5-FU), doxorubicin, and etoposide treatments, with no modification of Taxol and PS341 cytotoxic activities.	Fluorouracil	153-157	checkpoint kinase 1	Homo sapiens	19-23
18698031-5	2008	RESULTS: Transient Chk1 down-regulation sensitized HCT-116 cells, p53-/- more than the p53 wild-type counterpart, to DNA-damaging agents 5-fluorouracil (5-FU), doxorubicin, and etoposide treatments, with no modification of Taxol and PS341 cytotoxic activities.	Doxorubicin	160-171	checkpoint kinase 1	Homo sapiens	19-23
18698031-5	2008	RESULTS: Transient Chk1 down-regulation sensitized HCT-116 cells, p53-/- more than the p53 wild-type counterpart, to DNA-damaging agents 5-fluorouracil (5-FU), doxorubicin, and etoposide treatments, with no modification of Taxol and PS341 cytotoxic activities.	Etoposide	177-186	checkpoint kinase 1	Homo sapiens	19-23
18698031-5	2008	RESULTS: Transient Chk1 down-regulation sensitized HCT-116 cells, p53-/- more than the p53 wild-type counterpart, to DNA-damaging agents 5-fluorouracil (5-FU), doxorubicin, and etoposide treatments, with no modification of Taxol and PS341 cytotoxic activities.	Paclitaxel	223-228	checkpoint kinase 1	Homo sapiens	19-23
18433847-13	2008	Although phosphorylation of Chk1 and Chk2 both increases after treatment, loss of Chk1 suppresses, whereas loss of Chk2 enhances, stilbene 5c-induced cell death.	Stilbenes	130-138	checkpoint kinase 1	Homo sapiens	28-32
18433847-13	2008	Although phosphorylation of Chk1 and Chk2 both increases after treatment, loss of Chk1 suppresses, whereas loss of Chk2 enhances, stilbene 5c-induced cell death.	Stilbenes	130-138	checkpoint kinase 1	Homo sapiens	82-86
18247328-0	2008	Involvement of the role of Chk1 in lithium-induced G2/M phase cell cycle arrest in hepatocellular carcinoma cells.	Lithium	35-42	checkpoint kinase 1	Homo sapiens	27-31
18247328-4	2008	Checkpoint kinase 1 (Chk1), a critical enzyme in DNA damage-induced G2/M arrest, was at least partially responsible for the lithium action.	Lithium	124-131	checkpoint kinase 1	Homo sapiens	0-19
18247328-4	2008	Checkpoint kinase 1 (Chk1), a critical enzyme in DNA damage-induced G2/M arrest, was at least partially responsible for the lithium action.	Lithium	124-131	checkpoint kinase 1	Homo sapiens	21-25
18247328-5	2008	The lithium-induced phosphorylation of cdc2 and G2/M arrest was abrogated largely by SB218078, a potent Chk1 inhibitor, as well as by Chk1 siRNA or the over-expression of kinase dead Chk1.	Lithium	4-11	checkpoint kinase 1	Homo sapiens	104-108
18247328-5	2008	The lithium-induced phosphorylation of cdc2 and G2/M arrest was abrogated largely by SB218078, a potent Chk1 inhibitor, as well as by Chk1 siRNA or the over-expression of kinase dead Chk1.	Lithium	4-11	checkpoint kinase 1	Homo sapiens	134-138
18247328-5	2008	The lithium-induced phosphorylation of cdc2 and G2/M arrest was abrogated largely by SB218078, a potent Chk1 inhibitor, as well as by Chk1 siRNA or the over-expression of kinase dead Chk1.	Lithium	4-11	checkpoint kinase 1	Homo sapiens	134-138
18247328-5	2008	The lithium-induced phosphorylation of cdc2 and G2/M arrest was abrogated largely by SB218078, a potent Chk1 inhibitor, as well as by Chk1 siRNA or the over-expression of kinase dead Chk1.	SB 218078	85-93	checkpoint kinase 1	Homo sapiens	104-108
18247328-6	2008	Furthermore, lithium-induced cdc25C phosphorylation in 7721 cells and in vitro kinase assay showed that the activity of Chk1 was enhanced after lithium treatment.	Lithium	13-20	checkpoint kinase 1	Homo sapiens	120-124
18247328-6	2008	Furthermore, lithium-induced cdc25C phosphorylation in 7721 cells and in vitro kinase assay showed that the activity of Chk1 was enhanced after lithium treatment.	Lithium	144-151	checkpoint kinase 1	Homo sapiens	120-124
18247328-7	2008	Interestingly, the increase of Chk1 activity by lithium may be independent of ataxia telangiectasia mutated (ATM)/ATM and Rad3-related (ATR) kinase.	Lithium	48-55	checkpoint kinase 1	Homo sapiens	31-35
18247328-10	2008	Our study"s results revealed the role of Chk1 in lithium-induced G2/M arrest.	Lithium	49-56	checkpoint kinase 1	Homo sapiens	41-45
18247328-11	2008	Given that Chk1 has been proposed to be a novel tumor suppressor, we suggest that the effect of lithium on Chk1 and cell cycle is useful in tumor prevention and therapy.	Lithium	96-103	checkpoint kinase 1	Homo sapiens	11-15
18247328-11	2008	Given that Chk1 has been proposed to be a novel tumor suppressor, we suggest that the effect of lithium on Chk1 and cell cycle is useful in tumor prevention and therapy.	Lithium	96-103	checkpoint kinase 1	Homo sapiens	107-111
18448427-4	2008	Binding between Chk1 and PCNA was reduced in the presence of hydroxyurea, suggesting that the interaction is regulated by replication stress.	Hydroxyurea	61-72	checkpoint kinase 1	Homo sapiens	16-20
18448427-6	2008	The intact PIP box is required for efficient DNA damage-induced phosphorylation and release of activated Chk1 from chromatin.	pip	11-14	checkpoint kinase 1	Homo sapiens	105-109
18448427-8	2008	In addition, we show that mutations in the PIP box of Chk1 lead to decreased rates of replication fork progression and increased aberrant replication.	pip	43-46	checkpoint kinase 1	Homo sapiens	54-58
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	checkpoint kinase 1	Homo sapiens	121-125
17869387-0	2008	Synthesis and structure-activity relationships of N-6 substituted analogues of 9-hydroxy-4-phenylpyrrolo[3,4-c]carbazole-1,3(2H,6H)-diones as inhibitors of Wee1 and Chk1 checkpoint kinases.	n-6	50-53	checkpoint kinase 1	Homo sapiens	165-169
17869387-0	2008	Synthesis and structure-activity relationships of N-6 substituted analogues of 9-hydroxy-4-phenylpyrrolo[3,4-c]carbazole-1,3(2H,6H)-diones as inhibitors of Wee1 and Chk1 checkpoint kinases.	9-hydroxy-4-phenylpyrrolo[3,4-c]carbazole-1,3(2h,6h)-diones	79-138	checkpoint kinase 1	Homo sapiens	165-169
18566216-0	2008	Chk1 and Chk2 are differentially involved in homologous recombination repair and cell cycle arrest in response to DNA double-strand breaks induced by camptothecins.	Camptothecin	150-163	checkpoint kinase 1	Homo sapiens	0-4
18566216-6	2008	Using RNA interference, we further showed that Chk2 was essential to G(2)-M arrest, whereas Chk1 was mainly required for HR repair in CPT-treated HCT116 cells.	Camptothecin	134-137	checkpoint kinase 1	Homo sapiens	92-96
18084324-4	2008	HU-induced Chk1 activation is also impaired in human cancer cell lines in which Cdc7 is depleted by siRNA, and Cdc7-depleted cells are more sensitive to HU treatment.	Hydroxyurea	0-2	checkpoint kinase 1	Homo sapiens	11-15
18071310-0	2008	Hsp90-inhibitor geldanamycin abrogates G2 arrest in p53-negative leukemia cell lines through the depletion of Chk1.	geldanamycin	16-28	checkpoint kinase 1	Homo sapiens	110-114
18071310-2	2008	Treatment with 100 nM geldanamycin (GM) for 24 h markedly reduced the Chk1 amount in Jurkat and ML-1 leukemia cell lines.	geldanamycin	22-34	checkpoint kinase 1	Homo sapiens	70-74
18071310-2	2008	Treatment with 100 nM geldanamycin (GM) for 24 h markedly reduced the Chk1 amount in Jurkat and ML-1 leukemia cell lines.	geldanamycin	36-38	checkpoint kinase 1	Homo sapiens	70-74
18071310-3	2008	Because Chk1 plays a central role in G2 checkpoint, we added GM to G2-arrested Jurkat and HL-60 cells pretreated with 50 nM doxorubicin for 24 h. GM slowly released both cell lines from doxorubicin-induced G2 arrest into G1 phase.	geldanamycin	61-63	checkpoint kinase 1	Homo sapiens	8-12
18071310-3	2008	Because Chk1 plays a central role in G2 checkpoint, we added GM to G2-arrested Jurkat and HL-60 cells pretreated with 50 nM doxorubicin for 24 h. GM slowly released both cell lines from doxorubicin-induced G2 arrest into G1 phase.	geldanamycin	146-148	checkpoint kinase 1	Homo sapiens	8-12
18071310-5	2008	Western blot analysis showed that addition of GM attenuates doxorubicin- and ICRF-193-induced Chk1 phosphorylation at Ser345.	geldanamycin	46-48	checkpoint kinase 1	Homo sapiens	94-98
18071310-5	2008	Western blot analysis showed that addition of GM attenuates doxorubicin- and ICRF-193-induced Chk1 phosphorylation at Ser345.	Doxorubicin	60-71	checkpoint kinase 1	Homo sapiens	94-98
18289623-9	2008	Mafosfamide caused p53 stabilization by phosphorylation of Ser15, 20 and 37, and activation of ATM/ATR and Chk1/Chk2.	mafosfamide	0-11	checkpoint kinase 1	Homo sapiens	107-111
18289623-10	2008	Inhibition of ATM/ATR, PI3-kinase and Chk1/Chk2 by CGK733, wortmannin and DBH, respectively, attenuated the apoptotic response in p53(wt) but not p53(mt) cells.	Wortmannin	59-69	checkpoint kinase 1	Homo sapiens	38-42
18342518-1	2008	We describe here an efficient synthesis of new 5-azaindolocarbazoles designed for cytotoxic and Chk1 inhibiting properties.	5-azaindolocarbazoles	47-68	checkpoint kinase 1	Homo sapiens	96-100
18642443-4	2008	The siRNA-mediated downregulation and pharmacological inhibition of p38alpha MAPK (with SB 203580) also reduces cell death induced by Chk1 knockdown or UCN-01.	SB 203580	88-97	checkpoint kinase 1	Homo sapiens	134-138
18321713-0	2008	Synthesis, checkpoint kinase 1 inhibitory properties and in vitro antiproliferative activities of new pyrrolocarbazoles.	pyrrolocarbazoles	102-119	checkpoint kinase 1	Homo sapiens	11-30
18358720-0	2008	Investigation of novel 7,8-disubstituted-5,10-dihydro-dibenzo[b,e][1,4]diazepin-11-ones as potent Chk1 inhibitors.	7,8-disubstituted-5,10-dihydro-dibenzo[b,e][1,4]diazepin-11-ones	23-87	checkpoint kinase 1	Homo sapiens	98-102
18358720-1	2008	The synthesis and structure-activity relationships (SAR) of Chk1 inhibitors based on a 5,10-dihydro-dibenzo[b,e][1,4]diazepin-11-one core are described.	5,10-dihydro-11H-dibenzo[b,e][1,4]diazepin-11-one	87-132	checkpoint kinase 1	Homo sapiens	60-64
18413794-5	2008	The 2-DG-mediated Akt phosphorylation also led to the phosphorylation of Akt downstream targets, such as Foxo3a, GSK3beta, and Chk1.	Deoxyglucose	4-8	checkpoint kinase 1	Homo sapiens	127-131
18339864-2	2008	Here, we found that the Hsp72-depleted cells show defect in phosphorylation and activation of the protein kinase Chk1 by genotoxic stresses, such as UVC irradiation or camptothecin.	Camptothecin	168-180	checkpoint kinase 1	Homo sapiens	113-117
18191399-0	2008	Synthesis and structure-activity relationships of soluble 8-substituted 4-(2-chlorophenyl)-9-hydroxypyrrolo[3,4-c]carbazole-1,3(2H,6H)-diones as inhibitors of the Wee1 and Chk1 checkpoint kinases.	8-substituted 4-(2-chlorophenyl)-9-hydroxypyrrolo[3,4-c]carbazole-1,3(2h,6h)-diones	58-141	checkpoint kinase 1	Homo sapiens	172-176
18191399-1	2008	Pyrrolo[3,4-c]carbazoles bearing solubilising basic side chains at the 8-position retain potent Wee1 and Chk1 inhibitory properties in isolated enzyme assays, and evidence of G2/M checkpoint abrogation in several cellular assays.	pyrrolo[3,4-c]carbazoles	0-24	checkpoint kinase 1	Homo sapiens	105-109
17502122-0	2008	Synthesis, in vitro antiproliferative activities, and Chk1 inhibitory properties of pyrrolo[3,4-a]carbazole-1,3-diones, pyrrolo[3,4-c]carbazole-1,3-diones, and 2-aminopyridazino[3,4-a]pyrrolo[3,4-c]carbazole-1,3,4,7-tetraone.	pyrrolo[3,4-a]carbazole-1,3-diones	84-118	checkpoint kinase 1	Homo sapiens	54-58
17502122-4	2008	The ATP binding pocket of Chk1 seems to be adaptable to substitution of the nitrogen of the imide E heterocycle with a hydroxymethyl group, allowing the fundamental hydrogen bond with the Glu(85) residue of the enzyme.	Adenosine Triphosphate	4-7	checkpoint kinase 1	Homo sapiens	26-30
17502122-4	2008	The ATP binding pocket of Chk1 seems to be adaptable to substitution of the nitrogen of the imide E heterocycle with a hydroxymethyl group, allowing the fundamental hydrogen bond with the Glu(85) residue of the enzyme.	Nitrogen	76-84	checkpoint kinase 1	Homo sapiens	26-30
17502122-4	2008	The ATP binding pocket of Chk1 seems to be adaptable to substitution of the nitrogen of the imide E heterocycle with a hydroxymethyl group, allowing the fundamental hydrogen bond with the Glu(85) residue of the enzyme.	Hydrogen	165-173	checkpoint kinase 1	Homo sapiens	26-30
17502122-4	2008	The ATP binding pocket of Chk1 seems to be adaptable to substitution of the nitrogen of the imide E heterocycle with a hydroxymethyl group, allowing the fundamental hydrogen bond with the Glu(85) residue of the enzyme.	Glutamic Acid	188-191	checkpoint kinase 1	Homo sapiens	26-30
18642443-1	2008	We have previously shown that tetraploid cancer cells succumb through a p53-dependent apoptotic pathway when checkpoint kinase 1 (Chk1) is depleted by small interfering RNAs (siRNAs) or inhibited with 7-hydroxystaurosporine (UCN-01).	7-hydroxystaurosporine	201-223	checkpoint kinase 1	Homo sapiens	109-128
18642443-1	2008	We have previously shown that tetraploid cancer cells succumb through a p53-dependent apoptotic pathway when checkpoint kinase 1 (Chk1) is depleted by small interfering RNAs (siRNAs) or inhibited with 7-hydroxystaurosporine (UCN-01).	7-hydroxystaurosporine	201-223	checkpoint kinase 1	Homo sapiens	130-134
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	checkpoint kinase 1	Homo sapiens	239-243
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	checkpoint kinase 1	Homo sapiens	239-243
18289945-5	2008	In poleta-deficient cells, drug treatment leads to prolonged S-phase arrest, and increased phosphorylation of the phosphatidylinositol-3-kinase-related protein kinase (PIKK) substrates Chk1, p95/Nbs1 and RPA2, the 34kDa subunit of replication protein A.	poleta	3-9	checkpoint kinase 1	Homo sapiens	185-189
17594092-8	2008	Pemetrexed sensitization by caffeine was associated with an increase in pemetrexed-induced phosphorylation of ataxia-telangiectasia-mutated (ATM) and Chk1.	Pemetrexed	0-10	checkpoint kinase 1	Homo sapiens	150-154
17594092-8	2008	Pemetrexed sensitization by caffeine was associated with an increase in pemetrexed-induced phosphorylation of ataxia-telangiectasia-mutated (ATM) and Chk1.	Caffeine	28-36	checkpoint kinase 1	Homo sapiens	150-154
17594092-8	2008	Pemetrexed sensitization by caffeine was associated with an increase in pemetrexed-induced phosphorylation of ataxia-telangiectasia-mutated (ATM) and Chk1.	Pemetrexed	72-82	checkpoint kinase 1	Homo sapiens	150-154
18823530-11	2008	However, deletion of distal chromosome 11q, defined as downregulation of the marker Chk1 (checkpoint kinase 1), was associated with an impaired tamoxifen response, and interestingly with low proliferative breast cancer of low grade.	Tamoxifen	144-153	checkpoint kinase 1	Homo sapiens	84-88
18159231-7	2007	Chk1 inhibition reversed the cisplatin resistance of tetraploid cells in vitro and in vivo, in xenografted human cancers.	Cisplatin	29-38	checkpoint kinase 1	Homo sapiens	0-4
17976513-4	2007	THIF treatment also led to an inhibition of cdc2, which was accompanied by the phosphorylation of both p53 (Ser15) and Chk1 (Ser296) and the de-activation of cdc25C phosphatase.	orobol	0-4	checkpoint kinase 1	Homo sapiens	119-123
17976513-5	2007	We suggest the anti-proliferative actions of THIF may be mediated by initial oxidative DNA damage, activation of ATR and downstream regulation of the p53 and Chk1 pathways leading to cell cycle arrest in G2-M.	orobol	45-49	checkpoint kinase 1	Homo sapiens	158-162
18089794-3	2007	Here, we present clear insights in the different responses of tumor and non-transformed cells to the inhibition of DNA replication with hydroxyurea in combination with checkpoint abrogation via inhibition of Ataxia telangiectasia-mutated- (ATM) and Rad3-related/ATM (ATR/ATM) and Chk1 kinases.	Hydroxyurea	136-147	checkpoint kinase 1	Homo sapiens	280-284
18089794-6	2007	Our results show that p38 is activated in response to hydroxyurea treatment and collaborates with Chk1 to prevent mitotic entry in non-transformed cell lines by maintaining cyclin B1/Cdk1 complexes inactive.	Hydroxyurea	54-65	checkpoint kinase 1	Homo sapiens	98-102
17931867-1	2007	A variety of macrocyclic urea compounds were prepared as potent Chk1 inhibitors by modifying the C5 position of the benzene ring of the macrocyclic urea with ether moieties, aliphatic carbon chains, amide and halides.	Benzene	116-123	checkpoint kinase 1	Homo sapiens	64-68
17931867-1	2007	A variety of macrocyclic urea compounds were prepared as potent Chk1 inhibitors by modifying the C5 position of the benzene ring of the macrocyclic urea with ether moieties, aliphatic carbon chains, amide and halides.	Ether	158-163	checkpoint kinase 1	Homo sapiens	64-68
17931867-1	2007	A variety of macrocyclic urea compounds were prepared as potent Chk1 inhibitors by modifying the C5 position of the benzene ring of the macrocyclic urea with ether moieties, aliphatic carbon chains, amide and halides.	Carbon	184-190	checkpoint kinase 1	Homo sapiens	64-68
17931867-1	2007	A variety of macrocyclic urea compounds were prepared as potent Chk1 inhibitors by modifying the C5 position of the benzene ring of the macrocyclic urea with ether moieties, aliphatic carbon chains, amide and halides.	Amides	199-204	checkpoint kinase 1	Homo sapiens	64-68
17931867-1	2007	A variety of macrocyclic urea compounds were prepared as potent Chk1 inhibitors by modifying the C5 position of the benzene ring of the macrocyclic urea with ether moieties, aliphatic carbon chains, amide and halides.	halides	209-216	checkpoint kinase 1	Homo sapiens	64-68
17935989-1	2007	A new series of potent macrocyclic urea-based Chk1 inhibitors are described.	Urea	35-39	checkpoint kinase 1	Homo sapiens	46-50
17935989-2	2007	A detailed SAR study on the 4-position of the phenyl ring of the 14-member macrocyclic ureas 1a and d led to the identification of the potent Chk1 inhibitors 2, 5-7, 10, 13, 14, 19-21, 25, 27, and 31-34.	Urea	87-92	checkpoint kinase 1	Homo sapiens	142-146
17935989-3	2007	These compounds significantly sensitize tumor cells to the DNA-damaging antitumor agent doxorubicin in a cell-based assay and efficiently abrogate the doxorubicin-induced G2/M and camptothecin-induced S checkpoints, indicating that the potent biological activities of these compounds are mechanism-based through Chk1 inhibition.	Doxorubicin	151-162	checkpoint kinase 1	Homo sapiens	312-316
17935989-3	2007	These compounds significantly sensitize tumor cells to the DNA-damaging antitumor agent doxorubicin in a cell-based assay and efficiently abrogate the doxorubicin-induced G2/M and camptothecin-induced S checkpoints, indicating that the potent biological activities of these compounds are mechanism-based through Chk1 inhibition.	Camptothecin	180-192	checkpoint kinase 1	Homo sapiens	312-316
17935989-4	2007	Kinome profiling analysis of a representative macrocyclic urea 25 against a panel of 120 kinases indicates that these novel macrocyclic ureas are highly selective Chk1 inhibitors.	Urea	58-62	checkpoint kinase 1	Homo sapiens	163-167
17935989-4	2007	Kinome profiling analysis of a representative macrocyclic urea 25 against a panel of 120 kinases indicates that these novel macrocyclic ureas are highly selective Chk1 inhibitors.	Urea	136-141	checkpoint kinase 1	Homo sapiens	163-167
17881774-6	2007	In contrast, the phosphorylation of Chk1 efficiently occurs in cells treated with dacarbazine as well as with ACNU, the former being in MLH1-dependent manner, whereas the latter in MLH1-independent manner.	Dacarbazine	82-93	checkpoint kinase 1	Homo sapiens	36-40
17881774-6	2007	In contrast, the phosphorylation of Chk1 efficiently occurs in cells treated with dacarbazine as well as with ACNU, the former being in MLH1-dependent manner, whereas the latter in MLH1-independent manner.	Nimustine	110-114	checkpoint kinase 1	Homo sapiens	36-40
17616687-8	2007	Interestingly, ATR and Chk1 siRNA transfection in BRCA1-positive cells shows similar levels of 6-TG cytotoxicity as the control transfectant, whereas MSH2 and MLH1 siRNA transfectants show 6-TG resistance as expected.	Thioguanine	95-99	checkpoint kinase 1	Homo sapiens	23-27
18281511-2	2008	The Chk1 inhibitor 7-hydroxystaurosporine (UCN-01) can overcome both S and G(2) arrest and drive cells through a lethal mitosis.	7-hydroxystaurosporine	19-41	checkpoint kinase 1	Homo sapiens	4-8
18281511-2	2008	The Chk1 inhibitor 7-hydroxystaurosporine (UCN-01) can overcome both S and G(2) arrest and drive cells through a lethal mitosis.	7-hydroxystaurosporine	43-49	checkpoint kinase 1	Homo sapiens	4-8
18088187-7	2007	Chk1 phosphorylation was maintained only in the presence of staurosporine and UCN-01 in p53+/+ cells.	Staurosporine	60-73	checkpoint kinase 1	Homo sapiens	0-4
17986860-7	2007	In human colon carcinoma cells treated with the topoisomerase I inhibitor camptothecin, DNA replication is inhibited both at the level of initiation and at the level of elongation through a Chk1-dependent checkpoint mechanism.	Camptothecin	74-86	checkpoint kinase 1	Homo sapiens	190-194
17900801-5	2007	Combining the Chk1 inhibitor UCN-01 dramatically enhanced the response to AG490 in p53-mutated or deleted glioma cells.	7-hydroxystaurosporine	29-35	checkpoint kinase 1	Homo sapiens	14-18
17900801-5	2007	Combining the Chk1 inhibitor UCN-01 dramatically enhanced the response to AG490 in p53-mutated or deleted glioma cells.	alpha-cyano-(3,4-dihydroxy)-N-benzylcinnamide	74-79	checkpoint kinase 1	Homo sapiens	14-18
17827013-0	2007	Discovery of 4"-(1,4-dihydro-indeno[1,2-c]pyrazol-3-yl)-benzonitriles and 4"-(1,4-dihydro-indeno[1,2-c]pyrazol-3-yl)-pyridine-2"-carbonitriles as potent checkpoint kinase 1 (Chk1) inhibitors.	4"-(1,4-dihydro-indeno[1,2-c]pyrazol-3-yl)-benzonitriles	13-69	checkpoint kinase 1	Homo sapiens	153-172
17827013-0	2007	Discovery of 4"-(1,4-dihydro-indeno[1,2-c]pyrazol-3-yl)-benzonitriles and 4"-(1,4-dihydro-indeno[1,2-c]pyrazol-3-yl)-pyridine-2"-carbonitriles as potent checkpoint kinase 1 (Chk1) inhibitors.	4"-(1,4-dihydro-indeno[1,2-c]pyrazol-3-yl)-benzonitriles	13-69	checkpoint kinase 1	Homo sapiens	174-178
17827013-0	2007	Discovery of 4"-(1,4-dihydro-indeno[1,2-c]pyrazol-3-yl)-benzonitriles and 4"-(1,4-dihydro-indeno[1,2-c]pyrazol-3-yl)-pyridine-2"-carbonitriles as potent checkpoint kinase 1 (Chk1) inhibitors.	4"-(1,4-dihydro-indeno[1,2-c]pyrazol-3-yl)-pyridine-2"-carbonitriles	74-142	checkpoint kinase 1	Homo sapiens	153-172
17827013-0	2007	Discovery of 4"-(1,4-dihydro-indeno[1,2-c]pyrazol-3-yl)-benzonitriles and 4"-(1,4-dihydro-indeno[1,2-c]pyrazol-3-yl)-pyridine-2"-carbonitriles as potent checkpoint kinase 1 (Chk1) inhibitors.	4"-(1,4-dihydro-indeno[1,2-c]pyrazol-3-yl)-pyridine-2"-carbonitriles	74-142	checkpoint kinase 1	Homo sapiens	174-178
17827013-1	2007	An extensive structure-activity relationship study of the 3-position of a series of tricyclic pyrazole-based Chk1 inhibitors is described.	tricyclic pyrazole	84-102	checkpoint kinase 1	Homo sapiens	109-113
17887663-0	2007	Structure-based design and synthesis of (5-arylamino-2H-pyrazol-3-yl)-biphenyl-2",4"-diols as novel and potent human CHK1 inhibitors.	(5-arylamino-2h-pyrazol-3-yl)-biphenyl-2",4"-diols	40-90	checkpoint kinase 1	Homo sapiens	117-121
17912033-7	2007	We also observed higher levels of Chk1 protein in Plk2-deficient cells that were associated with reduced levels of Serine 317-phosphorylated Chk1.	Serine	115-121	checkpoint kinase 1	Homo sapiens	34-38
17912033-7	2007	We also observed higher levels of Chk1 protein in Plk2-deficient cells that were associated with reduced levels of Serine 317-phosphorylated Chk1.	Serine	115-121	checkpoint kinase 1	Homo sapiens	141-145
17912033-8	2007	In aphidicolin-treated cells, there were lower levels of Serine 317-phosphorylated Chk1 when Plk2 was knocked-down.	Aphidicolin	3-14	checkpoint kinase 1	Homo sapiens	83-87
17912033-8	2007	In aphidicolin-treated cells, there were lower levels of Serine 317-phosphorylated Chk1 when Plk2 was knocked-down.	Serine	57-63	checkpoint kinase 1	Homo sapiens	83-87
17912033-9	2007	Plk2 was demonstrated to interact with Chk2, Chk1, Serine 317-phosphorylated Chk1 and p53.	Serine	51-57	checkpoint kinase 1	Homo sapiens	77-81
17722905-0	2007	Synthesis and biological activities of new checkpoint kinase 1 inhibitors structurally related to granulatimide.	granulatimide	98-111	checkpoint kinase 1	Homo sapiens	43-62
17722905-3	2007	The results of molecular modeling in the ATP binding pocket of Chk1 are described.	Adenosine Triphosphate	41-44	checkpoint kinase 1	Homo sapiens	63-67
17722905-4	2007	Among the newly synthesized compounds, compounds 13 and 16, in which the imidazole was replaced by a quinone and a hydroquinone and which bear a hydroxy group on the indole moiety, are the most potent Chk1 inhibitors in this series with IC50 values of 27 and 23 nM, respectively.	imidazole	73-82	checkpoint kinase 1	Homo sapiens	201-205
17722905-4	2007	Among the newly synthesized compounds, compounds 13 and 16, in which the imidazole was replaced by a quinone and a hydroquinone and which bear a hydroxy group on the indole moiety, are the most potent Chk1 inhibitors in this series with IC50 values of 27 and 23 nM, respectively.	quinone	101-108	checkpoint kinase 1	Homo sapiens	201-205
17722905-4	2007	Among the newly synthesized compounds, compounds 13 and 16, in which the imidazole was replaced by a quinone and a hydroquinone and which bear a hydroxy group on the indole moiety, are the most potent Chk1 inhibitors in this series with IC50 values of 27 and 23 nM, respectively.	hydroquinone	115-127	checkpoint kinase 1	Homo sapiens	201-205
17722905-4	2007	Among the newly synthesized compounds, compounds 13 and 16, in which the imidazole was replaced by a quinone and a hydroquinone and which bear a hydroxy group on the indole moiety, are the most potent Chk1 inhibitors in this series with IC50 values of 27 and 23 nM, respectively.	indole	166-172	checkpoint kinase 1	Homo sapiens	201-205
17517898-2	2007	To develop a Chk1-specific cell-based assay, stable clones were established in which Chk1 kinase domain fused at its N-terminus with p53 through 4 tandem repeats of Gly-Gly-Gly-Gly-Ser was expressed in an inducible manner.	Serine	181-184	checkpoint kinase 1	Homo sapiens	13-17
17517898-2	2007	To develop a Chk1-specific cell-based assay, stable clones were established in which Chk1 kinase domain fused at its N-terminus with p53 through 4 tandem repeats of Gly-Gly-Gly-Gly-Ser was expressed in an inducible manner.	Serine	181-184	checkpoint kinase 1	Homo sapiens	85-89
17530733-6	2007	Strikingly, DMCs increased cytotoxicity was not associated with an increase in DNA double-strand breaks but was associated with early poly(ADP-ribose) polymerase (PARP) activation and Chk1 kinase depletion.	methyl carbonate	12-16	checkpoint kinase 1	Homo sapiens	184-188
17879369-2	2007	ATR and CHEK1 contain mononucleotide microsatellite repeat regions, which are mutational targets in tumors with defective mismatch repair (MMR).	mononucleotide	22-36	checkpoint kinase 1	Homo sapiens	8-13
18088187-8	2007	In the presence of caffeine Chk1 phosphorylation was inhibited regardless of p53 status.	Caffeine	19-27	checkpoint kinase 1	Homo sapiens	28-32
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.	Staurosporine	152-165	checkpoint kinase 1	Homo sapiens	15-19
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	checkpoint kinase 1	Homo sapiens	15-19
18088187-10	2007	Moreover, sustained phosphorylation of Chk1 in the presence of staurosporine and UCN-01 is strongly related to phosphorylation of p53.	Staurosporine	63-76	checkpoint kinase 1	Homo sapiens	39-43
17900896-0	2007	Synthesis and evaluation of substituted benzoisoquinolinones as potent inhibitors of Chk1 kinase.	benzoisoquinolinones	40-60	checkpoint kinase 1	Homo sapiens	85-89
17900896-1	2007	From HTS lead 1, a novel benzoisoquinolinone class of ATP-competitive Chk1 inhibitors was devised and synthesized via a photochemical route.	benzoisoquinolinone	25-44	checkpoint kinase 1	Homo sapiens	70-74
17900896-1	2007	From HTS lead 1, a novel benzoisoquinolinone class of ATP-competitive Chk1 inhibitors was devised and synthesized via a photochemical route.	Adenosine Triphosphate	54-57	checkpoint kinase 1	Homo sapiens	70-74
17804227-0	2007	Optimization of a pyrazoloquinolinone class of Chk1 kinase inhibitors.	pyrazoloquinolinone	18-37	checkpoint kinase 1	Homo sapiens	47-51
17804227-1	2007	The development of 2,5-dihydro-4H-pyrazolo[4,3-c]quinolin-4-ones as inhibitors of Chk1 kinase is described.	2,5-dihydro-4h-pyrazolo[4,3-c]quinolin-4-ones	19-64	checkpoint kinase 1	Homo sapiens	82-86
17804227-2	2007	Introduction of a fused ring at the C7/C8 positions of the pyrazoloquinolinone provided an increase in potency while guidance from overlapping inhibitor bound Chk1 X-ray crystal structures contributed to the discovery of a potent and solubilizing propyl amine moiety in compound 52 (Chk1 IC(50)=3.1 nM).	pyrazoloquinolinone	59-78	checkpoint kinase 1	Homo sapiens	159-163
17804227-2	2007	Introduction of a fused ring at the C7/C8 positions of the pyrazoloquinolinone provided an increase in potency while guidance from overlapping inhibitor bound Chk1 X-ray crystal structures contributed to the discovery of a potent and solubilizing propyl amine moiety in compound 52 (Chk1 IC(50)=3.1 nM).	pyrazoloquinolinone	59-78	checkpoint kinase 1	Homo sapiens	283-287
17804227-2	2007	Introduction of a fused ring at the C7/C8 positions of the pyrazoloquinolinone provided an increase in potency while guidance from overlapping inhibitor bound Chk1 X-ray crystal structures contributed to the discovery of a potent and solubilizing propyl amine moiety in compound 52 (Chk1 IC(50)=3.1 nM).	Propylamines	247-259	checkpoint kinase 1	Homo sapiens	159-163
17804227-2	2007	Introduction of a fused ring at the C7/C8 positions of the pyrazoloquinolinone provided an increase in potency while guidance from overlapping inhibitor bound Chk1 X-ray crystal structures contributed to the discovery of a potent and solubilizing propyl amine moiety in compound 52 (Chk1 IC(50)=3.1 nM).	Propylamines	247-259	checkpoint kinase 1	Homo sapiens	283-287
17726372-3	2007	Here, we demonstrate that DNA damage caused by ultraviolet irradiation or hydroxyurea treatment leads to centrosomal accumulation of endogenous Chk1 in normal human BJ fibroblasts and in ATR- or ATM-deficient fibroblasts.	Hydroxyurea	74-85	checkpoint kinase 1	Homo sapiens	144-148
17726372-4	2007	Chemical inhibition of ATR/ATM by caffeine led to enhanced centrosomal Chk1 deposition associated with nuclear Chk1 depletion.	Caffeine	34-42	checkpoint kinase 1	Homo sapiens	71-75
17726372-4	2007	Chemical inhibition of ATR/ATM by caffeine led to enhanced centrosomal Chk1 deposition associated with nuclear Chk1 depletion.	Caffeine	34-42	checkpoint kinase 1	Homo sapiens	111-115
17704656-6	2007	Sublethal concentrations of BrdU evoke a DNA damage response in these cells that involves the activation of Chk1, Chk2 and p53.	Bromodeoxyuridine	28-32	checkpoint kinase 1	Homo sapiens	108-112
17517898-2	2007	To develop a Chk1-specific cell-based assay, stable clones were established in which Chk1 kinase domain fused at its N-terminus with p53 through 4 tandem repeats of Gly-Gly-Gly-Gly-Ser was expressed in an inducible manner.	glycyl-glycyl-glycyl-glycine	165-180	checkpoint kinase 1	Homo sapiens	13-17
17517898-2	2007	To develop a Chk1-specific cell-based assay, stable clones were established in which Chk1 kinase domain fused at its N-terminus with p53 through 4 tandem repeats of Gly-Gly-Gly-Gly-Ser was expressed in an inducible manner.	glycyl-glycyl-glycyl-glycine	165-180	checkpoint kinase 1	Homo sapiens	85-89
17690534-10	2007	The genes showing significantly lower expressions after X-ray irradiation rather than after carbon-ion beam irradiation were RAD50, BRCA1, MRE11A, XRCC3, CHEK1, MLH1, CCNB1, CCNB2 and LIG4.	Carbon	92-98	checkpoint kinase 1	Homo sapiens	154-159
17658776-0	2007	Design, synthesis, and biological activity of 5,10-dihydro-dibenzo[b,e][1,4]diazepin-11-one-based potent and selective Chk-1 inhibitors.	5,10-dihydro-11H-dibenzo[b,e][1,4]diazepin-11-one	46-91	checkpoint kinase 1	Homo sapiens	119-124
17658776-1	2007	A novel series of 5,10-dihydro-dibenzo[b,e][1,4]diazepin-11-ones have been synthesized as potent and selective checkpoint kinase 1 (Chk1) inhibitors via structure-based design.	5,10-dihydro-dibenzo[b,e][1,4]diazepin-11-ones	18-64	checkpoint kinase 1	Homo sapiens	111-130
17658776-1	2007	A novel series of 5,10-dihydro-dibenzo[b,e][1,4]diazepin-11-ones have been synthesized as potent and selective checkpoint kinase 1 (Chk1) inhibitors via structure-based design.	5,10-dihydro-dibenzo[b,e][1,4]diazepin-11-ones	18-64	checkpoint kinase 1	Homo sapiens	132-136
17658776-5	2007	Two important binding interactions between compound 46b and Chk1 kinase, revealed by X-ray cocrystal structure, were hydrogen bonds between the hinge region and the amide bond of the core structure and a hydrogen bond between the methoxy group and Lys38 of the protein.	Hydrogen	117-125	checkpoint kinase 1	Homo sapiens	60-64
17658776-5	2007	Two important binding interactions between compound 46b and Chk1 kinase, revealed by X-ray cocrystal structure, were hydrogen bonds between the hinge region and the amide bond of the core structure and a hydrogen bond between the methoxy group and Lys38 of the protein.	Amides	165-170	checkpoint kinase 1	Homo sapiens	60-64
17658776-5	2007	Two important binding interactions between compound 46b and Chk1 kinase, revealed by X-ray cocrystal structure, were hydrogen bonds between the hinge region and the amide bond of the core structure and a hydrogen bond between the methoxy group and Lys38 of the protein.	Hydrogen	204-212	checkpoint kinase 1	Homo sapiens	60-64
17320279-1	2007	Protein kinase C (PKC) alpha/betaI isoenzyme inhibitor Go6976 has been suggested to be a G2 checkpoint abrogator by direct Chk1 inhibition.	Go 6976	55-61	checkpoint kinase 1	Homo sapiens	123-127
17544271-0	2007	Synthesis and biological evaluation of 4"-(6,7-disubstituted-2,4-dihydro-indeno[1,2-c]pyrazol-3-yl)-biphenyl-4-ol as potent Chk1 inhibitors.	4"-(6,7-disubstituted-2,4-dihydro-indeno[1,2-c]pyrazol-3-yl)-biphenyl-4-ol	39-113	checkpoint kinase 1	Homo sapiens	124-128
17544271-1	2007	A new series of potent tricyclic pyrazole-based Chk1 inhibitors are described.	tricyclic pyrazole	23-41	checkpoint kinase 1	Homo sapiens	48-52
17544271-6	2007	These compounds significantly potentiate the cytotoxicity of DNA-damaging antitumor agents in a cell-based assay and efficiently abrogate the doxorubicin-induced G2/M and the camptothecin-induced S checkpoints, suggesting that their potent biological activities are mechanism-based through Chk1 inhibition.	Doxorubicin	142-153	checkpoint kinase 1	Homo sapiens	290-294
17544271-6	2007	These compounds significantly potentiate the cytotoxicity of DNA-damaging antitumor agents in a cell-based assay and efficiently abrogate the doxorubicin-induced G2/M and the camptothecin-induced S checkpoints, suggesting that their potent biological activities are mechanism-based through Chk1 inhibition.	Camptothecin	175-187	checkpoint kinase 1	Homo sapiens	290-294
17329004-0	2007	Tubulozole-induced G2/M cell cycle arrest in human colon cancer cells through formation of microtubule polymerization mediated by ERK1/2 and Chk1 kinase activation.	tubulazole	0-10	checkpoint kinase 1	Homo sapiens	141-145
17329004-1	2007	Our studies demonstrated that human colon cancer cells (COLO 205), with higher expression level of check point kinase 1 (Chk1), were more sensitive to microtubule damage agent Tubulozole (TUBU) induced G2/M phase arrest than normal human colon epithelial (CRL) cells.	tubulazole	176-186	checkpoint kinase 1	Homo sapiens	121-125
17329004-4	2007	In addition, TUBU induced phosphorylation of the Cdc25C (Ser-216) and Bad (Ser-155) proteins were blocked by Chk1 SiRNA-transfection.	Serine	57-60	checkpoint kinase 1	Homo sapiens	109-113
17329004-4	2007	In addition, TUBU induced phosphorylation of the Cdc25C (Ser-216) and Bad (Ser-155) proteins were blocked by Chk1 SiRNA-transfection.	Serine	75-78	checkpoint kinase 1	Homo sapiens	109-113
17329004-6	2007	We further demonstrated that extracellular signal-regulated kinase (ERK) activation by TUBU was needed for Chk1 kinase activation and microtubule formation as shown by the attenuation of these responses by the ERK1/2 specific inhibitor PD98059.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	236-243	checkpoint kinase 1	Homo sapiens	107-111
17663721-4	2007	Here, we show that checkpoint kinases, Chk1 and Chk2, as well as their upstream ATM kinase are phosphorylated and activated following MG treatment of cultured cells.	Pyruvaldehyde	134-136	checkpoint kinase 1	Homo sapiens	39-43
17663721-5	2007	This MG-induced activation of Chk1 and Chk2 were inhibited by either aminoguanidine (AG), an inhibitor of production of advanced glycation end products (AGEs) or N-acetyl-l-cysteine (NAC), an anti-oxidant in dose dependent manners, indicating that oxidative stress via AGEs is involved critically in the activation of Chk1 and Chk2 by MG.	pimagedine	69-83	checkpoint kinase 1	Homo sapiens	30-34
17663721-5	2007	This MG-induced activation of Chk1 and Chk2 were inhibited by either aminoguanidine (AG), an inhibitor of production of advanced glycation end products (AGEs) or N-acetyl-l-cysteine (NAC), an anti-oxidant in dose dependent manners, indicating that oxidative stress via AGEs is involved critically in the activation of Chk1 and Chk2 by MG.	pimagedine	69-83	checkpoint kinase 1	Homo sapiens	318-322
17663721-5	2007	This MG-induced activation of Chk1 and Chk2 were inhibited by either aminoguanidine (AG), an inhibitor of production of advanced glycation end products (AGEs) or N-acetyl-l-cysteine (NAC), an anti-oxidant in dose dependent manners, indicating that oxidative stress via AGEs is involved critically in the activation of Chk1 and Chk2 by MG.	Pyruvaldehyde	5-7	checkpoint kinase 1	Homo sapiens	30-34
17663721-5	2007	This MG-induced activation of Chk1 and Chk2 were inhibited by either aminoguanidine (AG), an inhibitor of production of advanced glycation end products (AGEs) or N-acetyl-l-cysteine (NAC), an anti-oxidant in dose dependent manners, indicating that oxidative stress via AGEs is involved critically in the activation of Chk1 and Chk2 by MG.	Pyruvaldehyde	5-7	checkpoint kinase 1	Homo sapiens	318-322
17611684-0	2007	Zoledronate-induced S phase arrest and apoptosis accompanied by DNA damage and activation of the ATM/Chk1/cdc25 pathway in human osteosarcoma cells.	Zoledronic Acid	0-11	checkpoint kinase 1	Homo sapiens	101-105
17611684-7	2007	When HOS cells were treated with zoledronate, ATM kinase and its substrate, check-point kinase (Chk)1, were phosphorylated.	Zoledronic Acid	33-44	checkpoint kinase 1	Homo sapiens	76-101
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	checkpoint kinase 1	Homo sapiens	98-102
17611684-10	2007	As gamma-H2AX accumulates at dsDNA breaks, these results demonstrate that zoledronate induced DNA damage and S phase arrest, accompanied by activation of the ATM/Chk1/cdc25 pathway in a human osteosarcoma cell line.	gamma-h2ax	3-13	checkpoint kinase 1	Homo sapiens	162-166
17611684-10	2007	As gamma-H2AX accumulates at dsDNA breaks, these results demonstrate that zoledronate induced DNA damage and S phase arrest, accompanied by activation of the ATM/Chk1/cdc25 pathway in a human osteosarcoma cell line.	Zoledronic Acid	74-85	checkpoint kinase 1	Homo sapiens	162-166
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	checkpoint kinase 1	Homo sapiens	52-71
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	checkpoint kinase 1	Homo sapiens	73-77
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	checkpoint kinase 1	Homo sapiens	29-33
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	checkpoint kinase 1	Homo sapiens	32-36
17634129-9	2007	p30 expression in Jurkat T-cells resulted in an increase in phosphorylation at serine 216 of nuclear cell division cycle 25C (Cdc25C), had enhanced checkpoint kinase 1 (Chk1) serine 345 phosphorylation, reduced expression of polo-like kinase 1 (PLK1), diminished phosphorylation of PLK1 at tyrosine 210 and reduced phosphorylation of Cdc25C at serine 198.	Serine	175-181	checkpoint kinase 1	Homo sapiens	169-173
17634129-9	2007	p30 expression in Jurkat T-cells resulted in an increase in phosphorylation at serine 216 of nuclear cell division cycle 25C (Cdc25C), had enhanced checkpoint kinase 1 (Chk1) serine 345 phosphorylation, reduced expression of polo-like kinase 1 (PLK1), diminished phosphorylation of PLK1 at tyrosine 210 and reduced phosphorylation of Cdc25C at serine 198.	Serine	175-181	checkpoint kinase 1	Homo sapiens	169-173
17630511-4	2007	The BPDE-induced S phase block, but not the G(2)/M phase arrest, was significantly attenuated by knockdown of Chk1 protein level.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	4-8	checkpoint kinase 1	Homo sapiens	110-114
17630511-5	2007	The BPDE-mediated accumulation of sub-diploid fraction (apoptotic cells) was significantly decreased in H1299 cells transiently transfected with both Chk1 and Chk2 specific siRNAs.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	4-8	checkpoint kinase 1	Homo sapiens	150-154
17638866-1	2007	We previously showed that checkpoint kinase 1 (Chk1) and Claspin, two DNA-damage checkpoint proteins, were down-regulated by 1,25-dihydroxyvitamin D(3), a known inhibitor of cell proliferation.	1,25-dihydroxyvitamin D	125-148	checkpoint kinase 1	Homo sapiens	26-45
17638866-1	2007	We previously showed that checkpoint kinase 1 (Chk1) and Claspin, two DNA-damage checkpoint proteins, were down-regulated by 1,25-dihydroxyvitamin D(3), a known inhibitor of cell proliferation.	1,25-dihydroxyvitamin D	125-148	checkpoint kinase 1	Homo sapiens	47-51
17297454-5	2007	Moreover, incubation of cells with caffeine, which inhibits ataxia telangiectasia mutated (ATM)/ATR, or transfection of cells with short interfering RNA targeting ATR abrogated IR-induced Chk1 phosphorylation and G2/M arrest but had no effect on IR-induced ERK1/2 activation.	Caffeine	35-43	checkpoint kinase 1	Homo sapiens	188-192
17616687-8	2007	Interestingly, ATR and Chk1 siRNA transfection in BRCA1-positive cells shows similar levels of 6-TG cytotoxicity as the control transfectant, whereas MSH2 and MLH1 siRNA transfectants show 6-TG resistance as expected.	Thioguanine	189-193	checkpoint kinase 1	Homo sapiens	23-27
17563398-6	2007	Additionally, DFO treatment also led to the activation of Chk1, p53, and Akt, where DFO-induced activation of p53, Chk1, and Akt occurred in both PKCdelta-dependent and -independent manners.	Deferoxamine	14-17	checkpoint kinase 1	Homo sapiens	58-62
17418864-10	2007	We also found that an inhibitory CHK1 phosphorylation at Ser-280 was dramatically increased upon COX-2 overexpression in MCF10A cells, thus explaining the mechanism of inactivation of an important cell cycle checkpoint.	Serine	57-60	checkpoint kinase 1	Homo sapiens	33-37
17563398-6	2007	Additionally, DFO treatment also led to the activation of Chk1, p53, and Akt, where DFO-induced activation of p53, Chk1, and Akt occurred in both PKCdelta-dependent and -independent manners.	Deferoxamine	14-17	checkpoint kinase 1	Homo sapiens	115-119
17563398-6	2007	Additionally, DFO treatment also led to the activation of Chk1, p53, and Akt, where DFO-induced activation of p53, Chk1, and Akt occurred in both PKCdelta-dependent and -independent manners.	Deferoxamine	84-87	checkpoint kinase 1	Homo sapiens	58-62
17563398-6	2007	Additionally, DFO treatment also led to the activation of Chk1, p53, and Akt, where DFO-induced activation of p53, Chk1, and Akt occurred in both PKCdelta-dependent and -independent manners.	Deferoxamine	84-87	checkpoint kinase 1	Homo sapiens	115-119
17292679-2	2007	The combination of MMS+4-AN results in accumulation of cells in S-phase of the cell cycle and activation of Chk1.	mms+4-an	19-27	checkpoint kinase 1	Homo sapiens	108-112
17292679-5	2007	Consistent with this hypothesis, the inhibitors caffeine and UCN-01 also abrogate the ATR- and Chk1-mediated delay in progression through S-phase.	Caffeine	48-56	checkpoint kinase 1	Homo sapiens	95-99
17292679-5	2007	Consistent with this hypothesis, the inhibitors caffeine and UCN-01 also abrogate the ATR- and Chk1-mediated delay in progression through S-phase.	7-hydroxystaurosporine	61-67	checkpoint kinase 1	Homo sapiens	95-99
17339337-5	2007	Evaluation of these calcium calmodulin kinase superfamily members as candidate Ser(20) kinases in vivo has shown that only CHK1 or DAPK-1 can stimulate p53 transactivation and induce Ser(20) phosphorylation of p53.	Serine	79-82	checkpoint kinase 1	Homo sapiens	123-127
17290426-8	2007	We modulated checkpoint-related gene expression in testis using the anti-metabolite, 5-fluorouracil, resulting in increased apoptosis and upregulation of Chk1 (P<0.0001) and Cdc2 (P<0.02) mRNA.	Fluorouracil	85-99	checkpoint kinase 1	Homo sapiens	154-158
16978863-0	2006	3-(Indol-2-yl)indazoles as Chek1 kinase inhibitors: Optimization of potency and selectivity via substitution at C6.	3-(indol-2-yl)indazoles	0-23	checkpoint kinase 1	Homo sapiens	27-32
17352464-5	2007	Compounds 5b, 5c, 5f, 15, 16d, 17g, 17h, 17k, 18d, and 22 were identified as ideal Chk1 inhibitors, which showed little or no single-agent activity but significantly potentiate the cytotoxicities of the DNA-damaging antitumor agents doxorubicin and camptothecin.	Doxorubicin	233-244	checkpoint kinase 1	Homo sapiens	83-87
17352464-5	2007	Compounds 5b, 5c, 5f, 15, 16d, 17g, 17h, 17k, 18d, and 22 were identified as ideal Chk1 inhibitors, which showed little or no single-agent activity but significantly potentiate the cytotoxicities of the DNA-damaging antitumor agents doxorubicin and camptothecin.	Camptothecin	249-261	checkpoint kinase 1	Homo sapiens	83-87
17352464-6	2007	These novel Chk1 inhibitors abrogate the doxorubicin-induced G2 and camptothecin-induced S checkpoint arrests, confirming that their potent biological activities are mechanism-based through Chk1 inhibition.	Doxorubicin	41-52	checkpoint kinase 1	Homo sapiens	12-16
17352464-6	2007	These novel Chk1 inhibitors abrogate the doxorubicin-induced G2 and camptothecin-induced S checkpoint arrests, confirming that their potent biological activities are mechanism-based through Chk1 inhibition.	Doxorubicin	41-52	checkpoint kinase 1	Homo sapiens	190-194
17352464-6	2007	These novel Chk1 inhibitors abrogate the doxorubicin-induced G2 and camptothecin-induced S checkpoint arrests, confirming that their potent biological activities are mechanism-based through Chk1 inhibition.	Camptothecin	68-80	checkpoint kinase 1	Homo sapiens	12-16
17352464-6	2007	These novel Chk1 inhibitors abrogate the doxorubicin-induced G2 and camptothecin-induced S checkpoint arrests, confirming that their potent biological activities are mechanism-based through Chk1 inhibition.	Camptothecin	68-80	checkpoint kinase 1	Homo sapiens	190-194
17287122-0	2007	Discovery of 1,4-dihydroindeno[1,2-c]pyrazoles as a novel class of potent and selective checkpoint kinase 1 inhibitors.	1,4-dihydroindeno[1,2-c]pyrazoles	13-46	checkpoint kinase 1	Homo sapiens	88-107
17287122-1	2007	A new class of checkpoint kinase 1 (CHK-1) inhibitors bearing a 1,4-dihydroindeno[1,2-c]pyrazole core was developed after initial hits from high throughput screening.	2,4-dihydroindeno[1,2-c]pyrazole	64-96	checkpoint kinase 1	Homo sapiens	15-34
17287122-1	2007	A new class of checkpoint kinase 1 (CHK-1) inhibitors bearing a 1,4-dihydroindeno[1,2-c]pyrazole core was developed after initial hits from high throughput screening.	2,4-dihydroindeno[1,2-c]pyrazole	64-96	checkpoint kinase 1	Homo sapiens	36-41
17296736-3	2007	Here, we show that, in response to DNA damage, Chk1 directly phosphorylates the FANCE subunit of the FA core complex on two conserved sites (threonine 346 and serine 374).	Threonine	141-150	checkpoint kinase 1	Homo sapiens	47-51
17296736-3	2007	Here, we show that, in response to DNA damage, Chk1 directly phosphorylates the FANCE subunit of the FA core complex on two conserved sites (threonine 346 and serine 374).	Serine	159-165	checkpoint kinase 1	Homo sapiens	47-51
17384638-4	2007	ATR phosphorylation is known to both activate Chk1 and target it for proteolytic degradation, and depleting ATR or mutation of Chk1 at Ser 345 restored Chk1 protein levels in HCLK2-depleted cells.	Serine	135-138	checkpoint kinase 1	Homo sapiens	127-131
17384638-4	2007	ATR phosphorylation is known to both activate Chk1 and target it for proteolytic degradation, and depleting ATR or mutation of Chk1 at Ser 345 restored Chk1 protein levels in HCLK2-depleted cells.	Serine	135-138	checkpoint kinase 1	Homo sapiens	127-131
17406032-9	2007	Exposure of previously gemcitabine-treated cultures to the Chk1 inhibitor 7-hydroxystaurosporine (UCN-01) caused a 10-fold increase in H2AX phosphorylation, which was displayed as an even pan-nuclear staining.	gemcitabine	23-34	checkpoint kinase 1	Homo sapiens	59-63
17406032-9	2007	Exposure of previously gemcitabine-treated cultures to the Chk1 inhibitor 7-hydroxystaurosporine (UCN-01) caused a 10-fold increase in H2AX phosphorylation, which was displayed as an even pan-nuclear staining.	7-hydroxystaurosporine	74-96	checkpoint kinase 1	Homo sapiens	59-63
17406032-9	2007	Exposure of previously gemcitabine-treated cultures to the Chk1 inhibitor 7-hydroxystaurosporine (UCN-01) caused a 10-fold increase in H2AX phosphorylation, which was displayed as an even pan-nuclear staining.	7-hydroxystaurosporine	98-104	checkpoint kinase 1	Homo sapiens	59-63
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	checkpoint kinase 1	Homo sapiens	132-136
17210576-1	2007	ATM and Rad3-related (ATR) is a regulatory kinase that, when activated by hydroxyurea, UV, or human immunodeficiency virus-1 Vpr, causes cell cycle arrest through Chk1-Ser(345) phosphorylation.	Hydroxyurea	74-85	checkpoint kinase 1	Homo sapiens	163-167
17210576-1	2007	ATM and Rad3-related (ATR) is a regulatory kinase that, when activated by hydroxyurea, UV, or human immunodeficiency virus-1 Vpr, causes cell cycle arrest through Chk1-Ser(345) phosphorylation.	Serine	168-171	checkpoint kinase 1	Homo sapiens	163-167
17210576-2	2007	We demonstrate here that of these three agents only Vpr requires protein phosphatase type 2A (PP2A) to activate ATR for Chk1-Ser(345) phosphorylation.	Serine	125-128	checkpoint kinase 1	Homo sapiens	120-124
17210576-7	2007	Conversely, H2AX down-regulation had little effect on PP2A(Aalpha/Cbeta)-mediated G(2) arrest and Chk1-Ser(345) phosphorylation by Vpr.	Serine	103-106	checkpoint kinase 1	Homo sapiens	98-102
16978863-3	2006	Enzyme potency against Chek1 was optimized by the incorporation of a hydroxymethyl triazole moiety in compound 21 (Chek1 IC(50)=0.30nM) that was shown by X-ray crystallography to displace one of three highly conserved water molecules in the HI region of the ATP-binding cleft.	Adenosine Triphosphate	258-261	checkpoint kinase 1	Homo sapiens	115-120
17490879-0	2007	1,4-Dihydroindeno[1,2-c]pyrazoles as potent checkpoint kinase 1 inhibitors: extended exploration on phenyl ring substitutions and preliminary ADME/PK studies.	1,4-dihydroindeno[1,2-c]pyrazoles	0-33	checkpoint kinase 1	Homo sapiens	44-63
17490879-1	2007	A study on substitutions at the four open positions on the phenyl ring of the 1,4-dihydroindeno[1,2-c]pyrazoles as potent CHK-1 inhibitors is described.	1,4-dihydroindeno[1,2-c]pyrazoles	78-111	checkpoint kinase 1	Homo sapiens	122-127
17268080-2	2007	Here, we show that Chk1 is cleaved in the treatment of apoptotic dose of etoposide (ETP) or cisplatin (CIS) but not of viable dose in HeLa S3 cells.	Etoposide	73-82	checkpoint kinase 1	Homo sapiens	19-23
17268080-2	2007	Here, we show that Chk1 is cleaved in the treatment of apoptotic dose of etoposide (ETP) or cisplatin (CIS) but not of viable dose in HeLa S3 cells.	Etoposide	84-87	checkpoint kinase 1	Homo sapiens	19-23
17268080-2	2007	Here, we show that Chk1 is cleaved in the treatment of apoptotic dose of etoposide (ETP) or cisplatin (CIS) but not of viable dose in HeLa S3 cells.	Cisplatin	92-101	checkpoint kinase 1	Homo sapiens	19-23
17268080-3	2007	The cleavage of Chk1 was completely inhibited by an irreversible and cell-permeable pan-caspase inhibitor, N-benzyloxycarbonyl-Val-Ala-Asp (OMe) fluoromethylketone (z-VAD-fmk).	n-benzyloxycarbonyl-val-ala-asp (ome) fluoromethylketone	107-163	checkpoint kinase 1	Homo sapiens	16-20
17268080-3	2007	The cleavage of Chk1 was completely inhibited by an irreversible and cell-permeable pan-caspase inhibitor, N-benzyloxycarbonyl-Val-Ala-Asp (OMe) fluoromethylketone (z-VAD-fmk).	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	165-174	checkpoint kinase 1	Homo sapiens	16-20
17276342-2	2007	Here, we show that Chk1, a component of the DNA damage and replication checkpoints, protects vertebrate cells against spontaneous chromosome missegregation and is required to sustain anaphase delay when spindle function is disrupted by taxol, but not when microtubules are completely depolymerized by nocodazole.	Paclitaxel	236-241	checkpoint kinase 1	Homo sapiens	19-23
17276342-2	2007	Here, we show that Chk1, a component of the DNA damage and replication checkpoints, protects vertebrate cells against spontaneous chromosome missegregation and is required to sustain anaphase delay when spindle function is disrupted by taxol, but not when microtubules are completely depolymerized by nocodazole.	Nocodazole	301-311	checkpoint kinase 1	Homo sapiens	19-23
17276342-6	2007	In addition, Chk1-deficient cells exhibit increased resistance to taxol.	Paclitaxel	66-71	checkpoint kinase 1	Homo sapiens	13-17
17134696-0	2007	Bis-imide granulatimide analogues as potent Checkpoint 1 kinase inhibitors.	bis-imide	0-9	checkpoint kinase 1	Homo sapiens	44-63
17134696-0	2007	Bis-imide granulatimide analogues as potent Checkpoint 1 kinase inhibitors.	granulatimide	10-23	checkpoint kinase 1	Homo sapiens	44-63
17134696-1	2007	Granulatimide and isogranulatimide, natural products isolated from an ascidian, were found to be abrogators of the cell cycle G2-M phase checkpoint by inhibition of Checkpoint 1 kinase (Chk1).	granulatimide	0-13	checkpoint kinase 1	Homo sapiens	165-184
17134696-1	2007	Granulatimide and isogranulatimide, natural products isolated from an ascidian, were found to be abrogators of the cell cycle G2-M phase checkpoint by inhibition of Checkpoint 1 kinase (Chk1).	granulatimide	0-13	checkpoint kinase 1	Homo sapiens	186-190
17134696-1	2007	Granulatimide and isogranulatimide, natural products isolated from an ascidian, were found to be abrogators of the cell cycle G2-M phase checkpoint by inhibition of Checkpoint 1 kinase (Chk1).	isogranulatimide	18-34	checkpoint kinase 1	Homo sapiens	165-184
17134696-1	2007	Granulatimide and isogranulatimide, natural products isolated from an ascidian, were found to be abrogators of the cell cycle G2-M phase checkpoint by inhibition of Checkpoint 1 kinase (Chk1).	isogranulatimide	18-34	checkpoint kinase 1	Homo sapiens	186-190
17134696-5	2007	Compared to those of granulatimide and isogranulatimide, the Chk1 inhibitory activities of some of the bis-imide carbazoles were stronger.	granulatimide	21-34	checkpoint kinase 1	Homo sapiens	61-65
17134696-5	2007	Compared to those of granulatimide and isogranulatimide, the Chk1 inhibitory activities of some of the bis-imide carbazoles were stronger.	isogranulatimide	39-55	checkpoint kinase 1	Homo sapiens	61-65
17134696-5	2007	Compared to those of granulatimide and isogranulatimide, the Chk1 inhibitory activities of some of the bis-imide carbazoles were stronger.	bis-imide	103-112	checkpoint kinase 1	Homo sapiens	61-65
17134696-5	2007	Compared to those of granulatimide and isogranulatimide, the Chk1 inhibitory activities of some of the bis-imide carbazoles were stronger.	Carbazoles	113-123	checkpoint kinase 1	Homo sapiens	61-65
17088865-7	2006	Lovastatin attenuated the doxorubicin-induced increase in p53 as well as activation of checkpoint kinase (Chk-1) and stress-activated protein kinase/c-Jun-N-terminal kinase (SAPK/JNK).	Lovastatin	0-10	checkpoint kinase 1	Homo sapiens	106-111
16978863-1	2006	The development of 3-(indol-2-yl)indazoles as inhibitors of Chek1 kinase is described.	3-(indol-2-yl)indazoles	19-42	checkpoint kinase 1	Homo sapiens	60-65
16978863-2	2006	Introduction of amides and heteroaryl groups at the C6 position of the indazole ring system provided sufficient Chek1 potency and selectivity over Cdk7 to permit escape from DNA damage-induced arrest in a cellular assay.	Amides	16-22	checkpoint kinase 1	Homo sapiens	112-117
16978863-2	2006	Introduction of amides and heteroaryl groups at the C6 position of the indazole ring system provided sufficient Chek1 potency and selectivity over Cdk7 to permit escape from DNA damage-induced arrest in a cellular assay.	Indazoles	71-79	checkpoint kinase 1	Homo sapiens	112-117
16978863-3	2006	Enzyme potency against Chek1 was optimized by the incorporation of a hydroxymethyl triazole moiety in compound 21 (Chek1 IC(50)=0.30nM) that was shown by X-ray crystallography to displace one of three highly conserved water molecules in the HI region of the ATP-binding cleft.	hydroxymethyl triazole	69-91	checkpoint kinase 1	Homo sapiens	23-28
16978863-3	2006	Enzyme potency against Chek1 was optimized by the incorporation of a hydroxymethyl triazole moiety in compound 21 (Chek1 IC(50)=0.30nM) that was shown by X-ray crystallography to displace one of three highly conserved water molecules in the HI region of the ATP-binding cleft.	hydroxymethyl triazole	69-91	checkpoint kinase 1	Homo sapiens	115-120
16978863-3	2006	Enzyme potency against Chek1 was optimized by the incorporation of a hydroxymethyl triazole moiety in compound 21 (Chek1 IC(50)=0.30nM) that was shown by X-ray crystallography to displace one of three highly conserved water molecules in the HI region of the ATP-binding cleft.	Water	218-223	checkpoint kinase 1	Homo sapiens	23-28
16978863-3	2006	Enzyme potency against Chek1 was optimized by the incorporation of a hydroxymethyl triazole moiety in compound 21 (Chek1 IC(50)=0.30nM) that was shown by X-ray crystallography to displace one of three highly conserved water molecules in the HI region of the ATP-binding cleft.	Water	218-223	checkpoint kinase 1	Homo sapiens	115-120
16978863-3	2006	Enzyme potency against Chek1 was optimized by the incorporation of a hydroxymethyl triazole moiety in compound 21 (Chek1 IC(50)=0.30nM) that was shown by X-ray crystallography to displace one of three highly conserved water molecules in the HI region of the ATP-binding cleft.	Adenosine Triphosphate	258-261	checkpoint kinase 1	Homo sapiens	23-28
16996169-0	2006	Synthesis, in vitro antiproliferative activities, and Chk1 inhibitory properties of indolylpyrazolones and indolylpyridazinedione.	indolylpyridazinedione	107-129	checkpoint kinase 1	Homo sapiens	54-58
17134696-6	2007	In particular, 1,3,4,6-tetrahydro-10-hydroxy-7H-dipyrrolo[3,4-a:3,4-c]carbazole-1,3,4,6-tetraone 11 exhibited an IC(50) value on purified full length Chk1 of 2 nM, which makes it a more potent Chk1 inhibitor than granulatimide and isogranulatimide.	1,3,4,6-tetrahydro-10-hydroxy-7h-dipyrrolo[3,4-a	15-63	checkpoint kinase 1	Homo sapiens	150-154
17134696-6	2007	In particular, 1,3,4,6-tetrahydro-10-hydroxy-7H-dipyrrolo[3,4-a:3,4-c]carbazole-1,3,4,6-tetraone 11 exhibited an IC(50) value on purified full length Chk1 of 2 nM, which makes it a more potent Chk1 inhibitor than granulatimide and isogranulatimide.	1,3,4,6-tetrahydro-10-hydroxy-7h-dipyrrolo[3,4-a	15-63	checkpoint kinase 1	Homo sapiens	193-197
16996169-4	2006	The IC(50) values toward Chk1 of the two indolylpyrazolones are identical and are in the micromolar range, but the cytotoxicities of 4-indolylpyrazol-3-one are significantly stronger than those of 5-indolylpyrazol-3-one.	indolylpyrazolones	41-59	checkpoint kinase 1	Homo sapiens	25-29
17134696-6	2007	In particular, 1,3,4,6-tetrahydro-10-hydroxy-7H-dipyrrolo[3,4-a:3,4-c]carbazole-1,3,4,6-tetraone 11 exhibited an IC(50) value on purified full length Chk1 of 2 nM, which makes it a more potent Chk1 inhibitor than granulatimide and isogranulatimide.	3,4-c]carbazole-1,3,4,6-tetraone	64-96	checkpoint kinase 1	Homo sapiens	150-154
17134696-6	2007	In particular, 1,3,4,6-tetrahydro-10-hydroxy-7H-dipyrrolo[3,4-a:3,4-c]carbazole-1,3,4,6-tetraone 11 exhibited an IC(50) value on purified full length Chk1 of 2 nM, which makes it a more potent Chk1 inhibitor than granulatimide and isogranulatimide.	3,4-c]carbazole-1,3,4,6-tetraone	64-96	checkpoint kinase 1	Homo sapiens	193-197
16996169-5	2006	Since 4-indolylpyrazol-3-one and 5-indolylpyrazol-3-one can present several conformers and tautomeric forms, molecular modelling in the ATP binding site of Chk1 has been carried out to investigate which form could induce the best stabilization in the active site of the enzyme.	4-indolylpyrazol-3-one	6-28	checkpoint kinase 1	Homo sapiens	156-160
17134696-6	2007	In particular, 1,3,4,6-tetrahydro-10-hydroxy-7H-dipyrrolo[3,4-a:3,4-c]carbazole-1,3,4,6-tetraone 11 exhibited an IC(50) value on purified full length Chk1 of 2 nM, which makes it a more potent Chk1 inhibitor than granulatimide and isogranulatimide.	granulatimide	213-226	checkpoint kinase 1	Homo sapiens	150-154
17134696-6	2007	In particular, 1,3,4,6-tetrahydro-10-hydroxy-7H-dipyrrolo[3,4-a:3,4-c]carbazole-1,3,4,6-tetraone 11 exhibited an IC(50) value on purified full length Chk1 of 2 nM, which makes it a more potent Chk1 inhibitor than granulatimide and isogranulatimide.	granulatimide	213-226	checkpoint kinase 1	Homo sapiens	193-197
16996169-5	2006	Since 4-indolylpyrazol-3-one and 5-indolylpyrazol-3-one can present several conformers and tautomeric forms, molecular modelling in the ATP binding site of Chk1 has been carried out to investigate which form could induce the best stabilization in the active site of the enzyme.	5-indolylpyrazol-3-one	33-55	checkpoint kinase 1	Homo sapiens	156-160
17134696-6	2007	In particular, 1,3,4,6-tetrahydro-10-hydroxy-7H-dipyrrolo[3,4-a:3,4-c]carbazole-1,3,4,6-tetraone 11 exhibited an IC(50) value on purified full length Chk1 of 2 nM, which makes it a more potent Chk1 inhibitor than granulatimide and isogranulatimide.	isogranulatimide	231-247	checkpoint kinase 1	Homo sapiens	150-154
16996169-5	2006	Since 4-indolylpyrazol-3-one and 5-indolylpyrazol-3-one can present several conformers and tautomeric forms, molecular modelling in the ATP binding site of Chk1 has been carried out to investigate which form could induce the best stabilization in the active site of the enzyme.	Adenosine Triphosphate	136-139	checkpoint kinase 1	Homo sapiens	156-160
17134696-6	2007	In particular, 1,3,4,6-tetrahydro-10-hydroxy-7H-dipyrrolo[3,4-a:3,4-c]carbazole-1,3,4,6-tetraone 11 exhibited an IC(50) value on purified full length Chk1 of 2 nM, which makes it a more potent Chk1 inhibitor than granulatimide and isogranulatimide.	isogranulatimide	231-247	checkpoint kinase 1	Homo sapiens	193-197
17204173-2	2006	After treatment with adrimycin for six hours, the cell cycle distribution was detected by flow cytometry; the Chk1mRNA expression was detected by RT-PCR and the Chk1 phosphorylation level was detected by Western blot.	adrimycin	21-30	checkpoint kinase 1	Homo sapiens	110-114
16996169-0	2006	Synthesis, in vitro antiproliferative activities, and Chk1 inhibitory properties of indolylpyrazolones and indolylpyridazinedione.	indolylpyrazolones	84-102	checkpoint kinase 1	Homo sapiens	54-58
17204173-7	2006	It is concluded that the increased chk1 activity that delay the progress of cell cycle are associated with cellular resistance to adrimycin in the K562/A02 cell line.	adrimycin	130-139	checkpoint kinase 1	Homo sapiens	35-39
17204173-3	2006	Under the condition of down-regulation of Chk1mRNA expression in cells transfected with Chk1 short hairpin RNA, the cell apoptosis rates were detected by flow-cytometry following adrimycin.	adrimycin	179-188	checkpoint kinase 1	Homo sapiens	42-46
17204173-3	2006	Under the condition of down-regulation of Chk1mRNA expression in cells transfected with Chk1 short hairpin RNA, the cell apoptosis rates were detected by flow-cytometry following adrimycin.	adrimycin	179-188	checkpoint kinase 1	Homo sapiens	88-92
17204173-5	2006	No evident difference of the Chk1mRNA expression was observed between K562 and K562/A02 cell lines, while elevated Chk1 phosphorylation following DNA damage induced by adriamycin was observed in the K562/A02 cell line (0.79 +/- 0.56), significantly higher than that in K562 cell line (0.27 +/- 1.47).	Doxorubicin	168-178	checkpoint kinase 1	Homo sapiens	115-119
17055492-0	2006	Anandamide inhibits Cdk2 and activates Chk1 leading to cell cycle arrest in human breast cancer cells.	anandamide	0-10	checkpoint kinase 1	Homo sapiens	39-43
16940414-0	2006	Dissecting the roles of checkpoint kinase 1/CDC2 and mitogen-activated protein kinase kinase 1/2/extracellular signal-regulated kinase 1/2 in relation to 7-hydroxystaurosporine-induced apoptosis in human multiple myeloma cells.	7-hydroxystaurosporine	154-176	checkpoint kinase 1	Homo sapiens	24-43
16940414-6	2006	It is interesting that Chk1 knockdown reduced basal ERK1/2 activation and antagonized the ability of UCN-01 to activate ERK1/2.	7-hydroxystaurosporine	101-107	checkpoint kinase 1	Homo sapiens	23-27
16940414-8	2006	Together, these findings indicate that although UCN-01-mediated Chk1 inhibition and Cdc2 activation are unlikely to be responsible for MEK1/2/ERK1/2 activation, both of these events contribute functionally to enhanced lethality in cells coexposed to MEK inhibitors.	7-hydroxystaurosporine	48-54	checkpoint kinase 1	Homo sapiens	64-68
16990002-0	2006	Development of 6-substituted indolylquinolinones as potent Chek1 kinase inhibitors.	6-substituted indolylquinolinones	15-48	checkpoint kinase 1	Homo sapiens	59-64
16990002-1	2006	Through a comparison of X-ray co-crystallographic data for 1 and 2 in the Chek1 active site, it was hypothesized that the affinity of the indolylquinolinone series (2) for Chek1 kinase would be improved via C6 substitution into the hydrophobic region I (HI) pocket.	indolylquinolinone	138-156	checkpoint kinase 1	Homo sapiens	74-79
16990002-1	2006	Through a comparison of X-ray co-crystallographic data for 1 and 2 in the Chek1 active site, it was hypothesized that the affinity of the indolylquinolinone series (2) for Chek1 kinase would be improved via C6 substitution into the hydrophobic region I (HI) pocket.	indolylquinolinone	138-156	checkpoint kinase 1	Homo sapiens	172-177
16990002-3	2006	A general trend was observed among these low nanomolar Chek1 inhibitors that compounds with multiple basic amines, or elevated polar surface area (PSA) exhibited poor cell potency.	Amines	107-113	checkpoint kinase 1	Homo sapiens	55-60
16990002-4	2006	Minimization of these parameters (basic amines, PSA) resulted in Chek1 inhibitors with improved cell potency, and preliminary pharmacokinetic data are presented for several of these compounds.	basic amines	34-46	checkpoint kinase 1	Homo sapiens	65-70
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	checkpoint kinase 1	Homo sapiens	120-124
17015476-3	2006	In response to genotoxic stress, Chk1 is phosphorylated on serines 317 (S317) and 345 (S345) by the ataxia-telangiectasia-related (ATR) protein kinase.	Serine	59-66	checkpoint kinase 1	Homo sapiens	33-37
16963448-6	2006	In addition, we found that Thr-916 on Claspin is phosphorylated by Chk1, suggesting that Chk1 regulates Claspin during checkpoint response.	Threonine	27-30	checkpoint kinase 1	Homo sapiens	67-71
16963448-6	2006	In addition, we found that Thr-916 on Claspin is phosphorylated by Chk1, suggesting that Chk1 regulates Claspin during checkpoint response.	Threonine	27-30	checkpoint kinase 1	Homo sapiens	89-93
17085670-11	2006	DMAG-mediated down-regulation of CHK1, a known HSP90 client, forced doxorubicin-treated cells into premature mitosis followed by apoptosis.	17-(dimethylaminoethylamino)-17-demethoxygeldanamycin	0-4	checkpoint kinase 1	Homo sapiens	33-37
17085670-11	2006	DMAG-mediated down-regulation of CHK1, a known HSP90 client, forced doxorubicin-treated cells into premature mitosis followed by apoptosis.	Doxorubicin	68-79	checkpoint kinase 1	Homo sapiens	33-37
17085670-12	2006	A CHK1 inhibitor, SB-218078, reproduced the effect of DMAG.	SB 218078	18-27	checkpoint kinase 1	Homo sapiens	2-6
17085670-12	2006	A CHK1 inhibitor, SB-218078, reproduced the effect of DMAG.	17-(dimethylaminoethylamino)-17-demethoxygeldanamycin	54-58	checkpoint kinase 1	Homo sapiens	2-6
16912045-1	2006	DNA damage induced by the carcinogen benzo[a]pyrene dihydrodiol epoxide (BPDE) induces a Chk1-dependent S-phase checkpoint.	benzo[a]pyrene dihydrodiol epoxide	37-71	checkpoint kinase 1	Homo sapiens	89-93
16912045-1	2006	DNA damage induced by the carcinogen benzo[a]pyrene dihydrodiol epoxide (BPDE) induces a Chk1-dependent S-phase checkpoint.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	73-77	checkpoint kinase 1	Homo sapiens	89-93
16912045-3	2006	Chk1-dependent inhibition of DNA synthesis in BPDE-treated cells occurred without detectable changes in Cdc25A levels, Cdk2 activity, or Cdc7/Dbf4 interaction.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	46-50	checkpoint kinase 1	Homo sapiens	0-4
16912045-6	2006	The levels of chromatin-associated Cdc45 (but not soluble Cdc45) were reduced concomitantly with BPDE-induced Chk1 activation and inhibition of DNA synthesis.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	97-101	checkpoint kinase 1	Homo sapiens	110-114
16912045-10	2006	The inhibitory effects of BPDE on DNA synthesis, Cdc45/Mcm7 associations, and interactions between Cdc45 and the beta-globin locus were abrogated by the Chk1 inhibitor UCN-01.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	26-30	checkpoint kinase 1	Homo sapiens	153-157
16652144-4	2006	Different from a classical senescent arrest in G(1), the ROS-induced arrest was predominantly in the G(2) phase of the cell cycle, and its establishment depended at least in part on an intact Chk1-dependent checkpoint.	Reactive Oxygen Species	57-60	checkpoint kinase 1	Homo sapiens	192-196
17015476-4	2006	Phosphorylation of Chk1 on these C-terminal serine residues is used as an indicator of Chk1 activation in vivo.	Serine	44-50	checkpoint kinase 1	Homo sapiens	19-23
17015476-4	2006	Phosphorylation of Chk1 on these C-terminal serine residues is used as an indicator of Chk1 activation in vivo.	Serine	44-50	checkpoint kinase 1	Homo sapiens	87-91
17036110-1	2006	From a structure-activity relationship perspective, the new indolocarbazoles 11 and 12 have been synthesized and evaluated biologically as novel Chk1 inhibitors.	indolocarbazoles	60-76	checkpoint kinase 1	Homo sapiens	145-149
16849332-6	2006	The results obtained from the Western blot experiment showed that NER defects resulted in enhanced CHK1 phosphorylation and p21 induction after cisplatin treatment.	Cisplatin	144-153	checkpoint kinase 1	Homo sapiens	99-103
16928871-0	2006	The Chk1/Cdc25A pathway as activators of the cell cycle in neuronal death induced by camptothecin.	Camptothecin	85-97	checkpoint kinase 1	Homo sapiens	4-8
16931916-3	2006	We designed a study to test whether the simultaneous depletion of Chk1 and Chk2 would sensitize cells to FdUrd- and gemcitabine-induced cytotoxicity to a greater extent than Chk1 depletion alone and to determine the contribution of premature mitosis to cytotoxicity.	gemcitabine	116-127	checkpoint kinase 1	Homo sapiens	66-70
16931916-4	2006	We found that RNAi-mediated Chk1 depletion enhanced FdUrd- and gemcitabine-mediated cytotoxicity (2- to 3-fold) in Panc-1 and SW620 cells.	gemcitabine	63-74	checkpoint kinase 1	Homo sapiens	28-32
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	checkpoint kinase 1	Homo sapiens	38-42
16931916-6	2006	The simultaneous depletion of Chk1 and Chk2 inhibited Cdc25A degradation, induced premature mitotic entry and enhanced cytotoxicity in response to FdUrd and gemcitabine to a similar extent as Chk1 depletion alone.	5-fluoro-2'-deoxyuridine	147-152	checkpoint kinase 1	Homo sapiens	30-34
16931916-6	2006	The simultaneous depletion of Chk1 and Chk2 inhibited Cdc25A degradation, induced premature mitotic entry and enhanced cytotoxicity in response to FdUrd and gemcitabine to a similar extent as Chk1 depletion alone.	gemcitabine	157-168	checkpoint kinase 1	Homo sapiens	30-34
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	checkpoint kinase 1	Homo sapiens	37-41
16884302-5	2006	While retention of the maleimide ring and pendant 4-phenyl group is necessary for potency, replacement of the carbazole nitrogen by oxygen is well tolerated and results in improved Wee1 selectivity against the related checkpoint kinase Chk1.	carbazole	110-119	checkpoint kinase 1	Homo sapiens	236-240
16914589-9	2006	Radiation-induced checkpoint kinase (Chk) 1 and Chk2 phosphorylation were inhibited by celecoxib and gefitinib treatment, respectively.	Celecoxib	87-96	checkpoint kinase 1	Homo sapiens	18-43
16914589-9	2006	Radiation-induced checkpoint kinase (Chk) 1 and Chk2 phosphorylation were inhibited by celecoxib and gefitinib treatment, respectively.	Gefitinib	101-110	checkpoint kinase 1	Homo sapiens	18-43
16884302-5	2006	While retention of the maleimide ring and pendant 4-phenyl group is necessary for potency, replacement of the carbazole nitrogen by oxygen is well tolerated and results in improved Wee1 selectivity against the related checkpoint kinase Chk1.	Nitrogen	120-128	checkpoint kinase 1	Homo sapiens	236-240
16884302-5	2006	While retention of the maleimide ring and pendant 4-phenyl group is necessary for potency, replacement of the carbazole nitrogen by oxygen is well tolerated and results in improved Wee1 selectivity against the related checkpoint kinase Chk1.	Oxygen	132-138	checkpoint kinase 1	Homo sapiens	236-240
16884302-6	2006	Wee1 potency and selectivity are also enhanced by the incorporation of lipophilic functionality at the 2"-position of the 4-phenyl ring, and Wee1 selectivity against Chk1 is favored by C3-C5 alkyl substitution of the carbazole nitrogen.	carbazole	217-226	checkpoint kinase 1	Homo sapiens	166-170
16884302-6	2006	Wee1 potency and selectivity are also enhanced by the incorporation of lipophilic functionality at the 2"-position of the 4-phenyl ring, and Wee1 selectivity against Chk1 is favored by C3-C5 alkyl substitution of the carbazole nitrogen.	Nitrogen	227-235	checkpoint kinase 1	Homo sapiens	166-170
16928813-7	2006	Our result showed that only the down-regulation of Chk1, but not of Chk2 or MK2, abrogated camptothecin- or 5-fluorouracil-induced S-phase arrest or doxorubicin-induced G(2)-phase arrest.	Camptothecin	91-103	checkpoint kinase 1	Homo sapiens	51-55
16928813-7	2006	Our result showed that only the down-regulation of Chk1, but not of Chk2 or MK2, abrogated camptothecin- or 5-fluorouracil-induced S-phase arrest or doxorubicin-induced G(2)-phase arrest.	Fluorouracil	108-122	checkpoint kinase 1	Homo sapiens	51-55
16928813-7	2006	Our result showed that only the down-regulation of Chk1, but not of Chk2 or MK2, abrogated camptothecin- or 5-fluorouracil-induced S-phase arrest or doxorubicin-induced G(2)-phase arrest.	Doxorubicin	149-160	checkpoint kinase 1	Homo sapiens	51-55
16828751-4	2006	In response to hydroxyurea, UV or aphidicolin, Claspin is phosphorylated in the Chk1-binding domain and its protein levels are increased in an ATR-dependent manner.	Aphidicolin	34-45	checkpoint kinase 1	Homo sapiens	80-84
16732333-5	2006	We demonstrate that both CHK1 and CHK2 are activated following treatment of cells with low doses of aphidicolin that induce fragile site breakage.	Aphidicolin	100-111	checkpoint kinase 1	Homo sapiens	25-29
16629900-8	2006	Treatment with Cdk inhibitor butyrolactone I induced the reduction of Chk1-S301 phosphorylation, although treatment with p38-specific inhibitor SB203580 or siRNA did not.	4-Butyrolactone	29-42	checkpoint kinase 1	Homo sapiens	70-74
16801388-3	2006	The expression of tCdc6 perturbs the loading of Mcm2 but not Orc2 onto chromatin and activates ataxia telangiectasia mutated (ATM) and ATM and Rad-3 related (ATR) kinase activities with kinetics similar to that of the phosphorylation of Chk1/2.	tcdc6	18-23	checkpoint kinase 1	Homo sapiens	237-243
16603354-0	2006	4-(Aminoalkylamino)-3-benzimidazole-quinolinones as potent CHK-1 inhibitors.	4-(aminoalkylamino)-3-benzimidazole-quinolinones	0-48	checkpoint kinase 1	Homo sapiens	59-64
16603354-2	2006	Novel 4-(amino-alkylamino)-3-benzimidazole-quinolinones were prepared and assayed for their ability to inhibit CHK-1.	4-(amino-alkylamino)-3-benzimidazole-quinolinones	6-55	checkpoint kinase 1	Homo sapiens	111-116
16603354-3	2006	These compounds are potent cell permeable CHK-1 inhibitors and showed synergistic effect with a DNA-damaging agent, camptothecin.	Camptothecin	116-128	checkpoint kinase 1	Homo sapiens	42-47
16713580-5	2006	Furthermore, ATR kinase is activated to phosphorylate Chk1 in the presence of O(6)-meG/T mispairs and MMR proteins.	o(6)	78-82	checkpoint kinase 1	Homo sapiens	54-58
16407843-6	2006	The cell cycle checkpoint abrogator and Chk1/Chk2 inhibitor 7-hydroxystaurosporine (UCN-01) also increases camptothecin-induced gammaH2AX formation and inhibits camptothecin-induced p21(CDKN1A) upregulation in HCT116 wt cells.	7-hydroxystaurosporine	60-82	checkpoint kinase 1	Homo sapiens	40-44
16407843-6	2006	The cell cycle checkpoint abrogator and Chk1/Chk2 inhibitor 7-hydroxystaurosporine (UCN-01) also increases camptothecin-induced gammaH2AX formation and inhibits camptothecin-induced p21(CDKN1A) upregulation in HCT116 wt cells.	7-hydroxystaurosporine	84-90	checkpoint kinase 1	Homo sapiens	40-44
16407843-6	2006	The cell cycle checkpoint abrogator and Chk1/Chk2 inhibitor 7-hydroxystaurosporine (UCN-01) also increases camptothecin-induced gammaH2AX formation and inhibits camptothecin-induced p21(CDKN1A) upregulation in HCT116 wt cells.	Camptothecin	107-119	checkpoint kinase 1	Homo sapiens	40-44
16407843-6	2006	The cell cycle checkpoint abrogator and Chk1/Chk2 inhibitor 7-hydroxystaurosporine (UCN-01) also increases camptothecin-induced gammaH2AX formation and inhibits camptothecin-induced p21(CDKN1A) upregulation in HCT116 wt cells.	Camptothecin	161-173	checkpoint kinase 1	Homo sapiens	40-44
16721053-2	2006	In the presence of genotoxic stress, the PI3 kinase-like kinase ATR rapidly phosphorylates Chk1 on conserved serine residues, thereby triggering kinase activation through the release of an auto-inhibitory region present at its C-terminus and by regulating interactions with other proteins.	Serine	109-115	checkpoint kinase 1	Homo sapiens	91-95
16414312-4	2006	Our results show that, following introduction of the oligonucleotide, the DNA-damage response pathway is activated, evidenced by the presence of phosphorylated p53, Chk1 and Chk2, respectively.	Oligonucleotides	53-68	checkpoint kinase 1	Homo sapiens	165-169
16618811-6	2006	These are further subclassified to proteins that connect DSBs with the rest of the nucleus (Chk1 and -2), that assemble at unprocessed DSBs (DNA-PK/Ku70), and that exist on chromatin as preassembled complexes but become locally modified after DNA damage (Smc1/Smc3).	dsbs	57-61	checkpoint kinase 1	Homo sapiens	92-103
16446090-0	2006	Synthesis and biological evaluation of 1-(2,4,5-trisubstituted phenyl)-3-(5-cyanopyrazin-2-yl)ureas as potent Chk1 kinase inhibitors.	1-(2,4,5-trisubstituted phenyl)-3-(5-cyanopyrazin-2-yl)ureas	39-99	checkpoint kinase 1	Homo sapiens	110-114
16446090-1	2006	Based on the X-ray crystallography of our lead compound 1-(5-chloro-2,4-dimethoxyphenyl)-3-(5-cyanopyrazin-2-yl)urea in the checkpoint kinase 1 (Chk1) enzyme, we modified R4, and to a lesser extent, R2, and R5 of the phenyl ring, and made a variety of N-aryl-N"-pyrazinylurea Chk1 inhibitors.	1-(5-Chloro-2,4-Dimethoxyphenyl)-3-(5-Cyanopyrazin-2-Yl)urea	56-116	checkpoint kinase 1	Homo sapiens	124-143
16446090-1	2006	Based on the X-ray crystallography of our lead compound 1-(5-chloro-2,4-dimethoxyphenyl)-3-(5-cyanopyrazin-2-yl)urea in the checkpoint kinase 1 (Chk1) enzyme, we modified R4, and to a lesser extent, R2, and R5 of the phenyl ring, and made a variety of N-aryl-N"-pyrazinylurea Chk1 inhibitors.	1-(5-Chloro-2,4-Dimethoxyphenyl)-3-(5-Cyanopyrazin-2-Yl)urea	56-116	checkpoint kinase 1	Homo sapiens	145-149
16446090-1	2006	Based on the X-ray crystallography of our lead compound 1-(5-chloro-2,4-dimethoxyphenyl)-3-(5-cyanopyrazin-2-yl)urea in the checkpoint kinase 1 (Chk1) enzyme, we modified R4, and to a lesser extent, R2, and R5 of the phenyl ring, and made a variety of N-aryl-N"-pyrazinylurea Chk1 inhibitors.	1-(5-Chloro-2,4-Dimethoxyphenyl)-3-(5-Cyanopyrazin-2-Yl)urea	56-116	checkpoint kinase 1	Homo sapiens	276-280
16446090-1	2006	Based on the X-ray crystallography of our lead compound 1-(5-chloro-2,4-dimethoxyphenyl)-3-(5-cyanopyrazin-2-yl)urea in the checkpoint kinase 1 (Chk1) enzyme, we modified R4, and to a lesser extent, R2, and R5 of the phenyl ring, and made a variety of N-aryl-N"-pyrazinylurea Chk1 inhibitors.	n-aryl-n"-pyrazinylurea	252-275	checkpoint kinase 1	Homo sapiens	124-143
16446090-1	2006	Based on the X-ray crystallography of our lead compound 1-(5-chloro-2,4-dimethoxyphenyl)-3-(5-cyanopyrazin-2-yl)urea in the checkpoint kinase 1 (Chk1) enzyme, we modified R4, and to a lesser extent, R2, and R5 of the phenyl ring, and made a variety of N-aryl-N"-pyrazinylurea Chk1 inhibitors.	n-aryl-n"-pyrazinylurea	252-275	checkpoint kinase 1	Homo sapiens	145-149
16574416-2	2006	We report how computational docking of a large electronic catalogue of compounds to an X-ray structure of the Chk1 ATP-binding site allowed prioritisation of a small subset of these compounds for assay.	Adenosine Triphosphate	115-118	checkpoint kinase 1	Homo sapiens	110-114
16574416-11	2006	The structural models for these ligands in the Chk1 ATP-binding site will facilitate further medicinal chemistry efforts targeting this kinase.	Adenosine Triphosphate	52-55	checkpoint kinase 1	Homo sapiens	47-51
16414312-7	2006	We suggest that gene repair directed by oligonucleotides activates a pathway that prevents corrected cells from proliferating in cell culture through the activation of Chk1 and Chk2.	Oligonucleotides	40-56	checkpoint kinase 1	Homo sapiens	168-172
16431910-2	2006	Here we show that Chk1 phosphorylation in response to hydroxyurea and ultraviolet radiation is ATR-dependent and ATM- and Mre11-independent.	Hydroxyurea	54-65	checkpoint kinase 1	Homo sapiens	18-22
16511572-5	2006	Interestingly, in response to UV irradiation, the wild-type, but not the kinase-dead mutant, Chk1 phosphorylated MDMX at serine 367, enhanced the 14-3-3gamma-MDMX binding and the cytoplasmic retaining of MDMX.	Serine	121-127	checkpoint kinase 1	Homo sapiens	93-97
16511572-6	2006	The Chk1 specific inhibitor UCN-01 repressed all of these effects.	7-hydroxystaurosporine	28-34	checkpoint kinase 1	Homo sapiens	4-8
16289938-2	2006	We report how computational modelling predicted the binding mode of ligands of special interest to the Chk1 ATP site, for representatives of an indazole series and debromohymenialdisine.	Adenosine Triphosphate	108-111	checkpoint kinase 1	Homo sapiens	103-107
16533058-4	2006	Like ionizing radiation (IR) and other radiomimetics, breaks induced by C-1027 efficiently activate ATM by phosphorylation at Ser1981, yet unlike other radiomimetics and IR, DNA breaks induced by C-1027 result in normal phosphorylation of p53 and the cell cycle checkpoint kinases (Chk1 and Chk2) in the absence of ATM.	Carbon	72-73	checkpoint kinase 1	Homo sapiens	282-286
16533058-5	2006	In the presence of ATM, but under ATM and Rad3-related kinase (ATR) deficient conditions, C-1027 treatment resulted in a decrease in the level of Chk1 phosphorylation but not in the level of p53 and Chk2 phosphorylation.	C 1027	90-96	checkpoint kinase 1	Homo sapiens	146-150
16293603-1	2006	Chk1 and Akt signaling facilitate survival of cells treated with nucleoside analogues.	Nucleosides	65-75	checkpoint kinase 1	Homo sapiens	0-4
16289938-2	2006	We report how computational modelling predicted the binding mode of ligands of special interest to the Chk1 ATP site, for representatives of an indazole series and debromohymenialdisine.	Indazoles	144-152	checkpoint kinase 1	Homo sapiens	103-107
16293603-2	2006	Activation of Chk1 in response to cytarabine (ara-C) induced an S-phase checkpoint characterized by the inhibition of Cdk2, cell cycle arrest, no change in constitutively active Akt, or low-stress kinase signaling in ML-1 cells.	Cytarabine	34-44	checkpoint kinase 1	Homo sapiens	14-18
16293603-2	2006	Activation of Chk1 in response to cytarabine (ara-C) induced an S-phase checkpoint characterized by the inhibition of Cdk2, cell cycle arrest, no change in constitutively active Akt, or low-stress kinase signaling in ML-1 cells.	Cytarabine	46-51	checkpoint kinase 1	Homo sapiens	14-18
16289938-2	2006	We report how computational modelling predicted the binding mode of ligands of special interest to the Chk1 ATP site, for representatives of an indazole series and debromohymenialdisine.	debromohymenialdisine	164-185	checkpoint kinase 1	Homo sapiens	103-107
16293603-8	2006	Thus, use of UCN-01 in combination with ara-C decreases Chk1 phosphorylation, inhibits the Akt survival pathway, and activates JNK during the course of therapy, offering a rationale for the cytotoxic action of this combination during AML treatment.	Cytarabine	40-45	checkpoint kinase 1	Homo sapiens	56-60
16289938-5	2006	These interactions are formed in a buried pocket at the periphery of the ATP-binding site, the importance of which has previously been overlooked for ligand design against Chk1.	Adenosine Triphosphate	73-76	checkpoint kinase 1	Homo sapiens	172-176
16289938-8	2006	Structural overlays of known inhibitors complexed with Chk1 show that only the indazole series utilizes the pocket of interest.	Indazoles	79-87	checkpoint kinase 1	Homo sapiens	55-59
16452227-0	2006	The dispersal of replication proteins after Etoposide treatment requires the cooperation of Nbs1 with the ataxia telangiectasia Rad3-related/Chk1 pathway.	Etoposide	44-53	checkpoint kinase 1	Homo sapiens	141-145
16461339-5	2006	Whereas ATM signals DSBs arising from ionizing radiation (IR) through a Chk2-dependent pathway, ATR is activated in a variety of replication-linked DSBs and leads to activation of the checkpoints in a Chk1 kinase-dependent manner.	dsbs	148-152	checkpoint kinase 1	Homo sapiens	201-205
16284058-1	2006	BACKGROUND: 7-Hydroxystaurosporine (UCN-01) inhibits serine-threonine kinases including the Ca2+ and phospholipid-dependent protein kinase C (PKC), CDKs 2, 4, 6, Chk-1 and PDK1.	7-hydroxystaurosporine	12-34	checkpoint kinase 1	Homo sapiens	162-167
16414131-8	2006	NH2Cl also inhibited the phosphorylation of Chk1 (Ser345).	chloramine	0-5	checkpoint kinase 1	Homo sapiens	44-48
16075279-9	2006	Western blotting showed that PXL exposure followed by 5-FU up-regulated Chk1 and Wee1 protein expressions until PXL removal and 5-FU exposure, when these expressions gradually decreased to their basal levels.	Fluorouracil	54-58	checkpoint kinase 1	Homo sapiens	72-76
16467108-10	2006	Lovastatin affected various IR-induced stress responses in HUVEC: It attenuated the increase in p53/p21 protein level and impaired the activation of nuclear factor-kappaB, Chk-1, and Akt kinase but did not inhibit extracellular signal-regulated kinase activation.	Lovastatin	0-10	checkpoint kinase 1	Homo sapiens	172-177
16293623-5	2006	The UV light- and hydroxyurea-induced phosphorylation of CREB was delayed in comparison to the canonical ATR substrate CHK1, suggesting potentially different mechanisms of phosphorylation.	Hydroxyurea	18-29	checkpoint kinase 1	Homo sapiens	119-123
16242328-2	2006	Analogs of the Chk1 inhibitor, 3-ethylidene-1,3-dihydro-indol-2-one, were synthesized and tested in vitro for their inhibitory activities.	3-ethylidene-1H-indol-2-one	31-67	checkpoint kinase 1	Homo sapiens	15-19
16424027-5	2006	The mechanism through which cisplatin achieves these effects is different to daunorubicin and UV light but shows great similarity to the RelA regulatory pathway induced by the ARF tumor suppressor: cisplatin regulation of RelA requires ATR/Chk1 activity, represses Bcl-x(L) but not XIAP expression, and results in phosphorylation of RelA at Thr(505).	Cisplatin	28-37	checkpoint kinase 1	Homo sapiens	240-244
16263812-9	2006	CEP-751 induced a loss in the induction of the DNA repair program marked by phospho-H2AX and the checkpoint pathway marked by the activated Chk1 pathway.	CEP 751	0-7	checkpoint kinase 1	Homo sapiens	140-144
16126823-6	2005	Cells lacking Rad9, Chk1, or ATR were more sensitive to gemcitabine and cytarabine, consistent with the fact that these agents stall replication forks, and this sensitization was independent of p53 status.	gemcitabine	56-67	checkpoint kinase 1	Homo sapiens	20-24
16126823-6	2005	Cells lacking Rad9, Chk1, or ATR were more sensitive to gemcitabine and cytarabine, consistent with the fact that these agents stall replication forks, and this sensitization was independent of p53 status.	Cytarabine	72-82	checkpoint kinase 1	Homo sapiens	20-24
16424027-5	2006	The mechanism through which cisplatin achieves these effects is different to daunorubicin and UV light but shows great similarity to the RelA regulatory pathway induced by the ARF tumor suppressor: cisplatin regulation of RelA requires ATR/Chk1 activity, represses Bcl-x(L) but not XIAP expression, and results in phosphorylation of RelA at Thr(505).	Cisplatin	198-207	checkpoint kinase 1	Homo sapiens	240-244
15975956-5	2005	The involvement of these molecules in resveratrol-induced S phase was also supported by the studies showing that addition of ATM/ATR inhibitor caffeine reverses resveratrol-caused activation of ATM/ATR-Chk1/2 as well as phosphorylation of Cdc25C, Cdc2 and H2A.X, and S phase arrest.	Caffeine	143-151	checkpoint kinase 1	Homo sapiens	202-208
15975956-5	2005	The involvement of these molecules in resveratrol-induced S phase was also supported by the studies showing that addition of ATM/ATR inhibitor caffeine reverses resveratrol-caused activation of ATM/ATR-Chk1/2 as well as phosphorylation of Cdc25C, Cdc2 and H2A.X, and S phase arrest.	Resveratrol	161-172	checkpoint kinase 1	Homo sapiens	202-208
15975956-0	2005	Resveratrol causes Cdc2-tyr15 phosphorylation via ATM/ATR-Chk1/2-Cdc25C pathway as a central mechanism for S phase arrest in human ovarian carcinoma Ovcar-3 cells.	Resveratrol	0-11	checkpoint kinase 1	Homo sapiens	58-62
15975956-7	2005	These findings for the first time identify that resveratrol causes Cdc2-tyr15 phosphorylation via ATM/ATR-Chk1/2-Cdc25C pathway as a central mechanism for DNA damage and S phase arrest selectively in ovarian cancer cells, and provide a rationale for the potential efficacy of ATM/ATR agonists in the prevention and intervention of cancer.	Resveratrol	48-59	checkpoint kinase 1	Homo sapiens	106-110
15975956-5	2005	The involvement of these molecules in resveratrol-induced S phase was also supported by the studies showing that addition of ATM/ATR inhibitor caffeine reverses resveratrol-caused activation of ATM/ATR-Chk1/2 as well as phosphorylation of Cdc25C, Cdc2 and H2A.X, and S phase arrest.	Resveratrol	38-49	checkpoint kinase 1	Homo sapiens	202-208
16123041-4	2005	In cells, induction of DNA damage by etoposide at first produced rapid phosphorylation of Chk1 at a site targeted by ATR.	Etoposide	37-46	checkpoint kinase 1	Homo sapiens	90-94
16099423-0	2005	Geldanamycin-induced degradation of Chk1 is mediated by proteasome.	geldanamycin	0-12	checkpoint kinase 1	Homo sapiens	36-40
15994368-4	2005	We document that this arrest is sensitive to the pharmacological agents caffeine and 7-hydroxystaurosporine (UCN-01) that inhibit the checkpoint kinases ATM/ATM and Rad-3-related (ATR) and Chk1/Chk2, respectively.	Caffeine	72-80	checkpoint kinase 1	Homo sapiens	189-193
15994368-4	2005	We document that this arrest is sensitive to the pharmacological agents caffeine and 7-hydroxystaurosporine (UCN-01) that inhibit the checkpoint kinases ATM/ATM and Rad-3-related (ATR) and Chk1/Chk2, respectively.	7-hydroxystaurosporine	85-107	checkpoint kinase 1	Homo sapiens	189-193
16099423-3	2005	In this report, we analyzed the mechanisms of Chk1 regulation in U87MG glioblastoma cells using Geldanamycin (GA), which interferes with the function of Hsp90.	geldanamycin	96-108	checkpoint kinase 1	Homo sapiens	46-50
16099423-3	2005	In this report, we analyzed the mechanisms of Chk1 regulation in U87MG glioblastoma cells using Geldanamycin (GA), which interferes with the function of Hsp90.	geldanamycin	110-112	checkpoint kinase 1	Homo sapiens	46-50
16099423-5	2005	Co-treatment with GA and cycloheximide (CHX), a protein synthesis inhibitor, induced a decrease of half-life of the Chk1 protein to 3h and resulted in Chk1 down-regulation.	geldanamycin	18-20	checkpoint kinase 1	Homo sapiens	116-120
16099423-5	2005	Co-treatment with GA and cycloheximide (CHX), a protein synthesis inhibitor, induced a decrease of half-life of the Chk1 protein to 3h and resulted in Chk1 down-regulation.	geldanamycin	18-20	checkpoint kinase 1	Homo sapiens	151-155
16099423-5	2005	Co-treatment with GA and cycloheximide (CHX), a protein synthesis inhibitor, induced a decrease of half-life of the Chk1 protein to 3h and resulted in Chk1 down-regulation.	Cycloheximide	25-38	checkpoint kinase 1	Homo sapiens	116-120
16099423-5	2005	Co-treatment with GA and cycloheximide (CHX), a protein synthesis inhibitor, induced a decrease of half-life of the Chk1 protein to 3h and resulted in Chk1 down-regulation.	Cycloheximide	25-38	checkpoint kinase 1	Homo sapiens	151-155
16099423-5	2005	Co-treatment with GA and cycloheximide (CHX), a protein synthesis inhibitor, induced a decrease of half-life of the Chk1 protein to 3h and resulted in Chk1 down-regulation.	Cycloheximide	40-43	checkpoint kinase 1	Homo sapiens	116-120
16099423-5	2005	Co-treatment with GA and cycloheximide (CHX), a protein synthesis inhibitor, induced a decrease of half-life of the Chk1 protein to 3h and resulted in Chk1 down-regulation.	Cycloheximide	40-43	checkpoint kinase 1	Homo sapiens	151-155
16099423-8	2005	In addition, GA-induced down-regulation of Chk1 was reversed by MG132, a specific proteasome inhibitor.	geldanamycin	13-15	checkpoint kinase 1	Homo sapiens	43-47
16099423-8	2005	In addition, GA-induced down-regulation of Chk1 was reversed by MG132, a specific proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	64-69	checkpoint kinase 1	Homo sapiens	43-47
16099423-10	2005	These results have indicated that degradation of Chk1 by GA was mediated by the ubiquitin-proteasome pathway in U87MG glioblastoma cells.	geldanamycin	57-59	checkpoint kinase 1	Homo sapiens	49-53
16082213-8	2005	Finally, we show that bypass of the G2/M checkpoint by the CHK1 kinase inhibitor UCN-01 results in the activation of Aurora-A and phosphorylation of CDC25B on S353.	7-hydroxystaurosporine	81-87	checkpoint kinase 1	Homo sapiens	59-63
16137618-3	2005	This response is triggered by phosphorylation of Chk1 at Ser-345, a known target site for the upstream activating kinase ATR.	Serine	57-60	checkpoint kinase 1	Homo sapiens	49-53
16137618-5	2005	Treatment of cells with the anticancer agent camptothecin (CPT) triggers Chk1 destruction, which blocks recovery from drug-induced S phase arrest and leads to cell death.	Camptothecin	45-57	checkpoint kinase 1	Homo sapiens	73-77
16137618-5	2005	Treatment of cells with the anticancer agent camptothecin (CPT) triggers Chk1 destruction, which blocks recovery from drug-induced S phase arrest and leads to cell death.	Camptothecin	59-62	checkpoint kinase 1	Homo sapiens	73-77
16137618-7	2005	Proteolysis of activated Chk1 may promote checkpoint termination under normal conditions, and may play an important role in the cytotoxic effects of CPT and related anticancer drugs.	Camptothecin	149-152	checkpoint kinase 1	Homo sapiens	25-29
15961392-0	2005	Checkpoint kinase 1 regulates diallyl trisulfide-induced mitotic arrest in human prostate cancer cells.	diallyl trisulfide	30-48	checkpoint kinase 1	Homo sapiens	0-19
16123041-5	2005	Subsequently, etoposide caused activation of caspase-7, cleavage of Claspin, and dephosphorylation of Chk1.	Etoposide	14-23	checkpoint kinase 1	Homo sapiens	102-106
15961392-3	2005	The DATS treatment caused activation of checkpoint kinase 1 and checkpoint kinase 2, which are intermediaries of DNA damage checkpoints and implicated in Ser(216) phosphorylation of Cdc25C.	Serine	154-157	checkpoint kinase 1	Homo sapiens	40-59
16061666-0	2005	Role of checkpoint kinase 1 in preventing premature mitosis in response to gemcitabine.	gemcitabine	75-86	checkpoint kinase 1	Homo sapiens	8-27
15784732-1	2005	Previous studies demonstrated that ataxia telangiectasia mutated- and Rad3-related (ATR) kinase and its downstream target checkpoint kinase 1 (Chk1) facilitate survival of cells treated with nucleoside analogs and other replication inhibitors.	Nucleosides	191-201	checkpoint kinase 1	Homo sapiens	122-141
15961392-7	2005	In conclusion, the results of the present study suggest existence of a checkpoint kinase 1-dependent mechanism for diallyl trisulfide-induced mitotic arrest in human prostate cancer cells.	diallyl trisulfide	115-133	checkpoint kinase 1	Homo sapiens	71-90
15870702-2	2005	LD doxorubicin-induced SLP was preceded by multinucleation and downregulation of multiple proteins with mitotic checkpoint function, including CENP-A, Mad2, BubR1, and Chk1.	Doxorubicin	3-14	checkpoint kinase 1	Homo sapiens	168-172
16061666-4	2005	We hypothesized that gemcitabine might induce Chk1 or Chk2 signal transduction pathways that mediate S-phase arrest.	gemcitabine	21-32	checkpoint kinase 1	Homo sapiens	46-50
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	checkpoint kinase 1	Homo sapiens	100-104
15784732-1	2005	Previous studies demonstrated that ataxia telangiectasia mutated- and Rad3-related (ATR) kinase and its downstream target checkpoint kinase 1 (Chk1) facilitate survival of cells treated with nucleoside analogs and other replication inhibitors.	Nucleosides	191-201	checkpoint kinase 1	Homo sapiens	143-147
16061666-6	2005	Depletion of Chk1 from Panc-1 cells prevented the down-regulation of Cdc25A in response to gemcitabine.	gemcitabine	91-102	checkpoint kinase 1	Homo sapiens	13-17
16061666-7	2005	Furthermore, Chk1 depletion permitted Panc-1 and SW620 cells treated with gemcitabine to enter mitosis despite incomplete DNA synthesis.	gemcitabine	74-85	checkpoint kinase 1	Homo sapiens	13-17
15784732-2	2005	Recent results also demonstrated that Chk1 is depleted when cells are treated with heat shock protein 90 (Hsp90) inhibitor 17-allylamino-17-demethoxygeldanamycin (17-AAG).	tanespimycin	123-161	checkpoint kinase 1	Homo sapiens	38-42
16061666-9	2005	These results provide evidence that Chk1 negatively regulates entry into mitosis in response to gemcitabine.	gemcitabine	96-107	checkpoint kinase 1	Homo sapiens	36-40
16061666-10	2005	Furthermore, these data imply that Chk1 acts to coordinate the cell cycle with DNA synthesis, thus preventing premature mitotic entry in gemcitabine-treated cells.	gemcitabine	137-148	checkpoint kinase 1	Homo sapiens	35-39
16061671-8	2005	Inhibition of Chk1 kinase with 7-hydroxystaurosporine (UCN-01) abrogated the checkpoint pathway as indicated by dephosphorylation of checkpoint proteins and progression of cells through mitosis and into G1.	7-hydroxystaurosporine	31-53	checkpoint kinase 1	Homo sapiens	14-18
16061671-8	2005	Inhibition of Chk1 kinase with 7-hydroxystaurosporine (UCN-01) abrogated the checkpoint pathway as indicated by dephosphorylation of checkpoint proteins and progression of cells through mitosis and into G1.	7-hydroxystaurosporine	55-61	checkpoint kinase 1	Homo sapiens	14-18
15707391-4	2005	In this system, double-stranded DNA oligonucleotides induce the phosphorylation of Chk1 at activating sites targeted by ATR [ATM (ataxia telangiectasia mutated)- and Rad3-related] and ATM kinases.	double-stranded dna oligonucleotides	16-52	checkpoint kinase 1	Homo sapiens	83-87
15688426-7	2005	Here we show that downregulation of Chk1 sensitizes tumor cells to the toxicity of paclitaxel in cell proliferation assay.	Paclitaxel	83-93	checkpoint kinase 1	Homo sapiens	36-40
15688426-8	2005	Fluorescence microscopy showed that Chk1 knockdown augments mitotic catastrophe and apoptosis in paclitaxel-treated cancer cells.	Paclitaxel	97-107	checkpoint kinase 1	Homo sapiens	36-40
15688426-10	2005	Chk1 inhibition facilitates paclitaxel-induced M-phase entry by activation of Cdc2 kinase and accumulation of cyclin B1, the required cofactor for Cdc2 kinase activity.	Paclitaxel	28-38	checkpoint kinase 1	Homo sapiens	0-4
15688426-13	2005	We show that Chk1 elimination attenuates the paclitaxel-induced activation of the anti-apoptotic p42/p44 (ERK1/2) MAP kinase pathway, additionally contributing to the sensitization.	Paclitaxel	45-55	checkpoint kinase 1	Homo sapiens	13-17
15974586-0	2005	Structure-based design of novel Chk1 inhibitors: insights into hydrogen bonding and protein-ligand affinity.	Hydrogen	63-71	checkpoint kinase 1	Homo sapiens	32-36
15974586-1	2005	We report the discovery, synthesis, and crystallographic binding mode of novel furanopyrimidine and pyrrolopyrimidine inhibitors of the Chk1 kinase, an oncology target.	furanopyrimidine	79-95	checkpoint kinase 1	Homo sapiens	136-140
15974586-1	2005	We report the discovery, synthesis, and crystallographic binding mode of novel furanopyrimidine and pyrrolopyrimidine inhibitors of the Chk1 kinase, an oncology target.	pyrrolopyrimidine	100-117	checkpoint kinase 1	Homo sapiens	136-140
15974586-2	2005	These inhibitors are synthetically tractable and inhibit Chk1 by competing for its ATP site.	Adenosine Triphosphate	83-86	checkpoint kinase 1	Homo sapiens	57-61
15970704-6	2005	ARF-induced Chk1 phosphorylates RelA on threonine 505, a residue in its transactivation domain, thus inhibiting NF-kappaB"s ability to stimulate anti-apoptotic gene expression.	Threonine	40-49	checkpoint kinase 1	Homo sapiens	12-16
15930307-4	2005	Temozolomide-treated control cells activated the DNA damage signal transducers Chk1, Chk2, and p38, leading to Cdc25C and Cdc2 inactivation, prolonged G2 arrest, and loss of clonagenicity by a combination of senescence and mitotic catastrophe.	Temozolomide	0-12	checkpoint kinase 1	Homo sapiens	79-83
15805289-7	2005	Combining ATM knockdown with the Chk1 inhibitor UCN-01 further increased doxorubicin sensitivity in these cells.	Doxorubicin	73-84	checkpoint kinase 1	Homo sapiens	33-37
15782134-2	2005	The Chk1 inhibitor, 7-hydroxystaurosporine (UCN-01), overcomes both S and G(2) arrest preferentially in cells mutated for p53, driving cells through a lethal mitosis and thereby enhancing cytotoxicity.	7-hydroxystaurosporine	20-42	checkpoint kinase 1	Homo sapiens	4-8
15870257-3	2005	PPM1D binds Chk1 and dephosphorylates the ATR-targeted phospho-Ser 345, leading to decreased Chk1 kinase activity.	Serine	63-66	checkpoint kinase 1	Homo sapiens	93-97
15857116-0	2005	1-(5-Chloro-2-alkoxyphenyl)-3-(5-cyanopyrazin-2-yl)ureas [correction of cyanopyrazi] as potent and selective inhibitors of Chk1 kinase: synthesis, preliminary SAR, and biological activities.	1-(5-chloro-2-alkoxyphenyl)-3-(5-cyanopyrazin-2-yl)ureas	0-56	checkpoint kinase 1	Homo sapiens	123-127
15857116-0	2005	1-(5-Chloro-2-alkoxyphenyl)-3-(5-cyanopyrazin-2-yl)ureas [correction of cyanopyrazi] as potent and selective inhibitors of Chk1 kinase: synthesis, preliminary SAR, and biological activities.	cyanopyrazi	33-44	checkpoint kinase 1	Homo sapiens	123-127
15857116-1	2005	The discovery of 1-(5-chloro-2-alkoxyphenyl)-3-(5-cyanopyrazin-2-yl)ureas as a new class of potent (IC(50) values of 3-10 nM) and selective inhibitors of Chk1 kinase was described.	1-(5-chloro-2-alkoxyphenyl)-3-(5-cyanopyrazin-2-yl)ureas	17-73	checkpoint kinase 1	Homo sapiens	154-158
15699047-5	2005	Colony forming assays demonstrated that down-regulation of ATR or Chk1 sensitized cells to SN-38 and camptothecin.	Irinotecan	91-96	checkpoint kinase 1	Homo sapiens	66-70
15699047-5	2005	Colony forming assays demonstrated that down-regulation of ATR or Chk1 sensitized cells to SN-38 and camptothecin.	Camptothecin	101-113	checkpoint kinase 1	Homo sapiens	66-70
15699047-7	2005	Additional experiments demonstrated that the Hsp90 inhibitor 17-allylamino-17-demethoxygeldanamycin, which down-regulates Chk1, also sensitized a variety of human carcinoma cell lines to SN-38.	tanespimycin	61-99	checkpoint kinase 1	Homo sapiens	122-126
15805289-10	2005	In addition, knockdown of the G(2) checkpoint regulators ATR and Chk1 also sensitized PC3 cells to doxorubicin and increased the expression of the E2F target gene PCNA.	Doxorubicin	99-110	checkpoint kinase 1	Homo sapiens	65-69
15389625-4	2005	By using a pair of transformed rat fibroblast cell lines, we show that compared with their counterpart B4 cells, A1-5 cells with higher CHK1 expression are more resistant to taxotere, a microtubule stabilizer, but are more sensitive to nocodazole, a microtubule destabilizer.	Docetaxel	174-182	checkpoint kinase 1	Homo sapiens	136-140
15784732-3	2005	The present study examined the effects of 17-AAG and its major metabolite, 17-aminogeldanamycin (17-AG), on Chk1 levels and cellular responses to cytarabine in human acute myelogenous leukemia (AML) cell lines and clinical isolates.	17-aminogeldanamycin	75-95	checkpoint kinase 1	Homo sapiens	108-112
15784732-3	2005	The present study examined the effects of 17-AAG and its major metabolite, 17-aminogeldanamycin (17-AG), on Chk1 levels and cellular responses to cytarabine in human acute myelogenous leukemia (AML) cell lines and clinical isolates.	17-aminogeldanamycin	97-102	checkpoint kinase 1	Homo sapiens	108-112
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	checkpoint kinase 1	Homo sapiens	84-88
15784732-6	2005	Additional studies demonstrated that small inhibitory RNA (siRNA) depletion of Chk1 also sensitized cells to cytarabine, whereas disruption of the phosphatidylinositol 3-kinase (PI3k) signaling pathway, which is also blocked by Hsp90 inhibition, did not.	Cytarabine	109-119	checkpoint kinase 1	Homo sapiens	79-83
15389625-7	2005	Taken together, these results indicate that CHK1 is one of the factors affecting cell resistance to taxotere and sensitiveness to nocodazole, suggesting that CHK1 is involved in affecting microtubule dynamics and could be inhibited for taxotere sensitization in CHK1 highly expressed tumor cells.	Docetaxel	100-108	checkpoint kinase 1	Homo sapiens	44-48
15389625-7	2005	Taken together, these results indicate that CHK1 is one of the factors affecting cell resistance to taxotere and sensitiveness to nocodazole, suggesting that CHK1 is involved in affecting microtubule dynamics and could be inhibited for taxotere sensitization in CHK1 highly expressed tumor cells.	Docetaxel	100-108	checkpoint kinase 1	Homo sapiens	158-162
15389625-7	2005	Taken together, these results indicate that CHK1 is one of the factors affecting cell resistance to taxotere and sensitiveness to nocodazole, suggesting that CHK1 is involved in affecting microtubule dynamics and could be inhibited for taxotere sensitization in CHK1 highly expressed tumor cells.	Docetaxel	100-108	checkpoint kinase 1	Homo sapiens	158-162
15389625-7	2005	Taken together, these results indicate that CHK1 is one of the factors affecting cell resistance to taxotere and sensitiveness to nocodazole, suggesting that CHK1 is involved in affecting microtubule dynamics and could be inhibited for taxotere sensitization in CHK1 highly expressed tumor cells.	Nocodazole	130-140	checkpoint kinase 1	Homo sapiens	44-48
15389625-7	2005	Taken together, these results indicate that CHK1 is one of the factors affecting cell resistance to taxotere and sensitiveness to nocodazole, suggesting that CHK1 is involved in affecting microtubule dynamics and could be inhibited for taxotere sensitization in CHK1 highly expressed tumor cells.	Nocodazole	130-140	checkpoint kinase 1	Homo sapiens	158-162
15389625-7	2005	Taken together, these results indicate that CHK1 is one of the factors affecting cell resistance to taxotere and sensitiveness to nocodazole, suggesting that CHK1 is involved in affecting microtubule dynamics and could be inhibited for taxotere sensitization in CHK1 highly expressed tumor cells.	Nocodazole	130-140	checkpoint kinase 1	Homo sapiens	158-162
15389625-7	2005	Taken together, these results indicate that CHK1 is one of the factors affecting cell resistance to taxotere and sensitiveness to nocodazole, suggesting that CHK1 is involved in affecting microtubule dynamics and could be inhibited for taxotere sensitization in CHK1 highly expressed tumor cells.	Docetaxel	236-244	checkpoint kinase 1	Homo sapiens	44-48
15389625-7	2005	Taken together, these results indicate that CHK1 is one of the factors affecting cell resistance to taxotere and sensitiveness to nocodazole, suggesting that CHK1 is involved in affecting microtubule dynamics and could be inhibited for taxotere sensitization in CHK1 highly expressed tumor cells.	Docetaxel	236-244	checkpoint kinase 1	Homo sapiens	158-162
15389625-7	2005	Taken together, these results indicate that CHK1 is one of the factors affecting cell resistance to taxotere and sensitiveness to nocodazole, suggesting that CHK1 is involved in affecting microtubule dynamics and could be inhibited for taxotere sensitization in CHK1 highly expressed tumor cells.	Docetaxel	236-244	checkpoint kinase 1	Homo sapiens	158-162
15775976-3	2005	Here we demonstrate that ARF induces the ATR- and Chk1-dependent phosphorylation of the RelA transactivation domain at threonine 505, a site required for ARF-dependent repression of RelA transcriptional activity.	Threonine	119-128	checkpoint kinase 1	Homo sapiens	50-54
15494423-0	2005	Farnesyltransferase inhibitors interact synergistically with the Chk1 inhibitor UCN-01 to induce apoptosis in human leukemia cells through interruption of both Akt and MEK/ERK pathways and activation of SEK1/JNK.	7-hydroxystaurosporine	80-86	checkpoint kinase 1	Homo sapiens	65-69
15674326-0	2005	Hematopoietic cytokines enhance Chk1-dependent G2/M checkpoint activation by etoposide through the Akt/GSK3 pathway to inhibit apoptosis.	Etoposide	77-86	checkpoint kinase 1	Homo sapiens	32-36
15674326-4	2005	Erythropoietin or IL-3 significantly enhanced etoposide-induced activation-specific phosphorylation of Chk1, a checkpoint kinase that inhibits Cdc2 activation by Cdc25 phosphatases, and led to the inhibition of Cdc2 kinase activity with the persistent inhibitory phosphorylation on Tyr15.	Etoposide	46-55	checkpoint kinase 1	Homo sapiens	103-107
15674326-5	2005	The inhibitory Cdc2 phosphorylation and G2/M block by etoposide were enhanced or inhibited by overexpression of Chk1 or by the specific Chk1 inhibitor SB218078, respectively.	Etoposide	54-63	checkpoint kinase 1	Homo sapiens	112-116
15674326-5	2005	The inhibitory Cdc2 phosphorylation and G2/M block by etoposide were enhanced or inhibited by overexpression of Chk1 or by the specific Chk1 inhibitor SB218078, respectively.	Etoposide	54-63	checkpoint kinase 1	Homo sapiens	136-140
15674326-5	2005	The inhibitory Cdc2 phosphorylation and G2/M block by etoposide were enhanced or inhibited by overexpression of Chk1 or by the specific Chk1 inhibitor SB218078, respectively.	SB 218078	151-159	checkpoint kinase 1	Homo sapiens	136-140
15674326-7	2005	Furthermore, SB216763 or LiCl, a specific inhibitor for the GSK3 kinase inhibited by Akt, enhanced the Chk1 phosphorylation and G2/M arrest by etoposide.	SB 216763	13-21	checkpoint kinase 1	Homo sapiens	103-107
15674326-7	2005	Furthermore, SB216763 or LiCl, a specific inhibitor for the GSK3 kinase inhibited by Akt, enhanced the Chk1 phosphorylation and G2/M arrest by etoposide.	Lithium Chloride	25-29	checkpoint kinase 1	Homo sapiens	103-107
15674326-7	2005	Furthermore, SB216763 or LiCl, a specific inhibitor for the GSK3 kinase inhibited by Akt, enhanced the Chk1 phosphorylation and G2/M arrest by etoposide.	Etoposide	143-152	checkpoint kinase 1	Homo sapiens	103-107
15674326-8	2005	These results indicate that hematopoietic cytokines protect etoposide-treated cells from DNA damage-induced apoptosis by promoting, through the PI3K/Akt/GSK3 signaling pathway, G2/M checkpoint that is dependent on Chk1-mediated inhibition of Cdc2.	Etoposide	60-69	checkpoint kinase 1	Homo sapiens	214-218
15608676-2	2005	We have previously shown that inhibition of Chk1 sensitizes tumor cells to topoisomerase inhibitors such as camptothecin and doxorubicin through abrogation of cell-cycle arrest (S or G2/M checkpoints).	Camptothecin	108-120	checkpoint kinase 1	Homo sapiens	44-48
15608676-2	2005	We have previously shown that inhibition of Chk1 sensitizes tumor cells to topoisomerase inhibitors such as camptothecin and doxorubicin through abrogation of cell-cycle arrest (S or G2/M checkpoints).	Doxorubicin	125-136	checkpoint kinase 1	Homo sapiens	44-48
15608676-5	2005	Here we demonstrate that 5-FU activates Chk1 and induces an early S-phase arrest.	Fluorouracil	25-29	checkpoint kinase 1	Homo sapiens	40-44
15608676-6	2005	Chk1 downregulation abrogates this arrest and dramatically sensitizes tumor cells to the cytotoxic effects of 5-FU.	Fluorouracil	110-114	checkpoint kinase 1	Homo sapiens	0-4
15608676-7	2005	5-FU confers S-phase arrest through Chk1-mediated Cdc25A proteolysis leading to inhibition of Cdk2.	Fluorouracil	0-4	checkpoint kinase 1	Homo sapiens	36-40
15608676-9	2005	As a result, downregulation of Chk1 potentiates 5-FU efficacy through induction of premature chromosomal condensation followed by apoptosis.	Fluorouracil	48-52	checkpoint kinase 1	Homo sapiens	31-35
15608676-14	2005	Additionally, we show that Chk1 deficiency potentiates 5-FU efficacy through the preferential induction of the caspase-8 pathway and subsequent caspase-3 activation.	Fluorouracil	55-59	checkpoint kinase 1	Homo sapiens	27-31
15707569-0	2005	The relative contribution of CHK1 and CHK2 to Adriamycin-induced checkpoint.	Doxorubicin	46-56	checkpoint kinase 1	Homo sapiens	29-33
15707569-2	2005	Adriamycin-induced DNA damage checkpoint activates ATM and ATR, which could in turn inhibit the cell cycle engine through either CHK1 or CHK2.	Doxorubicin	0-10	checkpoint kinase 1	Homo sapiens	129-133
15707569-3	2005	In this study, we characterized whether CHK1 or CHK2 is required for Adriamycin-induced checkpoint.	Doxorubicin	69-79	checkpoint kinase 1	Homo sapiens	40-44
15707569-4	2005	We found that both CHK1 and CHK2 were phosphorylated after Adriamycin treatment.	Doxorubicin	59-69	checkpoint kinase 1	Homo sapiens	19-23
15707569-5	2005	Several lines of evidence from dominant-negative mutants, short hairpin RNA (shRNA), and knockout cells indicated that CHK1, but not CHK2, is critical for Adriamycin-induced cell cycle arrest.	Doxorubicin	155-165	checkpoint kinase 1	Homo sapiens	119-123
15707569-6	2005	Disruption of CHK1 function bypassed the checkpoint, as manifested by the increase in CDC25A, activation of CDC2, increase in histone H3 phosphorylation, and reduction in cell survival after Adriamycin treatment.	Doxorubicin	191-201	checkpoint kinase 1	Homo sapiens	14-18
15494423-1	2005	Interactions between the Chk1 inhibitor UCN-01 and the farnesyltransferase inhibitor L744832 were examined in human leukemia cells.	7-hydroxystaurosporine	40-46	checkpoint kinase 1	Homo sapiens	25-29
15710331-2	2005	The checkpoint defect was traced to the ability of AKT to phosphorylate CHK1 at serine 280, since a nonphosphorylated mutant of CHK1 (S280A) complemented the checkpoint defect and restored CDC25A degradation.	Serine	80-86	checkpoint kinase 1	Homo sapiens	72-76
15705874-9	2005	Finally, both Cdk and Chk1 inhibitors enhanced the cytotoxity of etoposide, a DNA-damaging agent.	Etoposide	65-74	checkpoint kinase 1	Homo sapiens	22-26
15710331-2	2005	The checkpoint defect was traced to the ability of AKT to phosphorylate CHK1 at serine 280, since a nonphosphorylated mutant of CHK1 (S280A) complemented the checkpoint defect and restored CDC25A degradation.	Serine	80-86	checkpoint kinase 1	Homo sapiens	128-132
15710331-3	2005	CHK1 phosphorylation at serine 280 led to covalent binding of 1 to 2 molecules of ubiquitin and cytoplasmic CHK1 localization.	Serine	24-30	checkpoint kinase 1	Homo sapiens	0-4
15710331-3	2005	CHK1 phosphorylation at serine 280 led to covalent binding of 1 to 2 molecules of ubiquitin and cytoplasmic CHK1 localization.	Serine	24-30	checkpoint kinase 1	Homo sapiens	108-112
15489221-10	2004	In contrast, preincubation of cells with the hydroxyl radical scavenger, N-acetylcysteine, significantly attenuated the doxorubicin-mediated phosphorylation and accumulation of p53, p53-DNA binding, and the phosphorylation of H2AX, Nbs1, SMC1, Chk1, and Chk2, suggesting that hydroxyl radicals contribute to the doxorubicin-induced activation of ATM-dependent pathways.	Hydroxyl Radical	45-61	checkpoint kinase 1	Homo sapiens	244-248
15676021-4	2005	We next found that Ara-C activates Chk1 and Chk2 in the cells, and that the activation of Chk1, but not of Chk2, was almost completely inhibited by caffeine.	Caffeine	148-156	checkpoint kinase 1	Homo sapiens	90-94
15676021-6	2005	To directly observe the effects of checkpoint kinase activation in Ara-C-induced differentiation, we suppressed Chk1 or Chk2 with the Chk1-specific inhibitor Go6976, by generating cell lines stably over-expressing dominant-negative forms of Chk2, or by siRNA-mediated knock-down of the Chk1 or the Chk2 gene.	Go 6976	158-164	checkpoint kinase 1	Homo sapiens	134-138
15676021-6	2005	To directly observe the effects of checkpoint kinase activation in Ara-C-induced differentiation, we suppressed Chk1 or Chk2 with the Chk1-specific inhibitor Go6976, by generating cell lines stably over-expressing dominant-negative forms of Chk2, or by siRNA-mediated knock-down of the Chk1 or the Chk2 gene.	Go 6976	158-164	checkpoint kinase 1	Homo sapiens	134-138
15665856-4	2005	Abrogation of Chk1 function with small interfering RNA or chemical antagonists inhibits HRR, leading to persistent unrepaired DNA double-strand breaks (DSBs) and cell death after replication inhibition with hydroxyurea or DNA-damage caused by camptothecin.	Camptothecin	243-255	checkpoint kinase 1	Homo sapiens	14-18
15665856-6	2005	We demonstrate that Chk1 interacts with RAD51, and that RAD51 is phosphorylated on Thr 309 in a Chk1-dependent manner.	Threonine	83-86	checkpoint kinase 1	Homo sapiens	20-24
15665856-6	2005	We demonstrate that Chk1 interacts with RAD51, and that RAD51 is phosphorylated on Thr 309 in a Chk1-dependent manner.	Threonine	83-86	checkpoint kinase 1	Homo sapiens	96-100
15665856-7	2005	Consistent with a functional interplay between Chk1 and RAD51, Chk1-depleted cells failed to form RAD51 nuclear foci after exposure to hydroxyurea, and cells expressing a phosphorylation-deficient mutant RAD51(T309A) were hypersensitive to hydroxyurea.	Hydroxyurea	135-146	checkpoint kinase 1	Homo sapiens	63-67
15533933-4	2005	Phosphorylation on Chk1(Ser-345), Chk2(Thr-68), and p53(Ser-15) following oxidative damage by IR involved both ATM and ATR.	Serine	24-27	checkpoint kinase 1	Homo sapiens	19-23
15533933-7	2005	Consistent with ATM or ATR activation, hyperoxia induced wortmannin-sensitive phosphorylation of Chk1, Chk2, and p53.	Wortmannin	57-67	checkpoint kinase 1	Homo sapiens	97-101
15603752-10	2005	Further, high NaCl impairs activation of several components of the classical DNA damage response such as Mre11, H2AX and Chk1 leading to inhibition of DNA repair.	Sodium Chloride	14-18	checkpoint kinase 1	Homo sapiens	121-125
15539958-3	2005	In this manuscript we investigated the potential of chemo-sensitization via ablation of Chk1 in cells treated with anti-metabolite cancer drugs, hydroxyurea (HU) and cytosine arabinoside (ara-C).	Hydroxyurea	145-156	checkpoint kinase 1	Homo sapiens	88-92
15539958-3	2005	In this manuscript we investigated the potential of chemo-sensitization via ablation of Chk1 in cells treated with anti-metabolite cancer drugs, hydroxyurea (HU) and cytosine arabinoside (ara-C).	Cytarabine	166-186	checkpoint kinase 1	Homo sapiens	88-92
15615778-3	2005	The p53-independent pathway involves a phosphorylation cascade that activates the Chk1 effector kinase and induces G2 arrest through inhibitory tyrosine phosphorylation of Cdc2.	Tyrosine	144-152	checkpoint kinase 1	Homo sapiens	82-86
15489221-7	2004	Doxorubicin treatment also stimulated ATM autophosphorylation on serine 1981 and the ATM-dependent phosphorylation of numerous effectors in the ATM-signaling pathway, including Nbs1 (Ser(343)), SMC1 (Ser(957)), Chk1 (Ser(317) and Ser(345)), and Chk2 (Ser(33/35) and Thr(68)).	Doxorubicin	0-11	checkpoint kinase 1	Homo sapiens	211-215
15489221-10	2004	In contrast, preincubation of cells with the hydroxyl radical scavenger, N-acetylcysteine, significantly attenuated the doxorubicin-mediated phosphorylation and accumulation of p53, p53-DNA binding, and the phosphorylation of H2AX, Nbs1, SMC1, Chk1, and Chk2, suggesting that hydroxyl radicals contribute to the doxorubicin-induced activation of ATM-dependent pathways.	Acetylcysteine	73-89	checkpoint kinase 1	Homo sapiens	244-248
15489221-10	2004	In contrast, preincubation of cells with the hydroxyl radical scavenger, N-acetylcysteine, significantly attenuated the doxorubicin-mediated phosphorylation and accumulation of p53, p53-DNA binding, and the phosphorylation of H2AX, Nbs1, SMC1, Chk1, and Chk2, suggesting that hydroxyl radicals contribute to the doxorubicin-induced activation of ATM-dependent pathways.	Doxorubicin	120-131	checkpoint kinase 1	Homo sapiens	244-248
15381075-5	2004	We also found that methyl methanesulfonate induces phosphorylation of Ser-317 in protein kinase Chk1 and Ser-139 in histone H2AX and stimulates formation of single-stranded DNA at replication foci.	Methyl Methanesulfonate	19-42	checkpoint kinase 1	Homo sapiens	96-100
15459181-4	2004	Thymidine induces ATM-mediated phosphorylation of Chk2 and NBS1 and an ATM-independent phosphorylation of Chk1 and SMC1.	Thymidine	0-9	checkpoint kinase 1	Homo sapiens	106-110
15538388-3	2004	In HeLa cells, depletion of either hRad17 or hMCM7 with small-interfering RNA suppressed ultraviolet (UV) light- or aphidicolin-induced hChk1 phosphorylation, and abolished UV-induced S-phase checkpoint activation.	Aphidicolin	116-127	checkpoint kinase 1	Homo sapiens	136-141
15736430-2	2004	Chk1 phosphorylates Cdc25C at serine-216, a major regulatory site, in response to DNA damage.	Serine	30-36	checkpoint kinase 1	Homo sapiens	0-4
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	checkpoint kinase 1	Homo sapiens	13-17
15736430-8	2004	Our results suggest that Chk1 associates with BAD and phosphorylates the BAD protein at serine-155.	Serine	88-94	checkpoint kinase 1	Homo sapiens	25-29
15381075-5	2004	We also found that methyl methanesulfonate induces phosphorylation of Ser-317 in protein kinase Chk1 and Ser-139 in histone H2AX and stimulates formation of single-stranded DNA at replication foci.	Serine	70-73	checkpoint kinase 1	Homo sapiens	96-100
15456844-4	2004	Iron depletion induces DNA double-strand breaks in treated cells, and activates a DNA damage response that results in focal phosphorylation of histone H2AX, focal accumulation of replication protein A (RPA) and ATR (ATM and Rad3-related kinase), and activation of CHK1 kinase.	Iron	0-4	checkpoint kinase 1	Homo sapiens	264-268
15486189-0	2004	Inhibition of Chk1 by the G2 DNA damage checkpoint inhibitor isogranulatimide.	isogranulatimide	61-77	checkpoint kinase 1	Homo sapiens	14-18
15486189-4	2004	Isogranulatimide shows structural resemblance to the aglycon of UCN-01, a potent bisindolemaleimide inhibitor of protein kinase C beta (IC(50), 0.001 micromol/L) and of the checkpoint kinase Chk1 (IC(50), 0.007 micromol/L).	isogranulatimide	0-16	checkpoint kinase 1	Homo sapiens	191-195
15486189-5	2004	In vitro kinase assays show that isogranulatimide inhibits Chk1 (IC(50), 0.1 micromol/L) but not protein kinase C beta.	isogranulatimide	33-49	checkpoint kinase 1	Homo sapiens	59-63
15486189-7	2004	We determined the crystal structure of the Chk1 catalytic domain complexed with isogranulatimide.	isogranulatimide	80-96	checkpoint kinase 1	Homo sapiens	43-47
15486189-8	2004	Like UCN-01, isogranulatimide binds in the ATP-binding pocket of Chk1 and hydrogen bonds with the backbone carbonyl oxygen of Glu(85) and the amide nitrogen of Cys(87).	7-hydroxystaurosporine	5-11	checkpoint kinase 1	Homo sapiens	65-69
15486189-8	2004	Like UCN-01, isogranulatimide binds in the ATP-binding pocket of Chk1 and hydrogen bonds with the backbone carbonyl oxygen of Glu(85) and the amide nitrogen of Cys(87).	isogranulatimide	13-29	checkpoint kinase 1	Homo sapiens	65-69
15486189-8	2004	Like UCN-01, isogranulatimide binds in the ATP-binding pocket of Chk1 and hydrogen bonds with the backbone carbonyl oxygen of Glu(85) and the amide nitrogen of Cys(87).	Adenosine Triphosphate	43-46	checkpoint kinase 1	Homo sapiens	65-69
15486189-8	2004	Like UCN-01, isogranulatimide binds in the ATP-binding pocket of Chk1 and hydrogen bonds with the backbone carbonyl oxygen of Glu(85) and the amide nitrogen of Cys(87).	Oxygen	116-122	checkpoint kinase 1	Homo sapiens	65-69
15486189-8	2004	Like UCN-01, isogranulatimide binds in the ATP-binding pocket of Chk1 and hydrogen bonds with the backbone carbonyl oxygen of Glu(85) and the amide nitrogen of Cys(87).	Glutamic Acid	126-129	checkpoint kinase 1	Homo sapiens	65-69
15486189-10	2004	The mechanism by which isogranulatimide inhibits Chk1 and its favorable kinase selectivity profile make it a promising candidate for modulating checkpoint responses in tumors for therapeutic benefit.	isogranulatimide	23-39	checkpoint kinase 1	Homo sapiens	49-53
15467443-7	2004	In non-stressed CML cells, serine 20 of p53 is constitutively phosphorylated by Chk1, and is inhibited by STI571.	Serine	27-33	checkpoint kinase 1	Homo sapiens	80-84
15367709-6	2004	Furthermore, we show that CHK2 is hyperphosphorylated at later times following 6-TG treatment and the phosphorylation of CHK2 seems to be ATM independent but up-regulated when ATR or CHK1 is reduced.	Thioguanine	79-83	checkpoint kinase 1	Homo sapiens	183-187
15498111-0	2004	[Influence of antisense oligonucleotide targeting Chk1/2 on apoptosis of K562 cell induced by DDP].	Oligonucleotides	24-39	checkpoint kinase 1	Homo sapiens	50-56
15498111-1	2004	In order to investigate the change of cell-cycle of K562 cells induced by cisplatin (DDP) and role of antisense oligonucleotide targeting Chk1/2 on apoptosis of K562 cell induced by DDP, the change of cell-cycle was observed by means of flow cytometry after different intervals in which the K562 cell were treated by DDP.	Oligonucleotides	112-127	checkpoint kinase 1	Homo sapiens	138-144
15498111-2	2004	Chk1/2 protein expression was investigated by Western blot and confocal microscopy in best condition of transfection of antisense oligonucleotide targeting Chk1/2 by lipofection.	Oligonucleotides	130-145	checkpoint kinase 1	Homo sapiens	0-6
15498111-2	2004	Chk1/2 protein expression was investigated by Western blot and confocal microscopy in best condition of transfection of antisense oligonucleotide targeting Chk1/2 by lipofection.	Oligonucleotides	130-145	checkpoint kinase 1	Homo sapiens	0-4
15498111-3	2004	Apoptosis of K562 induced by DDP was investigated by flow cytometry after transfection of antisense oligonucleotide targeting Chk1/2.	Oligonucleotides	100-115	checkpoint kinase 1	Homo sapiens	126-132
15498111-5	2004	Transfection with antisense oligonucleotide targeting Chk1/2 could inhibit expression of Chk1/2 at different levels.	Oligonucleotides	28-43	checkpoint kinase 1	Homo sapiens	54-60
15498111-5	2004	Transfection with antisense oligonucleotide targeting Chk1/2 could inhibit expression of Chk1/2 at different levels.	Oligonucleotides	28-43	checkpoint kinase 1	Homo sapiens	54-58
15498111-6	2004	The frequency of apoptosis induced by DDP was increased when transfected with antisense oligonucleotide targeting Chk1 and/or Chk2.	Oligonucleotides	88-103	checkpoint kinase 1	Homo sapiens	114-118
15498111-7	2004	The effect of antisense oligonucleotide targeting Chk1 and Chk2 synchronously exceeded that of antisense oligonucleotide targeting either Chk1 or Chk2 alone.	Oligonucleotides	24-39	checkpoint kinase 1	Homo sapiens	50-54
15498111-7	2004	The effect of antisense oligonucleotide targeting Chk1 and Chk2 synchronously exceeded that of antisense oligonucleotide targeting either Chk1 or Chk2 alone.	Oligonucleotides	105-120	checkpoint kinase 1	Homo sapiens	50-54
15326376-4	2004	We here show that inhibition of Chk1 but not of Chk2 in p21(-/-) and p53(-/-) cells caused a greater abrogation of G(2) block induced by ionizing radiation and cis-diamine-dichloroplatinum treatments and a greater sensitization to the same treatments than in the parental cell line with p53 and p21 wild type proteins.	cis-diamine	160-171	checkpoint kinase 1	Homo sapiens	32-36
15326376-4	2004	We here show that inhibition of Chk1 but not of Chk2 in p21(-/-) and p53(-/-) cells caused a greater abrogation of G(2) block induced by ionizing radiation and cis-diamine-dichloroplatinum treatments and a greater sensitization to the same treatments than in the parental cell line with p53 and p21 wild type proteins.	Platinum(II) chloride	172-188	checkpoint kinase 1	Homo sapiens	32-36
15367709-0	2004	CHK1 and CHK2 are differentially involved in mismatch repair-mediated 6-thioguanine-induced cell cycle checkpoint responses.	Thioguanine	70-83	checkpoint kinase 1	Homo sapiens	0-4
15367709-3	2004	We show that, in response to 6-TG (3 micromol/L x 24 hours), activating phosphorylation of CHK1 at Ser317 [CHK1(pS317)] and CHK2 at Thr68 [CHK2(pT68)] are induced differentially during a prolonged course (up to 6 days) of MMR-mediated cell cycle arrests following 6-TG treatment, with CHK1(pS317) being induced within 1 day and CHK2(pT68) being induced later.	Thioguanine	29-33	checkpoint kinase 1	Homo sapiens	91-95
15367709-3	2004	We show that, in response to 6-TG (3 micromol/L x 24 hours), activating phosphorylation of CHK1 at Ser317 [CHK1(pS317)] and CHK2 at Thr68 [CHK2(pT68)] are induced differentially during a prolonged course (up to 6 days) of MMR-mediated cell cycle arrests following 6-TG treatment, with CHK1(pS317) being induced within 1 day and CHK2(pT68) being induced later.	Thioguanine	29-33	checkpoint kinase 1	Homo sapiens	107-111
15367709-3	2004	We show that, in response to 6-TG (3 micromol/L x 24 hours), activating phosphorylation of CHK1 at Ser317 [CHK1(pS317)] and CHK2 at Thr68 [CHK2(pT68)] are induced differentially during a prolonged course (up to 6 days) of MMR-mediated cell cycle arrests following 6-TG treatment, with CHK1(pS317) being induced within 1 day and CHK2(pT68) being induced later.	Thioguanine	29-33	checkpoint kinase 1	Homo sapiens	107-111
15367709-3	2004	We show that, in response to 6-TG (3 micromol/L x 24 hours), activating phosphorylation of CHK1 at Ser317 [CHK1(pS317)] and CHK2 at Thr68 [CHK2(pT68)] are induced differentially during a prolonged course (up to 6 days) of MMR-mediated cell cycle arrests following 6-TG treatment, with CHK1(pS317) being induced within 1 day and CHK2(pT68) being induced later.	Thioguanine	264-268	checkpoint kinase 1	Homo sapiens	91-95
15367709-7	2004	Thus, our data suggest that CHK1(pS317) is involved in a MMR-mediated 6-TG-induced G2 arrest, whereas CHK2(pT68) seems to be involved in a subsequent tetraploid G1-S checkpoint.	Thioguanine	70-74	checkpoint kinase 1	Homo sapiens	28-32
15367709-4	2004	Using chemical inhibitors and small interfering RNA of the signaling kinases, we show that a MMR-mediated 6-TG-induced G2 arrest is ATR/CHK1 dependent but ATM/CHK2 independent and that ATR/CHK1 signaling is responsible for both initiation and maintenance of the G2 arrest.	Thioguanine	106-110	checkpoint kinase 1	Homo sapiens	136-140
15190204-7	2004	ATR ablation also inhibited the activatory phosphorylation of Chk1 on serine 345.	Serine	70-76	checkpoint kinase 1	Homo sapiens	62-66
15367709-4	2004	Using chemical inhibitors and small interfering RNA of the signaling kinases, we show that a MMR-mediated 6-TG-induced G2 arrest is ATR/CHK1 dependent but ATM/CHK2 independent and that ATR/CHK1 signaling is responsible for both initiation and maintenance of the G2 arrest.	Thioguanine	106-110	checkpoint kinase 1	Homo sapiens	189-193
15110787-0	2004	Mismatch repair-mediated G2/M arrest by 6-thioguanine involves the ATR-Chk1 pathway.	Thioguanine	40-53	checkpoint kinase 1	Homo sapiens	71-75
15169628-0	2004	Abrogation of Chk1-mediated S/G2 checkpoint by UCN-01 enhances ara-C-induced cytotoxicity in human colon cancer cells.	Cytarabine	63-68	checkpoint kinase 1	Homo sapiens	14-18
15169628-6	2004	Measurements of cyclin A and B protein levels, Cdk2 and Cdc2 kinase activities, Cdc25C phosphorylation, and Chk1 kinase activity were consistent with UCN-01-induced abrogation of the S/G2-phase checkpoint in ara-C treated cells.	7-hydroxystaurosporine	150-156	checkpoint kinase 1	Homo sapiens	108-112
15200121-0	2004	Cooperative function of Chk1 and p38 pathways in activating G2 arrest following exposure to temozolomide.	Temozolomide	92-104	checkpoint kinase 1	Homo sapiens	24-28
15200121-1	2004	OBJECT: The Chk1 and p38 mitogen-activated protein kinase (MAPK) pathways play key roles in the G2 arrest caused by exposing glioma cells to temozolomide (TMZ).	Temozolomide	141-153	checkpoint kinase 1	Homo sapiens	12-16
15200121-1	2004	OBJECT: The Chk1 and p38 mitogen-activated protein kinase (MAPK) pathways play key roles in the G2 arrest caused by exposing glioma cells to temozolomide (TMZ).	Temozolomide	155-158	checkpoint kinase 1	Homo sapiens	12-16
15200121-3	2004	METHODS: The authors pharmacologically inhibited the Chk1 and/or p38 pathways in U87MG human glioma cells prior to and/or after exposure to TMZ; thereafter, effects on the TMZ-induced G2 arrest pathway and toxicity were monitored.	Temozolomide	140-143	checkpoint kinase 1	Homo sapiens	53-57
15200121-4	2004	The p38 inhibitor SB203580 or the Chk1 inhibitor UCN-01 or their combination blocked TMZ-mediated inactivation of cdc25C and cdc2, suggesting that p38 and Chk1 pathways work cooperatively and are both necessary to inactivate cdc25C and cdc2.	SB 203580	18-26	checkpoint kinase 1	Homo sapiens	155-159
15200121-4	2004	The p38 inhibitor SB203580 or the Chk1 inhibitor UCN-01 or their combination blocked TMZ-mediated inactivation of cdc25C and cdc2, suggesting that p38 and Chk1 pathways work cooperatively and are both necessary to inactivate cdc25C and cdc2.	7-hydroxystaurosporine	49-52	checkpoint kinase 1	Homo sapiens	34-38
15200121-4	2004	The p38 inhibitor SB203580 or the Chk1 inhibitor UCN-01 or their combination blocked TMZ-mediated inactivation of cdc25C and cdc2, suggesting that p38 and Chk1 pathways work cooperatively and are both necessary to inactivate cdc25C and cdc2.	7-hydroxystaurosporine	49-52	checkpoint kinase 1	Homo sapiens	155-159
15200121-4	2004	The p38 inhibitor SB203580 or the Chk1 inhibitor UCN-01 or their combination blocked TMZ-mediated inactivation of cdc25C and cdc2, suggesting that p38 and Chk1 pathways work cooperatively and are both necessary to inactivate cdc25C and cdc2.	Temozolomide	85-88	checkpoint kinase 1	Homo sapiens	34-38
15200121-4	2004	The p38 inhibitor SB203580 or the Chk1 inhibitor UCN-01 or their combination blocked TMZ-mediated inactivation of cdc25C and cdc2, suggesting that p38 and Chk1 pathways work cooperatively and are both necessary to inactivate cdc25C and cdc2.	Temozolomide	85-88	checkpoint kinase 1	Homo sapiens	155-159
15200121-7	2004	The two pathways, however, are not functionally identical; the Chk1 pathway was required for both the initiation and maintenance of TMZ-induced G2 arrest, whereas the p38 pathway played a role only in the initiation.	Temozolomide	132-135	checkpoint kinase 1	Homo sapiens	63-67
15200121-8	2004	CONCLUSIONS: The Chk1 and p38 pathways cooperate to bring about TMZ-induced G2 arrest, and the inhibition of either pathway alone is sufficient to sensitize U87MG glioma cells to TMZ-induced cytotoxicity.	Temozolomide	64-67	checkpoint kinase 1	Homo sapiens	17-21
15200121-8	2004	CONCLUSIONS: The Chk1 and p38 pathways cooperate to bring about TMZ-induced G2 arrest, and the inhibition of either pathway alone is sufficient to sensitize U87MG glioma cells to TMZ-induced cytotoxicity.	Temozolomide	179-182	checkpoint kinase 1	Homo sapiens	17-21
15110787-3	2004	In this study, we found that prolonged (up to 4 days) treatment with 6-TG (3microM) resulted in a progressive phosphorylation of Chk1 and Chk2 in MMR(+) HeLa cells, correlating temporally with a drug-induced G2/M arrest.	Thioguanine	69-73	checkpoint kinase 1	Homo sapiens	129-133
15159417-4	2004	We found a CHK1-dependent checkpoint to be activated in rereplicating cells accompanied by formation of gammaH2AX and RAD51 nuclear foci.	gammah2ax	104-113	checkpoint kinase 1	Homo sapiens	11-15
15110787-4	2004	Transfection of HeLa cells with small interfering RNA (siRNA) against the ataxia telangiectasia-related (ATR) kinase or against the Chk1 kinase destroyed the G2/M checkpoint and enhanced the apoptosis following 6-TG treatment.	Thioguanine	211-215	checkpoint kinase 1	Homo sapiens	132-136
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	checkpoint kinase 1	Homo sapiens	283-287
15107605-1	2004	We have shown recently that DNA damage effector kinase Chk1 is phosphorylated in vitro by protein kinase B/Akt (PKB/Akt) on serine 280.	Serine	124-130	checkpoint kinase 1	Homo sapiens	55-59
15107605-3	2004	In this study we show that Chk1 is phosphorylated by PKB in vivo, and that increased phosphorylation by PKB on serine 280 correlates with impairment of Chk1 activation by DNA damage.	Serine	111-117	checkpoint kinase 1	Homo sapiens	27-31
15107605-3	2004	In this study we show that Chk1 is phosphorylated by PKB in vivo, and that increased phosphorylation by PKB on serine 280 correlates with impairment of Chk1 activation by DNA damage.	Serine	111-117	checkpoint kinase 1	Homo sapiens	152-156
15107605-4	2004	Our results indicate a likely mechanism for the negative effects that phosphorylation of serine 280 has on activation of Chk1.	Serine	89-95	checkpoint kinase 1	Homo sapiens	121-125
15107605-5	2004	The Chk1 protein phosphorylated by PKB on serine 280 does not enter into protein complexes after replication arrest.	Serine	42-48	checkpoint kinase 1	Homo sapiens	4-8
15141015-6	2004	DNA damage checkpoint proteins including p53, chk1, and chk2 were differentially activated by hedamycin depending on the concentration and duration of treatment.	hedamycin	94-103	checkpoint kinase 1	Homo sapiens	46-50
14681223-6	2004	Unlike the full-length protein, C-terminally truncated CHK1 displays autophosphorylation, phosphorylates CDC25C on Ser(216), and delays cell cycle progression.	Serine	115-118	checkpoint kinase 1	Homo sapiens	55-59
12959929-10	2004	We also show that checkpoint kinase 1 (Chk1) is phosphorylated on Ser345 in response to hyperoxia, which could be inhibited by caffeine or wortmannin, potent inhibitors of phosphoinositide 3-kinase-related kinases.	Caffeine	127-135	checkpoint kinase 1	Homo sapiens	18-37
15274354-8	2004	Within 24 hours of treatment, HMJ-38 influenced the CDK/cyclin B activity by increasing Chk1, Wee1 and p21 and decreasing Cdc25C protein levels.	2-(3'-methoxyphenyl)-6-pyrrolidinyl-4-quinazolinone	30-36	checkpoint kinase 1	Homo sapiens	88-92
12959929-10	2004	We also show that checkpoint kinase 1 (Chk1) is phosphorylated on Ser345 in response to hyperoxia, which could be inhibited by caffeine or wortmannin, potent inhibitors of phosphoinositide 3-kinase-related kinases.	Caffeine	127-135	checkpoint kinase 1	Homo sapiens	39-43
12959929-10	2004	We also show that checkpoint kinase 1 (Chk1) is phosphorylated on Ser345 in response to hyperoxia, which could be inhibited by caffeine or wortmannin, potent inhibitors of phosphoinositide 3-kinase-related kinases.	Wortmannin	139-149	checkpoint kinase 1	Homo sapiens	18-37
12959929-10	2004	We also show that checkpoint kinase 1 (Chk1) is phosphorylated on Ser345 in response to hyperoxia, which could be inhibited by caffeine or wortmannin, potent inhibitors of phosphoinositide 3-kinase-related kinases.	Wortmannin	139-149	checkpoint kinase 1	Homo sapiens	39-43
14585975-5	2003	Consistent with this, we discovered that endogenous p73alpha interacts with Chk1 and is phosphorylated by Chk1 at serine 47 in vitro and in vivo.	Serine	114-120	checkpoint kinase 1	Homo sapiens	106-110
14681206-8	2003	SCFbeta-TRCP promotes Chk1-dependent Cdc25A ubiquitination in vitro, and this involves serine 76, a known Chk1 phosphorylation site.	Serine	87-93	checkpoint kinase 1	Homo sapiens	106-110
14643438-3	2003	Treatment by aphidicolin and HU resulted in phosphorylation of Chk1, while HU, but not aphidicolin, induced focalization of gamma-H2AX and RPA.	Aphidicolin	13-24	checkpoint kinase 1	Homo sapiens	63-67
14504477-2	2003	Chk1 has been shown to be transcriptionally down-regulated in response to cis-dichloro-diamino platinum treatment in a p53-dependent manner.	cis-dichloro-diamino platinum	74-103	checkpoint kinase 1	Homo sapiens	0-4
14585975-4	2003	We found that endogenous p73alpha is serine phosphorylated by endogenous Chk1 upon DNA damage, which is a mechanism required for the apoptotic-inducing function of p73alpha.	Serine	37-43	checkpoint kinase 1	Homo sapiens	73-77
14585975-7	2003	Moreover, mutation of serine 47 abolishes both Chk1-dependent phosphorylation of p73alpha upon DNA damage in vivo and the ability of Chk1 to upregulate the transactivation capacity of p73alpha.	Serine	22-28	checkpoint kinase 1	Homo sapiens	47-51
14585975-7	2003	Moreover, mutation of serine 47 abolishes both Chk1-dependent phosphorylation of p73alpha upon DNA damage in vivo and the ability of Chk1 to upregulate the transactivation capacity of p73alpha.	Serine	22-28	checkpoint kinase 1	Homo sapiens	133-137
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	checkpoint kinase 1	Homo sapiens	0-4
12847089-4	2003	Surprisingly, I have found that multiple ATM-ATR substrates including CHK1 and -2 are hyperphosphorylated in cells treated with caffeine and genotoxic agents such as hydroxyurea or ionizing radiation.	Caffeine	128-136	checkpoint kinase 1	Homo sapiens	70-81
12847089-4	2003	Surprisingly, I have found that multiple ATM-ATR substrates including CHK1 and -2 are hyperphosphorylated in cells treated with caffeine and genotoxic agents such as hydroxyurea or ionizing radiation.	Hydroxyurea	166-177	checkpoint kinase 1	Homo sapiens	70-81
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	checkpoint kinase 1	Homo sapiens	69-73
12756247-4	2003	Chk1 stimulates the kinase activity of DNA-PK (protein kinase) complexes, which leads to increased phosphorylation of p53 on Ser-15 and Ser-37.	Serine	125-128	checkpoint kinase 1	Homo sapiens	0-4
12756247-4	2003	Chk1 stimulates the kinase activity of DNA-PK (protein kinase) complexes, which leads to increased phosphorylation of p53 on Ser-15 and Ser-37.	Serine	136-139	checkpoint kinase 1	Homo sapiens	0-4
12759351-2	2003	In response to ionizing radiation, Cdc25A is phosphorylated by both Chk1 and Chk2 on Ser-123.	Serine	85-88	checkpoint kinase 1	Homo sapiens	68-72
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	checkpoint kinase 1	Homo sapiens	55-59
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	checkpoint kinase 1	Homo sapiens	88-92
12684226-10	2003	Also, high NaCl prevents ionizing and UV radiation-induced phosphorylation of chk1, but cell cycle arrest still occurs, indicating the existence of alternative mechanisms for the S and G2/M delays.	Sodium Chloride	11-15	checkpoint kinase 1	Homo sapiens	78-82
12897801-5	2003	Although CHK2 has a basal Ser 20 kinase activity that is predominantly activated towards Thr 18, CHK1 has constitutive Thr 18 kinase activity that is predominantly activated in trans towards Ser 20.	Threonine	119-122	checkpoint kinase 1	Homo sapiens	97-101
14570880-3	2003	Consistent with Chk1 being an Hsp90 client, we also found that Chk1 but not Chk2 is destabilized in cells treated with the Hsp90 inhibitor 17-allylamino-17-demethoxygeldanamycin (17-AAG).	tanespimycin	139-177	checkpoint kinase 1	Homo sapiens	16-20
14570880-3	2003	Consistent with Chk1 being an Hsp90 client, we also found that Chk1 but not Chk2 is destabilized in cells treated with the Hsp90 inhibitor 17-allylamino-17-demethoxygeldanamycin (17-AAG).	tanespimycin	139-177	checkpoint kinase 1	Homo sapiens	63-67
14570880-3	2003	Consistent with Chk1 being an Hsp90 client, we also found that Chk1 but not Chk2 is destabilized in cells treated with the Hsp90 inhibitor 17-allylamino-17-demethoxygeldanamycin (17-AAG).	tanespimycin	179-185	checkpoint kinase 1	Homo sapiens	16-20
14570880-3	2003	Consistent with Chk1 being an Hsp90 client, we also found that Chk1 but not Chk2 is destabilized in cells treated with the Hsp90 inhibitor 17-allylamino-17-demethoxygeldanamycin (17-AAG).	tanespimycin	179-185	checkpoint kinase 1	Homo sapiens	63-67
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	checkpoint kinase 1	Homo sapiens	16-20
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	checkpoint kinase 1	Homo sapiens	49-53
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	checkpoint kinase 1	Homo sapiens	49-53
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	checkpoint kinase 1	Homo sapiens	16-20
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	checkpoint kinase 1	Homo sapiens	49-53
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	checkpoint kinase 1	Homo sapiens	49-53
14570880-5	2003	Finally, 17-AAG-mediated disruption of Chk1 activation dramatically sensitized various tumor cells to gemcitabine, an S phase-active chemotherapeutic agent.	tanespimycin	9-15	checkpoint kinase 1	Homo sapiens	39-43
14570880-5	2003	Finally, 17-AAG-mediated disruption of Chk1 activation dramatically sensitized various tumor cells to gemcitabine, an S phase-active chemotherapeutic agent.	gemcitabine	102-113	checkpoint kinase 1	Homo sapiens	39-43
12740909-9	2003	An inverse relationship with p21(WAF1) modulation was found for CHK1 in parental cells treated with both agents and in resistant cells treated with cisplatin.	Cisplatin	148-157	checkpoint kinase 1	Homo sapiens	64-68
12676962-0	2003	Regulation of Chk1 includes chromatin association and 14-3-3 binding following phosphorylation on Ser-345.	Serine	98-101	checkpoint kinase 1	Homo sapiens	14-18
12676962-3	2003	Chk1 is phosphorylated on Ser-317 and Ser-345 following a checkpoint signal, a process that is regulated by Atr, and by the sensor complexes containing Rad17 and Hus1.	Serine	26-29	checkpoint kinase 1	Homo sapiens	0-4
12676962-3	2003	Chk1 is phosphorylated on Ser-317 and Ser-345 following a checkpoint signal, a process that is regulated by Atr, and by the sensor complexes containing Rad17 and Hus1.	Serine	38-41	checkpoint kinase 1	Homo sapiens	0-4
12676962-5	2003	The UV-induced Ser-345-phosphorylated forms of Chk1 that appear minutes after treatment are predominantly associated with chromatin.	Serine	15-18	checkpoint kinase 1	Homo sapiens	47-51
12676962-6	2003	The Ser-345 site is in a 14-3-3 consensus binding motif and is required for nuclear retention of Chk1 following an hydroxyurea-induced checkpoint signal; nonetheless, Ser-345 or Ser-317 are not required for the chromatin association of Chk1.	Serine	4-7	checkpoint kinase 1	Homo sapiens	97-101
12676962-6	2003	The Ser-345 site is in a 14-3-3 consensus binding motif and is required for nuclear retention of Chk1 following an hydroxyurea-induced checkpoint signal; nonetheless, Ser-345 or Ser-317 are not required for the chromatin association of Chk1.	Serine	4-7	checkpoint kinase 1	Homo sapiens	236-240
12676962-6	2003	The Ser-345 site is in a 14-3-3 consensus binding motif and is required for nuclear retention of Chk1 following an hydroxyurea-induced checkpoint signal; nonetheless, Ser-345 or Ser-317 are not required for the chromatin association of Chk1.	Hydroxyurea	115-126	checkpoint kinase 1	Homo sapiens	97-101
12676962-7	2003	Hus1, a member of the proliferating cell nuclear antigen-like damage recognition complex plays a role in the phosphorylation of Chk1 on Ser-345, however, Hus1 is not required for phosphorylation on Ser-317 or for Chk1 localization to chromatin.	Serine	136-139	checkpoint kinase 1	Homo sapiens	128-132
12676962-7	2003	Hus1, a member of the proliferating cell nuclear antigen-like damage recognition complex plays a role in the phosphorylation of Chk1 on Ser-345, however, Hus1 is not required for phosphorylation on Ser-317 or for Chk1 localization to chromatin.	Serine	136-139	checkpoint kinase 1	Homo sapiens	213-217
12676962-7	2003	Hus1, a member of the proliferating cell nuclear antigen-like damage recognition complex plays a role in the phosphorylation of Chk1 on Ser-345, however, Hus1 is not required for phosphorylation on Ser-317 or for Chk1 localization to chromatin.	Serine	198-201	checkpoint kinase 1	Homo sapiens	128-132
12676962-8	2003	These results indicate that there is more than one step in Chk1 activation and that the regulation of this checkpoint signaling is achieved at least in part through phosphorylation of Ser-345, which serves to localize Chk1 in the nucleus presumably by blocking Crm1-dependent nuclear export.	Serine	184-187	checkpoint kinase 1	Homo sapiens	59-63
12676962-8	2003	These results indicate that there is more than one step in Chk1 activation and that the regulation of this checkpoint signaling is achieved at least in part through phosphorylation of Ser-345, which serves to localize Chk1 in the nucleus presumably by blocking Crm1-dependent nuclear export.	Serine	184-187	checkpoint kinase 1	Homo sapiens	218-222
12714602-3	2003	The data presented here indicate that the consecutive actions of ATR-CHK1 and CDK2 kinases are involved in this phosphorylation in the presence of hydroxyurea.	Hydroxyurea	147-158	checkpoint kinase 1	Homo sapiens	69-73
12742232-6	2003	Checkpoint kinases, Chk1/2, and MAPK became phosphorylated after stimulation with bisphosphonates in the myeloma cells.	Diphosphonates	82-97	checkpoint kinase 1	Homo sapiens	20-26
12676925-6	2003	However, the involvement of Chk1 is far from clear, because caffeine is a rather nonspecific inhibitor of the ATR/Chk1 signaling pathway.	Caffeine	60-68	checkpoint kinase 1	Homo sapiens	114-118
12588868-0	2003	Ataxia-telangiectasia-mutated (ATM) and NBS1-dependent phosphorylation of Chk1 on Ser-317 in response to ionizing radiation.	Serine	82-85	checkpoint kinase 1	Homo sapiens	74-78
12689636-5	2003	Total alkali-soluble hexose from the cell wall of the chk1 mutant (strain CHK21) was significantly reduced.	Hexoses	21-27	checkpoint kinase 1	Homo sapiens	54-58
12588868-6	2003	Phosphorylation of Chk1 on Ser-317 in response to IR is ATM-dependent.	Serine	27-30	checkpoint kinase 1	Homo sapiens	19-23
12660173-5	2003	Chk1 phosphorylates Tlk1 on serine 695 (S695) in vitro, and this UCN-01- and caffeine-sensitive site is phosphorylated in vivo in response to DNA damage.	Serine	28-34	checkpoint kinase 1	Homo sapiens	0-4
12859877-0	2003	[Transfection of chk1/2 antisense oligonucleotide to HL-60 cell line increases the apoptotic sensitivity to irradiation].	Oligonucleotides	34-49	checkpoint kinase 1	Homo sapiens	17-23
12660173-5	2003	Chk1 phosphorylates Tlk1 on serine 695 (S695) in vitro, and this UCN-01- and caffeine-sensitive site is phosphorylated in vivo in response to DNA damage.	Caffeine	77-85	checkpoint kinase 1	Homo sapiens	0-4
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	checkpoint kinase 1	Homo sapiens	71-75
12676583-4	2003	IR-induced acceleration of Cdc25A proteolysis correlated with increased phosphate incorporation into these residues generated by a combined action of Chk1 and Chk2 kinases.	Phosphates	72-81	checkpoint kinase 1	Homo sapiens	150-154
12678913-6	2003	Identification of the targets of caffeine and UCN-01 to be key-players of the G(2) checkpoint (ATM/ATR and Chk1, respectively) promoted the search for novel inhibitors of this checkpoint.	Caffeine	33-41	checkpoint kinase 1	Homo sapiens	107-111
12554670-5	2003	An inhibitor of Chk1 kinase activity, UCN-01, overcomes the HuCdc6 mediated G(2) arrest indicating that HuCdc6 blocks cells in G(2) phase via a checkpoint pathway involving Chk1.	hucdc6	60-66	checkpoint kinase 1	Homo sapiens	16-20
12554670-5	2003	An inhibitor of Chk1 kinase activity, UCN-01, overcomes the HuCdc6 mediated G(2) arrest indicating that HuCdc6 blocks cells in G(2) phase via a checkpoint pathway involving Chk1.	hucdc6	60-66	checkpoint kinase 1	Homo sapiens	173-177
12446774-5	2002	Pretreatment of normal and AT fibroblasts with caffeine or UCN-01, inhibitors of ATR (AT mutated and Rad3 related) and Chk1, respectively, abolished the S checkpoint response to UVC.	Caffeine	47-55	checkpoint kinase 1	Homo sapiens	119-123
12446774-5	2002	Pretreatment of normal and AT fibroblasts with caffeine or UCN-01, inhibitors of ATR (AT mutated and Rad3 related) and Chk1, respectively, abolished the S checkpoint response to UVC.	7-hydroxystaurosporine	59-65	checkpoint kinase 1	Homo sapiens	119-123
12244092-2	2002	UCN-01 (7-hydroxystaurosporine), currently in clinical trials, has recently been shown to be a potent Chk1 inhibitor that abrogates the G(2)/M checkpoint induced by DNA-damaging agents.	7-hydroxystaurosporine	0-6	checkpoint kinase 1	Homo sapiens	102-106
12244092-2	2002	UCN-01 (7-hydroxystaurosporine), currently in clinical trials, has recently been shown to be a potent Chk1 inhibitor that abrogates the G(2)/M checkpoint induced by DNA-damaging agents.	7-hydroxystaurosporine	8-30	checkpoint kinase 1	Homo sapiens	102-106
12244092-3	2002	To understand the structural basis of Chk1 inhibition by UCN-01, we determined the crystal structure of the Chk1 kinase domain in complex with UCN-01.	7-hydroxystaurosporine	57-63	checkpoint kinase 1	Homo sapiens	38-42
12244092-3	2002	To understand the structural basis of Chk1 inhibition by UCN-01, we determined the crystal structure of the Chk1 kinase domain in complex with UCN-01.	7-hydroxystaurosporine	57-63	checkpoint kinase 1	Homo sapiens	108-112
12244092-4	2002	Chk1 structures with staurosporine and its analog SB-218078 were also determined.	Staurosporine	21-34	checkpoint kinase 1	Homo sapiens	0-4
12244092-4	2002	Chk1 structures with staurosporine and its analog SB-218078 were also determined.	SB 218078	50-59	checkpoint kinase 1	Homo sapiens	0-4
12244092-5	2002	All three compounds bind in the ATP-binding pocket of Chk1, producing only slight changes in the protein conformation.	Adenosine Triphosphate	32-35	checkpoint kinase 1	Homo sapiens	54-58
12244092-6	2002	Selectivity of UCN-01 toward Chk1 over cyclin-dependent kinases can be explained by the presence of a hydroxyl group in the lactam moiety interacting with the ATP-binding pocket.	Lactams	124-130	checkpoint kinase 1	Homo sapiens	29-33
12244092-6	2002	Selectivity of UCN-01 toward Chk1 over cyclin-dependent kinases can be explained by the presence of a hydroxyl group in the lactam moiety interacting with the ATP-binding pocket.	Adenosine Triphosphate	159-162	checkpoint kinase 1	Homo sapiens	29-33
12244092-7	2002	Hydrophobic interactions and hydrogen-bonding interactions were observed in the structures between UCN-01 and the Chk1 kinase domain.	Hydrogen	29-37	checkpoint kinase 1	Homo sapiens	114-118
12370755-0	2002	Phosphorylation of chk1 at serine-345 affected by topoisomerase I poison SN-38.	Serine	27-33	checkpoint kinase 1	Homo sapiens	19-23
12414624-8	2002	Treatment with Chk1 antisense oligonucleotide abolishes the stronger G(2) checkpoint response and sensitizes Ku80(-/-) cells to IR.	Oligonucleotides	30-45	checkpoint kinase 1	Homo sapiens	15-19
12370755-0	2002	Phosphorylation of chk1 at serine-345 affected by topoisomerase I poison SN-38.	Irinotecan	73-78	checkpoint kinase 1	Homo sapiens	19-23
12370755-6	2002	Increased chk1 phosphorylation at Ser345 induced by SN-38 was accompanied by the observed G2 phase arrest in the A253 cell line, while significant downregulation of chk1 and cdc25C phosphorylation, which resulted in the abrogation of G2/M checkpoint arrest, was noted in FaDu cells at this timepoint.	Irinotecan	52-57	checkpoint kinase 1	Homo sapiens	10-14
12370755-7	2002	These results suggest that alterations of chk1 signaling are associated with the response to topoisomerase I poison SN-38.	Irinotecan	116-121	checkpoint kinase 1	Homo sapiens	42-46
12384533-3	2002	Here we show that UCN-01 prevented IR-induced p53 up-regulation and p53 phosphorylation on serine 20, a site previously identified for Chk2 (or/and Chk1) kinase.	Serine	91-97	checkpoint kinase 1	Homo sapiens	148-152
11980637-0	2002	Ku affects the ataxia and Rad 3-related/CHK1-dependent S phase checkpoint response after camptothecin treatment.	Camptothecin	89-101	checkpoint kinase 1	Homo sapiens	40-44
12150968-6	2002	Elevated chk1 phosphorylation at Ser(345) following DNA damage induced by BNP1350 was accompanied by G(2) accumulation in the A253/BNPR cell line, while exposure to equimolar concentrations of BNP1350 (0.7 microM) induced S-phase arrest and no increased phosphorylation of chk1 at Ser(345) in the A253 cell line.	Serine	33-36	checkpoint kinase 1	Homo sapiens	9-13
12150968-6	2002	Elevated chk1 phosphorylation at Ser(345) following DNA damage induced by BNP1350 was accompanied by G(2) accumulation in the A253/BNPR cell line, while exposure to equimolar concentrations of BNP1350 (0.7 microM) induced S-phase arrest and no increased phosphorylation of chk1 at Ser(345) in the A253 cell line.	Serine	281-284	checkpoint kinase 1	Homo sapiens	9-13
12150968-10	2002	Chk1 antisense oligonucleotide can sensitize the A253/BNPR cells to killing by topo I inhibitor BNP1350, but no significant sensitization of BNP1350-induced growth inhibition was observed in the drug-sensitive cell line.	Oligonucleotides	15-30	checkpoint kinase 1	Homo sapiens	0-4
12429947-5	2002	Potentiation of PMA-mediated apoptosis was partially mimicked by caffeine suggesting the involvement of Chk1 in the potentiation of apoptosis.	Caffeine	65-73	checkpoint kinase 1	Homo sapiens	104-108
12071807-4	2002	UCN-01 (7-hydroxystaurosporine), a CHEK1 inhibitor that abrogates the G(2) block, has been reported to enhance radiation toxicity in human lymphoma and colon cancer cell lines.	7-hydroxystaurosporine	0-6	checkpoint kinase 1	Homo sapiens	35-40
12071807-4	2002	UCN-01 (7-hydroxystaurosporine), a CHEK1 inhibitor that abrogates the G(2) block, has been reported to enhance radiation toxicity in human lymphoma and colon cancer cell lines.	7-hydroxystaurosporine	8-30	checkpoint kinase 1	Homo sapiens	35-40
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	checkpoint kinase 1	Homo sapiens	47-51
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	checkpoint kinase 1	Homo sapiens	47-51
12181445-6	2002	The addition of the Chk1 kinase inhibitor 7-hydroxystaurosporine (UCN-01) to F-ara-A-arrested S-phase cells resulted in a rapid decrease in the fraction of cells with an S-phase DNA content and a corresponding increase in the fraction of apoptotic cells.	7-hydroxystaurosporine	42-64	checkpoint kinase 1	Homo sapiens	20-24
12181445-6	2002	The addition of the Chk1 kinase inhibitor 7-hydroxystaurosporine (UCN-01) to F-ara-A-arrested S-phase cells resulted in a rapid decrease in the fraction of cells with an S-phase DNA content and a corresponding increase in the fraction of apoptotic cells.	7-hydroxystaurosporine	66-72	checkpoint kinase 1	Homo sapiens	20-24
12181445-6	2002	The addition of the Chk1 kinase inhibitor 7-hydroxystaurosporine (UCN-01) to F-ara-A-arrested S-phase cells resulted in a rapid decrease in the fraction of cells with an S-phase DNA content and a corresponding increase in the fraction of apoptotic cells.	fludarabine	77-84	checkpoint kinase 1	Homo sapiens	20-24
12181445-7	2002	Under these conditions, the kinase activity of Chk1 was reduced, Cdc25A phosphatase activity was increased, the level of Tyr(15) phosphorylation of Cdk2 was reduced, and the kinase activity associated with immunoprecipitates of Cdk2 and cyclin A was reactivated.	Tyrosine	121-124	checkpoint kinase 1	Homo sapiens	47-51
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	checkpoint kinase 1	Homo sapiens	92-96
12171907-8	2002	Exposure of WSU-CLL cells to 4 and 5 nM CA4P was associated with overproduction of total p53 and no dramatic change in MDM2, 14-3-3sigma, GADD45, the cyclin-dependent kinase cdc2, its inhibitory phosphorylation, the cdc2-inhibitory kinase (wee1), chk1, or cdc25 hyperphosphorylation.	CA4P	40-44	checkpoint kinase 1	Homo sapiens	247-251
12171907-10	2002	Our findings suggest that CA4P induces mitotic catastrophe and arrest of WSU-CLL cells mostly in the M phase independent of p53 and independent of chk1 and cdc2 phosphorylation pathways.	CA4P	26-30	checkpoint kinase 1	Homo sapiens	147-151
11953432-7	2002	UCN-01 inhibits Chk1/2, which should activate the mitosis-inducing phosphatase Cdc25C, yet this phosphatase remained inactive during S phase progression induced by low concentrations of UCN-01, probably because Cdc25C is also inhibited by the constitutive kinase, C-TAK1.	7-hydroxystaurosporine	0-6	checkpoint kinase 1	Homo sapiens	16-22
11953432-8	2002	High concentrations of UCN-01 caused rapid activation of Cdc25C, which is attributed to inhibition of C-TAK1, as well as Chk1/2.	7-hydroxystaurosporine	23-29	checkpoint kinase 1	Homo sapiens	121-127
11980637-8	2002	Not only caffeine, the nonspecific inhibitor of ATR, or UCN-01, the nonspecific inhibitor of CHK1, but also the specific CHK1 antisense oligonucleotide abolished the stronger inhibition of DNA replication in CPT-treated Ku80-/- cells.	7-hydroxystaurosporine	56-62	checkpoint kinase 1	Homo sapiens	93-97
11980637-8	2002	Not only caffeine, the nonspecific inhibitor of ATR, or UCN-01, the nonspecific inhibitor of CHK1, but also the specific CHK1 antisense oligonucleotide abolished the stronger inhibition of DNA replication in CPT-treated Ku80-/- cells.	Oligonucleotides	136-151	checkpoint kinase 1	Homo sapiens	121-125
11912127-3	2002	The slow response of S-phase checkpoint, which is resistant to wortmannin, sensitive to caffeine and UCN-01, and related to cyclin-dependent kinase phosphorylation, is much stronger in CHK1 overexpressed cells, and it could be abolished by Chk1 antisense oligonucleotides.	Wortmannin	63-73	checkpoint kinase 1	Homo sapiens	185-189
11912127-3	2002	The slow response of S-phase checkpoint, which is resistant to wortmannin, sensitive to caffeine and UCN-01, and related to cyclin-dependent kinase phosphorylation, is much stronger in CHK1 overexpressed cells, and it could be abolished by Chk1 antisense oligonucleotides.	Wortmannin	63-73	checkpoint kinase 1	Homo sapiens	240-244
11912127-3	2002	The slow response of S-phase checkpoint, which is resistant to wortmannin, sensitive to caffeine and UCN-01, and related to cyclin-dependent kinase phosphorylation, is much stronger in CHK1 overexpressed cells, and it could be abolished by Chk1 antisense oligonucleotides.	Caffeine	88-96	checkpoint kinase 1	Homo sapiens	185-189
11912127-3	2002	The slow response of S-phase checkpoint, which is resistant to wortmannin, sensitive to caffeine and UCN-01, and related to cyclin-dependent kinase phosphorylation, is much stronger in CHK1 overexpressed cells, and it could be abolished by Chk1 antisense oligonucleotides.	Caffeine	88-96	checkpoint kinase 1	Homo sapiens	240-244
11912127-3	2002	The slow response of S-phase checkpoint, which is resistant to wortmannin, sensitive to caffeine and UCN-01, and related to cyclin-dependent kinase phosphorylation, is much stronger in CHK1 overexpressed cells, and it could be abolished by Chk1 antisense oligonucleotides.	Oligonucleotides	255-271	checkpoint kinase 1	Homo sapiens	185-189
11912127-3	2002	The slow response of S-phase checkpoint, which is resistant to wortmannin, sensitive to caffeine and UCN-01, and related to cyclin-dependent kinase phosphorylation, is much stronger in CHK1 overexpressed cells, and it could be abolished by Chk1 antisense oligonucleotides.	Oligonucleotides	255-271	checkpoint kinase 1	Homo sapiens	240-244
11553781-0	2001	Serine-345 is required for Rad3-dependent phosphorylation and function of checkpoint kinase Chk1 in fission yeast.	Serine	0-6	checkpoint kinase 1	Homo sapiens	92-96
11841447-7	2002	We found that the expression of the cell cycle checkpoint protein Chk1 was reduced in the etoposide-treated p53-transfected cells by 24 h, and this correlated with a reduction in the extent of etoposide-induced phosphorylation of CDK1 at tyrosine 15 (Y15).	Etoposide	90-99	checkpoint kinase 1	Homo sapiens	66-70
11841447-7	2002	We found that the expression of the cell cycle checkpoint protein Chk1 was reduced in the etoposide-treated p53-transfected cells by 24 h, and this correlated with a reduction in the extent of etoposide-induced phosphorylation of CDK1 at tyrosine 15 (Y15).	Etoposide	193-202	checkpoint kinase 1	Homo sapiens	66-70
11841447-7	2002	We found that the expression of the cell cycle checkpoint protein Chk1 was reduced in the etoposide-treated p53-transfected cells by 24 h, and this correlated with a reduction in the extent of etoposide-induced phosphorylation of CDK1 at tyrosine 15 (Y15).	Tyrosine	238-246	checkpoint kinase 1	Homo sapiens	66-70
11841447-8	2002	We conclude, therefore, that p53 overrides the strong G2 checkpoint response to etoposide in K562 cells, by directly or indirectly downregulating Chk1 expression, which, in turn, contributes to the proapoptotic effect of p53.	Etoposide	80-89	checkpoint kinase 1	Homo sapiens	146-150
11864911-4	2002	The checkpoint kinase Chk1 (but not Chk2) was phosphorylated after treatment with low doses of BPDE.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	95-99	checkpoint kinase 1	Homo sapiens	22-26
11864911-5	2002	High concentrations of BPDE elicited phosphorylation of both Chk1 and Chk2.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	23-27	checkpoint kinase 1	Homo sapiens	61-65
11864911-6	2002	Adenovirus-mediated expression of "dominant-negative" Chk1 (but not dominant-negative Chk2) and the Chk1 inhibitor UCN-01 abrogated the S-phase delay elicited by low doses of BPDE.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	175-179	checkpoint kinase 1	Homo sapiens	54-58
11864911-6	2002	Adenovirus-mediated expression of "dominant-negative" Chk1 (but not dominant-negative Chk2) and the Chk1 inhibitor UCN-01 abrogated the S-phase delay elicited by low doses of BPDE.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	175-179	checkpoint kinase 1	Homo sapiens	100-104
11864911-7	2002	Consistent with a role for the caffeine-sensitive ATM or ATR protein kinase in low-dose BPDE-induced S-phase arrest, both Chk1 phosphorylation and S-phase arrest were abrogated by caffeine.	Caffeine	31-39	checkpoint kinase 1	Homo sapiens	122-126
11864911-7	2002	Consistent with a role for the caffeine-sensitive ATM or ATR protein kinase in low-dose BPDE-induced S-phase arrest, both Chk1 phosphorylation and S-phase arrest were abrogated by caffeine.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	88-92	checkpoint kinase 1	Homo sapiens	122-126
11864911-7	2002	Consistent with a role for the caffeine-sensitive ATM or ATR protein kinase in low-dose BPDE-induced S-phase arrest, both Chk1 phosphorylation and S-phase arrest were abrogated by caffeine.	Caffeine	180-188	checkpoint kinase 1	Homo sapiens	122-126
11864911-8	2002	However, low doses of BPDE elicited Chk1 phosphorylation and S-phase arrest in AT cells (from ataxia telangiectasia patients), demonstrating that ATM is dispensable for S-phase checkpoint responses to this genotoxin.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	22-26	checkpoint kinase 1	Homo sapiens	36-40
11864911-9	2002	BPDE-induced Chk1 phosphorylation and S-phase arrest were abrogated by caffeine treatment in AT cells, suggesting that a caffeine-sensitive kinase other than ATM is an important mediator of responses to BPDE-adducted DNA.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	0-4	checkpoint kinase 1	Homo sapiens	13-17
11864911-9	2002	BPDE-induced Chk1 phosphorylation and S-phase arrest were abrogated by caffeine treatment in AT cells, suggesting that a caffeine-sensitive kinase other than ATM is an important mediator of responses to BPDE-adducted DNA.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	203-207	checkpoint kinase 1	Homo sapiens	13-17
11864911-10	2002	Overall, our data demonstrate the existence of a caffeine-sensitive, Chk1-mediated, S-phase checkpoint that is operational in response to BPDE.	Caffeine	49-57	checkpoint kinase 1	Homo sapiens	69-73
11864911-10	2002	Overall, our data demonstrate the existence of a caffeine-sensitive, Chk1-mediated, S-phase checkpoint that is operational in response to BPDE.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	138-142	checkpoint kinase 1	Homo sapiens	69-73
12191604-8	2002	Comparison of the ATP-binding site of CDK2 with that of other kinases reveals that in Chk1 kinase, a major target for UCN-01 in the cell, one of the surrounding residues, Ala144 in CDK2, is a serine in Chk1, thus providing a possible explanation for the effectiveness of UCN-01 against this kinase.	Adenosine Triphosphate	18-21	checkpoint kinase 1	Homo sapiens	86-90
12191604-8	2002	Comparison of the ATP-binding site of CDK2 with that of other kinases reveals that in Chk1 kinase, a major target for UCN-01 in the cell, one of the surrounding residues, Ala144 in CDK2, is a serine in Chk1, thus providing a possible explanation for the effectiveness of UCN-01 against this kinase.	Adenosine Triphosphate	18-21	checkpoint kinase 1	Homo sapiens	202-206
12191604-8	2002	Comparison of the ATP-binding site of CDK2 with that of other kinases reveals that in Chk1 kinase, a major target for UCN-01 in the cell, one of the surrounding residues, Ala144 in CDK2, is a serine in Chk1, thus providing a possible explanation for the effectiveness of UCN-01 against this kinase.	Serine	192-198	checkpoint kinase 1	Homo sapiens	86-90
12191604-8	2002	Comparison of the ATP-binding site of CDK2 with that of other kinases reveals that in Chk1 kinase, a major target for UCN-01 in the cell, one of the surrounding residues, Ala144 in CDK2, is a serine in Chk1, thus providing a possible explanation for the effectiveness of UCN-01 against this kinase.	Serine	192-198	checkpoint kinase 1	Homo sapiens	202-206
12191604-8	2002	Comparison of the ATP-binding site of CDK2 with that of other kinases reveals that in Chk1 kinase, a major target for UCN-01 in the cell, one of the surrounding residues, Ala144 in CDK2, is a serine in Chk1, thus providing a possible explanation for the effectiveness of UCN-01 against this kinase.	7-hydroxystaurosporine	118-124	checkpoint kinase 1	Homo sapiens	86-90
12191604-8	2002	Comparison of the ATP-binding site of CDK2 with that of other kinases reveals that in Chk1 kinase, a major target for UCN-01 in the cell, one of the surrounding residues, Ala144 in CDK2, is a serine in Chk1, thus providing a possible explanation for the effectiveness of UCN-01 against this kinase.	7-hydroxystaurosporine	118-124	checkpoint kinase 1	Homo sapiens	202-206
11553781-5	2001	Fission yeast and human Chk1 proteins share two conserved SQ motifs at serine-345 and serine-367.	Serine	71-77	checkpoint kinase 1	Homo sapiens	24-28
11553781-5	2001	Fission yeast and human Chk1 proteins share two conserved SQ motifs at serine-345 and serine-367.	Serine	86-92	checkpoint kinase 1	Homo sapiens	24-28
11553781-6	2001	Serine-345 of human Chk1 is phosphorylated in response to DNA damage.	Serine	0-6	checkpoint kinase 1	Homo sapiens	20-24
11553781-7	2001	Here we report that Rad3 and ATM phosphorylate serine-345 of fission yeast Chk1.	Serine	47-53	checkpoint kinase 1	Homo sapiens	75-79
11553781-8	2001	Mutation of serine-345 (chk1-S345A) abrogates Rad3-dependent phosphorylation of Chk1 in vivo.	Serine	12-18	checkpoint kinase 1	Homo sapiens	24-28
11553781-8	2001	Mutation of serine-345 (chk1-S345A) abrogates Rad3-dependent phosphorylation of Chk1 in vivo.	Serine	12-18	checkpoint kinase 1	Homo sapiens	80-84
11553781-11	2001	These findings attest to the importance of serine-345 phosphorylation for Chk1 function and strengthen evidence that transduction of the DNA damage checkpoint signal requires direct phosphorylation of Chk1 by Rad3.	Serine	43-49	checkpoint kinase 1	Homo sapiens	74-78
11553781-11	2001	These findings attest to the importance of serine-345 phosphorylation for Chk1 function and strengthen evidence that transduction of the DNA damage checkpoint signal requires direct phosphorylation of Chk1 by Rad3.	Serine	43-49	checkpoint kinase 1	Homo sapiens	201-205
11535615-3	2001	We show that both Chk1 and Chk2 are phosphorylated and activated in a caffeine-sensitive signaling pathway during S phase, but only in response to replication blocks, not during normal S phase progression.	Caffeine	70-78	checkpoint kinase 1	Homo sapiens	18-22
11152453-1	2001	The levels of the human checkpoint gene hCHK1 were measured in human cancer cells growing in vitro after treatment with the DNA damaging agent cis-dichlorodiammine platinum(II) (DDP).	Cisplatin	143-172	checkpoint kinase 1	Homo sapiens	40-45
11481475-4	2001	We show that caffeine"s ability to inhibit ATR (but not ATM) causes PCC, that ATR (but not ATM) prevents PCC, and that ATR prevents PCC via Chk-1 regulation.	Caffeine	13-21	checkpoint kinase 1	Homo sapiens	140-145
11390642-5	2001	Furthermore, phosphorylation of Chk1 on serines 317 and 345 in vivo was ATR dependent.	Serine	40-47	checkpoint kinase 1	Homo sapiens	32-36
11390642-6	2001	Mutants of Chk1 containing alanine in place of serines 317 and 345 were poorly activated in response to replication blocks or genotoxic stress in vivo, were poorly phosphorylated by ATR in vitro, and were not found in faster-eluting fractions by gel filtration.	Alanine	27-34	checkpoint kinase 1	Homo sapiens	11-15
11390642-7	2001	These findings demonstrate that the activation of Chk1 in response to replication blocks and certain forms of genotoxic stress involves phosphorylation of serines 317 and 345.	Serine	155-162	checkpoint kinase 1	Homo sapiens	50-54
11279124-7	2001	DBH inhibited the checkpoint kinases Chk1 (IC(50) = 3 micrometer) and Chk2 (IC(50) = 3.5 micrometer) but not ataxia-telangiectasia mutated (ATM), ATM-Rad3-related protein, or DNA-dependent protein kinase in vitro, indicating that it blocks two major branches of the checkpoint pathway downstream of ATM.	debromohymenialdisine	0-3	checkpoint kinase 1	Homo sapiens	37-41
11533665-3	2001	Here we show that this complex is required for phosphorylation and activation of the Rad53 and Chk1 checkpoint kinases specifically in response to DSBs.	dsbs	147-151	checkpoint kinase 1	Homo sapiens	95-99
11687952-4	2001	We report that blocking Chk1 expression by antisense or ribozymes in mammalian cells induces apoptosis and interferes with the G2/M arrest induced by adriamycin.	Doxorubicin	150-160	checkpoint kinase 1	Homo sapiens	24-28
11687952-5	2001	The Chk1 inhibitor UCN-01 also blocks the G2 arrest after DNA damage and renders cells more susceptible to adriamycin.	7-hydroxystaurosporine	19-25	checkpoint kinase 1	Homo sapiens	4-8
11687952-5	2001	The Chk1 inhibitor UCN-01 also blocks the G2 arrest after DNA damage and renders cells more susceptible to adriamycin.	Doxorubicin	107-117	checkpoint kinase 1	Homo sapiens	4-8
11488607-8	2001	Vanadate also increased p21 and Chk1 levels and reduced Cdc25C expression, leading to phosphorylation of Cdc2 and a slight increase in cyclin B1 expression as analyzed by Western blot.	Vanadates	0-8	checkpoint kinase 1	Homo sapiens	32-36
11488607-9	2001	Catalase, a specific antioxidant for H2O2, decreased vanadate-induced expression of p21 and Chk1, reduced phosphorylation of Cdc2Tyr15, and decreased cyclin B1 levels.	Vanadates	53-61	checkpoint kinase 1	Homo sapiens	92-96
11479224-0	2001	Abrogation of the Chk1-mediated G(2) checkpoint pathway potentiates temozolomide-induced toxicity in a p53-independent manner in human glioblastoma cells.	Temozolomide	68-80	checkpoint kinase 1	Homo sapiens	18-22
11479224-6	2001	U87MG glioma cells treated with TMZ underwent G(2)-M arrest associated with Chk1 activation and phosphorylation of both cdc25C and cdc2.	Temozolomide	32-35	checkpoint kinase 1	Homo sapiens	76-80
11479224-7	2001	These TMZ-induced effects were inhibited by the Chk1 kinase inhibitor UCN-01.	Temozolomide	6-9	checkpoint kinase 1	Homo sapiens	48-52
11479224-7	2001	These TMZ-induced effects were inhibited by the Chk1 kinase inhibitor UCN-01.	7-hydroxystaurosporine	70-76	checkpoint kinase 1	Homo sapiens	48-52
11479224-9	2001	In addition to enhancing TMZ-induced cytotoxicity in p53-proficient cells, UCN-01 also blocked TMZ-induced Chk1 activation and transient G(2)-M arrest in p53-deficient U87MG-E6 cells and similarly enhanced TMZ-induced mitotic catastrophe and cell death.	Temozolomide	95-98	checkpoint kinase 1	Homo sapiens	107-111
11479224-9	2001	In addition to enhancing TMZ-induced cytotoxicity in p53-proficient cells, UCN-01 also blocked TMZ-induced Chk1 activation and transient G(2)-M arrest in p53-deficient U87MG-E6 cells and similarly enhanced TMZ-induced mitotic catastrophe and cell death.	Temozolomide	95-98	checkpoint kinase 1	Homo sapiens	107-111
11152453-2	2001	Treatment of human cancer cell lines with DDP induced a decrease in the hCHK1 protein levels starting 6 h after treatment, with a further decline at 24 and 48 h. A similar decrease in the levels of hCHK1 was found at the mRNA level by using Northern blot analysis.	Cisplatin	42-45	checkpoint kinase 1	Homo sapiens	72-77
11152453-2	2001	Treatment of human cancer cell lines with DDP induced a decrease in the hCHK1 protein levels starting 6 h after treatment, with a further decline at 24 and 48 h. A similar decrease in the levels of hCHK1 was found at the mRNA level by using Northern blot analysis.	Cisplatin	42-45	checkpoint kinase 1	Homo sapiens	198-203
11158294-5	2001	We found that induction of p53 either by diverse stress signals or ectopically using a tetracycline-regulated promoter causes a marked reduction in CHK1 protein levels.	Tetracycline	87-99	checkpoint kinase 1	Homo sapiens	148-152
10761933-2	2000	The 1.7 A resolution crystal structures of the human Chk1 kinase domain and its binary complex with an ATP analog has revealed an identical open kinase conformation.	Adenosine Triphosphate	103-106	checkpoint kinase 1	Homo sapiens	53-57
10859164-5	2000	We show that in human cells, Chk1 is phosphorylated on serine 345 (S345) in response to UV, IR, and hydroxyurea (HU).	Serine	55-61	checkpoint kinase 1	Homo sapiens	29-33
10786669-0	2000	The radiosensitizing agent 7-hydroxystaurosporine (UCN-01) inhibits the DNA damage checkpoint kinase hChk1.	7-hydroxystaurosporine	27-49	checkpoint kinase 1	Homo sapiens	101-106
11027648-7	2000	Chk1 phosphorylates cdc25C on serine 216 and inactivates it whereas cdc25C dephosphorylates tyrosine 15 phosphate of cdc2 and activates the cdc2-cyclin B complex.	Serine	30-36	checkpoint kinase 1	Homo sapiens	0-4
10692484-0	2000	Characterization of protein kinase chk1 essential for the cell cycle checkpoint after exposure of human head and neck carcinoma A253 cells to a novel topoisomerase I inhibitor BNP1350.	cositecan	176-183	checkpoint kinase 1	Homo sapiens	35-39
10676638-0	2000	An indolocarbazole inhibitor of human checkpoint kinase (Chk1) abrogates cell cycle arrest caused by DNA damage.	Indolocarbazole	3-18	checkpoint kinase 1	Homo sapiens	57-61
10681541-5	2000	The checkpoint kinases, Chk1 and Cds1, are proposed to regulate the interactions between human Cdc25C and 14-3-3 proteins by phosphorylating Cdc25C on serine 216.	Serine	151-157	checkpoint kinase 1	Homo sapiens	24-28
10673501-8	2000	The human homolog of the second S. pombe checkpoint kinase, Cds1 (CHK2/hCds1), phosphorylates tetrameric p53 but not monomeric p53 in vitro at sites similar to those phosphorylated by hCHK1 kinase, suggesting that both checkpoint kinases can play roles in regulating p53 after DNA damage.	cds1	60-64	checkpoint kinase 1	Homo sapiens	184-189
10676638-8	2000	Chk1 phosphorylates the dual specificity phosphatase cdc25C on Ser-216, and this may be involved in preventing cdc25 from activating cdc2/cyclinB and initiating mitosis.	Serine	63-66	checkpoint kinase 1	Homo sapiens	0-4
10676638-9	2000	To further study the role of Chk1 in G2 checkpoint control, we identified a potent and selective indolocarbazole inhibitor (SB-218078) of Chk1 kinase activity and used this compound to assess cell cycle checkpoint responses.	Indolocarbazole	97-112	checkpoint kinase 1	Homo sapiens	29-33
10676638-9	2000	To further study the role of Chk1 in G2 checkpoint control, we identified a potent and selective indolocarbazole inhibitor (SB-218078) of Chk1 kinase activity and used this compound to assess cell cycle checkpoint responses.	Indolocarbazole	97-112	checkpoint kinase 1	Homo sapiens	138-142
10676638-9	2000	To further study the role of Chk1 in G2 checkpoint control, we identified a potent and selective indolocarbazole inhibitor (SB-218078) of Chk1 kinase activity and used this compound to assess cell cycle checkpoint responses.	SB 218078	124-133	checkpoint kinase 1	Homo sapiens	29-33
10676638-9	2000	To further study the role of Chk1 in G2 checkpoint control, we identified a potent and selective indolocarbazole inhibitor (SB-218078) of Chk1 kinase activity and used this compound to assess cell cycle checkpoint responses.	SB 218078	124-133	checkpoint kinase 1	Homo sapiens	138-142
9543386-5	1998	C-TAK1 is ubiquitously expressed in human tissues and cell lines and is distinct from the DNA damage checkpoint kinase Chk1, shown previously to phosphorylate Cdc25C on serine 216.	Serine	169-175	checkpoint kinase 1	Homo sapiens	119-123
10391675-6	1999	Taken together with the findings that phosphorylation of Cdc25C on serine 216 is increased at the S to M phase, it is suggested that at this particular phase of the cell cycle, even in the absence of DNA damage, hChk1 phosphorylates Cdc25C on serine 216, which is considered to be a prerequisite for the G2/M checkpoint.	Serine	67-73	checkpoint kinase 1	Homo sapiens	212-217
10391675-6	1999	Taken together with the findings that phosphorylation of Cdc25C on serine 216 is increased at the S to M phase, it is suggested that at this particular phase of the cell cycle, even in the absence of DNA damage, hChk1 phosphorylates Cdc25C on serine 216, which is considered to be a prerequisite for the G2/M checkpoint.	Serine	243-249	checkpoint kinase 1	Homo sapiens	212-217
10391675-7	1999	Thus, hChk1 may play an important role in keeping Cdc25C prepared for responding to DNA damage by phosphorylating its serine residue at 216 during the S to M phase.	Serine	118-124	checkpoint kinase 1	Homo sapiens	6-11
10485486-8	1999	Likewise, the catalytic activity of the G2 checkpoint kinase, hChk1, was only marginally suppressed by caffeine but was inhibited potently by the structurally distinct radiosensitizer, UCN-01.	Caffeine	103-111	checkpoint kinase 1	Homo sapiens	62-67
10435585-7	1999	Using mass spectrometry, we found that, similar to Chk1, Chk2 can phosphorylate serine 216 in Cdc25C, a site known to be involved in negative regulation of Cdc25C.	Serine	80-86	checkpoint kinase 1	Homo sapiens	51-55
33807122-5	2021	A western blot analysis demonstrated the use of trametinib alone and trametinib in combination with ribociclib to decrease the expression of pERK, cMyc, Chk1, pChk2, pCDK1, CyclinD1, and c-myc in a time-dependent manner in NCI-H727 and QGP-1 cells.	trametinib	48-58	checkpoint kinase 1	Homo sapiens	153-157
33591599-2	2021	Herein, we describe the design, synthesis, and biological evaluation of a novel series of potent diaminopyrimidine CHK1 inhibitors.	2,4-diaminopyrimidine	97-114	checkpoint kinase 1	Homo sapiens	115-119
33591599-6	2021	Moreover, treatment of MV-4-11 cells with compound 13 for 2 h led to robust inhibition of CHK1 autophosphorylation on serine 296.	Serine	118-124	checkpoint kinase 1	Homo sapiens	90-94
9278511-5	1997	Chk1 phosphorylates Cdc25C on serine-216.	Serine	30-36	checkpoint kinase 1	Homo sapiens	0-4
33819647-7	2021	Moreover, we observed high similarity of phosphosite characteristics (e.g. 94% shared class 1 identifications) and deduced kinase activities (e.g. ATM, ATR, CHEK1/2, PRKDC).	phosphosite	41-52	checkpoint kinase 1	Homo sapiens	157-164
33807122-5	2021	A western blot analysis demonstrated the use of trametinib alone and trametinib in combination with ribociclib to decrease the expression of pERK, cMyc, Chk1, pChk2, pCDK1, CyclinD1, and c-myc in a time-dependent manner in NCI-H727 and QGP-1 cells.	trametinib	69-79	checkpoint kinase 1	Homo sapiens	153-157
34668620-5	2022	Importantly, we identified an inverse correlation between p90 RSK activity and CHK1 levels within the solid tumor mass, with lower levels of CHK1 and higher activity of p90 RSK in the center of the tumor where low glucose concentrations are often observed.	Glucose	214-221	checkpoint kinase 1	Homo sapiens	79-83
34974185-0	2022	Proline-serine-threonine-repeat region of MDC1 mediates Chk1 phosphorylation and the DNA double-strand break repair.	Proline	0-7	checkpoint kinase 1	Homo sapiens	56-60
34974185-0	2022	Proline-serine-threonine-repeat region of MDC1 mediates Chk1 phosphorylation and the DNA double-strand break repair.	Serine	8-14	checkpoint kinase 1	Homo sapiens	56-60
34974185-0	2022	Proline-serine-threonine-repeat region of MDC1 mediates Chk1 phosphorylation and the DNA double-strand break repair.	Threonine	15-24	checkpoint kinase 1	Homo sapiens	56-60
34773074-5	2022	Investigating the mechanism of synthetic lethality, we reveal that CHK1 inhibition in IGF-1R depleted or inhibited cells further downregulated RRM2, reduced dNTP supply and profoundly delayed replication fork progression.	Parathion	157-161	checkpoint kinase 1	Homo sapiens	67-71
34420220-11	2022	Butyrate stimulated ROS production and hemeoxygenase-1 (HO-1) expression as well as activating the Ac-H3, p-ATM, p-ATR, p-Chk1, p-Chk2, p-p38, and p-Akt expression of endothelial cells.	Butyrates	0-8	checkpoint kinase 1	Homo sapiens	122-126
34829893-7	2021	Although NNKOAc-induced DNA damage activated ATM-Rad3-related (ATR) and Chk1 kinase in BEAS-2B cells, pre-exposure of the cells with tested antioxidants prior to carcinogen challenge significantly reduced their activation and levels of gamma-H2AX (p <= 0.05).	4-(acetoxymethylnitrosamino)-1-(3-pyridyl)-1-butanone	9-15	checkpoint kinase 1	Homo sapiens	72-76
34953860-5	2022	Upon treatment with chemotherapeutic drugs (e.g., adriamycin), RBM28 is translocated from the nucleolus to the nucleoplasm, which is likely mediated via phosphorylation of RBM28 at Ser122 by DNA checkpoint kinases 1 and 2 (Chk1/2), indicating that RBM28 may act as a nucleolar stress sensor in response to DNA damage stress.	Doxorubicin	50-60	checkpoint kinase 1	Homo sapiens	195-221
34953860-5	2022	Upon treatment with chemotherapeutic drugs (e.g., adriamycin), RBM28 is translocated from the nucleolus to the nucleoplasm, which is likely mediated via phosphorylation of RBM28 at Ser122 by DNA checkpoint kinases 1 and 2 (Chk1/2), indicating that RBM28 may act as a nucleolar stress sensor in response to DNA damage stress.	Doxorubicin	50-60	checkpoint kinase 1	Homo sapiens	223-229
34893686-5	2021	Topotecan treatment induced different patterns of the DNA response network in SCLC cells: DNA damage response (DDR) was more prominently activated in SLFN11-deficient SCLC cell line H82 than in SLFN11-plentiful SCLC cell line DMS273, whereas topotecan induced significant accumulation of p-Chk1, p-RPA2 and Rad51 in H82 cells, but not in DMS273 cells.	Topotecan	0-9	checkpoint kinase 1	Homo sapiens	290-294
34893686-5	2021	Topotecan treatment induced different patterns of the DNA response network in SCLC cells: DNA damage response (DDR) was more prominently activated in SLFN11-deficient SCLC cell line H82 than in SLFN11-plentiful SCLC cell line DMS273, whereas topotecan induced significant accumulation of p-Chk1, p-RPA2 and Rad51 in H82 cells, but not in DMS273 cells.	Topotecan	242-251	checkpoint kinase 1	Homo sapiens	290-294
34782371-0	2022	Chk1 inhibition potently blocks STAT3 tyrosine705 phosphorylation, DNA binding activity, and activation of downstream targets in human multiple myeloma cells.	tyrosine705	38-49	checkpoint kinase 1	Homo sapiens	0-4
34908224-8	2022	Moreover, acrolein induced G0/G1phase arrest, promoted the expression of gamma-H2AX, activated the DDR signaling pathway (Ataxia-Telangiectasia-Mutated (ATM) and Rad-3-related/Chk1 and ATM/Chk2), and triggered the consequent cell cycle checkpoints.	Acrolein	10-18	checkpoint kinase 1	Homo sapiens	176-180
34886743-4	2022	These changes are likely driven by DNA strand breaks induced by 2-FaraA that activate protein kinases such as ATM, ATR and Chk1.	fludarabine	64-71	checkpoint kinase 1	Homo sapiens	123-127
34857765-0	2021	The cytosolic iron-sulfur cluster assembly (CIA) pathway is required for replication stress tolerance of cancer cells to Chk1 and ATR inhibitors.	ferrous sulfide	14-25	checkpoint kinase 1	Homo sapiens	121-125
34852220-3	2021	CHK1 inhibition also activates ERK and AMPK and increases autophagy, providing a mechanistic basis for increased efficacy of concurrent CHK1 and ERK inhibition and/or autophagy inhibition with chloroquine.	Chloroquine	193-204	checkpoint kinase 1	Homo sapiens	0-4
34807483-6	2022	Consistently, the MEK1/2 inhibitor, Trametinib, potentiated CHK1 inhibitor-mediated cell death in these cells.	trametinib	36-46	checkpoint kinase 1	Homo sapiens	60-64
34354944-6	2021	Enhancing CDK1/2 activity through the Wee1 inhibitor adavosertib or a combination of Wee1 and Chk1 inhibition resulted in an abrogation of the radiation-induced G2 cell cycle arrest and induction of replication stress as assessed by gammaH2AX and chromatin-bound RPA levels in S phase cells.	gammah2ax	233-242	checkpoint kinase 1	Homo sapiens	94-98
34719665-9	2021	Additionally, low expression of MCM2, EZH2, CENPK, and CHEK1 was correlated with increased sensitivity to cisplatin, but not etoposide.	Cisplatin	106-115	checkpoint kinase 1	Homo sapiens	55-60
34328261-6	2021	At physiologically relevant concentrations, acetaldehyde activated the ATR-Chk1 pathway, leading to S- and G2/M-phase delay with accumulation of the FA complementation group D2 protein (FANCD2) at the sites of DNA synthesis, suggesting that acetaldehyde impedes replication fork progression.	Acetaldehyde	44-56	checkpoint kinase 1	Homo sapiens	75-79
34328261-6	2021	At physiologically relevant concentrations, acetaldehyde activated the ATR-Chk1 pathway, leading to S- and G2/M-phase delay with accumulation of the FA complementation group D2 protein (FANCD2) at the sites of DNA synthesis, suggesting that acetaldehyde impedes replication fork progression.	Acetaldehyde	241-253	checkpoint kinase 1	Homo sapiens	75-79
34665631-0	2021	Discovery and Development of a Potent, Selective, and Orally Bioavailable CHK1 Inhibitor Candidate: 5-((4-((3-Amino-3-methylbutyl)amino)-5-(trifluoromethyl)pyrimidin-2-yl)amino)picolinonitrile.	5-((4-((3-amino-3-methylbutyl)amino)-5-(trifluoromethyl)pyrimidin-2-yl)amino)picolinonitrile	100-192	checkpoint kinase 1	Homo sapiens	74-78
34665631-2	2021	In this study, we used a strategy for trifluoromethyl substitution to obtain orally bioavailable CHK1 inhibitors to overcome the limitations of lead compound 1, which can only be administered intravenously.	lead compound	144-157	checkpoint kinase 1	Homo sapiens	97-101
34768325-16	2021	An analysis of CHK1, CHK2, and p-CHK2 expression suggested that the DNA damage checkpoint system seems also to be activated by RTA404 treatment in established U87MG cells.	rta404	127-133	checkpoint kinase 1	Homo sapiens	15-19
34314706-0	2021	One therapeutic approach for triple-negative breast cancer: Checkpoint kinase 1 inhibitor AZD7762 combination with neoadjuvant carboplatin.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	90-97	checkpoint kinase 1	Homo sapiens	60-79
34314706-3	2021	Here, we interestingly found that the combination treatment of carboplatin with the Chk1 inhibitor AZD7762 synergistically inhibits TNBC cell growth in multiple TNBC cell lines in vitro.	Carboplatin	63-74	checkpoint kinase 1	Homo sapiens	84-88
34314706-3	2021	Here, we interestingly found that the combination treatment of carboplatin with the Chk1 inhibitor AZD7762 synergistically inhibits TNBC cell growth in multiple TNBC cell lines in vitro.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	99-106	checkpoint kinase 1	Homo sapiens	84-88
34314706-4	2021	Mechanistically, we proved that prolonged carboplatin-treated induce cell mitotic arrest, and cells would fail to initiate the G2-M transition following the inhibition of the Chk1 pathway, leading to accumulation of DNA lesions.	Carboplatin	42-53	checkpoint kinase 1	Homo sapiens	175-179
34314706-6	2021	Thus, our findings not only propose Chk1 as a therapeutic target for combination therapy with DNA-damaging agents such as carboplatin in TNBC, but also highlight that the induction of mitotic catastrophe could be considered as an alternative strategy for TNBC therapy.	Carboplatin	122-133	checkpoint kinase 1	Homo sapiens	36-40
34144191-2	2021	When cells are exposed to exogenously added H2O2, ATR/CHK1 and ATM/CHK2 dependent DNA damage signaling is switched on, suggesting that H2O2 induces both single and double strand breaks.	Hydrogen Peroxide	44-48	checkpoint kinase 1	Homo sapiens	54-58
34144191-2	2021	When cells are exposed to exogenously added H2O2, ATR/CHK1 and ATM/CHK2 dependent DNA damage signaling is switched on, suggesting that H2O2 induces both single and double strand breaks.	Hydrogen Peroxide	135-139	checkpoint kinase 1	Homo sapiens	54-58
34360546-8	2021	Finally, we showed that inhibition of CHK1 phosphorylation further sensitized cancer cells to mitomycin C.	Mitomycin	94-105	checkpoint kinase 1	Homo sapiens	38-42
34841679-8	2021	Among them, miltefosine transcriptionally inhibited checkpoint kinase 1 (CHEK1), indicating that LR integrity is essential for CHEK1 expression regulation.	miltefosine	12-23	checkpoint kinase 1	Homo sapiens	52-71
34841679-8	2021	Among them, miltefosine transcriptionally inhibited checkpoint kinase 1 (CHEK1), indicating that LR integrity is essential for CHEK1 expression regulation.	miltefosine	12-23	checkpoint kinase 1	Homo sapiens	73-78
34841679-8	2021	Among them, miltefosine transcriptionally inhibited checkpoint kinase 1 (CHEK1), indicating that LR integrity is essential for CHEK1 expression regulation.	miltefosine	12-23	checkpoint kinase 1	Homo sapiens	127-132
34841679-8	2021	Among them, miltefosine transcriptionally inhibited checkpoint kinase 1 (CHEK1), indicating that LR integrity is essential for CHEK1 expression regulation.	Lawrencium	97-99	checkpoint kinase 1	Homo sapiens	52-71
34841679-8	2021	Among them, miltefosine transcriptionally inhibited checkpoint kinase 1 (CHEK1), indicating that LR integrity is essential for CHEK1 expression regulation.	Lawrencium	97-99	checkpoint kinase 1	Homo sapiens	73-78
34841679-8	2021	Among them, miltefosine transcriptionally inhibited checkpoint kinase 1 (CHEK1), indicating that LR integrity is essential for CHEK1 expression regulation.	Lawrencium	97-99	checkpoint kinase 1	Homo sapiens	127-132
34841679-10	2021	However, inhibition of the LR/CHEK1 axis by miltefosine released cell cycle checkpoints, forcing CSCs to enter inappropriate mitosis with accumulated DNA damage and resulting in catastrophic cell death.	miltefosine	44-55	checkpoint kinase 1	Homo sapiens	30-35
34841679-11	2021	CONCLUSION: Our findings underscore the therapeutic potential of LR-targeting APLs for CRC treatment that overcomes the therapy-resistant phenotype of CSCs, highlighting the importance of the LR/CHEK1 axis as a novel mechanism of APLs.	Lawrencium	65-67	checkpoint kinase 1	Homo sapiens	195-200
34571251-12	2021	Overall, SMG induced ROS, DNA damage and differential expression of DNA repair genes, and altered the overall DNA repair capacity which may activate ATM/ATR-Chk1/2 and Ku70/80 and DNA-PK-mediated apoptotic cell death.	N-SUCCINYL METHIONINE	9-12	checkpoint kinase 1	Homo sapiens	157-163
34596822-6	2022	Interaction with the Chk1/2 inhibitor AZD7762 confirm the differential effects of fascplysin and cisplatin.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	38-45	checkpoint kinase 1	Homo sapiens	21-27
34596822-6	2022	Interaction with the Chk1/2 inhibitor AZD7762 confirm the differential effects of fascplysin and cisplatin.	fascplysin	82-92	checkpoint kinase 1	Homo sapiens	21-27
34508175-6	2021	Suboptimal doses of the CHK1 inhibitor MK-8776 plus the PARP inhibitor olaparib led to a MYCN-dependent accumulation of DNA damage and cell death in vitro and significantly reduced the growth of four in vivo models of MYCN-driven tumors, without major toxicities.	MK-8776	39-46	checkpoint kinase 1	Homo sapiens	24-28
34572942-5	2021	Overexpression of the RAD50Q672X and RAD50L1264F missense mutation also sensitized cell death upon replication stress stimuli induced by formaldehyde treatment and the CHK1 inhibitor, AZD7762.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	184-191	checkpoint kinase 1	Homo sapiens	168-172
34519926-0	2021	Exploring the ATR-CHK1 pathway in the response of doxorubicin-induced DNA damages in acute lymphoblastic leukemia cells.	Doxorubicin	50-61	checkpoint kinase 1	Homo sapiens	18-22
34519926-4	2021	We evaluated the efficacy of a new drug schedule combining Dox and specific ATR (VE-821) or CHK1 (prexasertib, PX) inhibitors in the treatment of human B-/T cell precursor ALL cell lines and primary ALL leukemic cells.	prexasertib	98-109	checkpoint kinase 1	Homo sapiens	92-96
34519926-9	2021	In conclusion, we found that the ATR-CHK1 pathway is involved in the response to Dox-induced DNA damages and we demonstrated that our new in vitro drug schedule that combines Dox followed by ATR/CHK1 inhibitors can increase Dox cytotoxicity against ALL cells, while using lower drug doses.	Doxorubicin	81-84	checkpoint kinase 1	Homo sapiens	37-41
34519926-9	2021	In conclusion, we found that the ATR-CHK1 pathway is involved in the response to Dox-induced DNA damages and we demonstrated that our new in vitro drug schedule that combines Dox followed by ATR/CHK1 inhibitors can increase Dox cytotoxicity against ALL cells, while using lower drug doses.	Doxorubicin	81-84	checkpoint kinase 1	Homo sapiens	195-199
34519926-9	2021	In conclusion, we found that the ATR-CHK1 pathway is involved in the response to Dox-induced DNA damages and we demonstrated that our new in vitro drug schedule that combines Dox followed by ATR/CHK1 inhibitors can increase Dox cytotoxicity against ALL cells, while using lower drug doses.	Doxorubicin	175-178	checkpoint kinase 1	Homo sapiens	37-41
34519926-9	2021	In conclusion, we found that the ATR-CHK1 pathway is involved in the response to Dox-induced DNA damages and we demonstrated that our new in vitro drug schedule that combines Dox followed by ATR/CHK1 inhibitors can increase Dox cytotoxicity against ALL cells, while using lower drug doses.	Doxorubicin	224-227	checkpoint kinase 1	Homo sapiens	37-41
34519926-9	2021	In conclusion, we found that the ATR-CHK1 pathway is involved in the response to Dox-induced DNA damages and we demonstrated that our new in vitro drug schedule that combines Dox followed by ATR/CHK1 inhibitors can increase Dox cytotoxicity against ALL cells, while using lower drug doses.	Doxorubicin	224-227	checkpoint kinase 1	Homo sapiens	195-199
34519926-11	2021	ALL cells respond to doxorubicin-induced DNA damages by activating the ATR-CHK1 pathway.	Doxorubicin	21-32	checkpoint kinase 1	Homo sapiens	75-79
34519926-12	2021	The inhibition of the ATR-CHK1 pathway synergizes with doxorubicin in the induction of cytotoxicity in ALL cells.	Doxorubicin	55-66	checkpoint kinase 1	Homo sapiens	26-30
34519926-13	2021	The inhibition of ATR-CHK1 pathway induces aberrant chromosome segregation and mitotic spindle defects in doxorubicin-pretreated ALL cells.	Doxorubicin	106-117	checkpoint kinase 1	Homo sapiens	22-26
34388376-5	2021	Importantly, osimertinib resistance caused by epithelial-mesenchymal transition (EMT) activates the ATR-CHK1-Aurora B signaling cascade and thereby engenders hypersensitivity to respective kinase inhibitors by activating BIM-mediated mitotic catastrophe.	osimertinib	13-24	checkpoint kinase 1	Homo sapiens	104-108
34474677-11	2021	Moreover, we further demonstrated that CXCL2-mediated resistance to cisplatin could be saved by SB225002, the inhibitor of CXCL2 receptor, as well as be rescued by SAR-020106, the inhibitor of ATR/CHK1 signaling pathway.	Cisplatin	68-77	checkpoint kinase 1	Homo sapiens	197-201
34131002-0	2021	Phase 1 Combination Study of the CHK1 inhibitor prexasertib, and the PARP inhibitor olaparib, in high-grade serous ovarian cancer and other solid tumors.	prexasertib	48-59	checkpoint kinase 1	Homo sapiens	33-37
34131002-2	2021	In BRCA-deficient cancers with de novo or acquired PARP inhibitor resistance, the addition of the CHK1 inhibitor prexasertib to the PARP inhibitor olaparib compromises replication fork stability, as well as HR proficiency, allowing for sensitization to PARP inhibition.	prexasertib	113-124	checkpoint kinase 1	Homo sapiens	98-102
34131002-2	2021	In BRCA-deficient cancers with de novo or acquired PARP inhibitor resistance, the addition of the CHK1 inhibitor prexasertib to the PARP inhibitor olaparib compromises replication fork stability, as well as HR proficiency, allowing for sensitization to PARP inhibition.	olaparib	147-155	checkpoint kinase 1	Homo sapiens	98-102
34559360-1	2021	BACKGROUND: The checkpoint kinase 1 (CHK1) inhibitor prexasertib exhibited modest monotherapy antitumor activity in prior trials, suggesting that combination with chemotherapy or other targeted agents may be needed to maximize efficacy.	prexasertib	53-64	checkpoint kinase 1	Homo sapiens	16-35
34559360-1	2021	BACKGROUND: The checkpoint kinase 1 (CHK1) inhibitor prexasertib exhibited modest monotherapy antitumor activity in prior trials, suggesting that combination with chemotherapy or other targeted agents may be needed to maximize efficacy.	prexasertib	53-64	checkpoint kinase 1	Homo sapiens	37-41
34081985-3	2021	In this study, AZD7762 (Chk1/2 inhibitor) and SB218078 (Chk1 inhibitor) were used to uncover the joint roles of Chk1/2 and differentiate the importance of Chk1 and Chk2 during oocyte meiotic maturation.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	15-22	checkpoint kinase 1	Homo sapiens	24-30
34081985-3	2021	In this study, AZD7762 (Chk1/2 inhibitor) and SB218078 (Chk1 inhibitor) were used to uncover the joint roles of Chk1/2 and differentiate the importance of Chk1 and Chk2 during oocyte meiotic maturation.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	15-22	checkpoint kinase 1	Homo sapiens	112-118
34081985-3	2021	In this study, AZD7762 (Chk1/2 inhibitor) and SB218078 (Chk1 inhibitor) were used to uncover the joint roles of Chk1/2 and differentiate the importance of Chk1 and Chk2 during oocyte meiotic maturation.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	15-22	checkpoint kinase 1	Homo sapiens	155-159
34081985-3	2021	In this study, AZD7762 (Chk1/2 inhibitor) and SB218078 (Chk1 inhibitor) were used to uncover the joint roles of Chk1/2 and differentiate the importance of Chk1 and Chk2 during oocyte meiotic maturation.	SB 218078	46-54	checkpoint kinase 1	Homo sapiens	56-60
34081985-3	2021	In this study, AZD7762 (Chk1/2 inhibitor) and SB218078 (Chk1 inhibitor) were used to uncover the joint roles of Chk1/2 and differentiate the importance of Chk1 and Chk2 during oocyte meiotic maturation.	SB 218078	46-54	checkpoint kinase 1	Homo sapiens	112-118
34081985-3	2021	In this study, AZD7762 (Chk1/2 inhibitor) and SB218078 (Chk1 inhibitor) were used to uncover the joint roles of Chk1/2 and differentiate the importance of Chk1 and Chk2 during oocyte meiotic maturation.	SB 218078	46-54	checkpoint kinase 1	Homo sapiens	155-159
34376212-9	2021	RESULTS: Bufalin upregulated the expression of cytochrome C, cleaved caspase 3, p-Chk1 and p-p53 proteins to induce U251 cell apoptosis and cycle arrest in the S phase.	bufalin	9-16	checkpoint kinase 1	Homo sapiens	82-86
34423276-6	2021	LY2606368, the most selective of these CHK1i, was used in the current study.	prexasertib	0-9	checkpoint kinase 1	Homo sapiens	39-44
34226205-10	2022	Importantly, pharmacological inhibition of CHK1/2 using LY2606368 attenuated fibrosis and pulmonary vascular remodelling leading to improvement in respiratory mechanics and haemodynamic parameters in two animal models mimicking IPF and IPF+PH.	prexasertib	56-65	checkpoint kinase 1	Homo sapiens	43-49
34372559-8	2021	The role of Chk1, a protein kinase known to be involved in the replication stress-induced DDR, was examined by inhibition with the small molecule LY2603618 and by siRNA-mediated knockdown.	LY2603618	146-155	checkpoint kinase 1	Homo sapiens	12-16
34158506-1	2021	Atr is a serine/threonine kinase, known to sense single-stranded DNA breaks and activate the DNA damage checkpoint by phosphorylating Chek1, which inhibits Cdc25, causing cell cycle arrest.	Serine	9-15	checkpoint kinase 1	Homo sapiens	134-139
34206543-9	2021	KPT-8602 with or without olaparib was shown to reduce homologous recombination-regulated DNA damage response targets including BRCA1, BRCA2, CHEK1, EXO1, BLM, RAD51, LIG1, XRCC3 and RMI2.	olaparib	25-33	checkpoint kinase 1	Homo sapiens	141-146
34079223-12	2021	Docking results revealed that among the selected oncotargets, Chk1, CD73, Nrf2, PCAF and AT tip60 were more vulnerable to wedelolactone than their respective standard inhibitors.	wedelolactone	122-135	checkpoint kinase 1	Homo sapiens	62-66
34169240-0	2021	CHK1 inhibitor sensitizes resistant colorectal cancer stem cells to nortopsentin.	nortopsentin	68-80	checkpoint kinase 1	Homo sapiens	0-4
34169240-4	2021	In CR-CSphC-based organoids, NORA234 causes a genotoxic stress paralleled by G2-M cell cycle arrest and activation of CHK1, driving the DNA damage repair of CR-CSphCs, regardless of the mutational background, microsatellite stability, and consensus molecular subtype.	nora234	29-36	checkpoint kinase 1	Homo sapiens	118-122
34169240-5	2021	Synergistic combination of NORA234 and CHK1 (rabusertib) targeting is synthetic lethal inducing death of both CD44v6-negative and CD44v6-positive CRC stem cell fractions, aside from Wnt pathway activity.	LY2603618	45-55	checkpoint kinase 1	Homo sapiens	39-43
35526484-4	2022	Indeed, PARP and CHK1 inhibition by AZD2461 and UCN-01, by downregulating c-Myc, reduced the expression of XBP1s, constitutively expressed in these cells, and upregulated CHOP.	AZD2461	36-43	checkpoint kinase 1	Homo sapiens	17-21
34073837-13	2021	Further, inhibition of chk1 or homologous recombination enhanced dianhydrogalactiol-induced cytotoxicity in the cells.	dianhydrogalactiol	65-83	checkpoint kinase 1	Homo sapiens	23-27
35000525-4	2022	Then, pancreatic Capan-1 cells were repeatedly treated with the PARP1 inhibitor olaparib, the Chk1 inhibitor rabusertib or their combination for 211-214 days, during which the changes in drug sensitivity were monitored at a 35-day interval.	LY2603618	109-119	checkpoint kinase 1	Homo sapiens	94-98
35000525-11	2022	Our findings indicate that repeated treatments with the rabusertib/olaparib combination result in increased drug resistance and a more aggressive cell phenotype than those with either single agent, providing new clues for future clinical anticancer tests of PARP1 and Chk1 inhibitor combinations.	LY2603618	56-66	checkpoint kinase 1	Homo sapiens	268-272
35000525-11	2022	Our findings indicate that repeated treatments with the rabusertib/olaparib combination result in increased drug resistance and a more aggressive cell phenotype than those with either single agent, providing new clues for future clinical anticancer tests of PARP1 and Chk1 inhibitor combinations.	olaparib	67-75	checkpoint kinase 1	Homo sapiens	268-272
34134962-11	2021	The nanoparticles significantly increased the intracellular expression level of miR-16 (P < 0.001) and decreased the expression of Bcl-2 and Chk-1 proteins in ovarian cancer cells, thus enabling miR-16 to promote apoptosis and enhance cisplatin sensitivity of the cells.	Cisplatin	235-244	checkpoint kinase 1	Homo sapiens	141-146
35443722-0	2022	Artesunate improves venetoclax plus cytarabine AML cell targeting by regulating the Noxa/Bim/Mcl-1/p-Chk1 axis.	Artesunate	0-10	checkpoint kinase 1	Homo sapiens	101-105
35348291-0	2022	Circ_0011292 knockdown mitigates progression and drug resistance in PTX-resistant non-small-cell lung cancer cells by regulating miR-433-3p/CHEK1 axis.	Paclitaxel	68-71	checkpoint kinase 1	Homo sapiens	140-145
35348291-11	2022	Dual-luciferase reporter assay was carried out to verify the targeted interaction between miR-433-3p and circ_0011292 or CHEK1.	mir-433-3p	90-100	checkpoint kinase 1	Homo sapiens	121-126
35348291-14	2022	Circ_0011292 or CHEK1 knockdown enhanced PTX sensitivity and cell apoptosis, and repressed cell proliferation, migration, and invasion in PTX-resistant NSCLC cells.	Paclitaxel	41-44	checkpoint kinase 1	Homo sapiens	16-21
35348291-14	2022	Circ_0011292 or CHEK1 knockdown enhanced PTX sensitivity and cell apoptosis, and repressed cell proliferation, migration, and invasion in PTX-resistant NSCLC cells.	Paclitaxel	138-141	checkpoint kinase 1	Homo sapiens	16-21
35348291-16	2022	Meanwhile, silencing miR-433-3p or overexpressing CHEK1 respectively abrogated the impacts of circ_0011292 deletion or miR-433-3p introduction on PTX resistance and cell progression in PTX-resistant NSCLC cells in vitro.	Paclitaxel	146-149	checkpoint kinase 1	Homo sapiens	50-55
35348291-16	2022	Meanwhile, silencing miR-433-3p or overexpressing CHEK1 respectively abrogated the impacts of circ_0011292 deletion or miR-433-3p introduction on PTX resistance and cell progression in PTX-resistant NSCLC cells in vitro.	Paclitaxel	185-188	checkpoint kinase 1	Homo sapiens	50-55
35348291-19	2022	CONCLUSION: Circ_0011292 could accelerate PTX resistance and cell malignant progression of NSCLC cells partially through the regulation of circ_0011292/miR-433-3p/CHEK1 axis.	Paclitaxel	42-45	checkpoint kinase 1	Homo sapiens	163-168
35436464-6	2022	Furthermore, mutated LCL displayed lower levels of phospho-Chk1 and phospho-Chk2 following hydrogen peroxide-induced oxidative stress, indicating a poorly effective DNA damage checkpoint, as well as reduced basal levels of p53.	Hydrogen Peroxide	91-108	checkpoint kinase 1	Homo sapiens	59-63
35430566-5	2022	CHK1 and CHK2 phosphorylation was assessed by western blot and the effects of inhibiting CHK1/CHK2 by AZD7762 were examined.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	102-109	checkpoint kinase 1	Homo sapiens	89-93
35430566-8	2022	SLFN12 over-expression decreased CHK1 and CHK2 phosphorylation after treatment with the DNA damaging agent camptothecin (CPT).	Camptothecin	107-119	checkpoint kinase 1	Homo sapiens	33-37
35430566-8	2022	SLFN12 over-expression decreased CHK1 and CHK2 phosphorylation after treatment with the DNA damaging agent camptothecin (CPT).	Camptothecin	121-124	checkpoint kinase 1	Homo sapiens	33-37
35430566-9	2022	The CHK1/CHK2 inhibitor diminished the significant cytotoxicity difference between over-expression and baseline SLFN12 levels in response to carboplatin.	Carboplatin	141-152	checkpoint kinase 1	Homo sapiens	4-8
35631350-9	2022	Furthermore, HMN-214 induces apoptosis and significantly obstructs the cell cycle at the G2/M phase in NB cells by inhibiting multiple cell-cycle-related genes, such as PLK1, WEE1, CDK1, CDK2, Cyclin B1, CHK1, and CHK2.	(E)-4-(2-(2-(N-acetyl-N-(4-methoxybenzenesulfonyl)amino)stilbazole)) 1-oxide	13-20	checkpoint kinase 1	Homo sapiens	204-208
35443722-10	2022	We provide a new triple combination for AML treatment by targeting the Noxa/Mcl-1/Bim axis to reverse Mcl-1/p-Chk1 resistance of cytarabine therapy.	Cytarabine	129-139	checkpoint kinase 1	Homo sapiens	110-114
35443736-8	2022	Lastly, combined inhibition of SIK1 and CHEK1with small molecule inhibitors, YKL-05-099 and prexasertib, respectively, showed enhanced cytotoxicity in DSRCT cells compared to inhibition of either kinases alone.	prexasertib	92-103	checkpoint kinase 1	Homo sapiens	40-45
35428780-0	2022	Suppressive effects of umbilical cord mesenchymal stem cell-derived exosomal miR-15a-5p on the progression of cholangiocarcinoma by inhibiting CHEK1 expression.	mir-15a-5p	77-87	checkpoint kinase 1	Homo sapiens	143-148
35428780-8	2022	miR-15a-5p targeted CHEK1 and downregulated the expression of CHEK1.	mir-15a-5p	0-10	checkpoint kinase 1	Homo sapiens	20-25
35428780-8	2022	miR-15a-5p targeted CHEK1 and downregulated the expression of CHEK1.	mir-15a-5p	0-10	checkpoint kinase 1	Homo sapiens	62-67
35428780-11	2022	Overexpression of miR-15a-5p promoted apoptosis but suppressed malignancy and tumorigenicity of CCA cells as well as EMT through downregulating CHEK1.	mir-15a-5p	18-28	checkpoint kinase 1	Homo sapiens	144-149
35428780-12	2022	Our data suggested that miR-15a-5p in HUCMSCs-exo suppresses EMT and metastasis of CCA through targeting downregulation of CHEK1.	mir-15a-5p	24-34	checkpoint kinase 1	Homo sapiens	123-128
35418303-0	2022	Clinically relevant CHK1 inhibitors abrogate wild-type and Y537S mutant ERalpha expression and proliferation in luminal primary and metastatic breast cancer cells.	Phenobarbital	112-119	checkpoint kinase 1	Homo sapiens	20-24
35418303-4	2022	Robust-Z-score calculation identified AZD7762 (CHK1/CHK2 inhibitor) as a positive hit.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	38-45	checkpoint kinase 1	Homo sapiens	47-51
35418303-8	2022	Accordingly, CHK1 and ERalpha activations are correlated in ERalpha-positive BC cell lines, and the ATR:CHK1 pathway controls ERalpha stability and cell proliferation in luminal A BC cells.	Phenobarbital	170-177	checkpoint kinase 1	Homo sapiens	104-108
35418303-10	2022	Furthermore, CHK1 inhibition interferes with E2:ERalpha signaling to cell proliferation, and drugs approved for clinical treatment of primary and MBC (4OH-tamoxifen and the CDK4/CDK6 inhibitors abemaciclib and palbociclib) exert synergic effects with the CHK1 inhibitors in clinical trials for the treatment of solid tumors (AZD7762, MK8776, prexasertib) in preventing the proliferation of cells modeling primary and MBC.	Estetrol	151-154	checkpoint kinase 1	Homo sapiens	13-17
35443722-0	2022	Artesunate improves venetoclax plus cytarabine AML cell targeting by regulating the Noxa/Bim/Mcl-1/p-Chk1 axis.	Cytarabine	36-46	checkpoint kinase 1	Homo sapiens	101-105
35443722-3	2022	Cytarabine induces S phase arrest-mediated DNA damage with activation of DNA replication checkpoint kinase 1 (Chk1) through phosphorylation, while venetoclax induces B cell lymphoma 2 (Bcl-2)-interacting mediator of cell death (Bim)-mediated apoptotic DNA damage.	Cytarabine	0-10	checkpoint kinase 1	Homo sapiens	89-108
35443722-3	2022	Cytarabine induces S phase arrest-mediated DNA damage with activation of DNA replication checkpoint kinase 1 (Chk1) through phosphorylation, while venetoclax induces B cell lymphoma 2 (Bcl-2)-interacting mediator of cell death (Bim)-mediated apoptotic DNA damage.	Cytarabine	0-10	checkpoint kinase 1	Homo sapiens	110-114
35443722-7	2022	Silencing Mcl-1 or adding venetoclax/artesunate diminishes the cytarabine resistance pathway p-Chk1.	venetoclax	26-36	checkpoint kinase 1	Homo sapiens	95-99
35443722-7	2022	Silencing Mcl-1 or adding venetoclax/artesunate diminishes the cytarabine resistance pathway p-Chk1.	Artesunate	37-47	checkpoint kinase 1	Homo sapiens	95-99
35443722-7	2022	Silencing Mcl-1 or adding venetoclax/artesunate diminishes the cytarabine resistance pathway p-Chk1.	Cytarabine	63-73	checkpoint kinase 1	Homo sapiens	95-99
35190641-7	2022	The Chk1 inhibitor (AZD7762) tested showed good synergism with standard-of-care myeloma drugs, velcade and melphalan, thus further reinforcing the translational potential of this therapeutic approach.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	20-27	checkpoint kinase 1	Homo sapiens	4-8
35413091-8	2022	Mechanistic investigations showed that AZD6738 treatment inhibited the repair of gemcitabine-induced double-strand breaks by interfering with CHK1.	ceralasertib	39-46	checkpoint kinase 1	Homo sapiens	142-146
35413091-8	2022	Mechanistic investigations showed that AZD6738 treatment inhibited the repair of gemcitabine-induced double-strand breaks by interfering with CHK1.	gemcitabine	81-92	checkpoint kinase 1	Homo sapiens	142-146
35480096-0	2022	MUS81 Inhibition Enhances the Anticancer Efficacy of Talazoparib by Impairing ATR/CHK1 Signaling Pathway in Gastric Cancer.	talazoparib	53-64	checkpoint kinase 1	Homo sapiens	82-86
35480096-8	2022	In conclusion, these data suggested that MUS81 regulated ATR/CHK1 activation, a key signaling pathway in the G2M checkpoint, and targeting MUS81 enhanced the antitumor efficacy of talazoparib.	talazoparib	180-191	checkpoint kinase 1	Homo sapiens	61-65
35191521-6	2022	In vitro, the AZD6738/5-FU combination increased the number of mitotic cells according to flow cytometry, decreased the checkpoint kinase 1 phosphorylation levels and increased cleaved caspase-3 and phosphorylated form of H2A.X variant histone levels according to western blotting, and decreased the proliferation rate of four colon cancer cell lines according to cell viability experiments.	Fluorouracil	22-26	checkpoint kinase 1	Homo sapiens	120-139
35418303-10	2022	Furthermore, CHK1 inhibition interferes with E2:ERalpha signaling to cell proliferation, and drugs approved for clinical treatment of primary and MBC (4OH-tamoxifen and the CDK4/CDK6 inhibitors abemaciclib and palbociclib) exert synergic effects with the CHK1 inhibitors in clinical trials for the treatment of solid tumors (AZD7762, MK8776, prexasertib) in preventing the proliferation of cells modeling primary and MBC.	Tamoxifen	155-164	checkpoint kinase 1	Homo sapiens	13-17
35418303-10	2022	Furthermore, CHK1 inhibition interferes with E2:ERalpha signaling to cell proliferation, and drugs approved for clinical treatment of primary and MBC (4OH-tamoxifen and the CDK4/CDK6 inhibitors abemaciclib and palbociclib) exert synergic effects with the CHK1 inhibitors in clinical trials for the treatment of solid tumors (AZD7762, MK8776, prexasertib) in preventing the proliferation of cells modeling primary and MBC.	Tamoxifen	155-164	checkpoint kinase 1	Homo sapiens	255-259
35418303-10	2022	Furthermore, CHK1 inhibition interferes with E2:ERalpha signaling to cell proliferation, and drugs approved for clinical treatment of primary and MBC (4OH-tamoxifen and the CDK4/CDK6 inhibitors abemaciclib and palbociclib) exert synergic effects with the CHK1 inhibitors in clinical trials for the treatment of solid tumors (AZD7762, MK8776, prexasertib) in preventing the proliferation of cells modeling primary and MBC.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	325-332	checkpoint kinase 1	Homo sapiens	13-17
35418303-10	2022	Furthermore, CHK1 inhibition interferes with E2:ERalpha signaling to cell proliferation, and drugs approved for clinical treatment of primary and MBC (4OH-tamoxifen and the CDK4/CDK6 inhibitors abemaciclib and palbociclib) exert synergic effects with the CHK1 inhibitors in clinical trials for the treatment of solid tumors (AZD7762, MK8776, prexasertib) in preventing the proliferation of cells modeling primary and MBC.	MK-8776	334-340	checkpoint kinase 1	Homo sapiens	13-17
35418303-10	2022	Furthermore, CHK1 inhibition interferes with E2:ERalpha signaling to cell proliferation, and drugs approved for clinical treatment of primary and MBC (4OH-tamoxifen and the CDK4/CDK6 inhibitors abemaciclib and palbociclib) exert synergic effects with the CHK1 inhibitors in clinical trials for the treatment of solid tumors (AZD7762, MK8776, prexasertib) in preventing the proliferation of cells modeling primary and MBC.	prexasertib	342-353	checkpoint kinase 1	Homo sapiens	13-17
35418303-11	2022	CONCLUSIONS: CHK1 could be considered as an appealing novel pharmacological target for the treatment of luminal primary and MBCs.	Phenobarbital	104-111	checkpoint kinase 1	Homo sapiens	13-17
35190641-7	2022	The Chk1 inhibitor (AZD7762) tested showed good synergism with standard-of-care myeloma drugs, velcade and melphalan, thus further reinforcing the translational potential of this therapeutic approach.	Melphalan	107-116	checkpoint kinase 1	Homo sapiens	4-8
35216385-0	2022	VPA and TSA Interrupt the Interplay between mutp53 and HSP70, Leading to CHK1 and RAD51 Down-Regulation and Sensitizing Pancreatic Cancer Cells to AZD2461 PARP Inhibitor.	Valproic Acid	0-3	checkpoint kinase 1	Homo sapiens	73-77
35149548-8	2022	Additionally, treatment with DS-7300a and DXd induced phosphorylated checkpoint kinase 1, a DNA damage marker, and cleaved poly (ADP-ribose) polymerase, an apoptosis marker, in cancer cells.	ds-7300a	29-37	checkpoint kinase 1	Homo sapiens	69-88
35582533-4	2022	In the article by Lee et al., the authors identify that, while prexasertib (a CHK1 inhibitor) lacks efficacy alone, combination with an EGFR inhibitor provides synergistic anti-tumor effects.	prexasertib	63-74	checkpoint kinase 1	Homo sapiens	78-82
35078817-3	2022	Here, we found AZD6738 modulated CHK1 phosphorylation and induced ATM-dependent signaling (pRAD50) and the DNA damage marker gammaH2AX.	ceralasertib	15-22	checkpoint kinase 1	Homo sapiens	33-37
35220216-7	2022	Furthermore, cisplatin triggered the DNA damage response, via the ATM/ATR-Chk1/Chk2 signaling pathway.	Cisplatin	13-22	checkpoint kinase 1	Homo sapiens	74-78
35379057-2	2022	GDC-0575 is an ATP-competitive small-molecule inhibitor of ChK1 that is being developed by Genentech for the treatment of various human malignancies.2.	GDC-0575	0-8	checkpoint kinase 1	Homo sapiens	59-63
35379057-2	2022	GDC-0575 is an ATP-competitive small-molecule inhibitor of ChK1 that is being developed by Genentech for the treatment of various human malignancies.2.	Adenosine Triphosphate	15-18	checkpoint kinase 1	Homo sapiens	59-63
35216385-0	2022	VPA and TSA Interrupt the Interplay between mutp53 and HSP70, Leading to CHK1 and RAD51 Down-Regulation and Sensitizing Pancreatic Cancer Cells to AZD2461 PARP Inhibitor.	trichostatin A	8-11	checkpoint kinase 1	Homo sapiens	73-77
35216385-4	2022	At a molecular level, VPA and TSA down-regulated CHK1 and RAD51, which is correlated with the interruption of the cross-talk between mutp53 and HSP70.	Valproic Acid	22-25	checkpoint kinase 1	Homo sapiens	49-53
35216385-4	2022	At a molecular level, VPA and TSA down-regulated CHK1 and RAD51, which is correlated with the interruption of the cross-talk between mutp53 and HSP70.	trichostatin A	30-33	checkpoint kinase 1	Homo sapiens	49-53
35216385-5	2022	Moreover, VPA and to a lesser extent TSA reactivated wtp53 in these cells, which contributed to CHK1 and RAD51 reduction.	Valproic Acid	10-13	checkpoint kinase 1	Homo sapiens	96-100
35216385-5	2022	Moreover, VPA and to a lesser extent TSA reactivated wtp53 in these cells, which contributed to CHK1 and RAD51 reduction.	trichostatin A	37-40	checkpoint kinase 1	Homo sapiens	96-100
35100653-6	2022	The binding resulted in the generation of ROS, which consequently activated the oxidative stress-related cell cycle arrest and apoptotic pathways, viz., JNK/p38, p21Cip1/Chk1, and p21Cip1/Rb/E2F, as shown by microarray profiling.	ros	42-45	checkpoint kinase 1	Homo sapiens	170-174
35051747-2	2022	Until now, PARP inhibitors like olaparib are the first successful case of utilizing synthetic lethality-based therapy to treat cancers with DNA-repairing deficiency (e.g. BRCA1 or BRCA2 mutation), which has fueled the search for more targetable components in the DDR signaling pathway by exploiting synthetic lethality, including but not limited to DNA-PK, ATR, ATM, CHK1, and WEE1.	olaparib	32-40	checkpoint kinase 1	Homo sapiens	367-371
33953402-8	2021	Hydroxyurea-induced replication stress6,7 triggered ATR-CHK1- and p53-dependent cell extrusion from a mammalian epithelial monolayer.	Hydroxyurea	0-11	checkpoint kinase 1	Homo sapiens	56-60
35163511-4	2022	Treatment with MHY2245 decreased SIRT1 activity and caused DNA damage, leading to the upregulation of p53 acetylation, and increased levels of p53, phosphorylation of H2A histone family member X, ataxia telangiectasia and Rad3-related kinase, checkpoint kinase 1 (Chk1), and Chk2.	mhy2245	15-22	checkpoint kinase 1	Homo sapiens	243-262
35163511-4	2022	Treatment with MHY2245 decreased SIRT1 activity and caused DNA damage, leading to the upregulation of p53 acetylation, and increased levels of p53, phosphorylation of H2A histone family member X, ataxia telangiectasia and Rad3-related kinase, checkpoint kinase 1 (Chk1), and Chk2.	mhy2245	15-22	checkpoint kinase 1	Homo sapiens	264-268
35059477-7	2022	Results: The Chk1 inhibitor treatment promoted retinal differentiation from hPSCs, in combination with low-concentration rhBMP4.	rhbmp4	121-127	checkpoint kinase 1	Homo sapiens	13-17
35088107-8	2022	At a high YCl3-exposure concentration (120 muM), specific DNA damage sensors ATM/ATR-Chk1/Chk2 were significantly decreased.	yttrium chloride	10-14	checkpoint kinase 1	Homo sapiens	85-89
34043345-8	2021	The accumulated G2/M phase cells with increasing levels of phosphorylated CDC25C, CDC2, ATM/ATR, and CHK2/CHK1 confirmed the arrested cell cycle caused by bavachinin via a dose-dependent manner.	bavachinin	155-165	checkpoint kinase 1	Homo sapiens	106-110
33740539-3	2021	Treatment of adherent HT29 or HCC1937 cancer cells or suspension Jurkat or THP1 cells with a Chk1 inhibitor increased gammaH2AX in these cells.	gammah2ax	118-127	checkpoint kinase 1	Homo sapiens	93-97
32165486-5	2021	CUDC-907 downregulates CHK1, Wee1, RRM1, and c-Myc, which were found to play a role in venetoclax-induced apoptosis.	CUDC-907	0-8	checkpoint kinase 1	Homo sapiens	23-27
33870196-3	2021	Activation of the Chk1 arm of the replication stress response (RSR) was reduced when TDO activity was blocked prior to BCNU treatment, whereas phosphorylation of serine 33 (pS33) on replication protein A (RPA) was enhanced-indicative of increased fork collapse.	Serine	162-168	checkpoint kinase 1	Homo sapiens	18-22
33921638-6	2021	Here, we analyzed the impact of druggable DDR players in the response of patient-derived colorectal CSCs (CRC-SCs) to CHK1/2 inhibitor prexasertib, identifying RAD51 and MRE11 as sensitizing targets enhancing prexasertib efficacy.	ddr	42-45	checkpoint kinase 1	Homo sapiens	118-124
33921638-6	2021	Here, we analyzed the impact of druggable DDR players in the response of patient-derived colorectal CSCs (CRC-SCs) to CHK1/2 inhibitor prexasertib, identifying RAD51 and MRE11 as sensitizing targets enhancing prexasertib efficacy.	prexasertib	135-146	checkpoint kinase 1	Homo sapiens	118-124
33921638-6	2021	Here, we analyzed the impact of druggable DDR players in the response of patient-derived colorectal CSCs (CRC-SCs) to CHK1/2 inhibitor prexasertib, identifying RAD51 and MRE11 as sensitizing targets enhancing prexasertib efficacy.	prexasertib	209-220	checkpoint kinase 1	Homo sapiens	118-124
33921638-7	2021	We showed that combined inhibition of RAD51 and CHK1 (via B02+prexasertib) or MRE11 and CHK1 (via mirin+prexasertib) kills CSCs by affecting multiple genoprotective processes.	RAD51 inhibitor B02	58-61	checkpoint kinase 1	Homo sapiens	48-52
33921638-7	2021	We showed that combined inhibition of RAD51 and CHK1 (via B02+prexasertib) or MRE11 and CHK1 (via mirin+prexasertib) kills CSCs by affecting multiple genoprotective processes.	prexasertib	62-73	checkpoint kinase 1	Homo sapiens	48-52
33921638-7	2021	We showed that combined inhibition of RAD51 and CHK1 (via B02+prexasertib) or MRE11 and CHK1 (via mirin+prexasertib) kills CSCs by affecting multiple genoprotective processes.	6-(4-hydroxyphenyl)-2-thioxo-2,3-dihydro-4(1H)-pyrimidinone	98-103	checkpoint kinase 1	Homo sapiens	88-92
33921638-7	2021	We showed that combined inhibition of RAD51 and CHK1 (via B02+prexasertib) or MRE11 and CHK1 (via mirin+prexasertib) kills CSCs by affecting multiple genoprotective processes.	prexasertib	104-115	checkpoint kinase 1	Homo sapiens	88-92
33206174-5	2021	CHIR-124, a selective CHK1 inhibitor, impairs cell viability and induces remarkable synergistic lethality with mTOR inhibitor rapamycin in MYC-overexpressing cells.	CHIR-124	0-8	checkpoint kinase 1	Homo sapiens	22-26
33863777-4	2021	Here we report that TAK-243, a first-in-class ubiquitin activating enzyme UBA1 inhibitor in clinical development, causes preferential cytotoxicity in SLFN11-KO cells; this effect is associated with claspin-mediated DNA replication inhibition by CHK1 independently of ATR.	TAK-243	20-27	checkpoint kinase 1	Homo sapiens	245-249
33870196-3	2021	Activation of the Chk1 arm of the replication stress response (RSR) was reduced when TDO activity was blocked prior to BCNU treatment, whereas phosphorylation of serine 33 (pS33) on replication protein A (RPA) was enhanced-indicative of increased fork collapse.	Carmustine	119-123	checkpoint kinase 1	Homo sapiens	18-22
34034991-1	2021	BACKGROUND: This study assessed the checkpoint kinase 1 inhibitor prexasertib in patients with extensive-stage small-cell lung cancer (ED-SCLC).	prexasertib	66-77	checkpoint kinase 1	Homo sapiens	36-55
33881209-0	2021	A phase 1 study of prexasertib (LY2606368), a CHK1/2 inhibitor, in pediatric patients with recurrent or refractory solid tumors, including CNS tumors: A report from the Children"s Oncology Group Pediatric Early Phase Clinical Trials Network (ADVL1515).	prexasertib	19-30	checkpoint kinase 1	Homo sapiens	46-52
33881209-1	2021	BACKGROUND: Prexasertib (LY2606368) is a novel, second-generation, selective dual inhibitor of checkpoint kinase proteins 1 (CHK1) and 2 (CHK2).	prexasertib	12-23	checkpoint kinase 1	Homo sapiens	125-129
33915913-6	2021	Combination treatment with doxo and a small-molecule inhibitor of ATM showed a delay in regrowth in SK-N-DZ, of CHK1 in BE(2)-C, of Wee1 in SK-N-FI and BE(2)-C, and of p21 in Kelly and BE(2)-C. Further investigation revealed, in all tested cell lines, a subset of cells arrested in mitosis, indicating independence on the intra-S- and/or G2/M-checkpoints.	Doxorubicin	27-31	checkpoint kinase 1	Homo sapiens	112-116
33915913-6	2021	Combination treatment with doxo and a small-molecule inhibitor of ATM showed a delay in regrowth in SK-N-DZ, of CHK1 in BE(2)-C, of Wee1 in SK-N-FI and BE(2)-C, and of p21 in Kelly and BE(2)-C. Further investigation revealed, in all tested cell lines, a subset of cells arrested in mitosis, indicating independence on the intra-S- and/or G2/M-checkpoints.	Beryllium	120-123	checkpoint kinase 1	Homo sapiens	112-116
33987368-0	2021	Metastasis-associated gene 1 (MTA1) enhances cisplatin resistance of malignant pleural mesothelioma by ATR-Chk1-mediated DNA repair.	Cisplatin	45-54	checkpoint kinase 1	Homo sapiens	107-111
33987368-10	2021	Cisplatin stabilized the expression of the MTA1 protein by inhibiting its ubiquitination, and MTA1 enhanced G2/M cell cycle delay and regulated and protected the tumor genome from chemotherapeutic drugs via participating in the phosphorylation of the ataxia telangiectasia mutated and rad3 related-checkpoint kinase 1 (ATR-Chk1) pathway.	Cisplatin	0-9	checkpoint kinase 1	Homo sapiens	323-327
33987368-11	2021	Conclusions: These data suggest that MTA1 enhances cisplatin resistance by ATR-Chk1-mediated DNA damage repairment and cisplatin stabilizes MTA1 expression via affecting on the ubiquitination pathway of MTA1 in MPM.	Cisplatin	51-60	checkpoint kinase 1	Homo sapiens	79-83
33571504-5	2021	We established that WRN-depleted cells are dependent on a critical but compromised CHK1-mediated HRR-pathway for repairing ionizing radiation (IR) induced DSBs for their survival.	1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione	155-159	checkpoint kinase 1	Homo sapiens	83-87
33495309-1	2021	PURPOSE: Prexasertib, a checkpoint kinase-I inhibitor (CHK1), exhibited modest monotherapy antitumor activity in previous studies.	prexasertib	9-20	checkpoint kinase 1	Homo sapiens	55-59
33915913-6	2021	Combination treatment with doxo and a small-molecule inhibitor of ATM showed a delay in regrowth in SK-N-DZ, of CHK1 in BE(2)-C, of Wee1 in SK-N-FI and BE(2)-C, and of p21 in Kelly and BE(2)-C. Further investigation revealed, in all tested cell lines, a subset of cells arrested in mitosis, indicating independence on the intra-S- and/or G2/M-checkpoints.	Beryllium	120-122	checkpoint kinase 1	Homo sapiens	112-116
33320980-2	2021	As the cell cycle checkpoint kinase 1 (Chk1) plays a key role in DNA damage response to chemotherapeutic drugs, we explored the mechanisms of acquired drug resistance to the Chk1 inhibitor prexasertib in SCLC.	prexasertib	189-200	checkpoint kinase 1	Homo sapiens	39-43
33320980-2	2021	As the cell cycle checkpoint kinase 1 (Chk1) plays a key role in DNA damage response to chemotherapeutic drugs, we explored the mechanisms of acquired drug resistance to the Chk1 inhibitor prexasertib in SCLC.	prexasertib	189-200	checkpoint kinase 1	Homo sapiens	174-178
33686514-0	2022	CHK1 kinase inhibition: identification of allosteric hits using MD simulations, pharmacophore modeling, docking and MM-PBSA calculations.	poly(tetramethylene succinate-co-tetramethylene adipate)	119-123	checkpoint kinase 1	Homo sapiens	0-4
33782497-9	2021	In contrast, gammaH2AX induced by single agent ATRi and CHK1i requires a high threshold activity CDK2.	gammah2ax	13-22	checkpoint kinase 1	Homo sapiens	56-61
33789090-5	2021	Our data show that CLASPIN engages a conserved site on CHK1 adjacent to the substrate-binding cleft, involved in phosphate sensing in other kinases.	Phosphates	113-122	checkpoint kinase 1	Homo sapiens	55-59
33745032-0	2021	Immune modulating activity of the CHK1 inhibitor prexasertib and anti-PD-L1 antibody LY3300054 in patients with high-grade serous ovarian cancer and other solid tumors.	prexasertib	49-60	checkpoint kinase 1	Homo sapiens	34-38
33745032-3	2021	METHODS: This was an open-label phase 1 study evaluating the CHK1 inhibitor prexasertib and the anti-PD-L1 antibody LY3300054.	prexasertib	76-87	checkpoint kinase 1	Homo sapiens	61-65
33339894-6	2021	Combinations of DDA with DDRi targeting the replication-stress response (ATR, CHK1 and WEE1) could re-sensitise SLFN11-absent/low cancer models to the DDA treatment and were effective in upper gastrointestinal and genitourinary malignancies.	dda	16-19	checkpoint kinase 1	Homo sapiens	78-82
33339894-6	2021	Combinations of DDA with DDRi targeting the replication-stress response (ATR, CHK1 and WEE1) could re-sensitise SLFN11-absent/low cancer models to the DDA treatment and were effective in upper gastrointestinal and genitourinary malignancies.	dda	151-154	checkpoint kinase 1	Homo sapiens	78-82
33860197-0	2021	Comparative Activity and Off-Target Effects in Cells of the CHK1 Inhibitors MK-8776, SRA737, and LY2606368.	MK-8776	76-83	checkpoint kinase 1	Homo sapiens	60-64
33172976-4	2021	Here, we show that BGB324 (bemcentinib), a selective small-molecule AXL inhibitor, caused DNA damage and induced replication stress, indicated by ATR/CHK1 phosphorylation, more significantly in TP53-deficient NSCLC cell lines.	bemcentinib	19-25	checkpoint kinase 1	Homo sapiens	150-154
33172976-4	2021	Here, we show that BGB324 (bemcentinib), a selective small-molecule AXL inhibitor, caused DNA damage and induced replication stress, indicated by ATR/CHK1 phosphorylation, more significantly in TP53-deficient NSCLC cell lines.	bemcentinib	27-38	checkpoint kinase 1	Homo sapiens	150-154
33492002-4	2021	RECENT FINDINGS: Cells harboring splicing factor mutations have increased aberrant splicing leading to R-loop formation and cell cycle stalling that create dependencies on Checkpoint kinase 1 (CHK1) activation and canonical splicing maintained by protein arginine methyltransferase activity.	Arginine	255-263	checkpoint kinase 1	Homo sapiens	172-191
33492002-4	2021	RECENT FINDINGS: Cells harboring splicing factor mutations have increased aberrant splicing leading to R-loop formation and cell cycle stalling that create dependencies on Checkpoint kinase 1 (CHK1) activation and canonical splicing maintained by protein arginine methyltransferase activity.	Arginine	255-263	checkpoint kinase 1	Homo sapiens	193-197
33669867-10	2021	Doxorubicin with RIDR-PI-103 inhibited p-AktS473, upregulated p-CHK1/2 and p-P53.	Doxorubicin	0-11	checkpoint kinase 1	Homo sapiens	64-70
33860197-0	2021	Comparative Activity and Off-Target Effects in Cells of the CHK1 Inhibitors MK-8776, SRA737, and LY2606368.	SRA737	85-91	checkpoint kinase 1	Homo sapiens	60-64
33860197-0	2021	Comparative Activity and Off-Target Effects in Cells of the CHK1 Inhibitors MK-8776, SRA737, and LY2606368.	prexasertib	97-106	checkpoint kinase 1	Homo sapiens	60-64
33860197-8	2021	LY2606368 was far more potent at inhibiting CHK1 and inducing growth arrest, while all three CHK1i inhibited CHK2 at concentrations 10- (MK-8776 and SRA737) to 100- (LY2606368) fold higher.	prexasertib	0-9	checkpoint kinase 1	Homo sapiens	44-48
33860197-8	2021	LY2606368 was far more potent at inhibiting CHK1 and inducing growth arrest, while all three CHK1i inhibited CHK2 at concentrations 10- (MK-8776 and SRA737) to 100- (LY2606368) fold higher.	MK-8776	137-144	checkpoint kinase 1	Homo sapiens	93-98
33860197-8	2021	LY2606368 was far more potent at inhibiting CHK1 and inducing growth arrest, while all three CHK1i inhibited CHK2 at concentrations 10- (MK-8776 and SRA737) to 100- (LY2606368) fold higher.	SRA737	149-155	checkpoint kinase 1	Homo sapiens	93-98
33860197-10	2021	Acquired resistance to LY2606368 resulted in limited cross-resistance to other CHK1i.	prexasertib	23-32	checkpoint kinase 1	Homo sapiens	79-84
33860197-11	2021	LY2606368-resistant cells still abrogated DNA damage-induced S phase arrest, which requires low CDK2 activity, whereas inappropriately high CDK2 activity is responsible for sensitivity to CHK1i alone.	prexasertib	0-9	checkpoint kinase 1	Homo sapiens	188-193
33860197-13	2021	LY2606368 appears to be the most selective CHK1i, suggesting that further clinical development of this drug is warranted.	prexasertib	0-9	checkpoint kinase 1	Homo sapiens	43-48
33536335-3	2021	We found that inactivation of Ataxia Telangiectasia- and Rad3-related (ATR), CHK1, BRCA2, and RPA1 overcome chemoresistance to camptothecin (CPT) in SLFN11-KO cells.	Camptothecin	127-139	checkpoint kinase 1	Homo sapiens	77-81
33536335-4	2021	Accordingly, we validate that clinical inhibitors of ATR (M4344 and M6620) and CHK1 (SRA737) resensitize SLFN11-KO cells to topotecan, indotecan, etoposide, cisplatin, and talazoparib.	Topotecan	124-133	checkpoint kinase 1	Homo sapiens	79-83
33536335-4	2021	Accordingly, we validate that clinical inhibitors of ATR (M4344 and M6620) and CHK1 (SRA737) resensitize SLFN11-KO cells to topotecan, indotecan, etoposide, cisplatin, and talazoparib.	NSC 724998	135-144	checkpoint kinase 1	Homo sapiens	79-83
33536335-4	2021	Accordingly, we validate that clinical inhibitors of ATR (M4344 and M6620) and CHK1 (SRA737) resensitize SLFN11-KO cells to topotecan, indotecan, etoposide, cisplatin, and talazoparib.	Etoposide	146-155	checkpoint kinase 1	Homo sapiens	79-83
33536335-4	2021	Accordingly, we validate that clinical inhibitors of ATR (M4344 and M6620) and CHK1 (SRA737) resensitize SLFN11-KO cells to topotecan, indotecan, etoposide, cisplatin, and talazoparib.	Cisplatin	157-166	checkpoint kinase 1	Homo sapiens	79-83
33536335-4	2021	Accordingly, we validate that clinical inhibitors of ATR (M4344 and M6620) and CHK1 (SRA737) resensitize SLFN11-KO cells to topotecan, indotecan, etoposide, cisplatin, and talazoparib.	talazoparib	172-183	checkpoint kinase 1	Homo sapiens	79-83
33546122-5	2021	The radiosensitizing effect of AZD6738 was correlated with checkpoint kinase 1 (CHK1)-mediated abrogation of G2/M-arrest.	ceralasertib	31-38	checkpoint kinase 1	Homo sapiens	59-78
33542435-7	2021	A kinome shRNA screen revealed that carboplatin-resistant cells are vulnerable to the depletion of the mitotic checkpoint regulators, whereas the checkpoint kinases CHEK1 and WEE1 are indispensable for the survival of carboplatin-resistant cells in the presence of carboplatin.	Carboplatin	218-229	checkpoint kinase 1	Homo sapiens	165-170
33542435-7	2021	A kinome shRNA screen revealed that carboplatin-resistant cells are vulnerable to the depletion of the mitotic checkpoint regulators, whereas the checkpoint kinases CHEK1 and WEE1 are indispensable for the survival of carboplatin-resistant cells in the presence of carboplatin.	Carboplatin	218-229	checkpoint kinase 1	Homo sapiens	165-170
33546122-5	2021	The radiosensitizing effect of AZD6738 was correlated with checkpoint kinase 1 (CHK1)-mediated abrogation of G2/M-arrest.	ceralasertib	31-38	checkpoint kinase 1	Homo sapiens	80-84
33145616-9	2021	Model simulations indicated that concentrations of berzosertib exceeded p-Chk1 (proximal pharmacodynamic biomarker) IC50 at recommended phase II doses in combination with carboplatin, cisplatin, and gemcitabine.	berzosertib	51-62	checkpoint kinase 1	Homo sapiens	74-78
33529438-6	2021	In combination with cytotoxic chemotherapy such as gemcitabine or camptothecin, Chk1 inhibition increased cytoplasmic dsDNA compared to the cytotoxic alone but attenuated the cytotoxic chemotherapy-induced increase in IRF1 protein and STAT1 phosphorylation through inhibition of nuclear RelB translocation.	gemcitabine	51-62	checkpoint kinase 1	Homo sapiens	80-84
33529438-6	2021	In combination with cytotoxic chemotherapy such as gemcitabine or camptothecin, Chk1 inhibition increased cytoplasmic dsDNA compared to the cytotoxic alone but attenuated the cytotoxic chemotherapy-induced increase in IRF1 protein and STAT1 phosphorylation through inhibition of nuclear RelB translocation.	Camptothecin	66-78	checkpoint kinase 1	Homo sapiens	80-84
33378592-0	2021	Effects of checkpoint kinase 1 inhibition by prexasertib on the tumor immune microenvironment of head and neck squamous cell carcinoma.	prexasertib	45-56	checkpoint kinase 1	Homo sapiens	11-30
33321673-9	2021	ZnO particles activated ATM, ATR, Chk1, Chk2, gamma-H2AX, ERK and p38 phosphorylation as detected by immunofluorescent staining and western blotting.	Zinc Oxide	0-3	checkpoint kinase 1	Homo sapiens	34-38
33378592-4	2021	Prexasertib, a CHK1 inhibitor, induces DNA damage and cell death, however, its effect on the tumor immune microenvironment (TIME) is largely unknown.	prexasertib	0-11	checkpoint kinase 1	Homo sapiens	15-19
33501840-0	2021	Role of inhibiting Chk1-p53 pathway in hepatotoxicity caused by chronic arsenic exposure from coal-burning.	Arsenic	72-79	checkpoint kinase 1	Homo sapiens	19-23
32991949-2	2021	A critical component of this response is the serine/threonine kinase CHK1 which is encoded by the CHEK1 gene.	Serine	45-51	checkpoint kinase 1	Homo sapiens	69-73
32991949-2	2021	A critical component of this response is the serine/threonine kinase CHK1 which is encoded by the CHEK1 gene.	Serine	45-51	checkpoint kinase 1	Homo sapiens	98-103
33501840-5	2021	The results showed that arsenic induced liver damage, increased hepatocyte apoptosis and elevated the expression level of Chk1 and the ratios of p-p53/p53 and Bax/Bcl-2 in liver tissues, which were significantly attenuated by GBE.	Arsenic	24-31	checkpoint kinase 1	Homo sapiens	122-126
33513721-5	2021	Mechanistically, belotecan, a DNA-damaging agent, increased phospho-ATR (pATR) and phospho-Chk1 (pChk1) in consecutive order, indicating the activation of the DNA repair system.	belotecan	17-26	checkpoint kinase 1	Homo sapiens	91-95
33503415-4	2021	Chk1 activated by ataxia telangiectasia mutated (ATM) kinase on DNA breaks in G1 promotes NHEJ through direct phosphorylation of ASF1A at Ser-166.	Serine	138-141	checkpoint kinase 1	Homo sapiens	0-4
33466733-6	2021	Moreover, depletion of MBNL2 increases the phosphorylation levels of checkpoint kinase 1 (Chk1) serine 345 (S345) and DNA damage response, and the effect of MBNL2 on DNA damage response is p21-dependent.	Serine	96-102	checkpoint kinase 1	Homo sapiens	69-88
33472956-5	2021	We identified 45 effective compounds from the screen and found that cell cycle checkpoint kinase (CHK1/2) inhibition synergistically enhanced the cytotoxic activity of clinically used chemotherapeutics cyclophosphamide, cisplatin, and gemcitabine.	Cyclophosphamide	202-218	checkpoint kinase 1	Homo sapiens	68-96
33472956-5	2021	We identified 45 effective compounds from the screen and found that cell cycle checkpoint kinase (CHK1/2) inhibition synergistically enhanced the cytotoxic activity of clinically used chemotherapeutics cyclophosphamide, cisplatin, and gemcitabine.	Cyclophosphamide	202-218	checkpoint kinase 1	Homo sapiens	98-104
33472956-5	2021	We identified 45 effective compounds from the screen and found that cell cycle checkpoint kinase (CHK1/2) inhibition synergistically enhanced the cytotoxic activity of clinically used chemotherapeutics cyclophosphamide, cisplatin, and gemcitabine.	Cisplatin	220-229	checkpoint kinase 1	Homo sapiens	68-96
33472956-5	2021	We identified 45 effective compounds from the screen and found that cell cycle checkpoint kinase (CHK1/2) inhibition synergistically enhanced the cytotoxic activity of clinically used chemotherapeutics cyclophosphamide, cisplatin, and gemcitabine.	Cisplatin	220-229	checkpoint kinase 1	Homo sapiens	98-104
33472956-5	2021	We identified 45 effective compounds from the screen and found that cell cycle checkpoint kinase (CHK1/2) inhibition synergistically enhanced the cytotoxic activity of clinically used chemotherapeutics cyclophosphamide, cisplatin, and gemcitabine.	gemcitabine	235-246	checkpoint kinase 1	Homo sapiens	68-96
33472956-5	2021	We identified 45 effective compounds from the screen and found that cell cycle checkpoint kinase (CHK1/2) inhibition synergistically enhanced the cytotoxic activity of clinically used chemotherapeutics cyclophosphamide, cisplatin, and gemcitabine.	gemcitabine	235-246	checkpoint kinase 1	Homo sapiens	98-104
33466733-6	2021	Moreover, depletion of MBNL2 increases the phosphorylation levels of checkpoint kinase 1 (Chk1) serine 345 (S345) and DNA damage response, and the effect of MBNL2 on DNA damage response is p21-dependent.	Serine	96-102	checkpoint kinase 1	Homo sapiens	90-94
33412559-9	2021	We found that combining CHK1 inhibitor with olaparib results in restoration of sensitivity even when EMI1 expression is downregulated.	olaparib	44-52	checkpoint kinase 1	Homo sapiens	24-28
33301843-0	2021	Pristimerin synergizes with gemcitabine through abrogating Chk1/53BP1-mediated DNA repair in pancreatic cancer cells.	pristimerin	0-11	checkpoint kinase 1	Homo sapiens	59-63
33301843-0	2021	Pristimerin synergizes with gemcitabine through abrogating Chk1/53BP1-mediated DNA repair in pancreatic cancer cells.	gemcitabine	28-39	checkpoint kinase 1	Homo sapiens	59-63
33301843-4	2021	Interestingly, pristimerin induced lysosomal degradation of checkpoint kinase 1 (Chk1), decreased the percentage of cells at the G1/S boundary and triggered significant double-stranded DNA breaks compared to gemcitabine treatment alone.	pristimerin	15-26	checkpoint kinase 1	Homo sapiens	60-79
33301843-4	2021	Interestingly, pristimerin induced lysosomal degradation of checkpoint kinase 1 (Chk1), decreased the percentage of cells at the G1/S boundary and triggered significant double-stranded DNA breaks compared to gemcitabine treatment alone.	pristimerin	15-26	checkpoint kinase 1	Homo sapiens	81-85
33301843-5	2021	Moreover, gemcitabine activated the phosphorylation of Chk1 and induced the formation of poly (ADP-ribose) polymers (PARs) as well as the accumulation of 53BP1, which was either partially or completely impaired by pristimerin.	gemcitabine	10-21	checkpoint kinase 1	Homo sapiens	55-59
33301843-5	2021	Moreover, gemcitabine activated the phosphorylation of Chk1 and induced the formation of poly (ADP-ribose) polymers (PARs) as well as the accumulation of 53BP1, which was either partially or completely impaired by pristimerin.	pristimerin	214-225	checkpoint kinase 1	Homo sapiens	55-59
33269665-10	2020	Furthermore, CTC1 KO inhibited CHK1 phosphorylation following hydroxyurea-induced replication stress.	Hydroxyurea	62-73	checkpoint kinase 1	Homo sapiens	31-35
33854565-10	2020	Treatment of ovarian cancer cells with ATR specific siRNA or ATR inhibitor VE-822 led to significant apoptosis and inhibition of cellular proliferation, with reduced phosphorylation of Chk1 (p-Chk1), Cdc25c (p-Cdc25c), Cdc2 (p-Cdc2), and increased expression of cleaved PARP and gammaH2AX.	berzosertib	75-81	checkpoint kinase 1	Homo sapiens	185-189
33854565-10	2020	Treatment of ovarian cancer cells with ATR specific siRNA or ATR inhibitor VE-822 led to significant apoptosis and inhibition of cellular proliferation, with reduced phosphorylation of Chk1 (p-Chk1), Cdc25c (p-Cdc25c), Cdc2 (p-Cdc2), and increased expression of cleaved PARP and gammaH2AX.	berzosertib	75-81	checkpoint kinase 1	Homo sapiens	193-197
33065246-0	2021	Discovery and in silico evaluation of aminoarylbenzosuberene molecules as novel checkpoint kinase 1 inhibitor determinants.	aminoarylbenzosuberene	38-60	checkpoint kinase 1	Homo sapiens	80-99
33065246-4	2021	In this research, we considered a set of in-house plant based semi-synthetic aminoarylbenzosuberene molecules as potential CHK1 inhibitors.	aminoarylbenzosuberene	77-99	checkpoint kinase 1	Homo sapiens	123-127
33065246-7	2021	The computational strategy indicates that the Bch10 could be regarded as a potential CHK1 inhibitor in comparison with top five co-crystallize molecules.	bch10	46-51	checkpoint kinase 1	Homo sapiens	85-89
33065246-8	2021	Bch10 signifies a promising outlet for the development of potent inhibitors for CHK1.	bch10	0-5	checkpoint kinase 1	Homo sapiens	80-84
33408782-14	2021	Finally, in clinical samples, ovarian cancer patients with high levels of EZH2 and CHK1 not only were more resistant to platinum but also had a poorer prognosis.	Platinum	120-128	checkpoint kinase 1	Homo sapiens	83-87
33352723-3	2020	We hypothesized that the combination of olaparib with anticancer agents that disrupt HRR by targeting ataxia telangiectasia and Rad3-related protein (ATR) or checkpoint kinase 1 (CHK1) may be an effective strategy to reverse ovarian cancer resistance to olaparib.	olaparib	40-48	checkpoint kinase 1	Homo sapiens	158-177
33352723-3	2020	We hypothesized that the combination of olaparib with anticancer agents that disrupt HRR by targeting ataxia telangiectasia and Rad3-related protein (ATR) or checkpoint kinase 1 (CHK1) may be an effective strategy to reverse ovarian cancer resistance to olaparib.	olaparib	40-48	checkpoint kinase 1	Homo sapiens	179-183
33352723-3	2020	We hypothesized that the combination of olaparib with anticancer agents that disrupt HRR by targeting ataxia telangiectasia and Rad3-related protein (ATR) or checkpoint kinase 1 (CHK1) may be an effective strategy to reverse ovarian cancer resistance to olaparib.	olaparib	254-262	checkpoint kinase 1	Homo sapiens	179-183
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	checkpoint kinase 1	Homo sapiens	73-77
32510664-0	2020	A Phase II Single Arm Pilot Study of the CHK1 Inhibitor Prexasertib (LY2606368) in BRCA Wild-Type, Advanced Triple-Negative Breast Cancer.	prexasertib	56-67	checkpoint kinase 1	Homo sapiens	41-45
32510664-0	2020	A Phase II Single Arm Pilot Study of the CHK1 Inhibitor Prexasertib (LY2606368) in BRCA Wild-Type, Advanced Triple-Negative Breast Cancer.	prexasertib	69-78	checkpoint kinase 1	Homo sapiens	41-45
32510664-6	2020	We hypothesized the second-generation CHK1 inhibitor, prexasertib, would yield clinical activity in sporadic TNBC.	prexasertib	54-65	checkpoint kinase 1	Homo sapiens	38-42
32715947-0	2020	TRAIL-conjugated silver nanoparticles sensitize glioblastoma cells to TRAIL by regulating CHK1 in the DNA repair pathway.	Silver	17-23	checkpoint kinase 1	Homo sapiens	90-94
33014159-6	2020	The sensitizing effect of GA-13315 was associated with the alterations of topoisomerase 1 (Top1) protein expression, tyrosyl DNA phosphodiesterase 1 and checkpoint kinase 1.	13-chlorine-3,15-dioxy-gibberellic acid methyl ester	26-34	checkpoint kinase 1	Homo sapiens	153-172
33101488-7	2020	Furthermore, wortmannin and caffeine inhibited the 2,3-DCPE-mediated phosphorylation of Chk1 and the degradation of Cdc25A.	Wortmannin	13-23	checkpoint kinase 1	Homo sapiens	88-92
33101488-7	2020	Furthermore, wortmannin and caffeine inhibited the 2,3-DCPE-mediated phosphorylation of Chk1 and the degradation of Cdc25A.	Caffeine	28-36	checkpoint kinase 1	Homo sapiens	88-92
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	checkpoint kinase 1	Homo sapiens	88-92
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	61-69	checkpoint kinase 1	Homo sapiens	201-205
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	checkpoint kinase 1	Homo sapiens	201-205
33261142-0	2020	Checkpoint Kinase 1 Pharmacological Inhibition Synergizes with DNA-Damaging Agents and Overcomes Platinum Resistance in Basal-Like Breast Cancer.	Platinum	97-105	checkpoint kinase 1	Homo sapiens	0-19
33261142-9	2020	Lastly, the combination of CHK1 inhibitor with cisplatin and gemcitabine resulted in more activity than single or double combinations, leading to a higher apoptotic effect.	Cisplatin	47-56	checkpoint kinase 1	Homo sapiens	27-31
33261142-9	2020	Lastly, the combination of CHK1 inhibitor with cisplatin and gemcitabine resulted in more activity than single or double combinations, leading to a higher apoptotic effect.	gemcitabine	61-72	checkpoint kinase 1	Homo sapiens	27-31
33261142-10	2020	In conclusion, in our study we identify therapeutic options for the clinical development of CHK1 inhibitors, and confirm that the inhibition of this kinase can overcome acquired resistance to cisplatin.	Cisplatin	192-201	checkpoint kinase 1	Homo sapiens	92-96
32857208-0	2020	Radiosensitization of NSCLC cells to X-rays and carbon ions by the CHK1/CHK2 inhibitor AZD7762, Honokiol and Tunicamycin.	Carbon	48-54	checkpoint kinase 1	Homo sapiens	67-71
33176741-3	2020	Our previous studies demonstrated that 5-aminoimidazole-4-carboxamide ribonucleoside (AICAr) induced differentiation of monocytic cell lines by activating the ATR/Chk1 via pyrimidine depletion.	acadesine	39-84	checkpoint kinase 1	Homo sapiens	163-167
33176741-3	2020	Our previous studies demonstrated that 5-aminoimidazole-4-carboxamide ribonucleoside (AICAr) induced differentiation of monocytic cell lines by activating the ATR/Chk1 via pyrimidine depletion.	acadesine	86-91	checkpoint kinase 1	Homo sapiens	163-167
33176741-3	2020	Our previous studies demonstrated that 5-aminoimidazole-4-carboxamide ribonucleoside (AICAr) induced differentiation of monocytic cell lines by activating the ATR/Chk1 via pyrimidine depletion.	pyrimidine	172-182	checkpoint kinase 1	Homo sapiens	163-167
33155931-9	2021	RESULTS: The array-data demonstrated that dasatinib-treated K562 cells significantly caused the decrease of several genes (AURKA, AURKB, PLK, CHEK1, MYC, XPC, BCL2, and XRCC2).	Dasatinib	42-51	checkpoint kinase 1	Homo sapiens	142-147
33216839-6	2020	Consistently, the staining pattern of gammaH2AX-foci is significantly reduced in the cells exposed simultaneously to cisplatin and FH535; and (5) inhibition of Wnt/beta-catenin signalling impedes cisplatin-induced phosphorylation of Chk1, abrogates the G2/M phase arrest and impairs recombination-based DNA repair.	Cisplatin	117-126	checkpoint kinase 1	Homo sapiens	233-237
33216839-6	2020	Consistently, the staining pattern of gammaH2AX-foci is significantly reduced in the cells exposed simultaneously to cisplatin and FH535; and (5) inhibition of Wnt/beta-catenin signalling impedes cisplatin-induced phosphorylation of Chk1, abrogates the G2/M phase arrest and impairs recombination-based DNA repair.	FH535	131-136	checkpoint kinase 1	Homo sapiens	233-237
32653524-1	2020	Checkpoint kinase 1 (CHK1) is a serine/threonine-protein kinase that is involved in cell cycle regulation in eukaryotes.	Serine	32-38	checkpoint kinase 1	Homo sapiens	0-19
32653524-1	2020	Checkpoint kinase 1 (CHK1) is a serine/threonine-protein kinase that is involved in cell cycle regulation in eukaryotes.	Serine	32-38	checkpoint kinase 1	Homo sapiens	21-25
33097607-6	2020	Therefore, taken together with the previous report, we conclude that both IKKalpha- and CHK1-dependent p53 phosphorylation and acetylation contribute to mediating selective autophagy targeting feedback degradation of IKKalpha in arsenite-induced proapoptotic responses.	arsenite	229-237	checkpoint kinase 1	Homo sapiens	88-92
32901871-5	2020	In the present study, we demonstrated that shRNA-mediated CHK1 silencing suppressed cell proliferation and enhanced the cytotoxic effects of etoposide (VP16) in the chronic myeloid leukemia (CML) cell line K562 through the results of CCK-8, and comet assay.	Etoposide	141-150	checkpoint kinase 1	Homo sapiens	58-62
32901871-5	2020	In the present study, we demonstrated that shRNA-mediated CHK1 silencing suppressed cell proliferation and enhanced the cytotoxic effects of etoposide (VP16) in the chronic myeloid leukemia (CML) cell line K562 through the results of CCK-8, and comet assay.	Etoposide	152-156	checkpoint kinase 1	Homo sapiens	58-62
32901871-5	2020	In the present study, we demonstrated that shRNA-mediated CHK1 silencing suppressed cell proliferation and enhanced the cytotoxic effects of etoposide (VP16) in the chronic myeloid leukemia (CML) cell line K562 through the results of CCK-8, and comet assay.	Sincalide	234-239	checkpoint kinase 1	Homo sapiens	58-62
32901871-8	2020	Second, we tested the therapeutic effect of VP16 combined with CCT245737, an orally bioavailable CHK1 inhibitor, and observed strong synergistic anticancer effects in K562 cells.	Etoposide	44-48	checkpoint kinase 1	Homo sapiens	97-101
32901871-8	2020	Second, we tested the therapeutic effect of VP16 combined with CCT245737, an orally bioavailable CHK1 inhibitor, and observed strong synergistic anticancer effects in K562 cells.	CCT245737	63-72	checkpoint kinase 1	Homo sapiens	97-101
32857208-0	2020	Radiosensitization of NSCLC cells to X-rays and carbon ions by the CHK1/CHK2 inhibitor AZD7762, Honokiol and Tunicamycin.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	87-94	checkpoint kinase 1	Homo sapiens	67-71
32857208-3	2020	Cells pretreated with the CHK1/CHK2 inhibitor AZD7762, Honokiol or Tunicamycin were irradiated with low-LET X-rays and high-LET carbon ions.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	46-53	checkpoint kinase 1	Homo sapiens	26-30
32743678-0	2020	HOTAIR promotes paclitaxel resistance by regulating CHEK1 in ovarian cancer.	Paclitaxel	16-26	checkpoint kinase 1	Homo sapiens	52-57
32579780-0	2020	The CHK1 inhibitor MU380 significantly increases the sensitivity of human docetaxel-resistant prostate cancer cells to gemcitabine through the induction of mitotic catastrophe.	mu380	19-24	checkpoint kinase 1	Homo sapiens	4-8
32579780-0	2020	The CHK1 inhibitor MU380 significantly increases the sensitivity of human docetaxel-resistant prostate cancer cells to gemcitabine through the induction of mitotic catastrophe.	Docetaxel	74-83	checkpoint kinase 1	Homo sapiens	4-8
32579780-0	2020	The CHK1 inhibitor MU380 significantly increases the sensitivity of human docetaxel-resistant prostate cancer cells to gemcitabine through the induction of mitotic catastrophe.	gemcitabine	119-130	checkpoint kinase 1	Homo sapiens	4-8
32579780-3	2020	CHK1 has been associated with prostate cancer (PCa) induction, progression, and lethality, hence CHK1 inhibitors SCH900776 (also known as MK-8776) and the more effective SCH900776 analog MU380 may have clinical applications in the therapy of PCa.	MK-8776	113-122	checkpoint kinase 1	Homo sapiens	97-101
32579780-3	2020	CHK1 has been associated with prostate cancer (PCa) induction, progression, and lethality, hence CHK1 inhibitors SCH900776 (also known as MK-8776) and the more effective SCH900776 analog MU380 may have clinical applications in the therapy of PCa.	MK-8776	138-145	checkpoint kinase 1	Homo sapiens	0-4
32579780-3	2020	CHK1 has been associated with prostate cancer (PCa) induction, progression, and lethality, hence CHK1 inhibitors SCH900776 (also known as MK-8776) and the more effective SCH900776 analog MU380 may have clinical applications in the therapy of PCa.	MK-8776	138-145	checkpoint kinase 1	Homo sapiens	97-101
32579780-3	2020	CHK1 has been associated with prostate cancer (PCa) induction, progression, and lethality, hence CHK1 inhibitors SCH900776 (also known as MK-8776) and the more effective SCH900776 analog MU380 may have clinical applications in the therapy of PCa.	MK-8776	170-179	checkpoint kinase 1	Homo sapiens	0-4
32579780-3	2020	CHK1 has been associated with prostate cancer (PCa) induction, progression, and lethality, hence CHK1 inhibitors SCH900776 (also known as MK-8776) and the more effective SCH900776 analog MU380 may have clinical applications in the therapy of PCa.	mu380	187-192	checkpoint kinase 1	Homo sapiens	0-4
32579780-5	2020	Here we report, that such therapeutic approach may be exploited using the synergistic action of the antimetabolite gemcitabine and CHK1 inhibitors SCH900776 and MU380 in docetaxel-resistant mCRPC.	MK-8776	147-156	checkpoint kinase 1	Homo sapiens	131-135
32579780-5	2020	Here we report, that such therapeutic approach may be exploited using the synergistic action of the antimetabolite gemcitabine and CHK1 inhibitors SCH900776 and MU380 in docetaxel-resistant mCRPC.	mu380	161-166	checkpoint kinase 1	Homo sapiens	131-135
32579780-5	2020	Here we report, that such therapeutic approach may be exploited using the synergistic action of the antimetabolite gemcitabine and CHK1 inhibitors SCH900776 and MU380 in docetaxel-resistant mCRPC.	Docetaxel	170-179	checkpoint kinase 1	Homo sapiens	131-135
32579780-6	2020	Given the results, both CHK1 inhibitors significantly potentiated the sensitivity to gemcitabine in a panel of chemo-naive and matched docetaxel-resistant PCa cell lines under 2D conditions.	gemcitabine	85-96	checkpoint kinase 1	Homo sapiens	24-28
32579780-6	2020	Given the results, both CHK1 inhibitors significantly potentiated the sensitivity to gemcitabine in a panel of chemo-naive and matched docetaxel-resistant PCa cell lines under 2D conditions.	Docetaxel	135-144	checkpoint kinase 1	Homo sapiens	24-28
32579780-11	2020	Taken together, our data suggest that metabolically robust and selective CHK1 inhibitor MU380 can bypass docetaxel resistance and improve the effectiveness of gemcitabine in docetaxel-resistant mCRPC models.	mu380	88-93	checkpoint kinase 1	Homo sapiens	73-77
32579780-11	2020	Taken together, our data suggest that metabolically robust and selective CHK1 inhibitor MU380 can bypass docetaxel resistance and improve the effectiveness of gemcitabine in docetaxel-resistant mCRPC models.	Docetaxel	105-114	checkpoint kinase 1	Homo sapiens	73-77
32579780-11	2020	Taken together, our data suggest that metabolically robust and selective CHK1 inhibitor MU380 can bypass docetaxel resistance and improve the effectiveness of gemcitabine in docetaxel-resistant mCRPC models.	gemcitabine	159-170	checkpoint kinase 1	Homo sapiens	73-77
32579780-11	2020	Taken together, our data suggest that metabolically robust and selective CHK1 inhibitor MU380 can bypass docetaxel resistance and improve the effectiveness of gemcitabine in docetaxel-resistant mCRPC models.	Docetaxel	174-183	checkpoint kinase 1	Homo sapiens	73-77
32567031-0	2020	Bcl-2/Bcl-xL inhibitor navitoclax increases the antitumor effect of Chk1 inhibitor prexasertib by inducing apoptosis in pancreatic cancer cells via inhibition of Bcl-xL but not Bcl-2.	prexasertib	83-94	checkpoint kinase 1	Homo sapiens	68-72
32567031-1	2020	In our previous study, we showed that prexasertib, a checkpoint kinase 1 (Chk1) inhibitor, enhances the effects of standard drugs for pancreatic cancer, including gemcitabine (GEM), S-1, and the combination of GEM and S-1 (GS).	prexasertib	38-49	checkpoint kinase 1	Homo sapiens	53-72
32567031-1	2020	In our previous study, we showed that prexasertib, a checkpoint kinase 1 (Chk1) inhibitor, enhances the effects of standard drugs for pancreatic cancer, including gemcitabine (GEM), S-1, and the combination of GEM and S-1 (GS).	prexasertib	38-49	checkpoint kinase 1	Homo sapiens	74-78
32567031-8	2020	In addition, among the three cell lines, the combined effect of prexasertib and navitoclax resulted in increased apoptotic cell death because the protein expression levels of Bcl-xL and Chk1 were higher.	prexasertib	64-75	checkpoint kinase 1	Homo sapiens	186-190
32567031-8	2020	In addition, among the three cell lines, the combined effect of prexasertib and navitoclax resulted in increased apoptotic cell death because the protein expression levels of Bcl-xL and Chk1 were higher.	navitoclax	80-90	checkpoint kinase 1	Homo sapiens	186-190
32847043-6	2020	CLSPN c.1574A>G (p.Asn525Ser) was significantly associated with breast cancer and was shown to cause partial exon skipping and decreased Claspin expression and Chk1 activation in a minigene splicing assay and in signalling experiments, respectively.	asn525ser	19-28	checkpoint kinase 1	Homo sapiens	160-164
31782150-7	2020	Chk1 inhibition by prexasertib and its combination with the DNA damaging agent cisplatin and the PARP-inhibitor talazoparib thus emerges as a potential new treatment option for pediatric osteosarcoma which will now have to be tested in preclinical primary patient derived in vivo models and clinical studies.	Cisplatin	79-88	checkpoint kinase 1	Homo sapiens	0-4
31782150-7	2020	Chk1 inhibition by prexasertib and its combination with the DNA damaging agent cisplatin and the PARP-inhibitor talazoparib thus emerges as a potential new treatment option for pediatric osteosarcoma which will now have to be tested in preclinical primary patient derived in vivo models and clinical studies.	talazoparib	112-123	checkpoint kinase 1	Homo sapiens	0-4
33041328-0	2020	Inhibition of Chk1 by miR-320c increases oxaliplatin responsiveness in triple-negative breast cancer.	mir-320c	22-30	checkpoint kinase 1	Homo sapiens	14-18
33041328-0	2020	Inhibition of Chk1 by miR-320c increases oxaliplatin responsiveness in triple-negative breast cancer.	Oxaliplatin	41-52	checkpoint kinase 1	Homo sapiens	14-18
33041328-7	2020	We observed that overexpression of miR-320c in TNBC regulated the oxaliplatin responsiveness by mediating DNA damage repair through the negative regulation of Chk1 in vitro.	Oxaliplatin	66-77	checkpoint kinase 1	Homo sapiens	159-163
32652867-8	2020	Activation of the Wnt/beta-catenin pathway or overexpression of Chk1 abrogated the promoting effect of dbpA downregulation on 5-FU sensitivity of CRC cells.	Fluorouracil	126-130	checkpoint kinase 1	Homo sapiens	64-68
32652867-10	2020	Our study indicated that knockdown of dbpA enhanced the sensitivity of colorectal cancer cells to 5-FU via Wnt/beta-catenin/Chk1 pathway, and DbpA may be a potential therapeutic target to sensitize drug resistance colorectal cancer to 5-FU and L-OHP.	Fluorouracil	98-102	checkpoint kinase 1	Homo sapiens	124-128
32652867-10	2020	Our study indicated that knockdown of dbpA enhanced the sensitivity of colorectal cancer cells to 5-FU via Wnt/beta-catenin/Chk1 pathway, and DbpA may be a potential therapeutic target to sensitize drug resistance colorectal cancer to 5-FU and L-OHP.	Fluorouracil	235-239	checkpoint kinase 1	Homo sapiens	124-128
32652867-10	2020	Our study indicated that knockdown of dbpA enhanced the sensitivity of colorectal cancer cells to 5-FU via Wnt/beta-catenin/Chk1 pathway, and DbpA may be a potential therapeutic target to sensitize drug resistance colorectal cancer to 5-FU and L-OHP.	Oxaliplatin	244-249	checkpoint kinase 1	Homo sapiens	124-128
33007920-10	2020	Thus, PI3K/AKT signaling was activated, inhibiting CHK1 activity via phosphorylation of its serine 280 residue preventing the repair of damaged DNA.	Serine	92-98	checkpoint kinase 1	Homo sapiens	51-55
32729622-4	2020	Under ROS scavenging conditions, induction of DNA double-strand breaks (DSBs) increases the NRF2 protein level and recruits NRF2 to DNA damage sites where it interacts with ATR, resulting in activation of the ATR-CHK1-CDC2 signaling pathway.	Reactive Oxygen Species	6-9	checkpoint kinase 1	Homo sapiens	213-217
32729622-6	2020	The inhibition of NRF2 by brusatol increased the radiosensitivity of tumor cells in xenografts by perturbing ATR and CHK1 activation.	brusatol	26-34	checkpoint kinase 1	Homo sapiens	117-121
32878783-7	2020	In addition, this sclareol-induced growth arrest was associated with DNA damage as indicated by phosphorylation of H2AX, activation of ATR and Chk1.	sclareol	18-26	checkpoint kinase 1	Homo sapiens	143-147
32859084-8	2020	While the potentiation of CHK1i-mediated effects by BETi was BET-BRD4-dependent, MYC expression was BET-BRD4-independent.	beti	52-56	checkpoint kinase 1	Homo sapiens	26-31
32743678-12	2020	Strikingly, our results also revealed that HOTAIR plays a regulatory role in the expression of checkpoint kinase 1 (CHEK1), and that the restored paclitaxel sensitivity through knockdown of HOTAIR can be weakened by CHEK1 up-regulation.	Paclitaxel	146-156	checkpoint kinase 1	Homo sapiens	95-114
32743678-12	2020	Strikingly, our results also revealed that HOTAIR plays a regulatory role in the expression of checkpoint kinase 1 (CHEK1), and that the restored paclitaxel sensitivity through knockdown of HOTAIR can be weakened by CHEK1 up-regulation.	Paclitaxel	146-156	checkpoint kinase 1	Homo sapiens	116-121
32743678-12	2020	Strikingly, our results also revealed that HOTAIR plays a regulatory role in the expression of checkpoint kinase 1 (CHEK1), and that the restored paclitaxel sensitivity through knockdown of HOTAIR can be weakened by CHEK1 up-regulation.	Paclitaxel	146-156	checkpoint kinase 1	Homo sapiens	216-221
32743678-13	2020	Consistently, in vivo data confirmed that the therapeutic efficacy of paclitaxel can be enhanced through down-regulation of HOTAIR, and that CHEK1 is the down-stream target of HOTAIR in inducing paclitaxel resistance.	Paclitaxel	195-205	checkpoint kinase 1	Homo sapiens	141-146
32743678-14	2020	CONCLUSION: HOTAIR confers paclitaxel resistance in epithelial ovarian cancer by increasing the protein level of CHEK1.	Paclitaxel	27-37	checkpoint kinase 1	Homo sapiens	113-118
32647134-0	2020	Resistance to the CHK1 inhibitor prexasertib involves functionally distinct CHK1 activities in BRCA wild-type ovarian cancer.	prexasertib	33-44	checkpoint kinase 1	Homo sapiens	18-22
31707688-0	2020	A phase 1 dose-escalation study of checkpoint kinase 1 (CHK1) inhibitor prexasertib in combination with p38 mitogen-activated protein kinase (p38 MAPK) inhibitor ralimetinib in patients with advanced or metastatic cancer.	prexasertib	72-83	checkpoint kinase 1	Homo sapiens	35-54
31707688-0	2020	A phase 1 dose-escalation study of checkpoint kinase 1 (CHK1) inhibitor prexasertib in combination with p38 mitogen-activated protein kinase (p38 MAPK) inhibitor ralimetinib in patients with advanced or metastatic cancer.	prexasertib	72-83	checkpoint kinase 1	Homo sapiens	56-60
32060401-3	2020	Distinctly, prior to apoptosis, MEDI2228 activates DDRs in MM cells via phosphorylation of ATM/ATR kinases, CHK1/2, CDK1/2, and H2AX, associated with expression of DDR-related genes.	medi2228	32-40	checkpoint kinase 1	Homo sapiens	108-114
31707688-1	2020	Purpose The primary objective was to determine the recommended Phase 2 dose (RP2D) of checkpoint kinase 1 inhibitor, prexasertib, in combination with the p38 mitogen-activated protein kinase inhibitor, ralimetinib, which may be safely administered to patients with advanced cancer.	prexasertib	117-128	checkpoint kinase 1	Homo sapiens	86-105
32647134-0	2020	Resistance to the CHK1 inhibitor prexasertib involves functionally distinct CHK1 activities in BRCA wild-type ovarian cancer.	prexasertib	33-44	checkpoint kinase 1	Homo sapiens	76-80
32647134-3	2020	We recently reported a promising clinical activity of the CHK1 inhibitor (CHK1i) prexasertib monotherapy in BRCA wild-type (BRCAwt) HGSOC patients.	prexasertib	81-92	checkpoint kinase 1	Homo sapiens	58-62
32647134-7	2020	Therefore, CHK1i sensitizes CHK1i-resistant cells to DNA damaging agents such as gemcitabine or hydroxyurea by inhibition of HR.	gemcitabine	81-92	checkpoint kinase 1	Homo sapiens	11-15
32647134-7	2020	Therefore, CHK1i sensitizes CHK1i-resistant cells to DNA damaging agents such as gemcitabine or hydroxyurea by inhibition of HR.	Hydroxyurea	96-107	checkpoint kinase 1	Homo sapiens	11-15
32267018-6	2020	Key DNA damage response proteins including RPA, ATR, ATM, CHK1, and BRCA1 were activated in lung cells exposed to THS, consistent with replication stress.	THYMIDINE-5'-(DITHIO)PHOSPHATE	114-117	checkpoint kinase 1	Homo sapiens	58-62
32689938-7	2020	Our results further showed that melatonin can downregulate the expression levels of 5-FU resistance-related genes, such as thymidylate synthase in GC and ATR, CHEK1, BAX and MYC in CRC.	Melatonin	32-41	checkpoint kinase 1	Homo sapiens	159-164
32689938-7	2020	Our results further showed that melatonin can downregulate the expression levels of 5-FU resistance-related genes, such as thymidylate synthase in GC and ATR, CHEK1, BAX and MYC in CRC.	Fluorouracil	84-88	checkpoint kinase 1	Homo sapiens	159-164
32743161-6	2020	Accordingly, the combination of MT3 silencing and TMZ treatment increased the protein levels of checkpoint kinase-1, which was ultimately responsible for the lasting G1 arrest and death of double treated U87 cells.	Temozolomide	50-53	checkpoint kinase 1	Homo sapiens	96-115
32444488-4	2020	Strikingly, only 6-4PP lesions activated the ATR-Chk1 DNA damage response pathway.	6-4pp	17-22	checkpoint kinase 1	Homo sapiens	49-53
32610557-6	2020	Cisplatin-based chemotherapy combined with CHK1 inhibitor treatment synergistically inhibited cell proliferation by suppressing CHK1 phosphorylation and inducing PARP cleavage.	Cisplatin	0-9	checkpoint kinase 1	Homo sapiens	128-132
32459381-7	2020	Further, down-regulation of Wee1, CHK1, RRM1 and RRM2 contributed to CUDC-907-induced DNA damage and apoptosis.	CUDC-907	69-77	checkpoint kinase 1	Homo sapiens	34-38
32314919-2	2020	To elucidate the CHK1-regulated phosphorylation network, we performed a global quantitative phosphoproteomics analysis, which revealed 142 phosphosites whose phosphorylation levels were significantly different following treatment with the CHK1 inhibitor SCH 900776.	MK-8776	254-264	checkpoint kinase 1	Homo sapiens	17-21
32314919-2	2020	To elucidate the CHK1-regulated phosphorylation network, we performed a global quantitative phosphoproteomics analysis, which revealed 142 phosphosites whose phosphorylation levels were significantly different following treatment with the CHK1 inhibitor SCH 900776.	MK-8776	254-264	checkpoint kinase 1	Homo sapiens	239-243
32512734-10	2020	Our results indicate that SPOP deregulation plays a radiosensitizing role in PCa by impairing DDR via downregulation of RAD51 and CHK1.	ddr	94-97	checkpoint kinase 1	Homo sapiens	130-134
32371587-8	2020	Consequently, CHK1-inhibition by shRNA or treatment with the CHK1 inhibitor, prexasertib, markedly enhanced FTD-mediated DNA damage, represented by an increase of gamma-H2AX expression.	prexasertib	77-88	checkpoint kinase 1	Homo sapiens	14-18
32371587-8	2020	Consequently, CHK1-inhibition by shRNA or treatment with the CHK1 inhibitor, prexasertib, markedly enhanced FTD-mediated DNA damage, represented by an increase of gamma-H2AX expression.	prexasertib	77-88	checkpoint kinase 1	Homo sapiens	61-65
32371584-0	2020	CHK1/2 Inhibitor Prexasertib Suppresses NOTCH Signaling and Enhances Cytotoxicity of Cisplatin and Radiation in Head and Neck Squamous Cell Carcinoma.	prexasertib	17-28	checkpoint kinase 1	Homo sapiens	0-6
32424505-0	2020	Selected arylsulphonyl pyrazole derivatives as potential Chk1 kinase ligands-computational investigations.	arylsulphonyl pyrazole	9-31	checkpoint kinase 1	Homo sapiens	57-61
32371584-0	2020	CHK1/2 Inhibitor Prexasertib Suppresses NOTCH Signaling and Enhances Cytotoxicity of Cisplatin and Radiation in Head and Neck Squamous Cell Carcinoma.	Cisplatin	85-94	checkpoint kinase 1	Homo sapiens	0-6
32371584-3	2020	Checkpoint kinase 1 and 2 (CHK1/2) are serine/threonine kinases that activate cell cycle checkpoints and serve a critical role in the DNA-damage response (DDR).	Serine	39-45	checkpoint kinase 1	Homo sapiens	0-25
32371584-3	2020	Checkpoint kinase 1 and 2 (CHK1/2) are serine/threonine kinases that activate cell cycle checkpoints and serve a critical role in the DNA-damage response (DDR).	Serine	39-45	checkpoint kinase 1	Homo sapiens	27-33
32371584-4	2020	As resistance to cisplatin and radiation may involve a heightened DDR, we hypothesized that prexasertib, an inhibitor of CHK1/2, may enhance the cytotoxicity induced by cisplatin and irradiation in HNSCC.	prexasertib	92-103	checkpoint kinase 1	Homo sapiens	121-127
32371587-4	2020	Here, we propose a novel therapeutic strategy based on synthetic lethality combining trifluridine/tipiracil (FTD/TPI) and prexasertib (CHK1 inhibitor) as a treatment for ESCC.	prexasertib	122-133	checkpoint kinase 1	Homo sapiens	135-139
32371587-7	2020	Because CHK1-phosphorylation is considered to be induced as DDR for FTD-mediated DNA damage, we examined the effects of CHK1-inhibition on FTD treatment.	ddr	60-63	checkpoint kinase 1	Homo sapiens	8-12
32160976-5	2020	In particular, DCZ0847 induced DNA damage and triggered a DNA-damage response by enhancing the levels of gamma-H2A.X, phosphorylated (p)-ATM, p-ATR, p-Chk1, and p-Chk2.	dcz0847	15-22	checkpoint kinase 1	Homo sapiens	151-155
32424505-6	2020	The estimation of binding affinity seems to indicate that the indazole 5-substituted with 3,5-dimethylpyrazole 4 and condensed pyrazoloquinoline derivative 7 fit the best to the Chk1-binding pocket.	Indazoles	62-70	checkpoint kinase 1	Homo sapiens	178-182
32424505-5	2020	In the present study, in order to verify possibility of interactions of pyrazole and indazole derivatives with Chk1, we focused on the docking of selected tosyl derivatives of indazole and condensed pyrazole 1-7 to the Chk1 pocket, analysis of interactions involving optimized ligand-protein system using DFT formalism, and estimation of the interaction enthalpy of the ligand-protein complex by applying the PM7 method.	pyrazole	72-80	checkpoint kinase 1	Homo sapiens	111-115
32424505-5	2020	In the present study, in order to verify possibility of interactions of pyrazole and indazole derivatives with Chk1, we focused on the docking of selected tosyl derivatives of indazole and condensed pyrazole 1-7 to the Chk1 pocket, analysis of interactions involving optimized ligand-protein system using DFT formalism, and estimation of the interaction enthalpy of the ligand-protein complex by applying the PM7 method.	pyrazole	72-80	checkpoint kinase 1	Homo sapiens	219-223
32424505-6	2020	The estimation of binding affinity seems to indicate that the indazole 5-substituted with 3,5-dimethylpyrazole 4 and condensed pyrazoloquinoline derivative 7 fit the best to the Chk1-binding pocket.	3,5-dimethylpyrazole	90-110	checkpoint kinase 1	Homo sapiens	178-182
32424505-5	2020	In the present study, in order to verify possibility of interactions of pyrazole and indazole derivatives with Chk1, we focused on the docking of selected tosyl derivatives of indazole and condensed pyrazole 1-7 to the Chk1 pocket, analysis of interactions involving optimized ligand-protein system using DFT formalism, and estimation of the interaction enthalpy of the ligand-protein complex by applying the PM7 method.	Indazoles	85-93	checkpoint kinase 1	Homo sapiens	111-115
32424505-6	2020	The estimation of binding affinity seems to indicate that the indazole 5-substituted with 3,5-dimethylpyrazole 4 and condensed pyrazoloquinoline derivative 7 fit the best to the Chk1-binding pocket.	pyrazoloquinoline	127-144	checkpoint kinase 1	Homo sapiens	178-182
32424505-9	2020	Graphical Abstract Presentation of methods used to describe the interactions between arylsulphonyl pyrazole derivatives and Chk1 kinase.	arylsulphonyl pyrazole	85-107	checkpoint kinase 1	Homo sapiens	124-128
32424505-5	2020	In the present study, in order to verify possibility of interactions of pyrazole and indazole derivatives with Chk1, we focused on the docking of selected tosyl derivatives of indazole and condensed pyrazole 1-7 to the Chk1 pocket, analysis of interactions involving optimized ligand-protein system using DFT formalism, and estimation of the interaction enthalpy of the ligand-protein complex by applying the PM7 method.	Indazoles	85-93	checkpoint kinase 1	Homo sapiens	219-223
32424505-5	2020	In the present study, in order to verify possibility of interactions of pyrazole and indazole derivatives with Chk1, we focused on the docking of selected tosyl derivatives of indazole and condensed pyrazole 1-7 to the Chk1 pocket, analysis of interactions involving optimized ligand-protein system using DFT formalism, and estimation of the interaction enthalpy of the ligand-protein complex by applying the PM7 method.	Chloral Hydrate	155-160	checkpoint kinase 1	Homo sapiens	111-115
32424505-5	2020	In the present study, in order to verify possibility of interactions of pyrazole and indazole derivatives with Chk1, we focused on the docking of selected tosyl derivatives of indazole and condensed pyrazole 1-7 to the Chk1 pocket, analysis of interactions involving optimized ligand-protein system using DFT formalism, and estimation of the interaction enthalpy of the ligand-protein complex by applying the PM7 method.	Chloral Hydrate	155-160	checkpoint kinase 1	Homo sapiens	219-223
32424505-5	2020	In the present study, in order to verify possibility of interactions of pyrazole and indazole derivatives with Chk1, we focused on the docking of selected tosyl derivatives of indazole and condensed pyrazole 1-7 to the Chk1 pocket, analysis of interactions involving optimized ligand-protein system using DFT formalism, and estimation of the interaction enthalpy of the ligand-protein complex by applying the PM7 method.	Indazoles	176-184	checkpoint kinase 1	Homo sapiens	111-115
32424505-5	2020	In the present study, in order to verify possibility of interactions of pyrazole and indazole derivatives with Chk1, we focused on the docking of selected tosyl derivatives of indazole and condensed pyrazole 1-7 to the Chk1 pocket, analysis of interactions involving optimized ligand-protein system using DFT formalism, and estimation of the interaction enthalpy of the ligand-protein complex by applying the PM7 method.	Indazoles	176-184	checkpoint kinase 1	Homo sapiens	219-223
32424505-5	2020	In the present study, in order to verify possibility of interactions of pyrazole and indazole derivatives with Chk1, we focused on the docking of selected tosyl derivatives of indazole and condensed pyrazole 1-7 to the Chk1 pocket, analysis of interactions involving optimized ligand-protein system using DFT formalism, and estimation of the interaction enthalpy of the ligand-protein complex by applying the PM7 method.	pyrazole	199-207	checkpoint kinase 1	Homo sapiens	111-115
32424505-5	2020	In the present study, in order to verify possibility of interactions of pyrazole and indazole derivatives with Chk1, we focused on the docking of selected tosyl derivatives of indazole and condensed pyrazole 1-7 to the Chk1 pocket, analysis of interactions involving optimized ligand-protein system using DFT formalism, and estimation of the interaction enthalpy of the ligand-protein complex by applying the PM7 method.	pyrazole	199-207	checkpoint kinase 1	Homo sapiens	219-223
32393310-11	2020	The expression of P53 and phosphokinases including CHK1, CHK2, PLK1, and Aurora A increased after CoCl2 treatment.	cobaltous chloride	98-103	checkpoint kinase 1	Homo sapiens	51-55
32277442-6	2020	Exposure of asynchronous malignant granulosa cells to gemcitabine caused growth arrest, induced DNA damage and activated cellular stress pathways, cell cycle checkpoint sensors and triggered apoptosis as evidenced by increased expression of phospho-p38, gamma-histone H2AX, phospho-Chk-1/phospho-Chk-2, and cleaved forms of PARP and caspase-3 in a dose dependent manner.	gemcitabine	54-65	checkpoint kinase 1	Homo sapiens	282-287
32173365-0	2020	Targeting replication stress response using polypurine reverse hoogsteen hairpins directed against WEE1 and CHK1 genes in human cancer cells.	polypurine	44-54	checkpoint kinase 1	Homo sapiens	108-112
31713291-6	2020	We also identified multiple lysine residues on Chk1 that are poly-ubiquitinated by HUWE1 in vitro, many of which are within the kinase domain.	tyrosyl-lysine	28-34	checkpoint kinase 1	Homo sapiens	47-51
31713291-8	2020	Moreover, prolonged replication stress induced by hydroxyurea or camptothecin resulted in a reduction of Chk1 protein levels, which was rescued by HUWE1 knockdown.	Hydroxyurea	50-61	checkpoint kinase 1	Homo sapiens	105-109
31713291-8	2020	Moreover, prolonged replication stress induced by hydroxyurea or camptothecin resulted in a reduction of Chk1 protein levels, which was rescued by HUWE1 knockdown.	Camptothecin	65-77	checkpoint kinase 1	Homo sapiens	105-109
31904486-0	2020	All-trans retinoic acid exerts selective anti-FLT3-ITD acute myeloid leukemia efficacy through downregulating Chk1 kinase.	Tretinoin	0-23	checkpoint kinase 1	Homo sapiens	110-114
32161100-4	2020	We used the developmental clinical drug SRA737 in an unbiased large-scale siRNA screen to identify novel mediators of CHK1 inhibitor sensitivity and uncover potential combination therapies and biomarkers for patient selection.	SRA737	40-46	checkpoint kinase 1	Homo sapiens	118-122
31904486-2	2020	In this work, we report that ATRA causes fatal mitotic catastrophe in FLT3-ITD AML cells by degrading Chk1 kinase, and therefore preventing DNA damage repair.	Tretinoin	29-33	checkpoint kinase 1	Homo sapiens	102-106
31904486-6	2020	Taken together, our results indicate that ATRA down-regulates Chk1 in FLT3-ITD AML cells, and the combination of ATRA and SN38 significantly improves the anti-tumor effect of either ATRA or SN38 when used alone.	Tretinoin	42-46	checkpoint kinase 1	Homo sapiens	62-66
32355824-9	2020	All of the 10 hub genes (CCNA2, CCNB1, MAD2L1, BU1B, RACGAP1, CHEK1, BUB1, ASPM, NCAPG and TTK) have a strong association with lower overall survival in liver cancer patients and four genes (CCNA2, CCNB1, CHEK1 and BUB1) have reduced expression in metformin-treated samples.	Metformin	248-257	checkpoint kinase 1	Homo sapiens	62-67
32178478-8	2020	The molecular docking results showed that the CHEK1 gene can be regulated by microRNAs (miR-195-5p) due to the number of stable hydrogen atoms observed within the distance of 2.0 A and the favorable amino acids (Ala221, Ile353, Ile365, Ile756, Val797, Val70, Val154, Ile159, Val347, Tyr804, Phe811, Tyr815, and Phe156) identified in the binding pocket of the argonaute protein.	Hydrogen	128-136	checkpoint kinase 1	Homo sapiens	46-51
32178478-3	2020	The expression of CHEK1 was investigated using Oncomine analysis.	oncomine	47-55	checkpoint kinase 1	Homo sapiens	18-23
32355824-9	2020	All of the 10 hub genes (CCNA2, CCNB1, MAD2L1, BU1B, RACGAP1, CHEK1, BUB1, ASPM, NCAPG and TTK) have a strong association with lower overall survival in liver cancer patients and four genes (CCNA2, CCNB1, CHEK1 and BUB1) have reduced expression in metformin-treated samples.	Metformin	248-257	checkpoint kinase 1	Homo sapiens	205-210
31912675-5	2020	RESULTS: The PD-L1 expression was upregulated by C-ion beam in a dose-dependent manner in HeLa and SiHa cells through phosphorylated Chk1.	Carbon	49-50	checkpoint kinase 1	Homo sapiens	133-137
31289205-10	2020	Three kinases inhibitors (CHK1i, MELKi and PBKi) overcome resistance to Lenalidomide, while CHK1, PBK and DBF4 inhibitors re-sensitized Melphalan resistant cell line to this conventional therapeutic agent.	Lenalidomide	72-84	checkpoint kinase 1	Homo sapiens	26-30
31822519-3	2020	Specifically, we simultaneously inhibited checkpoint kinase 1 (Chk1) by prexasertib and the G9a histone methyltransferase with BRD4770, thereby targeting two key pathways for replication fork stability.	prexasertib	72-83	checkpoint kinase 1	Homo sapiens	42-61
31822519-3	2020	Specifically, we simultaneously inhibited checkpoint kinase 1 (Chk1) by prexasertib and the G9a histone methyltransferase with BRD4770, thereby targeting two key pathways for replication fork stability.	prexasertib	72-83	checkpoint kinase 1	Homo sapiens	63-67
31822519-3	2020	Specifically, we simultaneously inhibited checkpoint kinase 1 (Chk1) by prexasertib and the G9a histone methyltransferase with BRD4770, thereby targeting two key pathways for replication fork stability.	BRD4770	127-134	checkpoint kinase 1	Homo sapiens	42-61
31822519-3	2020	Specifically, we simultaneously inhibited checkpoint kinase 1 (Chk1) by prexasertib and the G9a histone methyltransferase with BRD4770, thereby targeting two key pathways for replication fork stability.	BRD4770	127-134	checkpoint kinase 1	Homo sapiens	63-67
32073931-3	2021	The aim of this study was to assess the ability of the PARP inhibitor niraparib (MK-4827) alone, or in combination with cell cycle checkpoint abrogating drugs targeting Chk1 (MK-8776) or Wee1 (MK-1775), to radiosensitize HNSCCs in the context of HPV status.Materials and Methods: PARP1, PARP2, Chk1 or Wee1 shRNA constructs were analyzed from an in vivo shRNA screen of HNSCC xenografts comparing radiosensitization differences between HPV(+) and HPV(-) tumors.	niraparib	70-79	checkpoint kinase 1	Homo sapiens	294-298
32034120-2	2020	Here we demonstrate that inhibition of dihydroorotate dehydrogenase (DHODH), a key enzyme of the de novo pyrimidine synthesis pathway, effectively decreases proliferation of cancer cells via induction of replication and ribosomal stress in a p53- and checkpoint kinase 1 (Chk1)-dependent manner.	pyrimidine	105-115	checkpoint kinase 1	Homo sapiens	251-270
32210727-5	2020	Results: In ER-/PR-/HER2- breast cancer, CHK1 inhibition enhanced adriamycin (ADR) chemosensitivity which was mediated by the mitotic checkpoint complex (MCC)-anaphase-promoting complex/cyclosome (APC/C)-cyclin B1 axis, Msh homeobox 2 (MSX2) and Bcl-2-like protein 11 (BIM).	Doxorubicin	66-76	checkpoint kinase 1	Homo sapiens	41-45
32075943-8	2020	Treatment by the ATR inhibitor VE-822 increased sensitivity to irinotecan in SLFN11-negative PDXs and abolished irinotecan-induced phosphorylation of checkpoint kinase 1 (CHK1).	irinotecan	112-122	checkpoint kinase 1	Homo sapiens	150-169
32075943-8	2020	Treatment by the ATR inhibitor VE-822 increased sensitivity to irinotecan in SLFN11-negative PDXs and abolished irinotecan-induced phosphorylation of checkpoint kinase 1 (CHK1).	irinotecan	112-122	checkpoint kinase 1	Homo sapiens	171-175
32071282-0	2020	The iron-sulfur helicase DDX11 promotes the generation of single-stranded DNA for CHK1 activation.	Sulfur	4-15	checkpoint kinase 1	Homo sapiens	82-86
32071282-6	2020	Accordingly, depletion of DDX11 causes reduced levels of single-stranded DNA, a reduction of chromatin-bound replication protein A, and impaired CHK1 phosphorylation at serine-345.	cholecystokinin C-terminal flanking peptide	169-175	checkpoint kinase 1	Homo sapiens	145-149
32034120-2	2020	Here we demonstrate that inhibition of dihydroorotate dehydrogenase (DHODH), a key enzyme of the de novo pyrimidine synthesis pathway, effectively decreases proliferation of cancer cells via induction of replication and ribosomal stress in a p53- and checkpoint kinase 1 (Chk1)-dependent manner.	pyrimidine	105-115	checkpoint kinase 1	Homo sapiens	272-276
32012873-5	2020	Subsequent analyses demonstrated potent combination activity between the CHK1/2 inhibitor LY2606268 (prexasertib), which eliminates a G2 checkpoint, and the WEE1 inhibitor AZD1775 (adavosertib), which promotes M-phase entry, in induction of DNA damage, mitotic catastrophe, and apoptosis, and reduction of anchorage independent growth and clonogenic capacity.	prexasertib	101-112	checkpoint kinase 1	Homo sapiens	73-79
31789403-1	2020	Our previous study demonstrated that gemcitabine (GEM), S-1, and a combination of GEM and S-1 (GS) induced S-phase arrest and increased the phosphorylation of checkpoint kinase 1 (Chk1), which is a critical mediator of cell survival under impaired DNA replication, in pancreatic cancer cell lines.	gemcitabine	37-48	checkpoint kinase 1	Homo sapiens	159-178
31789403-1	2020	Our previous study demonstrated that gemcitabine (GEM), S-1, and a combination of GEM and S-1 (GS) induced S-phase arrest and increased the phosphorylation of checkpoint kinase 1 (Chk1), which is a critical mediator of cell survival under impaired DNA replication, in pancreatic cancer cell lines.	gemcitabine	37-48	checkpoint kinase 1	Homo sapiens	180-184
31789403-1	2020	Our previous study demonstrated that gemcitabine (GEM), S-1, and a combination of GEM and S-1 (GS) induced S-phase arrest and increased the phosphorylation of checkpoint kinase 1 (Chk1), which is a critical mediator of cell survival under impaired DNA replication, in pancreatic cancer cell lines.	gemcitabine	50-53	checkpoint kinase 1	Homo sapiens	159-178
31789403-1	2020	Our previous study demonstrated that gemcitabine (GEM), S-1, and a combination of GEM and S-1 (GS) induced S-phase arrest and increased the phosphorylation of checkpoint kinase 1 (Chk1), which is a critical mediator of cell survival under impaired DNA replication, in pancreatic cancer cell lines.	gemcitabine	50-53	checkpoint kinase 1	Homo sapiens	180-184
32014904-10	2020	ELA32 treatment suppressed iodixanol-induced up-regulation of DNA damage-associated gene P-ATR and p-CHK1 as well as apoptosis-associated gene C-caspase 3 (p&lt;0.05).	iodixanol	27-36	checkpoint kinase 1	Homo sapiens	101-105
32042960-6	2020	Interestingly, we also observed an attenuated cell cycle response to gamma ionizing radiation (gamma-IR) via diminished phosphorylation of checkpoint kinase 1 (Chk1) on serine 345 in these cell lines.	cholecystokinin C-terminal flanking peptide	169-175	checkpoint kinase 1	Homo sapiens	139-158
32042960-6	2020	Interestingly, we also observed an attenuated cell cycle response to gamma ionizing radiation (gamma-IR) via diminished phosphorylation of checkpoint kinase 1 (Chk1) on serine 345 in these cell lines.	cholecystokinin C-terminal flanking peptide	169-175	checkpoint kinase 1	Homo sapiens	160-164
31889509-5	2019	The residual Chk1 activation in Cdc7-depleted cells is lost upon further depletion of casein kinase1 (CK1gamma1), previously reported to phosphorylate CKBD.	ckbd	151-155	checkpoint kinase 1	Homo sapiens	13-17
31512029-6	2020	Prexasertib (LY2606368) is a small ATP-competitive selective inhibitor of CHK1 and CHK2.	prexasertib	0-11	checkpoint kinase 1	Homo sapiens	74-78
31512029-6	2020	Prexasertib (LY2606368) is a small ATP-competitive selective inhibitor of CHK1 and CHK2.	prexasertib	13-22	checkpoint kinase 1	Homo sapiens	74-78
31512029-6	2020	Prexasertib (LY2606368) is a small ATP-competitive selective inhibitor of CHK1 and CHK2.	Adenosine Triphosphate	35-38	checkpoint kinase 1	Homo sapiens	74-78
32013837-7	2020	RESULTS: Here, we reported that pisosterol markedly induced G2/M arrest and apoptosis and decreased the cell viability and proliferation potential of glioma cells in a dose-dependent manner by increasing the expression of ATM, CASP3, CDK1, CDKN1A, CDKN2A, CDKN2B, CHEK1, p14ARF and TP53 and decreasing the expression of MYC, BCL2, BMI1 and MDM2.	pisosterol	32-42	checkpoint kinase 1	Homo sapiens	264-269
32281394-9	2020	Levels of the G2 phase-related molecules phosphorylated ATM, CHK1, CHK2, CDC25C, and cyclin B1 were increased in TLC388-treated cells.	TLC 388	113-119	checkpoint kinase 1	Homo sapiens	61-65
31760882-7	2020	The amount of repressive phosphorylation of CDK1 at tyrosine 15 (Y15) was decreased by Chk1 inhibitor treatment.	Tyrosine	52-60	checkpoint kinase 1	Homo sapiens	87-91
31932554-7	2020	Furthermore, our results demonstrated that the expression levels of gammaH2AX, p-Chk1 and p-Chk2 were significantly up-regulated, suggesting the induction of DNA damage responses in EJ-treated prostate cancer cells.	eupalinolide A	182-184	checkpoint kinase 1	Homo sapiens	81-85
31649026-1	2020	Inhibition of ribonucleotide reductase (RNR), the rate-limiting enzyme in the synthesis of deoxyribonucleotides, causes DNA replication stress and activates the ATR-CHK1 pathway.	Ribonucleotides	14-28	checkpoint kinase 1	Homo sapiens	165-169
31649026-1	2020	Inhibition of ribonucleotide reductase (RNR), the rate-limiting enzyme in the synthesis of deoxyribonucleotides, causes DNA replication stress and activates the ATR-CHK1 pathway.	Deoxyribonucleotides	91-111	checkpoint kinase 1	Homo sapiens	165-169
31610912-2	2019	In this study, we closely analyzed this kinetics using a CHK1 inhibitor (PF00477736) in HeLa cells expressing fluorescent ubiquitination-based cell cycle indicator (Fucci).	PF 00477736	73-83	checkpoint kinase 1	Homo sapiens	57-61
31759252-9	2019	Activation of DNA damage response pathways (ATM, Chk1, and Chk2) are decreased at 24 hours DOX-treatment in MMTV-PyMT;ApcMin/+ cells compared to control cells, but show activation at earlier time points.	Doxorubicin	91-94	checkpoint kinase 1	Homo sapiens	49-53
31783714-2	2019	The initial CHK1 inhibitor staurosporine analog, UCN01, entered clinical trials whilst it was still considered to act via PKC inhibition; only later were trials performed in a more focused fashion to determine whether CHK1 inhibition could dysregulate cell cycle checkpoints.	Staurosporine	27-40	checkpoint kinase 1	Homo sapiens	12-16
31783714-2	2019	The initial CHK1 inhibitor staurosporine analog, UCN01, entered clinical trials whilst it was still considered to act via PKC inhibition; only later were trials performed in a more focused fashion to determine whether CHK1 inhibition could dysregulate cell cycle checkpoints.	Staurosporine	27-40	checkpoint kinase 1	Homo sapiens	218-222
31470128-4	2019	METHODS AND RESULTS: Here, we show that combined treatment of SRA737, an oral CHK1 inhibitor, and anti-programmed death ligand 1 (PD-L1) leads to an antitumor response in multiple cancer models, including SCLC.	SRA737	62-68	checkpoint kinase 1	Homo sapiens	78-82
31686145-7	2019	Further studies suggested that autophagy suppression could obstruct the activation of checkpoint kinase 1 (Chk1) through elevating proteasomal activity and then impair the capacity of homologous recombination (HR), thereby improving the anti-LSCC efficiency of Niraparib.	niraparib	261-270	checkpoint kinase 1	Homo sapiens	86-105
31686145-7	2019	Further studies suggested that autophagy suppression could obstruct the activation of checkpoint kinase 1 (Chk1) through elevating proteasomal activity and then impair the capacity of homologous recombination (HR), thereby improving the anti-LSCC efficiency of Niraparib.	niraparib	261-270	checkpoint kinase 1	Homo sapiens	107-111
31533931-5	2019	Both 9-ING-41 and siRNA depletion of GSK-3 kinases impaired the activation of ATR leading to the phosphorylation and activation of Chk1.	9-ing	5-10	checkpoint kinase 1	Homo sapiens	131-135
31783584-5	2019	Moreover, transcriptional activation of ZEB1 facilitated GR cells to repair gemcitabine-mediated DNA damage via ATM/p-CHK1 signaling pathway.	gemcitabine	76-87	checkpoint kinase 1	Homo sapiens	118-122
30819918-7	2019	Downregulation of CHK1, Wee1, and RRM1, and induction of DNA damage also contributed to CUDC-907-induced apoptosis of acute myeloid leukemia cells.	CUDC-907	88-96	checkpoint kinase 1	Homo sapiens	18-22
31683862-8	2019	The Chk1 inhibitor MK-8776 was most effective, reducing viral DNA amplification by 90-99% and caused DNA damage and apoptosis, preferentially in HPV infected cells.	MK-8776	19-26	checkpoint kinase 1	Homo sapiens	4-8
31441116-10	2019	Cisplatin treatment resulted in increased autophosphorylation of ATR (T1989) and CHK1 (S345) phosphorylation that was markedly suppressed in the presence of WA.	Cisplatin	0-9	checkpoint kinase 1	Homo sapiens	81-85
31717700-6	2019	RESULTS: This study reports, for the first time, the efficacy of the concomitant inhibition of CHK1/CHK2 and WEE1 in ALL cell lines and primary leukemic B-ALL cells using two selective inhibitors: PF-0047736 (CHK1/CHK2 inhibitor) and AZD-1775 (WEE1 inhibitor).	Platelet Factor 3	197-207	checkpoint kinase 1	Homo sapiens	95-99
31431503-0	2019	The ribonucleoside AICAr induces differentiation of myeloid leukemia by activating the ATR/Chk1 kinase via pyrimidine depletion.	pyrimidine	107-117	checkpoint kinase 1	Homo sapiens	91-95
31444271-4	2019	RECQ1 loss led to defective ATR Ser/Thr kinase (ATR)/checkpoint kinase 1 (ChK1) activation and greater DNA damage accumulation in response to gemcitabine treatment.	gemcitabine	142-153	checkpoint kinase 1	Homo sapiens	74-78
31444271-6	2019	Consistent with defective checkpoint activation, a ChK1 inhibitor further sensitized RECQ1-deficient cells to gemcitabine and increased cell death.	gemcitabine	110-121	checkpoint kinase 1	Homo sapiens	51-55
31717700-6	2019	RESULTS: This study reports, for the first time, the efficacy of the concomitant inhibition of CHK1/CHK2 and WEE1 in ALL cell lines and primary leukemic B-ALL cells using two selective inhibitors: PF-0047736 (CHK1/CHK2 inhibitor) and AZD-1775 (WEE1 inhibitor).	adavosertib	234-242	checkpoint kinase 1	Homo sapiens	95-99
31601781-6	2019	Mechanistically, LINC02582 interacts with deubiquitinating enzyme ubiquitin specific peptidase 7 (USP7) to deubiquitinate and stabilize checkpoint kinase 1 (CHK1), a critical effector kinase in DNA damage response, thus promoting radioresistance.	linc02582	17-26	checkpoint kinase 1	Homo sapiens	136-155
31639020-0	2019	The Chk1 inhibitor SAR-020106 sensitizes human glioblastoma cells to irradiation, to temozolomide, and to decitabine treatment.	temozolomide	85-97	checkpoint kinase 1	Homo sapiens	4-8
31639020-0	2019	The Chk1 inhibitor SAR-020106 sensitizes human glioblastoma cells to irradiation, to temozolomide, and to decitabine treatment.	decitabine	106-116	checkpoint kinase 1	Homo sapiens	4-8
31409614-0	2019	The CHK1 Inhibitor Prexasertib Exhibits Monotherapy Activity in High-Grade Serous Ovarian Cancer Models and Sensitizes to PARP Inhibition.	prexasertib	19-30	checkpoint kinase 1	Homo sapiens	4-8
31409614-3	2019	We assessed the activity of prexasertib, a checkpoint kinase 1 (CHK1) inhibitor known to cause replication catastrophe, as monotherapy and in combination with the PARP inhibitor olaparib in preclinical models of HGSOC, including those with acquired PARP inhibitor resistance.Experimental Design: Prexasertib was tested as a single agent or in combination with olaparib in 14 clinically annotated and molecularly characterized luciferized HGSOC patient-derived xenograft (PDX) models and in a panel of ovarian cancer cell lines.	prexasertib	28-39	checkpoint kinase 1	Homo sapiens	43-62
31409614-3	2019	We assessed the activity of prexasertib, a checkpoint kinase 1 (CHK1) inhibitor known to cause replication catastrophe, as monotherapy and in combination with the PARP inhibitor olaparib in preclinical models of HGSOC, including those with acquired PARP inhibitor resistance.Experimental Design: Prexasertib was tested as a single agent or in combination with olaparib in 14 clinically annotated and molecularly characterized luciferized HGSOC patient-derived xenograft (PDX) models and in a panel of ovarian cancer cell lines.	prexasertib	28-39	checkpoint kinase 1	Homo sapiens	64-68
31601781-6	2019	Mechanistically, LINC02582 interacts with deubiquitinating enzyme ubiquitin specific peptidase 7 (USP7) to deubiquitinate and stabilize checkpoint kinase 1 (CHK1), a critical effector kinase in DNA damage response, thus promoting radioresistance.	linc02582	17-26	checkpoint kinase 1	Homo sapiens	157-161
31597105-7	2019	SENP6 deficiency impairs chromatin association of the ATR cofactor ATRIP, thereby compromising the activation of Chk1 signaling in response to aphidicolin-induced replicative stress and sensitizing cells to DNA damage.	Aphidicolin	143-154	checkpoint kinase 1	Homo sapiens	113-117
31271644-2	2019	This study has been attempted to elucidate the DNA damage response mechanism in a dermal model exposed to ZnO NPs through Ataxia Telangiectasia Mutated (ATM)-mediated ChK1-dependent G2/M arrest.	Zinc Oxide	106-109	checkpoint kinase 1	Homo sapiens	167-171
31337671-7	2019	We have also found that Chk1 plays a major role in the maintenance of genomic integrity following treatment with P-AscH-.	p-asch-	113-120	checkpoint kinase 1	Homo sapiens	24-28
31092016-3	2019	In cancer cells, overexpression of the serine/threonine-protein kinase CHK1 (checkpoint kinase 1) is exploited to counteract the excess of DNA damage insults they are exposed to.	Serine	39-45	checkpoint kinase 1	Homo sapiens	71-75
31519582-7	2019	Western blotting showed that Ro 90-7501 suppressed the phosphorylation of ATM and its downstream proteins, such as H2AX, Chk1, and Chk2, after irradiation.	ro 90	29-34	checkpoint kinase 1	Homo sapiens	121-125
31273061-5	2019	Temozolomide, unlike other alkylators, activated the ataxia telangiectasia and Rad3-related (ATR)-checkpoint kinase 1 (Chk1) axis in a manner that was highly dependent on MGMT status.	Temozolomide	0-12	checkpoint kinase 1	Homo sapiens	119-123
31273061-6	2019	Temozolomide induced growth delay, DNA double-strand breaks, and G2-M cell-cycle arrest, which led to ATR-dependent phosphorylation of Chk1; this effect was dependent on reduced MGMT expression.	Temozolomide	0-12	checkpoint kinase 1	Homo sapiens	135-139
31528122-0	2019	Long non-coding RNA LINC00485 acts as a microRNA-195 sponge to regulate the chemotherapy sensitivity of lung adenocarcinoma cells to cisplatin by regulating CHEK1.	Cisplatin	133-142	checkpoint kinase 1	Homo sapiens	157-162
31443367-0	2019	Chk1 Inhibitor MK-8776 Restores the Sensitivity of Chemotherapeutics in P-glycoprotein Overexpressing Cancer Cells.	MK-8776	15-22	checkpoint kinase 1	Homo sapiens	0-4
31443367-3	2019	Here, we report that checkpoint kinase (Chk) 1 inhibitor MK-8776, a drug candidate in clinical trial, can restore the sensitivity of chemotherapeutics that are substrates of P-gp in KB-C2, SW620/Ad300 cells and human embryonic kidney (HEK)293/ABCB1 cells that overexpress P-gp.	MK-8776	57-64	checkpoint kinase 1	Homo sapiens	21-46
30737777-5	2019	Following DNA damage, addition of the TLK specific inhibitor, thioridazine (THD), impairs ATR and Chk1 activation, establishing the existence of a ADT > TLK1 > NEK1 > ATR > Chk1, DDR pathway, while its abrogation leads to apoptosis.	Thioridazine	62-74	checkpoint kinase 1	Homo sapiens	98-102
30737777-5	2019	Following DNA damage, addition of the TLK specific inhibitor, thioridazine (THD), impairs ATR and Chk1 activation, establishing the existence of a ADT > TLK1 > NEK1 > ATR > Chk1, DDR pathway, while its abrogation leads to apoptosis.	Thioridazine	62-74	checkpoint kinase 1	Homo sapiens	173-177
31078603-6	2019	Furthermore, exposure to the Fe(II) complex led to excessive reactive oxygen species (ROS) accumulation by thioredoxin reductase (TrxR) inhibition and DNA double-strand breaks (DSBs), which in turn sequentially activated ATM, CHK1/2 and p53.	ammonium ferrous sulfate	29-35	checkpoint kinase 1	Homo sapiens	226-232
31078603-6	2019	Furthermore, exposure to the Fe(II) complex led to excessive reactive oxygen species (ROS) accumulation by thioredoxin reductase (TrxR) inhibition and DNA double-strand breaks (DSBs), which in turn sequentially activated ATM, CHK1/2 and p53.	Reactive Oxygen Species	61-84	checkpoint kinase 1	Homo sapiens	226-232
31078603-6	2019	Furthermore, exposure to the Fe(II) complex led to excessive reactive oxygen species (ROS) accumulation by thioredoxin reductase (TrxR) inhibition and DNA double-strand breaks (DSBs), which in turn sequentially activated ATM, CHK1/2 and p53.	Reactive Oxygen Species	86-89	checkpoint kinase 1	Homo sapiens	226-232
31092016-3	2019	In cancer cells, overexpression of the serine/threonine-protein kinase CHK1 (checkpoint kinase 1) is exploited to counteract the excess of DNA damage insults they are exposed to.	Serine	39-45	checkpoint kinase 1	Homo sapiens	77-96
31362335-6	2019	Interestingly, combined treatment with PF-477736 and the ATM inhibitor Ku55933 overcame the insensitivity of NB-39-nu and SK-N-BE cells to CHK1 inhibition and induced mitotic cell death.	pyrazofurin	39-41	checkpoint kinase 1	Homo sapiens	139-143
30786016-7	2019	Treatment of HPV8-CER expressing cells with the autophagy inhibitor Bafilomycin A1 rescued CHK1 expression and led to LC3B accumulation.	bafilomycin	68-79	checkpoint kinase 1	Homo sapiens	91-95
31839711-1	2019	Introduction: Cisplatin has been reported to elicit the DNA damage response (DDR) via activation of the ATR-Chk1 pathway, which in turn contributes to the induction of cisplatin resistance.	Cisplatin	14-23	checkpoint kinase 1	Homo sapiens	108-112
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	checkpoint kinase 1	Homo sapiens	154-159
31839711-1	2019	Introduction: Cisplatin has been reported to elicit the DNA damage response (DDR) via activation of the ATR-Chk1 pathway, which in turn contributes to the induction of cisplatin resistance.	Cisplatin	168-177	checkpoint kinase 1	Homo sapiens	108-112
31362335-6	2019	Interestingly, combined treatment with PF-477736 and the ATM inhibitor Ku55933 overcame the insensitivity of NB-39-nu and SK-N-BE cells to CHK1 inhibition and induced mitotic cell death.	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	71-78	checkpoint kinase 1	Homo sapiens	139-143
31839711-2	2019	Inhibition of ATR-Chk1 signaling reverses cisplatin resistance in some cancers.	Cisplatin	42-51	checkpoint kinase 1	Homo sapiens	18-22
31839711-3	2019	However, the influence of inhibiting ATR-Chk1 signaling on cisplatin resistance in chondrosarcoma cancer has not been reported.	Cisplatin	59-68	checkpoint kinase 1	Homo sapiens	41-45
31362335-7	2019	Similarly, co-treatment with PF-477736 and NU7441, a pharmacological inhibitor of DNA-PK, which is also essential for the DDR pathway, rendered the cells sensitive to CHK1 inhibition.	pyrazofurin	29-31	checkpoint kinase 1	Homo sapiens	167-171
31839711-7	2019	Results: We found that chondrosarcoma cells expressed very low basal levels of phosphorylated ATR, but cisplatin treatment induced the activation of ATR-Chk1 signaling in a dose- and time-dependent manner, suggesting the induction of DDR.	Cisplatin	103-112	checkpoint kinase 1	Homo sapiens	153-157
31362335-7	2019	Similarly, co-treatment with PF-477736 and NU7441, a pharmacological inhibitor of DNA-PK, which is also essential for the DDR pathway, rendered the cells sensitive to CHK1 inhibition.	8-dibenzothiophen-4-yl-2-morpholin-4-yl-chromen-4-one	43-49	checkpoint kinase 1	Homo sapiens	167-171
30514066-7	2019	AZD6738 blocked p-Chk1 and p-glycoprotein and increased gammaH2AX, a marker of DNA damage, in sensitive cells.	ceralasertib	0-7	checkpoint kinase 1	Homo sapiens	18-22
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	checkpoint kinase 1	Homo sapiens	180-184
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	checkpoint kinase 1	Homo sapiens	180-184
31372095-1	2019	Background: AZD7762 is a checkpoint kinase 1 (Chk 1) inhibitor, which has been reported to sensitize many tumor cells to DNA damage.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	12-19	checkpoint kinase 1	Homo sapiens	25-44
31372095-1	2019	Background: AZD7762 is a checkpoint kinase 1 (Chk 1) inhibitor, which has been reported to sensitize many tumor cells to DNA damage.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	12-19	checkpoint kinase 1	Homo sapiens	46-51
30478995-4	2019	In addition, the phosphorylation levels of Ser317 and Ser345 in Chk1 and of Ser216 in CDC25C were lower in CtIP-deficient HCT116 cells than in control cells after Eto treatment.	Etoposide	163-166	checkpoint kinase 1	Homo sapiens	64-68
31140586-0	2019	Fbxo6 confers drug-sensitization to cisplatin via inhibiting the activation of Chk1 in non-small cell lung cancer.	Cisplatin	36-45	checkpoint kinase 1	Homo sapiens	79-83
31140586-5	2019	Further in vitro experiments showed that Fbxo6 inhibits proliferation, facilitates apoptosis and promotes the sensitivity of cisplatin via decreased expression and phosphorylation of Chk1.	Cisplatin	125-134	checkpoint kinase 1	Homo sapiens	183-187
31061066-5	2019	Depletion of HMGB3 in cisplatin-sensitive and cisplatin-resistant cells resulted in transcriptional downregulation of the kinases ATR and CHK1, which attenuated the ATR/CHK1/p-CHK1 DNA damage signaling pathway.	Cisplatin	22-31	checkpoint kinase 1	Homo sapiens	138-142
31061066-5	2019	Depletion of HMGB3 in cisplatin-sensitive and cisplatin-resistant cells resulted in transcriptional downregulation of the kinases ATR and CHK1, which attenuated the ATR/CHK1/p-CHK1 DNA damage signaling pathway.	Cisplatin	22-31	checkpoint kinase 1	Homo sapiens	169-173
31061066-5	2019	Depletion of HMGB3 in cisplatin-sensitive and cisplatin-resistant cells resulted in transcriptional downregulation of the kinases ATR and CHK1, which attenuated the ATR/CHK1/p-CHK1 DNA damage signaling pathway.	Cisplatin	22-31	checkpoint kinase 1	Homo sapiens	169-173
31061066-5	2019	Depletion of HMGB3 in cisplatin-sensitive and cisplatin-resistant cells resulted in transcriptional downregulation of the kinases ATR and CHK1, which attenuated the ATR/CHK1/p-CHK1 DNA damage signaling pathway.	Cisplatin	46-55	checkpoint kinase 1	Homo sapiens	138-142
31061066-5	2019	Depletion of HMGB3 in cisplatin-sensitive and cisplatin-resistant cells resulted in transcriptional downregulation of the kinases ATR and CHK1, which attenuated the ATR/CHK1/p-CHK1 DNA damage signaling pathway.	Cisplatin	46-55	checkpoint kinase 1	Homo sapiens	169-173
31061066-5	2019	Depletion of HMGB3 in cisplatin-sensitive and cisplatin-resistant cells resulted in transcriptional downregulation of the kinases ATR and CHK1, which attenuated the ATR/CHK1/p-CHK1 DNA damage signaling pathway.	Cisplatin	46-55	checkpoint kinase 1	Homo sapiens	169-173
30986571-2	2019	Then a series of 5-(pyrimidin-2-ylamino)picolinonitrile derivatives as CHK1 inhibitors were discovered by further rational optimization.	5-(pyrimidin-2-ylamino)picolinonitrile	17-55	checkpoint kinase 1	Homo sapiens	71-75
31209198-6	2019	LY2603618 (Rabusertib), which specifically targets Chk1 kinase, kills HNSCC cells effectively and specifically.	LY2603618	0-9	checkpoint kinase 1	Homo sapiens	51-55
31044505-6	2019	Normal fibroblasts and haemopoietic cells retain viability and proliferative potential following exposure to CHK1 inhibitor plus low doses of HU, but normal cells exposed to CHK1 inhibitor combined with submicromolar concentrations of gemcitabine exhibited complete loss of proliferative potential.	gemcitabine	235-246	checkpoint kinase 1	Homo sapiens	174-178
31044505-7	2019	The effects of gemcitabine on normal tissue correlate with irreversible ATR-CHK1 pathway activation, whereas low doses of HU reversibly activate CHK1 independently of ATR.	gemcitabine	15-26	checkpoint kinase 1	Homo sapiens	76-80
31044505-7	2019	The effects of gemcitabine on normal tissue correlate with irreversible ATR-CHK1 pathway activation, whereas low doses of HU reversibly activate CHK1 independently of ATR.	Hydroxyurea	122-124	checkpoint kinase 1	Homo sapiens	145-149
31209198-6	2019	LY2603618 (Rabusertib), which specifically targets Chk1 kinase, kills HNSCC cells effectively and specifically.	LY2603618	11-21	checkpoint kinase 1	Homo sapiens	51-55
31209198-13	2019	In contrast, Wee1 inhibitor Adavosertib progresses the cell cycle and thereby increases lethality to Chk1 inhibition in HNSCC cell lines.	adavosertib	28-39	checkpoint kinase 1	Homo sapiens	101-105
31004705-4	2019	The present study aims to examine whether SN affects cell viability, cell cycle, redox balance, genomic stability, and expression of the DNA damage response (DDR)-related genes ATM, ATR, CHEK1, CHECK2, TP53, and SIRT1 in HepG2 cells - used as in vitro hepatocyte model.	Synephrine	42-44	checkpoint kinase 1	Homo sapiens	187-192
31017975-7	2019	In contrast, MG132-mediated proteasome inhibition, which induces rigorous autophagy, promotes p62 degradation but accumulation of the DNA repair proteins CHK1 and RAD51.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	checkpoint kinase 1	Homo sapiens	154-158
31078449-8	2019	Knockdown of RAD1, CHEK1 or FANCM led to a decrease in cellular viability and cells deficient in CHEK1, RAD1 or TP53I3 displayed increased sensitivity to cisplatin.	Cisplatin	154-163	checkpoint kinase 1	Homo sapiens	19-24
31078449-8	2019	Knockdown of RAD1, CHEK1 or FANCM led to a decrease in cellular viability and cells deficient in CHEK1, RAD1 or TP53I3 displayed increased sensitivity to cisplatin.	Cisplatin	154-163	checkpoint kinase 1	Homo sapiens	97-102
31213891-7	2019	At 48 hours, E2+Dox had induced a significant increase in the percentage of sub-G1 apoptotic cells, increased CHK1 expression, and decreased cyclin D1, CDK4, and CDK6 expression.	Doxorubicin	16-19	checkpoint kinase 1	Homo sapiens	110-114
31239709-6	2019	After BCSLCs were treated with norcantharidin (NCTD), the expression of Cdc6 and activation of the ATR-Chk1 pathway were detected by Western blotting.	norcantharidin	31-45	checkpoint kinase 1	Homo sapiens	103-107
30771522-0	2019	Checkpoint Kinase 1 Inhibition Enhances Cisplatin Cytotoxicity and Overcomes Cisplatin Resistance in SCLC by Promoting Mitotic Cell Death.	Cisplatin	40-49	checkpoint kinase 1	Homo sapiens	0-19
30771522-0	2019	Checkpoint Kinase 1 Inhibition Enhances Cisplatin Cytotoxicity and Overcomes Cisplatin Resistance in SCLC by Promoting Mitotic Cell Death.	Cisplatin	77-86	checkpoint kinase 1	Homo sapiens	0-19
30771522-4	2019	METHODS: We examined whether and how inhibition of checkpoint kinase 1 (Chk1) affects cisplatin cytotoxicity in SCLC cells with and without p53 mutations, and evaluated the effect of Chk1 inhibitor and cisplatin combination in cisplatin-sensitive and -resistant preclinical models.	Cisplatin	86-95	checkpoint kinase 1	Homo sapiens	51-70
30771522-4	2019	METHODS: We examined whether and how inhibition of checkpoint kinase 1 (Chk1) affects cisplatin cytotoxicity in SCLC cells with and without p53 mutations, and evaluated the effect of Chk1 inhibitor and cisplatin combination in cisplatin-sensitive and -resistant preclinical models.	Cisplatin	86-95	checkpoint kinase 1	Homo sapiens	72-76
30771522-7	2019	Furthermore, Chk1 inhibitors prexasertib and AZD7762 enhanced cisplatin antitumor activity and overcame cisplatin resistance in SCLC preclinical models in vitro an in vivo.	prexasertib	29-40	checkpoint kinase 1	Homo sapiens	13-17
30771522-7	2019	Furthermore, Chk1 inhibitors prexasertib and AZD7762 enhanced cisplatin antitumor activity and overcame cisplatin resistance in SCLC preclinical models in vitro an in vivo.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	45-52	checkpoint kinase 1	Homo sapiens	13-17
30771522-7	2019	Furthermore, Chk1 inhibitors prexasertib and AZD7762 enhanced cisplatin antitumor activity and overcame cisplatin resistance in SCLC preclinical models in vitro an in vivo.	Cisplatin	62-71	checkpoint kinase 1	Homo sapiens	13-17
30771522-7	2019	Furthermore, Chk1 inhibitors prexasertib and AZD7762 enhanced cisplatin antitumor activity and overcame cisplatin resistance in SCLC preclinical models in vitro an in vivo.	Cisplatin	104-113	checkpoint kinase 1	Homo sapiens	13-17
30771522-9	2019	CONCLUSIONS: Our data account Chk1 as a potential therapeutic target in SCLC, and rationalize clinical development of Chk1 inhibitor and cisplatin combinational strategy for the treatment of SCLC.	Cisplatin	137-146	checkpoint kinase 1	Homo sapiens	30-34
31017975-8	2019	However, pretreatment with an autophagy inhibitor offsets the effects of MG132 on CHK1 and RAD51 levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	73-78	checkpoint kinase 1	Homo sapiens	82-86
30607635-11	2019	We found that Chk1 suppressed IR-induced DSBs in these cells, which was dependent on H3K9me3/S10p-a chromatin mark previously found to indicate radioresistance in KRAS mutant cancers.	1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione	41-45	checkpoint kinase 1	Homo sapiens	14-18
30657978-5	2019	We demonstrate that loss of WRN leads to enhanced ATM phosphorylation upon prolonged exposure to aphidicolin, a specific inhibitor of DNA polymerases, resulting in CHK1 activation.	Aphidicolin	97-108	checkpoint kinase 1	Homo sapiens	164-168
32259055-6	2019	S phase arrest was induced with the topoisomerase I inhibitor SN38; the addition of CHK1i rapidly activated CDK2, inducing S phase progression that was inhibited by the CDK2 inhibitor CVT-313.	Irinotecan	62-66	checkpoint kinase 1	Homo sapiens	84-89
32259055-6	2019	S phase arrest was induced with the topoisomerase I inhibitor SN38; the addition of CHK1i rapidly activated CDK2, inducing S phase progression that was inhibited by the CDK2 inhibitor CVT-313.	CVT 313	184-191	checkpoint kinase 1	Homo sapiens	84-89
30616058-6	2019	The genotoxic potency was confirmed in both HBEC and HepG2 cells following exposure to oxy-PAHs by an increased level of phospho-Chk1, a biomarker used to estimate the carcinogenic potency of PAHs in vitro.	oxy-pahs	87-95	checkpoint kinase 1	Homo sapiens	129-133
30943845-7	2019	Moreover, p21 deficiency sensitized to combined treatment of MK1775 and the CHK1-inhibitor AZD6772, and to the combination of MK1775 with ionizing radiation.	azd6772	91-98	checkpoint kinase 1	Homo sapiens	76-80
30837643-2	2019	Checkpoint kinase 1 (CHK1), which is activated by DNA damage and replication stress, diminishes sensitivity to cytarabine and anthracyclines as single agents, suggesting that CHK1 inhibitors might increase the effectiveness of CPX-351.	Cytarabine	111-121	checkpoint kinase 1	Homo sapiens	0-19
30837643-2	2019	Checkpoint kinase 1 (CHK1), which is activated by DNA damage and replication stress, diminishes sensitivity to cytarabine and anthracyclines as single agents, suggesting that CHK1 inhibitors might increase the effectiveness of CPX-351.	Cytarabine	111-121	checkpoint kinase 1	Homo sapiens	21-25
30837643-2	2019	Checkpoint kinase 1 (CHK1), which is activated by DNA damage and replication stress, diminishes sensitivity to cytarabine and anthracyclines as single agents, suggesting that CHK1 inhibitors might increase the effectiveness of CPX-351.	Cytarabine	111-121	checkpoint kinase 1	Homo sapiens	175-179
30837643-2	2019	Checkpoint kinase 1 (CHK1), which is activated by DNA damage and replication stress, diminishes sensitivity to cytarabine and anthracyclines as single agents, suggesting that CHK1 inhibitors might increase the effectiveness of CPX-351.	Anthracyclines	126-140	checkpoint kinase 1	Homo sapiens	0-19
30837643-2	2019	Checkpoint kinase 1 (CHK1), which is activated by DNA damage and replication stress, diminishes sensitivity to cytarabine and anthracyclines as single agents, suggesting that CHK1 inhibitors might increase the effectiveness of CPX-351.	Anthracyclines	126-140	checkpoint kinase 1	Homo sapiens	21-25
30837643-2	2019	Checkpoint kinase 1 (CHK1), which is activated by DNA damage and replication stress, diminishes sensitivity to cytarabine and anthracyclines as single agents, suggesting that CHK1 inhibitors might increase the effectiveness of CPX-351.	Anthracyclines	126-140	checkpoint kinase 1	Homo sapiens	175-179
30837643-2	2019	Checkpoint kinase 1 (CHK1), which is activated by DNA damage and replication stress, diminishes sensitivity to cytarabine and anthracyclines as single agents, suggesting that CHK1 inhibitors might increase the effectiveness of CPX-351.	CPX-351	227-234	checkpoint kinase 1	Homo sapiens	0-19
30837643-2	2019	Checkpoint kinase 1 (CHK1), which is activated by DNA damage and replication stress, diminishes sensitivity to cytarabine and anthracyclines as single agents, suggesting that CHK1 inhibitors might increase the effectiveness of CPX-351.	CPX-351	227-234	checkpoint kinase 1	Homo sapiens	21-25
30837643-2	2019	Checkpoint kinase 1 (CHK1), which is activated by DNA damage and replication stress, diminishes sensitivity to cytarabine and anthracyclines as single agents, suggesting that CHK1 inhibitors might increase the effectiveness of CPX-351.	CPX-351	227-234	checkpoint kinase 1	Homo sapiens	175-179
30837643-3	2019	The present studies show that CPX-351 activates CHK1 as well as the S and G2/M cell cycle checkpoints.	CPX-351	30-37	checkpoint kinase 1	Homo sapiens	48-52
30837643-4	2019	Conversely, CHK1 inhibition diminishes the cell cycle effects of CPX-351.	CPX-351	65-72	checkpoint kinase 1	Homo sapiens	12-16
30837643-5	2019	Moreover, CHK1 knockdown or addition of a CHK1 inhibitor such as MK-8776, rabusertib or prexasertib enhances CPX-351-induced apoptosis in multiple TP53-null and TP53-wildtype AML cell lines.	MK-8776	65-72	checkpoint kinase 1	Homo sapiens	42-46
30837643-5	2019	Moreover, CHK1 knockdown or addition of a CHK1 inhibitor such as MK-8776, rabusertib or prexasertib enhances CPX-351-induced apoptosis in multiple TP53-null and TP53-wildtype AML cell lines.	LY2603618	74-84	checkpoint kinase 1	Homo sapiens	42-46
30837643-5	2019	Moreover, CHK1 knockdown or addition of a CHK1 inhibitor such as MK-8776, rabusertib or prexasertib enhances CPX-351-induced apoptosis in multiple TP53-null and TP53-wildtype AML cell lines.	CPX-351	109-116	checkpoint kinase 1	Homo sapiens	10-14
30773012-7	2019	Apart from ABL kinases, we identified a number of other kinases whose ATP-binding affinities are markedly diminished upon imatinib treatment, including CHK1, a checkpoint kinase involved in DNA damage response signaling.	Adenosine Triphosphate	70-73	checkpoint kinase 1	Homo sapiens	152-156
30773012-7	2019	Apart from ABL kinases, we identified a number of other kinases whose ATP-binding affinities are markedly diminished upon imatinib treatment, including CHK1, a checkpoint kinase involved in DNA damage response signaling.	Imatinib Mesylate	122-130	checkpoint kinase 1	Homo sapiens	152-156
30837643-5	2019	Moreover, CHK1 knockdown or addition of a CHK1 inhibitor such as MK-8776, rabusertib or prexasertib enhances CPX-351-induced apoptosis in multiple TP53-null and TP53-wildtype AML cell lines.	CPX-351	109-116	checkpoint kinase 1	Homo sapiens	42-46
30837643-6	2019	Likewise, CHK1 inhibition increases the antiproliferative effect of CPX-351 on primary AML specimens ex vivo, offering the possibility that CPX-351 may be well suited to combine with CHK1-targeted agents.	CPX-351	68-75	checkpoint kinase 1	Homo sapiens	10-14
30837643-6	2019	Likewise, CHK1 inhibition increases the antiproliferative effect of CPX-351 on primary AML specimens ex vivo, offering the possibility that CPX-351 may be well suited to combine with CHK1-targeted agents.	CPX-351	140-147	checkpoint kinase 1	Homo sapiens	10-14
30616058-6	2019	The genotoxic potency was confirmed in both HBEC and HepG2 cells following exposure to oxy-PAHs by an increased level of phospho-Chk1, a biomarker used to estimate the carcinogenic potency of PAHs in vitro.	Polycyclic Aromatic Hydrocarbons	91-95	checkpoint kinase 1	Homo sapiens	129-133
30362603-6	2019	The enzyme-linked immunosorbent assay technique was used for the detection of phospho-Chk1 at ser 317 and caspase-3.	Serine	94-97	checkpoint kinase 1	Homo sapiens	86-90
30735747-7	2019	PG and PC alter the DDR and may promote ATR-Chk1 and ATM-Chk2 pathways, respectively.	catechol	7-9	checkpoint kinase 1	Homo sapiens	44-48
30735747-7	2019	PG and PC alter the DDR and may promote ATR-Chk1 and ATM-Chk2 pathways, respectively.	Pyrogallol	0-2	checkpoint kinase 1	Homo sapiens	44-48
30834235-0	2019	Chk1 Inhibition Restores Inotuzumab Ozogamicin Citotoxicity in CD22-Positive Cells Expressing Mutant p53.	OZOGAMICIN	36-46	checkpoint kinase 1	Homo sapiens	0-4
30665195-4	2019	Equal levels of cisplatin-DNA lesions caused stronger Chk1 activation in lung cells, leading to resistance.	Cisplatin	16-25	checkpoint kinase 1	Homo sapiens	54-58
30834235-5	2019	When we combined IO with the Chk1 inhibitor UCN-01, we successfully abrogated IO-induced G2/M arrest regardless of the underlying p53 status, indicating that the DNA damage response triggered by IO is also modulated by p53-independent mechanisms.	io	78-80	checkpoint kinase 1	Homo sapiens	29-33
30834235-5	2019	When we combined IO with the Chk1 inhibitor UCN-01, we successfully abrogated IO-induced G2/M arrest regardless of the underlying p53 status, indicating that the DNA damage response triggered by IO is also modulated by p53-independent mechanisms.	io	78-80	checkpoint kinase 1	Homo sapiens	29-33
30635443-4	2019	Here, we have established near-diploid HCT116 cell lines containing endogenous Chk1 protein tagged with a minimum auxin-inducible degron (mAID) through CRISPR/Cas9-based gene editing.	Indoleacetic Acids	114-119	checkpoint kinase 1	Homo sapiens	79-83
30633885-0	2019	Acetyl-macrocalin B suppresses tumor growth in esophageal squamous cell carcinoma and exhibits synergistic anti-cancer effects with the Chk1/2 inhibitor AZD7762.	acetyl-macrocalin b	0-19	checkpoint kinase 1	Homo sapiens	136-140
30633885-0	2019	Acetyl-macrocalin B suppresses tumor growth in esophageal squamous cell carcinoma and exhibits synergistic anti-cancer effects with the Chk1/2 inhibitor AZD7762.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	153-160	checkpoint kinase 1	Homo sapiens	136-140
30633885-8	2019	The cell growth inhibition induced by A-macB was further enhanced by AZD7762, a specific Chk1/Chk2 inhibitor, with a combination index (CI) of &lt;1.	a-macb	38-44	checkpoint kinase 1	Homo sapiens	89-93
30633885-8	2019	The cell growth inhibition induced by A-macB was further enhanced by AZD7762, a specific Chk1/Chk2 inhibitor, with a combination index (CI) of &lt;1.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	69-76	checkpoint kinase 1	Homo sapiens	89-93
30428154-8	2019	Our results provide a novel mechanism by which glucose metabolism regulates a DNA damage effector, and imply that glucose deprivation, which is often found in solid tumor microenvironments, may enhance mutagenesis, clonal expansion, and tumor progression by triggering CHK1 degradation.	Glucose	47-54	checkpoint kinase 1	Homo sapiens	269-273
30573684-0	2019	Inhibition of checkpoint kinase 1 following gemcitabine-mediated S phase arrest results in CDC7- and CDK2-dependent replication catastrophe.	gemcitabine	44-55	checkpoint kinase 1	Homo sapiens	14-33
30573684-4	2019	Here, we characterized the molecular mechanism of sensitization to gemcitabine by the CHK1i MK8776.	gemcitabine	67-78	checkpoint kinase 1	Homo sapiens	86-90
31011562-0	2019	In Silico Exploration of Aryl Halides Analogues as Checkpoint Kinase 1 Inhibitors by Using 3D QSAR, Molecular Docking Study, and ADMET Screening.	aryl halides	25-37	checkpoint kinase 1	Homo sapiens	51-70
31011562-1	2019	Purpose: In this review, a set of aryl halides analogs were identified as potent checkpoint kinase 1 (Chk1) inhibitors through a series of computer-aided drug design processes, to develop models with good predictive ability, highlight the important interactions between the ligand and the Chk1 receptor protein and determine properties of the new proposed drugs as Chk1 inhibitors agents.	aryl halides	34-46	checkpoint kinase 1	Homo sapiens	81-100
31011562-1	2019	Purpose: In this review, a set of aryl halides analogs were identified as potent checkpoint kinase 1 (Chk1) inhibitors through a series of computer-aided drug design processes, to develop models with good predictive ability, highlight the important interactions between the ligand and the Chk1 receptor protein and determine properties of the new proposed drugs as Chk1 inhibitors agents.	aryl halides	34-46	checkpoint kinase 1	Homo sapiens	102-106
31011562-1	2019	Purpose: In this review, a set of aryl halides analogs were identified as potent checkpoint kinase 1 (Chk1) inhibitors through a series of computer-aided drug design processes, to develop models with good predictive ability, highlight the important interactions between the ligand and the Chk1 receptor protein and determine properties of the new proposed drugs as Chk1 inhibitors agents.	aryl halides	34-46	checkpoint kinase 1	Homo sapiens	289-293
31011562-1	2019	Purpose: In this review, a set of aryl halides analogs were identified as potent checkpoint kinase 1 (Chk1) inhibitors through a series of computer-aided drug design processes, to develop models with good predictive ability, highlight the important interactions between the ligand and the Chk1 receptor protein and determine properties of the new proposed drugs as Chk1 inhibitors agents.	aryl halides	34-46	checkpoint kinase 1	Homo sapiens	289-293
30445466-6	2019	Depletion of RNF8 or expression of NONO with lysine to arginine substitutions at positions 279, 290 and 295 prolonged CHK1 phosphorylation over an extended period of time.	Lysine	45-51	checkpoint kinase 1	Homo sapiens	118-122
30445466-6	2019	Depletion of RNF8 or expression of NONO with lysine to arginine substitutions at positions 279, 290 and 295 prolonged CHK1 phosphorylation over an extended period of time.	Arginine	55-63	checkpoint kinase 1	Homo sapiens	118-122
30352905-0	2019	Enhancing Abiraterone Acetate Efficacy in Androgen Receptor-positive Triple-negative Breast Cancer: Chk1 as a Potential Target.	Abiraterone Acetate	10-29	checkpoint kinase 1	Homo sapiens	100-104
30361254-4	2019	Inhibitor experiments revealed that temozolomide-induced senescence was initiated by damage recognition through the MRN complex, activation of the ATR/CHK1 axis of the DNA damage response pathway, and mediated by degradation of CDC25c.	Temozolomide	36-48	checkpoint kinase 1	Homo sapiens	151-155
30361254-0	2019	Temozolomide Induces Senescence and Repression of DNA Repair Pathways in Glioblastoma Cells via Activation of ATR-CHK1, p21, and NF-kappaB.	Temozolomide	0-12	checkpoint kinase 1	Homo sapiens	114-118
30201826-8	2019	Treatment of cells with mTORC inhibitors and olaparib increases gamma-H2AX and 53BP1 foci, decreases BRCA1, RPA, and Rad51 foci, impairs phosphorylation of ATR/Chk1 kinases, and induces necroptosis.	olaparib	45-53	checkpoint kinase 1	Homo sapiens	160-164
30470507-7	2019	Additionally, ATR serine 428 phosphorylation is altered by H2S donor and H2S synthesis enzyme inhibition, while the oxidative-stress induced phosphorylation of the ATR-regulated protein CHK1 on serine 345 is increased by H2S synthesis enzyme inhibition.	Serine	18-24	checkpoint kinase 1	Homo sapiens	186-190
30470507-7	2019	Additionally, ATR serine 428 phosphorylation is altered by H2S donor and H2S synthesis enzyme inhibition, while the oxidative-stress induced phosphorylation of the ATR-regulated protein CHK1 on serine 345 is increased by H2S synthesis enzyme inhibition.	Serine	194-200	checkpoint kinase 1	Homo sapiens	186-190
30365046-9	2019	The present results identified that suppression of FOXM1 using Thiostrepton inhibited MDA-MB-231 cell proliferation and the expression of cell cycle-associated genes, including cyclin A2, cyclin B2, checkpoint kinase 1, centrosomal protein 55 and polo like kinase 1.	Thiostrepton	63-75	checkpoint kinase 1	Homo sapiens	199-218
29873020-6	2019	Additionally, we characterise the Chk1-mediated phosphosite, Ser242, as a regulator of DNA binding, with a S242D p50 phosphomimetic exhibiting a &gt; 10-fold reduction in DNA binding affinity.	phosphosite	48-59	checkpoint kinase 1	Homo sapiens	34-38
30726813-4	2019	Furthermore, MTBITC induced Chk1 and Akt phosphorylations and decreased p27 protein expression.	4-(methylthio)-3-butenyl isothiocyanate	13-19	checkpoint kinase 1	Homo sapiens	28-32
30510197-2	2018	We have identified two novel Chk1 auto-phosphorylation sites, threonines 378 and 382 (T378/382), located in a highly conserved motif within the C-terminal Kinase Associated 1 (KA1) domain.	Threonine	62-72	checkpoint kinase 1	Homo sapiens	29-33
30510197-3	2018	T378/382 occur within optimal consensus Chk1 phosphorylation motifs and substitution with phospho-mimetic aspartic acid residues results in a constitutively active mutant Chk1 kinase (Chk1-DD) that arrests cell cycle progression in G2 phase of the cell cycle in the absence of DNA damage.	Aspartic Acid	106-119	checkpoint kinase 1	Homo sapiens	171-175
30510197-3	2018	T378/382 occur within optimal consensus Chk1 phosphorylation motifs and substitution with phospho-mimetic aspartic acid residues results in a constitutively active mutant Chk1 kinase (Chk1-DD) that arrests cell cycle progression in G2 phase of the cell cycle in the absence of DNA damage.	Aspartic Acid	106-119	checkpoint kinase 1	Homo sapiens	171-175
30297535-8	2018	Furthermore, when modification of Chk1 was inhibited with AZ0108 in breast cancer cells, we observed marked upregulation of p-S345 Chk1 accompanied by defects in mitotic signaling.	AZ0108	58-64	checkpoint kinase 1	Homo sapiens	34-38
30297535-8	2018	Furthermore, when modification of Chk1 was inhibited with AZ0108 in breast cancer cells, we observed marked upregulation of p-S345 Chk1 accompanied by defects in mitotic signaling.	AZ0108	58-64	checkpoint kinase 1	Homo sapiens	131-135
30297535-9	2018	Together, these results establish proof-of-concept antitumor efficacy through PARP6 inhibition and highlight a novel function of PARP6 in maintaining centrosome integrity via direct ADP-ribosylation of Chk1 and modulation of its activity.	Adenosine Diphosphate	182-185	checkpoint kinase 1	Homo sapiens	202-206
30420613-11	2018	Silencing SOX9 significantly inhibited gemcitabine-induced phosphorylation of checkpoint kinase 1, a key cell cycle checkpoint protein that coordinates the DNA damage response and inhibited the expression of multidrug resistance genes.	gemcitabine	39-50	checkpoint kinase 1	Homo sapiens	78-97
30439567-0	2018	Thymineless Death by the Fluoropyrimidine Polymer F10 Involves Replication Fork Collapse and Is Enhanced by Chk1 Inhibition.	2-fluoropyrimidine	25-41	checkpoint kinase 1	Homo sapiens	108-112
30145203-9	2018	Additional network analysis of significantly altered proteins revealed CDK2, CHEK1, and ERBB2 as central regulators mediating cisplatin resistance.	Cisplatin	126-135	checkpoint kinase 1	Homo sapiens	77-82
30103170-0	2018	Metronomic oral doxorubicin in combination of Chk1 inhibitor MK-8776 for p53-deficient breast cancer treatment.	MK-8776	61-68	checkpoint kinase 1	Homo sapiens	46-50
30103170-3	2018	In this light, within the limits of p53-deficient breast cancer, we demonstrate the enhanced anticancer effect of metronomic chemotherapy using doxorubicin when combined with Chk1 inhibitor MK-8776 by specifically augmenting the direct cytotoxic effect on cancer cells.	MK-8776	190-197	checkpoint kinase 1	Homo sapiens	175-179
30103170-5	2018	MK-8776 selectively enhanced the cytotoxic effect of low-concentration doxorubicin in p53-deficient breast cancer cells by abrogating the Chk1-dependent cell cycle arrest in vitro.	MK-8776	0-7	checkpoint kinase 1	Homo sapiens	138-142
30103170-5	2018	MK-8776 selectively enhanced the cytotoxic effect of low-concentration doxorubicin in p53-deficient breast cancer cells by abrogating the Chk1-dependent cell cycle arrest in vitro.	Doxorubicin	71-82	checkpoint kinase 1	Homo sapiens	138-142
30297842-3	2018	DNA damage caused by ultraviolet light (UV) or alkylating agent methyl methanesulphonate (MMS) results in phosphorylation of small GTPase RhoB by Chk1.	Methyl Methanesulfonate	64-88	checkpoint kinase 1	Homo sapiens	146-150
30300823-10	2018	Further, PP242 suppressed GO-induced Chk1 activation and G2/M cell cycle arrest, which in turn triggered cell cycle promotion and cell death.	PP242	9-14	checkpoint kinase 1	Homo sapiens	37-41
30300823-11	2018	These results indicate that inhibition of mTORC1/2 kinase by PP242 enhanced the cytotoxicity of GO by increasing lysosomal compartments and promoting the cell cycle via suppression of GO-induced Chk1 activation.	PP242	61-66	checkpoint kinase 1	Homo sapiens	195-199
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	checkpoint kinase 1	Homo sapiens	36-40
30297842-3	2018	DNA damage caused by ultraviolet light (UV) or alkylating agent methyl methanesulphonate (MMS) results in phosphorylation of small GTPase RhoB by Chk1.	Methyl Methanesulfonate	90-93	checkpoint kinase 1	Homo sapiens	146-150
30040168-0	2018	Dose-finding study of the checkpoint kinase 1 inhibitor, prexasertib, in Japanese patients with advanced solid tumors.	prexasertib	57-68	checkpoint kinase 1	Homo sapiens	26-45
30040168-1	2018	Prexasertib is a novel inhibitor of checkpoint kinase 1.	prexasertib	0-11	checkpoint kinase 1	Homo sapiens	36-55
30237857-3	2018	TX-induced stress signal was transmitted by protein kinase (ATM &amp; ATR) and phosphorylation of its downstream targets CHK1, CHK2, ATM, and ATR, respectively at the Ser 345, Thr68, Ser1981 and Ser 428 residues involved in complex disruption and p53 up-regulation.	Serine	167-170	checkpoint kinase 1	Homo sapiens	121-125
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	checkpoint kinase 1	Homo sapiens	85-89
30119887-6	2018	CHK1 inhibitor abrogated radiation-induced G2 arrest, whereas radiation-induced phosphorylation of CHK1 at Ser 345 or Ser 296 was decreased by the IGF-IR inhibitor.	Serine	107-110	checkpoint kinase 1	Homo sapiens	99-103
30003927-6	2018	Nx potentiated growth inhibitory effects of IR by down regulating ribosomal protein S6K (RPS6KB1), CyclinD1, Chk1 and HIF-1 alpha and prolonging G2/M checkpoint block.	nx	0-2	checkpoint kinase 1	Homo sapiens	109-113
30085332-10	2018	The results of western blot analysis indicated that the expression levels of proteins related to the DNA damage response system (Ser1981p-ATM, Ser345p-Chk1, Thr68p-Chk2 and Ser139p-gammaH2AX) and the cell cycle (Tyr15p-Cdc2 and cyclin B1) exhibited the greatest increase in the combined group.	ser345p	143-150	checkpoint kinase 1	Homo sapiens	151-155
29890208-7	2018	Then, it was shown that VE-822 inhibited ATR-CHK1 pathway activation, leading to the accumulation of cisplatin-modified DNA.	berzosertib	24-30	checkpoint kinase 1	Homo sapiens	45-49
29890208-7	2018	Then, it was shown that VE-822 inhibited ATR-CHK1 pathway activation, leading to the accumulation of cisplatin-modified DNA.	Cisplatin	101-110	checkpoint kinase 1	Homo sapiens	45-49
29964052-13	2018	Finally, resveratrol increased ROS production to induce DNA damage with p-CHK1 up-regulation and result in cancer cellular senescence.	Resveratrol	9-20	checkpoint kinase 1	Homo sapiens	74-78
29964052-13	2018	Finally, resveratrol increased ROS production to induce DNA damage with p-CHK1 up-regulation and result in cancer cellular senescence.	ros	31-34	checkpoint kinase 1	Homo sapiens	74-78
29954829-4	2018	Furthermore, Chk1 phosphorylates human Src at serine 51, and phosphorylated Src localizes to actin patches, the cell membrane, or the nucleus.	Serine	46-52	checkpoint kinase 1	Homo sapiens	13-17
30237857-3	2018	TX-induced stress signal was transmitted by protein kinase (ATM &amp; ATR) and phosphorylation of its downstream targets CHK1, CHK2, ATM, and ATR, respectively at the Ser 345, Thr68, Ser1981 and Ser 428 residues involved in complex disruption and p53 up-regulation.	Serine	183-186	checkpoint kinase 1	Homo sapiens	121-125
29271513-0	2018	Chk1 activation attenuates sensitivity of lapatinib in HER2-positive gastric cancer.	Lapatinib	42-51	checkpoint kinase 1	Homo sapiens	0-4
30111797-5	2018	A microarray analysis revealed that the suppression of the checkpoint kinase 1 (CHK1) pathway explained the resistance to 5-FU, especially in p53 wild-type cancer cells such as HCT-8.	Fluorouracil	122-126	checkpoint kinase 1	Homo sapiens	59-78
30111797-5	2018	A microarray analysis revealed that the suppression of the checkpoint kinase 1 (CHK1) pathway explained the resistance to 5-FU, especially in p53 wild-type cancer cells such as HCT-8.	Fluorouracil	122-126	checkpoint kinase 1	Homo sapiens	80-84
30111797-6	2018	Our data also demonstrated that the CHK1 pathway is suppressed by the Wnt pathway in 5-FU-resistant cells.	Fluorouracil	85-89	checkpoint kinase 1	Homo sapiens	36-40
30111797-7	2018	In summary, we have discovered a novel mechanism for 5-FU resistance mediated by histone deacetylation, which also revealed the crosstalk between the Wnt pathway and CHK1 pathway.	Fluorouracil	53-57	checkpoint kinase 1	Homo sapiens	166-170
29643063-0	2018	Evaluation of Prexasertib, a Checkpoint Kinase 1 Inhibitor, in a Phase Ib Study of Patients with Squamous Cell Carcinoma.	prexasertib	14-25	checkpoint kinase 1	Homo sapiens	29-48
29643063-1	2018	Purpose: Prexasertib, a checkpoint kinase 1 inhibitor, demonstrated single-agent activity in patients with advanced squamous cell carcinoma (SCC) in the dose-escalation portion of a phase I study (NCT01115790).	prexasertib	9-20	checkpoint kinase 1	Homo sapiens	24-43
29704517-0	2018	DUOXA1-mediated ROS production promotes cisplatin resistance by activating ATR-Chk1 pathway in ovarian cancer.	Reactive Oxygen Species	16-19	checkpoint kinase 1	Homo sapiens	79-83
29704517-0	2018	DUOXA1-mediated ROS production promotes cisplatin resistance by activating ATR-Chk1 pathway in ovarian cancer.	Cisplatin	40-49	checkpoint kinase 1	Homo sapiens	79-83
29704517-5	2018	Elevated ROS level sustains the activation of ATR-Chk1 pathway, leading to resistance to cisplatin in ovarian cancer cells.	Reactive Oxygen Species	9-12	checkpoint kinase 1	Homo sapiens	50-54
29704517-5	2018	Elevated ROS level sustains the activation of ATR-Chk1 pathway, leading to resistance to cisplatin in ovarian cancer cells.	Cisplatin	89-98	checkpoint kinase 1	Homo sapiens	50-54
29704517-6	2018	Moreover, using qHTCS we identified two Chk1 inhibitors (PF-477736 and AZD7762) that re-sensitize resistant cells to cisplatin.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	71-78	checkpoint kinase 1	Homo sapiens	40-44
29704517-6	2018	Moreover, using qHTCS we identified two Chk1 inhibitors (PF-477736 and AZD7762) that re-sensitize resistant cells to cisplatin.	Cisplatin	117-126	checkpoint kinase 1	Homo sapiens	40-44
29704517-7	2018	Blocking this novel pathway by inhibiting ROS, DUOXA1, ATR or Chk1 effectively overcomes cisplatin resistance in vitro and in vivo.	Cisplatin	89-98	checkpoint kinase 1	Homo sapiens	62-66
29870138-10	2018	Daunorubicin, mycophenolic acid, and pyrvinium could potentially target the hub gene CHEK1 directly.	Daunorubicin	0-12	checkpoint kinase 1	Homo sapiens	85-90
29870138-10	2018	Daunorubicin, mycophenolic acid, and pyrvinium could potentially target the hub gene CHEK1 directly.	Mycophenolic Acid	14-31	checkpoint kinase 1	Homo sapiens	85-90
29870138-10	2018	Daunorubicin, mycophenolic acid, and pyrvinium could potentially target the hub gene CHEK1 directly.	pyrvinium	37-46	checkpoint kinase 1	Homo sapiens	85-90
29271513-3	2018	In this study, we explored the effect of ATR/Chk1 pathway on regulating lapatinib sensitivity in human epidermal growth factor receptor-2 (HER2)-positive gastric cancer cell lines.	Lapatinib	72-81	checkpoint kinase 1	Homo sapiens	45-49
29271513-6	2018	In NCI-N87 cells, lapatinib induced G1 arrest and reduced Chk1 phosphorylation through inhibiting the expression of DNA topoisomerase 2-binding protein 1 (TopBP1).	Lapatinib	18-27	checkpoint kinase 1	Homo sapiens	58-62
29271513-8	2018	Inhibition of Chk1 phosphorylation enhanced the lapatinib sensitivity of MKN7 cells, which was shown by potentiated anti-proliferative effect, G1 arrest, downregulation of phosphorylated AKT and ERK along with aggravated DNA damage.	Lapatinib	48-57	checkpoint kinase 1	Homo sapiens	14-18
29271513-9	2018	In addition, increased Chk1 phosphorylation in NCI-N87 cells attenuated lapatinib-induced anti-proliferative effect and G1 arrest, and abrogated reduced phosphorylated AKT and ERK.	Lapatinib	72-81	checkpoint kinase 1	Homo sapiens	23-27
29735549-0	2018	Mechanistic Distinctions between CHK1 and WEE1 Inhibition Guide the Scheduling of Triple Therapy with Gemcitabine.	gemcitabine	102-113	checkpoint kinase 1	Homo sapiens	33-37
29636547-4	2018	Inhibition of BRD4 by JQ1 or AZD5153 resulted in a rapid, time-dependent reduction in CHK1 phosphorylation and aberrant DNA replication re-initiation.	AZD5153	29-36	checkpoint kinase 1	Homo sapiens	86-90
29535131-1	2018	Purpose: Checkpoint kinase 1 inhibitors (CHEK1i) have single-agent activity in vitro and in vivo Here, we have investigated the molecular basis of this activity.Experimental Design: We have assessed a panel of melanoma cell lines for their sensitivity to the CHEK1i GNE-323 and GDC-0575 in vitro and in vivo The effects of these compounds on responses to DNA replication stress were analyzed in the hypersensitive cell lines.Results: A subset of melanoma cell lines is hypersensitive to CHEK1i-induced cell death in vitro, and the drug effectively inhibits tumor growth in vivo In the hypersensitive cell lines, GNE-323 triggers cell death without cells entering mitosis.	gne	266-269	checkpoint kinase 1	Homo sapiens	41-46
29535131-1	2018	Purpose: Checkpoint kinase 1 inhibitors (CHEK1i) have single-agent activity in vitro and in vivo Here, we have investigated the molecular basis of this activity.Experimental Design: We have assessed a panel of melanoma cell lines for their sensitivity to the CHEK1i GNE-323 and GDC-0575 in vitro and in vivo The effects of these compounds on responses to DNA replication stress were analyzed in the hypersensitive cell lines.Results: A subset of melanoma cell lines is hypersensitive to CHEK1i-induced cell death in vitro, and the drug effectively inhibits tumor growth in vivo In the hypersensitive cell lines, GNE-323 triggers cell death without cells entering mitosis.	GDC-0575	278-286	checkpoint kinase 1	Homo sapiens	41-46
29545477-0	2018	Therapeutic Effect of Quinacrine, an Antiprotozoan Drug, by Selective Suppression of p-CHK1/2 in p53-Negative Malignant Cancers.	Quinacrine	22-32	checkpoint kinase 1	Homo sapiens	87-93
29684894-0	2018	Synthesis and biological evaluation of 2,6-disubstituted-9H-purine, 2,4-disubstitued-thieno[3,2-d]pyrimidine and -7H-pyrrolo[2,3-d]pyrimidine analogues as novel CHK1 inhibitors.	2,6-disubstituted-9h-purine	39-66	checkpoint kinase 1	Homo sapiens	161-165
29735693-4	2018	Herein, we show that the K63-linked ubiquitin chain at CHK1"s K132 residue has an inhibitory effect on the kinase activity.	3-Bromo-4-fluorobenzotrifluoride	62-66	checkpoint kinase 1	Homo sapiens	55-59
29684894-0	2018	Synthesis and biological evaluation of 2,6-disubstituted-9H-purine, 2,4-disubstitued-thieno[3,2-d]pyrimidine and -7H-pyrrolo[2,3-d]pyrimidine analogues as novel CHK1 inhibitors.	2,4-disubstitued-thieno[3,2-d]pyrimidine	68-108	checkpoint kinase 1	Homo sapiens	161-165
29684894-3	2018	Compounds (3a, 3d, 3f and 3j-l) with 9H-purine core displayed more potent inhibition against CHK1.	purine	37-46	checkpoint kinase 1	Homo sapiens	93-97
29352966-11	2018	Our results indicated that Polyphyllin G induced cell arrest in oral cancer OECM-1 cells by inactivation of cdc25C-cdc22 via ATM-Chk 1/2 stimulation.	polyphyllin VII	27-40	checkpoint kinase 1	Homo sapiens	129-134
29695073-10	2018	Additionally, compounds 13 and 14 also showed significant inhibition for ATR and mTOR substrates, i.e., p-Chk1 Ser 317 and p70 S6K Thr 389, respectively.	Serine	111-114	checkpoint kinase 1	Homo sapiens	106-110
29788155-0	2018	Phase I study of the checkpoint kinase 1 inhibitor GDC-0575 in combination with gemcitabine in patients with refractory solid tumors.	GDC-0575	51-59	checkpoint kinase 1	Homo sapiens	21-40
29788155-2	2018	GDC-0575 is a highly-selective oral small-molecule Chk1 inhibitor that results in tumor shrinkage and growth delay in xenograft models.	GDC-0575	0-8	checkpoint kinase 1	Homo sapiens	51-55
28389531-8	2018	By inhibiting checkpoint kinase (CHK)1, LY2606368 affected DNA replication in most CRC-SCs, including RAS-mutated ones, forcing them into premature, lethal mitoses.	prexasertib	40-49	checkpoint kinase 1	Homo sapiens	14-38
29353882-3	2018	These include the tamoxifen resistance suppressors BMPR1B, CDK10, CDK5, EIF2AK1, and MAP2K5, and the tamoxifen resistance inducers CHEK1, PAK2, RPS6KC1, TTK, and TXK.	Tamoxifen	101-110	checkpoint kinase 1	Homo sapiens	131-136
29617433-7	2018	The HCIF-CETSA method appeared robust and a good correlation in target engagement measured by this method and CETSA for the selective Chk1 inhibitor V158411 was observed.	V158411	149-156	checkpoint kinase 1	Homo sapiens	134-138
29409053-3	2018	GDC-0575 is a selective ATP-competitive inhibitor of CHK1.	GDC-0575	0-8	checkpoint kinase 1	Homo sapiens	53-57
29409053-3	2018	GDC-0575 is a selective ATP-competitive inhibitor of CHK1.	Adenosine Triphosphate	24-27	checkpoint kinase 1	Homo sapiens	53-57
29326282-4	2018	Cell killing/replication stress induced by CHEK1 inhibition was evaluated in cells, with or without RNF126 knockdown, by MTT/colony formation, replication stress biomarker immunostaining and DNA fiber assays.Results: RNF126 protein expression was elevated in breast cancer tissue samples.	monooxyethylene trimethylolpropane tristearate	121-124	checkpoint kinase 1	Homo sapiens	43-48
29286153-0	2018	CHK1 inhibition sensitizes pancreatic cancer cells to gemcitabine via promoting CDK-dependent DNA damage and ribonucleotide reductase downregulation.	gemcitabine	54-65	checkpoint kinase 1	Homo sapiens	0-4
29203250-6	2018	Deprivation of CHK1 sensitized OR-CRC cells to oxaliplatin.	Oxaliplatin	47-58	checkpoint kinase 1	Homo sapiens	15-19
29203250-9	2018	Consistently, a high level of NFYB, E2F1, or CHK1 predicted poor survival in CRC patients, especially with oxaliplatin treatment.	Oxaliplatin	107-118	checkpoint kinase 1	Homo sapiens	45-49
29203250-10	2018	Collectively, the NFYB-E2F1 pathway displays a crucial role in the chemoresistance of OR-CRC by inducing the expression and activation of CHK1, providing a possible therapeutic target for oxaliplatin resistance in CRC.	Oxaliplatin	188-199	checkpoint kinase 1	Homo sapiens	138-142
29555944-7	2018	Scoulerine acted to inhibit proliferation through inducing G2 or M-phase cell cycle arrest, which correlates well with the observed breakdown of the microtubule network, increased Chk1 Ser345, Chk2 Thr68 and mitotic H3 Ser10 phosphorylation.	discretamine	0-10	checkpoint kinase 1	Homo sapiens	180-184
29286153-3	2018	In the present study, we explored the antitumor mechanism of LY2603618, a specific CHK1 inhibitor, alone or in combination with gemcitabine in 5 pancreatic cancer cell lines.	LY2603618	61-70	checkpoint kinase 1	Homo sapiens	83-87
29286153-7	2018	Mechanistic investigations showed that gemcitabine sensitization by CHK1 inhibition was associated with CDK-dependent RRM1/2 downregulation and DNA damage enhancement.	gemcitabine	39-50	checkpoint kinase 1	Homo sapiens	68-72
31957309-5	2018	The obtained tetrahydroprotoflavones were free of the cytotoxicity of their parent compounds, and, even though tetrahydroprotoapigenone 1-O-butyl ether showed a weak inhibition of DNA damage response through Chk1, neither compounds influenced the cytotoxicity of doxorubicin either.	tetrahydroprotoflavones	13-36	checkpoint kinase 1	Homo sapiens	208-212
29301085-3	2018	Scaffold morphing of thiophene carboxamide ureas (TCUs), such as AZD7762 (1) and a related series of triazoloquinolines (TZQs), led to the identification of fused-ring bicyclic CHK1 inhibitors, 7-carboxamide thienopyridines (7-CTPs), and 7-carboxamide indoles.	thiophene carboxamide ureas	21-48	checkpoint kinase 1	Homo sapiens	177-181
29301085-3	2018	Scaffold morphing of thiophene carboxamide ureas (TCUs), such as AZD7762 (1) and a related series of triazoloquinolines (TZQs), led to the identification of fused-ring bicyclic CHK1 inhibitors, 7-carboxamide thienopyridines (7-CTPs), and 7-carboxamide indoles.	tcus	50-54	checkpoint kinase 1	Homo sapiens	177-181
29301085-3	2018	Scaffold morphing of thiophene carboxamide ureas (TCUs), such as AZD7762 (1) and a related series of triazoloquinolines (TZQs), led to the identification of fused-ring bicyclic CHK1 inhibitors, 7-carboxamide thienopyridines (7-CTPs), and 7-carboxamide indoles.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	65-72	checkpoint kinase 1	Homo sapiens	177-181
29301085-3	2018	Scaffold morphing of thiophene carboxamide ureas (TCUs), such as AZD7762 (1) and a related series of triazoloquinolines (TZQs), led to the identification of fused-ring bicyclic CHK1 inhibitors, 7-carboxamide thienopyridines (7-CTPs), and 7-carboxamide indoles.	triazoloquinolines	101-119	checkpoint kinase 1	Homo sapiens	177-181
29301085-3	2018	Scaffold morphing of thiophene carboxamide ureas (TCUs), such as AZD7762 (1) and a related series of triazoloquinolines (TZQs), led to the identification of fused-ring bicyclic CHK1 inhibitors, 7-carboxamide thienopyridines (7-CTPs), and 7-carboxamide indoles.	tzqs	121-125	checkpoint kinase 1	Homo sapiens	177-181
29301085-5	2018	An intramolecular hydrogen bond to an indole NH was also effective in locking the carboxamide in the preferred bound conformation to CHK1.	Hydrogen	18-26	checkpoint kinase 1	Homo sapiens	133-137
29301085-5	2018	An intramolecular hydrogen bond to an indole NH was also effective in locking the carboxamide in the preferred bound conformation to CHK1.	indole nh	38-47	checkpoint kinase 1	Homo sapiens	133-137
29301085-5	2018	An intramolecular hydrogen bond to an indole NH was also effective in locking the carboxamide in the preferred bound conformation to CHK1.	carboxamide	82-93	checkpoint kinase 1	Homo sapiens	133-137
31957309-5	2018	The obtained tetrahydroprotoflavones were free of the cytotoxicity of their parent compounds, and, even though tetrahydroprotoapigenone 1-O-butyl ether showed a weak inhibition of DNA damage response through Chk1, neither compounds influenced the cytotoxicity of doxorubicin either.	butyl-4-nitrophenyl ether	111-151	checkpoint kinase 1	Homo sapiens	208-212
29258953-3	2018	Butein-induced G2/M phase arrest is associated with increased phosphorylation of ataxia telangiectasia mutated (ATM) and Chk1/2, and consequently, with reduced cdc25C levels.	butein	0-6	checkpoint kinase 1	Homo sapiens	121-127
28604942-4	2018	The pervasive APOBEC3 activation in the host genome which converts cytosine to uracile during RNA editing has been suggested to depend on ATR/chk1 pathways.	Cytosine	67-75	checkpoint kinase 1	Homo sapiens	142-146
29075961-2	2018	In breast cancer, CHEK1 expression has been associated with an aggressive tumour phenotype, the triple-negative breast cancer subtype, an aberrant response to tamoxifen, and poor prognosis.	Tamoxifen	159-168	checkpoint kinase 1	Homo sapiens	18-23
29895190-1	2018	Small molecule inhibitors of the checkpoint proteins CHK1 and WEE1 are currently in clinical development in combination with the antimetabolite gemcitabine.	gemcitabine	144-155	checkpoint kinase 1	Homo sapiens	53-57
29048945-0	2018	Cell Density Affects the Detection of Chk1 Target Engagement by the Selective Inhibitor V158411.	V158411	88-95	checkpoint kinase 1	Homo sapiens	38-42
29048945-2	2018	Here we have evaluated target engagement of Chk1 by the small-molecule inhibitor V158411 using two different target engagement methods (autophosphorylation and cellular thermal shift assay [CETSA]).	V158411	81-88	checkpoint kinase 1	Homo sapiens	44-48
30024813-0	2018	The CHK1 inhibitor SRA737 synergizes with PARP1 inhibitors to kill carcinoma cells.	SRA737	19-25	checkpoint kinase 1	Homo sapiens	4-8
30024813-2	2018	We determined whether the novel clinically relevant CHK1 inhibitor SRA737 interacted with PARP1 inhibitors to kill carcinoma cells.	SRA737	67-73	checkpoint kinase 1	Homo sapiens	52-56
29113759-8	2018	Inhibition of G9a HMT activity by BIX-01294 treatment or by shRNA attenuated the proliferation of HMEC-1, nuclear localization of phosphorylated Chk1, and induced cell cycle arrest in G1 phase.	BIX 01294	34-43	checkpoint kinase 1	Homo sapiens	145-149
30260263-0	2018	RNF138 confers cisplatin resistance in gastric cancer cells via activating Chk1 signaling pathway.	Cisplatin	15-24	checkpoint kinase 1	Homo sapiens	75-79
30260263-8	2018	Moreover, RNF138-dependent phosphorylation of Chk1 was seen in GC cells, indicating a novel connection between cisplatin-induced DNA damage and apoptosis.	Cisplatin	111-120	checkpoint kinase 1	Homo sapiens	46-50
29895190-3	2018	The goals of this study were to directly compare the relative efficacies of the CHK1 inhibitor MK8776 and the WEE1 inhibitor AZD1775 to sensitize pancreatic cancer cell lines to gemcitabine and to identify pharmacodynamic biomarkers predictive of chemosensitization.	MK-8776	95-101	checkpoint kinase 1	Homo sapiens	80-84
29969371-7	2018	Apoptotic ELISA and western blot analyses revealed that the combinations of cladribine and entinostat exerted a much more profound activity to induce apoptosis and DNA damage response, evidenced by enhanced phosphorylation of histone H2A.X and the DNA repair enzymes Chk1 and Chk2.	Cladribine	76-86	checkpoint kinase 1	Homo sapiens	267-271
29895190-10	2018	Furthermore, our results suggest that the effects of CHK1 and WEE1 inhibition on gemcitabine-mediated replication stress best predict chemosensitization and support the use of high-intensity or pan-nuclear gammaH2AX staining as a marker for therapeutic response.	gemcitabine	81-92	checkpoint kinase 1	Homo sapiens	53-57
29969371-7	2018	Apoptotic ELISA and western blot analyses revealed that the combinations of cladribine and entinostat exerted a much more profound activity to induce apoptosis and DNA damage response, evidenced by enhanced phosphorylation of histone H2A.X and the DNA repair enzymes Chk1 and Chk2.	entinostat	91-101	checkpoint kinase 1	Homo sapiens	267-271
30516086-8	2018	Etoposide-induced DNA damage affected the phosphorylation of gamma-H2AX, CHK1 and CHK2 without affecting cell viability.	Etoposide	0-9	checkpoint kinase 1	Homo sapiens	73-77
29725502-0	2018	Ciclopirox activates ATR-Chk1 signaling pathway leading to Cdc25A protein degradation.	Ciclopirox	0-10	checkpoint kinase 1	Homo sapiens	25-29
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	checkpoint kinase 1	Homo sapiens	171-175
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	checkpoint kinase 1	Homo sapiens	62-66
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	checkpoint kinase 1	Homo sapiens	62-66
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	checkpoint kinase 1	Homo sapiens	96-100
29725502-8	2018	In contrast, knockdown of ATR conferred high resistance to CPX-induced Chk1 phosphorylation and Cdc25A degradation.	Ciclopirox	59-62	checkpoint kinase 1	Homo sapiens	71-75
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	checkpoint kinase 1	Homo sapiens	109-113
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	checkpoint kinase 1	Homo sapiens	109-113
29115606-8	2018	Further research demonstrated that activation inhibition of CHK1 and AKT, as well as an increase in apoptosis, were involved in DNMT3a-mediated chemosensitivity to GEM and OXA.	gemcitabine	164-167	checkpoint kinase 1	Homo sapiens	60-64
30498558-5	2018	In high glucose conditions, the CHK1-mediated DNA damage response is not activated properly.	Glucose	8-15	checkpoint kinase 1	Homo sapiens	32-36
29115606-0	2018	DNA methyltransferase 3a modulates chemosensitivity to gemcitabine and oxaliplatin via CHK1 and AKT in p53-deficient pancreatic cancer cells.	Oxaliplatin	71-82	checkpoint kinase 1	Homo sapiens	87-91
29149649-0	2018	Chk1 inhibitors overcome imatinib resistance in chronic myeloid leukemia cells.	Imatinib Mesylate	25-33	checkpoint kinase 1	Homo sapiens	0-4
29149649-3	2018	In our study, Chk1 inhibitors, AZD7762 and MK-8776, had strong antitumor effects on CML cell line KBM5 and imatinib-resistant form KBM5T315I.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	31-38	checkpoint kinase 1	Homo sapiens	14-18
29149649-3	2018	In our study, Chk1 inhibitors, AZD7762 and MK-8776, had strong antitumor effects on CML cell line KBM5 and imatinib-resistant form KBM5T315I.	MK-8776	43-50	checkpoint kinase 1	Homo sapiens	14-18
29149649-3	2018	In our study, Chk1 inhibitors, AZD7762 and MK-8776, had strong antitumor effects on CML cell line KBM5 and imatinib-resistant form KBM5T315I.	Imatinib Mesylate	107-115	checkpoint kinase 1	Homo sapiens	14-18
29149649-4	2018	Moreover, Chk1 inhibitors showed a strong cytotoxic effect on leukemia cells from primary CML and imatinib-resistance CML patients, but low cytotoxic effect on normal human mononuclear cells.	Imatinib Mesylate	98-106	checkpoint kinase 1	Homo sapiens	10-14
29086369-5	2018	The pervasive APOBEC3s activation in the host genome converts cytosine to uracile on single-stranded DNA, which has been suggested to depend on ATR/chk1 pathways.	Cytosine	62-70	checkpoint kinase 1	Homo sapiens	148-152
29115606-8	2018	Further research demonstrated that activation inhibition of CHK1 and AKT, as well as an increase in apoptosis, were involved in DNMT3a-mediated chemosensitivity to GEM and OXA.	Oxaliplatin	172-175	checkpoint kinase 1	Homo sapiens	60-64
29210298-0	2017	Synthesis and preliminary structure-activity relationship study of 2-aryl-2H-pyrazolo[4,3-c]quinolin-3-ones as potential checkpoint kinase 1 (Chk1) inhibitors.	2-aryl-2h-pyrazolo[4,3-c]quinolin-3-ones	67-107	checkpoint kinase 1	Homo sapiens	121-140
28983768-5	2017	In addition, the combination of CBNPs and Pb(AC)2 induced a significant increase in MDA and reduced the activities of ROS, LDH, SOD, and GSH, with G1/S phase arrest via upregulation of Chk1 and downregulation of CDK6 and cyclin D1.	cbnps	32-37	checkpoint kinase 1	Homo sapiens	185-189
28983768-5	2017	In addition, the combination of CBNPs and Pb(AC)2 induced a significant increase in MDA and reduced the activities of ROS, LDH, SOD, and GSH, with G1/S phase arrest via upregulation of Chk1 and downregulation of CDK6 and cyclin D1.	pb(ac)2	42-49	checkpoint kinase 1	Homo sapiens	185-189
29092815-0	2017	The kinase domain residue serine 173 of Schizosaccharomyces pombe Chk1 kinase is critical for the response to DNA replication stress.	Serine	26-32	checkpoint kinase 1	Homo sapiens	66-70
29092815-2	2017	We report here that the mutation of serine 173 (S173A) in the kinase domain of fission yeast Chk1 abolishes the G1-M and S-M checkpoints with little impact on the G2-M arrest.	Serine	36-42	checkpoint kinase 1	Homo sapiens	93-97
29092815-3	2017	This separation-of-function mutation strongly reduces the Rad3-dependent phosphorylation of Chk1 at serine 345 during logarithmic growth, but not when cells experience exogenous DNA damage.	Serine	100-106	checkpoint kinase 1	Homo sapiens	92-96
29092815-5	2017	The chk1-S173A allele is uniquely sensitive to high MMS concentrations where it displays a partial checkpoint defect.	Methyl Methanesulfonate	52-55	checkpoint kinase 1	Homo sapiens	4-8
29092815-8	2017	We conclude that serine 173, which is equivalent to lysine 166 in the activation loop of human Chk1, is only critical in DNA polymerase mutants or when forks collapse in the absence of Cds1.	Serine	17-23	checkpoint kinase 1	Homo sapiens	95-99
29092815-8	2017	We conclude that serine 173, which is equivalent to lysine 166 in the activation loop of human Chk1, is only critical in DNA polymerase mutants or when forks collapse in the absence of Cds1.	Lysine	52-58	checkpoint kinase 1	Homo sapiens	95-99
29021254-3	2017	Here, we identified O-linked beta-N-acetylglucosamine (O-GlcNAc)-transferase (OGT) as one of Chk1"s substrates.	linked	22-28	checkpoint kinase 1	Homo sapiens	93-97
29021254-4	2017	We found that Chk1 interacts with and phosphorylates OGT at Ser-20, which not only stabilizes OGT, but also is required for cytokinesis.	Serine	60-63	checkpoint kinase 1	Homo sapiens	14-18
29210298-0	2017	Synthesis and preliminary structure-activity relationship study of 2-aryl-2H-pyrazolo[4,3-c]quinolin-3-ones as potential checkpoint kinase 1 (Chk1) inhibitors.	2-aryl-2h-pyrazolo[4,3-c]quinolin-3-ones	67-107	checkpoint kinase 1	Homo sapiens	142-146
29210298-3	2017	In the search for new Chk1 inhibitors, a congeneric series of 2-aryl-2 H-pyrazolo[4,3-c]quinolin-3-one (PQ) was evaluated by in-vitro and in-silico approaches for the first time.	2-aryl-2 h-pyrazolo[4,3-c]quinolin-3-one	62-102	checkpoint kinase 1	Homo sapiens	22-26
29162833-0	2017	The combination of CHK1 inhibitor with G-CSF overrides cytarabine resistance in human acute myeloid leukemia.	Cytarabine	55-65	checkpoint kinase 1	Homo sapiens	19-23
29162833-3	2017	Here we show that the CHK1 inhibitor (CHK1i) GDC-0575 enhances AraC-mediated killing of AML cells both in vitro and in vivo, thus abrogating any potential chemoresistance mechanisms involving DNA repair.	GDC-0575	45-53	checkpoint kinase 1	Homo sapiens	22-26
29162833-3	2017	Here we show that the CHK1 inhibitor (CHK1i) GDC-0575 enhances AraC-mediated killing of AML cells both in vitro and in vivo, thus abrogating any potential chemoresistance mechanisms involving DNA repair.	Cytarabine	63-67	checkpoint kinase 1	Homo sapiens	22-26
28620979-0	2017	An application of CIFAP for predicting the binding affinity of Chk1 inhibitors derived from 2-aminothiazole-4-carboxamide.	2-aminothiazole-4-carboxamide	92-121	checkpoint kinase 1	Homo sapiens	63-67
28991639-0	2017	Haemanthamine alters sodium butyrate-induced histone acetylation, p21WAF1/Cip1 expression, Chk1 and Chk2 activation and leads to increased growth inhibition and death in A2780 ovarian cancer cells.	hemanthamine	0-13	checkpoint kinase 1	Homo sapiens	91-95
28991639-0	2017	Haemanthamine alters sodium butyrate-induced histone acetylation, p21WAF1/Cip1 expression, Chk1 and Chk2 activation and leads to increased growth inhibition and death in A2780 ovarian cancer cells.	Butyric Acid	21-36	checkpoint kinase 1	Homo sapiens	91-95
28991639-12	2017	Unexpectedly, NaB in combination with HA suppressed the phosphorylation of Chk2 on threonine 68 and Chk1 on serine 345 in A2780 cells and downregulated p21WAF1/Cip1 in both tested cell lines.	nab	14-17	checkpoint kinase 1	Homo sapiens	100-104
28991639-12	2017	Unexpectedly, NaB in combination with HA suppressed the phosphorylation of Chk2 on threonine 68 and Chk1 on serine 345 in A2780 cells and downregulated p21WAF1/Cip1 in both tested cell lines.	Serine	108-114	checkpoint kinase 1	Homo sapiens	100-104
29290940-13	2017	LPC stimulated intracellular ROS production and ATM/Chk2, ATR/Chk1 and Akt activation.	Lysophosphatidylcholines	0-3	checkpoint kinase 1	Homo sapiens	62-66
29118324-0	2017	Suppression of the FA pathway combined with CHK1 inhibitor hypersensitize lung cancer cells to gemcitabine.	gemcitabine	95-106	checkpoint kinase 1	Homo sapiens	44-48
29118324-6	2017	Furthermore, we demonstrated that FANCD2 depletion combined with CHK1 inhibitor MK-8776 significantly potentiated the cytotoxicity of gemcitabine to the two LSC cell lines, compared to individual FANCD2 depletion or MK-8776 treatment.	MK-8776	80-87	checkpoint kinase 1	Homo sapiens	65-69
29118324-6	2017	Furthermore, we demonstrated that FANCD2 depletion combined with CHK1 inhibitor MK-8776 significantly potentiated the cytotoxicity of gemcitabine to the two LSC cell lines, compared to individual FANCD2 depletion or MK-8776 treatment.	gemcitabine	134-145	checkpoint kinase 1	Homo sapiens	65-69
29118324-8	2017	Our results indicate that the enhancement effect of FANCD2 depletion combined with CHK1 inhibitor in sensitizing the LCS cells to gemcitabine supports the FA pathway and CHK1 as two therapeutic targets for improvement of anti-tumor regimens in treatment of LSC.	gemcitabine	130-141	checkpoint kinase 1	Homo sapiens	83-87
29118324-8	2017	Our results indicate that the enhancement effect of FANCD2 depletion combined with CHK1 inhibitor in sensitizing the LCS cells to gemcitabine supports the FA pathway and CHK1 as two therapeutic targets for improvement of anti-tumor regimens in treatment of LSC.	gemcitabine	130-141	checkpoint kinase 1	Homo sapiens	170-174
28620979-7	2017	In the prediction phase, support vector regression (SVR) and partial least squares regression are used for testing the quality of the CIFAP method for predicting the binding affinity of 45 CHK1 inhibitors derived from 2-aminothiazole-4-carboxamide.	2-aminothiazole-4-carboxamide	218-247	checkpoint kinase 1	Homo sapiens	189-193
29111814-5	2017	However, both the redox inhibitor glutathione (GSH) and ERK inhibitor U0126 antagonized SW-induced phosphorylations of ATM, ATR, and CHK1 in AGS cells.	Glutathione	34-45	checkpoint kinase 1	Homo sapiens	133-137
29111814-5	2017	However, both the redox inhibitor glutathione (GSH) and ERK inhibitor U0126 antagonized SW-induced phosphorylations of ATM, ATR, and CHK1 in AGS cells.	Glutathione	47-50	checkpoint kinase 1	Homo sapiens	133-137
29111814-5	2017	However, both the redox inhibitor glutathione (GSH) and ERK inhibitor U0126 antagonized SW-induced phosphorylations of ATM, ATR, and CHK1 in AGS cells.	U 0126	70-75	checkpoint kinase 1	Homo sapiens	133-137
28698200-6	2017	AZD1775 acquired resistance models demonstrated upregulation of AXL, pS6, and MET, and resistance was overcome with the addition of AXL (TP0903), dual-AXL/MET (cabozantinib), or mTOR (RAD001) inhibitors.Conclusions: AXL promotes resistance to WEE1 inhibition via downstream mTOR signaling and resulting activation of a parallel DNA damage repair pathway, CHK1.	adavosertib	0-7	checkpoint kinase 1	Homo sapiens	355-359
29048622-0	2017	Enhancement of cytotoxic effects of gemcitabine by Dclk1 inhibition through suppression of Chk1 phosphorylation in human pancreatic cancer cells.	gemcitabine	36-47	checkpoint kinase 1	Homo sapiens	91-95
28986587-0	2017	The drinking water contaminant dibromoacetonitrile delays G1-S transition and suppresses Chk1 activation at broken replication forks.	Water	13-18	checkpoint kinase 1	Homo sapiens	89-93
28888100-0	2017	Chk1 Inhibitor SCH900776 Effectively Potentiates the Cytotoxic Effects of Platinum-Based Chemotherapeutic Drugs in Human Colon Cancer Cells.	MK-8776	15-24	checkpoint kinase 1	Homo sapiens	0-4
28986587-0	2017	The drinking water contaminant dibromoacetonitrile delays G1-S transition and suppresses Chk1 activation at broken replication forks.	dibromoacetonitrile	31-50	checkpoint kinase 1	Homo sapiens	89-93
28986587-6	2017	DBAN does not hinder ongoing DNA replication, but specifically blocks the serine 345 phosphorylation of the DNA damage checkpoint kinase Chk1 by Rad3 (ATR) at broken replication forks.	dibromoacetonitrile	0-4	checkpoint kinase 1	Homo sapiens	137-141
28986587-6	2017	DBAN does not hinder ongoing DNA replication, but specifically blocks the serine 345 phosphorylation of the DNA damage checkpoint kinase Chk1 by Rad3 (ATR) at broken replication forks.	Serine	74-80	checkpoint kinase 1	Homo sapiens	137-141
28986587-9	2017	We conclude that DBAN targets a process or protein that acts at the start of S phase and is required for Chk1 phosphorylation.	dibromoacetonitrile	17-21	checkpoint kinase 1	Homo sapiens	105-109
28986587-10	2017	Taken together, DBAN may precipitate cancer by perturbing S phase and by blocking the Chk1-dependent response to replication fork damage.	dibromoacetonitrile	16-20	checkpoint kinase 1	Homo sapiens	86-90
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	checkpoint kinase 1	Homo sapiens	115-119
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	checkpoint kinase 1	Homo sapiens	136-140
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	checkpoint kinase 1	Homo sapiens	136-140
28849003-8	2017	In addition, the cell cycle-related proteins, including p27, CHK1, cyclin D1, CDK1, p-AMP-activated protein kinase (AMPK) and p-protein kinase B (AKT), were regulated by chrysophanol nanoparticles to prevent human prostate cancer cell progression.	chrysophanic acid	170-182	checkpoint kinase 1	Homo sapiens	61-65
28888100-0	2017	Chk1 Inhibitor SCH900776 Effectively Potentiates the Cytotoxic Effects of Platinum-Based Chemotherapeutic Drugs in Human Colon Cancer Cells.	Platinum	74-82	checkpoint kinase 1	Homo sapiens	0-4
28888100-2	2017	Here we newly demonstrate the ability of one of the most specific Chk1 inhibitors, SCH900776 (MK-8776), to enhance human colon cancer cell sensitivity to the cytotoxic effects of platinum(II) cisplatin and platinum(IV)- LA-12 complexes.	MK-8776	83-92	checkpoint kinase 1	Homo sapiens	66-70
28888100-2	2017	Here we newly demonstrate the ability of one of the most specific Chk1 inhibitors, SCH900776 (MK-8776), to enhance human colon cancer cell sensitivity to the cytotoxic effects of platinum(II) cisplatin and platinum(IV)- LA-12 complexes.	MK-8776	94-101	checkpoint kinase 1	Homo sapiens	66-70
28888100-2	2017	Here we newly demonstrate the ability of one of the most specific Chk1 inhibitors, SCH900776 (MK-8776), to enhance human colon cancer cell sensitivity to the cytotoxic effects of platinum(II) cisplatin and platinum(IV)- LA-12 complexes.	Platinum	179-187	checkpoint kinase 1	Homo sapiens	66-70
28888100-2	2017	Here we newly demonstrate the ability of one of the most specific Chk1 inhibitors, SCH900776 (MK-8776), to enhance human colon cancer cell sensitivity to the cytotoxic effects of platinum(II) cisplatin and platinum(IV)- LA-12 complexes.	Cisplatin	192-201	checkpoint kinase 1	Homo sapiens	66-70
28888100-2	2017	Here we newly demonstrate the ability of one of the most specific Chk1 inhibitors, SCH900776 (MK-8776), to enhance human colon cancer cell sensitivity to the cytotoxic effects of platinum(II) cisplatin and platinum(IV)- LA-12 complexes.	Platinum	206-214	checkpoint kinase 1	Homo sapiens	66-70
28888100-2	2017	Here we newly demonstrate the ability of one of the most specific Chk1 inhibitors, SCH900776 (MK-8776), to enhance human colon cancer cell sensitivity to the cytotoxic effects of platinum(II) cisplatin and platinum(IV)- LA-12 complexes.	)- la-12	217-225	checkpoint kinase 1	Homo sapiens	66-70
28928376-5	2017	Subsequent administration of Oligo-Fucoidan to etoposide-treated cells promotes p53 accumulation, p21 expression and significant decreases in ataxia-telangiectasia-mutated (ATM), checkpoint kinase 1 (Chk1) and gamma-H2AX phosphorylation in p53+/+ cells compared with p53-/- cells.	oligo-fucoidan	29-43	checkpoint kinase 1	Homo sapiens	179-198
28957699-0	2017	Randomized phase II trial of cytosine arabinoside with and without the CHK1 inhibitor MK-8776 in relapsed and refractory acute myeloid leukemia.	MK-8776	86-93	checkpoint kinase 1	Homo sapiens	71-75
28957699-2	2017	Incorporation of AraC into DNA activates checkpoint kinase 1 (Chk1), leading to cell-cycle arrest and diminished AraC cytotoxicity, which can be reversed by the selective Chk1 inhibitor MK-8776.	Cytarabine	17-21	checkpoint kinase 1	Homo sapiens	41-60
28957699-2	2017	Incorporation of AraC into DNA activates checkpoint kinase 1 (Chk1), leading to cell-cycle arrest and diminished AraC cytotoxicity, which can be reversed by the selective Chk1 inhibitor MK-8776.	Cytarabine	17-21	checkpoint kinase 1	Homo sapiens	62-66
28957699-2	2017	Incorporation of AraC into DNA activates checkpoint kinase 1 (Chk1), leading to cell-cycle arrest and diminished AraC cytotoxicity, which can be reversed by the selective Chk1 inhibitor MK-8776.	Cytarabine	17-21	checkpoint kinase 1	Homo sapiens	171-175
28957699-2	2017	Incorporation of AraC into DNA activates checkpoint kinase 1 (Chk1), leading to cell-cycle arrest and diminished AraC cytotoxicity, which can be reversed by the selective Chk1 inhibitor MK-8776.	Cytarabine	113-117	checkpoint kinase 1	Homo sapiens	41-60
28957699-2	2017	Incorporation of AraC into DNA activates checkpoint kinase 1 (Chk1), leading to cell-cycle arrest and diminished AraC cytotoxicity, which can be reversed by the selective Chk1 inhibitor MK-8776.	Cytarabine	113-117	checkpoint kinase 1	Homo sapiens	62-66
28957699-2	2017	Incorporation of AraC into DNA activates checkpoint kinase 1 (Chk1), leading to cell-cycle arrest and diminished AraC cytotoxicity, which can be reversed by the selective Chk1 inhibitor MK-8776.	Cytarabine	113-117	checkpoint kinase 1	Homo sapiens	171-175
28957699-2	2017	Incorporation of AraC into DNA activates checkpoint kinase 1 (Chk1), leading to cell-cycle arrest and diminished AraC cytotoxicity, which can be reversed by the selective Chk1 inhibitor MK-8776.	MK-8776	186-193	checkpoint kinase 1	Homo sapiens	41-60
28957699-2	2017	Incorporation of AraC into DNA activates checkpoint kinase 1 (Chk1), leading to cell-cycle arrest and diminished AraC cytotoxicity, which can be reversed by the selective Chk1 inhibitor MK-8776.	MK-8776	186-193	checkpoint kinase 1	Homo sapiens	62-66
28957699-2	2017	Incorporation of AraC into DNA activates checkpoint kinase 1 (Chk1), leading to cell-cycle arrest and diminished AraC cytotoxicity, which can be reversed by the selective Chk1 inhibitor MK-8776.	MK-8776	186-193	checkpoint kinase 1	Homo sapiens	171-175
29163782-4	2017	ATR subsequently phosphorylates H2AX at serine 139 (gammaH2AX) and CHK1 at serine 345 (CHK1pS345), leading to phosphorylation of CDK1 at tyrosine 15 (CDK1pY15) and S-phase arrest.	Serine	75-81	checkpoint kinase 1	Homo sapiens	67-71
29163782-4	2017	ATR subsequently phosphorylates H2AX at serine 139 (gammaH2AX) and CHK1 at serine 345 (CHK1pS345), leading to phosphorylation of CDK1 at tyrosine 15 (CDK1pY15) and S-phase arrest.	Tyrosine	137-145	checkpoint kinase 1	Homo sapiens	67-71
28928376-5	2017	Subsequent administration of Oligo-Fucoidan to etoposide-treated cells promotes p53 accumulation, p21 expression and significant decreases in ataxia-telangiectasia-mutated (ATM), checkpoint kinase 1 (Chk1) and gamma-H2AX phosphorylation in p53+/+ cells compared with p53-/- cells.	oligo-fucoidan	29-43	checkpoint kinase 1	Homo sapiens	200-204
28928376-5	2017	Subsequent administration of Oligo-Fucoidan to etoposide-treated cells promotes p53 accumulation, p21 expression and significant decreases in ataxia-telangiectasia-mutated (ATM), checkpoint kinase 1 (Chk1) and gamma-H2AX phosphorylation in p53+/+ cells compared with p53-/- cells.	Etoposide	47-56	checkpoint kinase 1	Homo sapiens	179-198
28928376-5	2017	Subsequent administration of Oligo-Fucoidan to etoposide-treated cells promotes p53 accumulation, p21 expression and significant decreases in ataxia-telangiectasia-mutated (ATM), checkpoint kinase 1 (Chk1) and gamma-H2AX phosphorylation in p53+/+ cells compared with p53-/- cells.	Etoposide	47-56	checkpoint kinase 1	Homo sapiens	200-204
28928376-6	2017	Similarly, co-administration of Oligo-Fucoidan with etoposide inhibits ATM, Chk1 and gamma-H2AX phosphorylation, particularly in the presence of p53.	Etoposide	52-61	checkpoint kinase 1	Homo sapiens	76-80
29221122-6	2017	The main characteristic of this effect was the sustained accumulation of teriflunomide-induced DNA damage as cells displayed increased phospho serine 139 H2AX (gammaH2AX) levels and concentration-dependent phosphorylation of Chk1 on serine 345 upon exposure to the combination as compared with either inhibitor alone.	teriflunomide	73-86	checkpoint kinase 1	Homo sapiens	225-229
28766886-9	2017	Chk-1 inhibitors such as rabusertib increased the cytotoxicity of etoposide/carboplatin to the SCLC lines in an additive to greater than additive manner.	LY2603618	25-35	checkpoint kinase 1	Homo sapiens	0-5
28766886-9	2017	Chk-1 inhibitors such as rabusertib increased the cytotoxicity of etoposide/carboplatin to the SCLC lines in an additive to greater than additive manner.	Etoposide	66-75	checkpoint kinase 1	Homo sapiens	0-5
28766886-9	2017	Chk-1 inhibitors such as rabusertib increased the cytotoxicity of etoposide/carboplatin to the SCLC lines in an additive to greater than additive manner.	Carboplatin	76-87	checkpoint kinase 1	Homo sapiens	0-5
28270495-0	2017	The Checkpoint Kinase 1 Inhibitor Prexasertib Induces Regression of Preclinical Models of Human Neuroblastoma.	prexasertib	34-45	checkpoint kinase 1	Homo sapiens	4-23
28270495-8	2017	Decreased Ki67 and increased immunostaining of endothelial and pericyte markers were observed in xenografts after only 6 days of exposure to prexasertib, potentially indicating a swift reduction in tumor volume and/or a direct effect on tumor vasculature.Conclusions: Overall, these data demonstrate that prexasertib is a specific inhibitor of CHK1 in neuroblastoma and leads to DNA damage and cell death in preclinical models of this devastating pediatric malignancy.	prexasertib	141-152	checkpoint kinase 1	Homo sapiens	344-348
28591670-9	2017	Western blot analysis showed that compound 5b induces G2/M phase arrest via ROS mediated DNA-damage, which in turn, induces phosphorylation of Chk1/Cdc25c/Cdc2 pathway.	ros	76-79	checkpoint kinase 1	Homo sapiens	143-147
28490518-0	2017	CHK1 Inhibition in Small-Cell Lung Cancer Produces Single-Agent Activity in Biomarker-Defined Disease Subsets and Combination Activity with Cisplatin or Olaparib.	Cisplatin	140-149	checkpoint kinase 1	Homo sapiens	0-4
28490518-0	2017	CHK1 Inhibition in Small-Cell Lung Cancer Produces Single-Agent Activity in Biomarker-Defined Disease Subsets and Combination Activity with Cisplatin or Olaparib.	olaparib	153-161	checkpoint kinase 1	Homo sapiens	0-4
28490518-3	2017	Our studies employed RNAi-mediated attenuation or pharmacologic blockade with the novel second-generation CHK1 inhibitor prexasertib (LY2606368), currently in clinical trials.	prexasertib	121-132	checkpoint kinase 1	Homo sapiens	106-110
28490518-3	2017	Our studies employed RNAi-mediated attenuation or pharmacologic blockade with the novel second-generation CHK1 inhibitor prexasertib (LY2606368), currently in clinical trials.	prexasertib	134-143	checkpoint kinase 1	Homo sapiens	106-110
28490518-5	2017	Proteomic analysis identified CHK1 and MYC as top predictive biomarkers of LY2606368 sensitivity, suggesting that CHK1 inhibition may be especially effective in SCLC with MYC amplification or MYC protein overexpression.	prexasertib	75-84	checkpoint kinase 1	Homo sapiens	30-34
28490518-5	2017	Proteomic analysis identified CHK1 and MYC as top predictive biomarkers of LY2606368 sensitivity, suggesting that CHK1 inhibition may be especially effective in SCLC with MYC amplification or MYC protein overexpression.	prexasertib	75-84	checkpoint kinase 1	Homo sapiens	114-118
28818808-6	2017	Levels of cell cycle-DNA repair regulator p21, CHK1 and FANCD2 levels were markedly affected by givinostat treatment.	givinostat	96-106	checkpoint kinase 1	Homo sapiens	47-51
28814980-6	2017	Co-treatment with chidamide and the DNA-damaging agent IDA gave rise to the production of gammaH2A.X and inhibited posttranslationally but not transcriptionally the repair gene of ATM, BRCA1, and checkpoint kinase 1 (CHK1) and 2 (CHK2) phosphorylation.	N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide	18-27	checkpoint kinase 1	Homo sapiens	196-215
28814980-6	2017	Co-treatment with chidamide and the DNA-damaging agent IDA gave rise to the production of gammaH2A.X and inhibited posttranslationally but not transcriptionally the repair gene of ATM, BRCA1, and checkpoint kinase 1 (CHK1) and 2 (CHK2) phosphorylation.	N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide	18-27	checkpoint kinase 1	Homo sapiens	217-221
28915668-0	2017	NSC30049 inhibits Chk1 pathway in 5-FU-resistant CRC bulk and stem cell populations.	Fluorouracil	34-38	checkpoint kinase 1	Homo sapiens	18-22
28915668-12	2017	Thus, NSC49L as a single agent or combined with 5-FU can be developed as a therapeutic agent by targeting the Chk1 pathway in 5-FU-resistant CRC heterogeneous bulk and CRC stem cell populations.	Fluorouracil	48-52	checkpoint kinase 1	Homo sapiens	110-114
28915668-12	2017	Thus, NSC49L as a single agent or combined with 5-FU can be developed as a therapeutic agent by targeting the Chk1 pathway in 5-FU-resistant CRC heterogeneous bulk and CRC stem cell populations.	Fluorouracil	126-130	checkpoint kinase 1	Homo sapiens	110-114
29221122-6	2017	The main characteristic of this effect was the sustained accumulation of teriflunomide-induced DNA damage as cells displayed increased phospho serine 139 H2AX (gammaH2AX) levels and concentration-dependent phosphorylation of Chk1 on serine 345 upon exposure to the combination as compared with either inhibitor alone.	Serine	233-239	checkpoint kinase 1	Homo sapiens	225-229
28692309-0	2017	Development and validation of a LC-MS/MS method for the quantification of the checkpoint kinase 1 inhibitor SRA737 in human plasma.	SRA737	108-114	checkpoint kinase 1	Homo sapiens	78-97
28692309-1	2017	AIM: SRA737 is an orally active small-molecule inhibitor of checkpoint kinase 1 being investigated in an oncology setting.	SRA737	5-11	checkpoint kinase 1	Homo sapiens	60-79
28978069-0	2017	Cell cycle perturbation induced by gemcitabine in human tumor cells in cell culture, xenografts and bladder cancer patients: implications for clinical trial designs combining gemcitabine with a Chk1 inhibitor.	gemcitabine	35-46	checkpoint kinase 1	Homo sapiens	194-198
29152060-7	2017	Treatment of Ewing sarcoma cells with gemcitabine also results in activation of checkpoint kinase 1 (CHK1), which is a critical mediator of cell survival in the setting of impaired DNA replication.	gemcitabine	38-49	checkpoint kinase 1	Homo sapiens	101-105
28978069-7	2017	The Chk1 inhibitor MK-8776 sensitized cells to gemcitabine with the greatest cell killing when added 18 h after gemcitabine.	MK-8776	19-26	checkpoint kinase 1	Homo sapiens	4-8
28978069-7	2017	The Chk1 inhibitor MK-8776 sensitized cells to gemcitabine with the greatest cell killing when added 18 h after gemcitabine.	gemcitabine	47-58	checkpoint kinase 1	Homo sapiens	4-8
28978069-7	2017	The Chk1 inhibitor MK-8776 sensitized cells to gemcitabine with the greatest cell killing when added 18 h after gemcitabine.	gemcitabine	112-123	checkpoint kinase 1	Homo sapiens	4-8
29152060-0	2017	Inhibition of CHK1 sensitizes Ewing sarcoma cells to the ribonucleotide reductase inhibitor gemcitabine.	gemcitabine	92-103	checkpoint kinase 1	Homo sapiens	14-18
29152060-7	2017	Treatment of Ewing sarcoma cells with gemcitabine also results in activation of checkpoint kinase 1 (CHK1), which is a critical mediator of cell survival in the setting of impaired DNA replication.	gemcitabine	38-49	checkpoint kinase 1	Homo sapiens	80-99
28430840-5	2017	A checkpoint kinase 1 (Chk1)/checkpoint kinase 2 (Chk2) consensus phosphorylation motif was identified at Serine 671 of Med1 and Ser671 motif was primarily phosphorylated by Chk2 in vitro.	Serine	106-112	checkpoint kinase 1	Homo sapiens	2-21
28273598-7	2017	Results showed that endosulfan induced DNA damage and activated DNA damage response signaling pathway (ATM/Chk2 and ATR/Chk1) and consequent cell cycle checkpoint.	Endosulfan	20-30	checkpoint kinase 1	Homo sapiens	120-124
28430840-5	2017	A checkpoint kinase 1 (Chk1)/checkpoint kinase 2 (Chk2) consensus phosphorylation motif was identified at Serine 671 of Med1 and Ser671 motif was primarily phosphorylated by Chk2 in vitro.	Serine	106-112	checkpoint kinase 1	Homo sapiens	23-27
28625637-1	2017	This phase 2 portion of a phase 1/2 study examined the efficacy and safety of LY2603618, a selective checkpoint kinase 1 inhibitor, combined with pemetrexed and cisplatin (LY+Pem+Cis) in patients with advanced nonsquamous non-small cell lung cancer (NSCLC).	LY2603618	78-87	checkpoint kinase 1	Homo sapiens	101-120
28625637-0	2017	A randomized, phase 2 evaluation of the CHK1 inhibitor, LY2603618, administered in combination with pemetrexed and cisplatin in patients with advanced nonsquamous non-small cell lung cancer.	LY2603618	56-65	checkpoint kinase 1	Homo sapiens	40-44
28454371-8	2017	Combined PE and CDDP targeting synergistically enhanced the expression of markers of DDR (phosphorylation of ataxia-telangiectasia mutated, checkpoint kinase (Chk)-1, Chk-2, and gamma-H2A histone family member X) in cells.	pe	9-11	checkpoint kinase 1	Homo sapiens	140-165
27815358-2	2017	This phase I study evaluated the Chk1 inhibitor GDC-0425 given in combination with gemcitabine to patients with advanced solid tumors.Experimental Design: Patients received GDC-0425 alone for a 1-week lead-in followed by 21-day cycles of gemcitabine plus GDC-0425.	GDC-0425	48-56	checkpoint kinase 1	Homo sapiens	33-37
27815358-10	2017	There were two confirmed partial responses in patients with triple-negative breast cancer (TP53-mutated) and melanoma (n = 1 each) and one unconfirmed partial response in a patient with cancer of unknown primary origin.Conclusions: Chk1 inhibition with GDC-0425 in combination with gemcitabine was tolerated with manageable bone marrow suppression.	GDC-0425	253-261	checkpoint kinase 1	Homo sapiens	232-236
27815358-10	2017	There were two confirmed partial responses in patients with triple-negative breast cancer (TP53-mutated) and melanoma (n = 1 each) and one unconfirmed partial response in a patient with cancer of unknown primary origin.Conclusions: Chk1 inhibition with GDC-0425 in combination with gemcitabine was tolerated with manageable bone marrow suppression.	gemcitabine	282-293	checkpoint kinase 1	Homo sapiens	232-236
28042876-0	2017	The Chk1 inhibitor MK-8776 increases the radiosensitivity of human triple-negative breast cancer by inhibiting autophagy.	MK-8776	19-26	checkpoint kinase 1	Homo sapiens	4-8
28138028-3	2017	We hypothesized that Chk1/2 inhibition (CHKi) with prexasertib may enhance cytotoxicity from EGFR inhibition plus radiotherapy in head and neck squamous cell carcinoma (HNSCC).	prexasertib	51-62	checkpoint kinase 1	Homo sapiens	21-27
28454371-8	2017	Combined PE and CDDP targeting synergistically enhanced the expression of markers of DDR (phosphorylation of ataxia-telangiectasia mutated, checkpoint kinase (Chk)-1, Chk-2, and gamma-H2A histone family member X) in cells.	Cisplatin	16-20	checkpoint kinase 1	Homo sapiens	140-165
28440428-7	2017	As expected, treatment of pancreatic cancer cell lines with AZ20 caused decreased phosphorylation of CHK1 (S-345).	AZ20	60-64	checkpoint kinase 1	Homo sapiens	101-105
28042876-1	2017	MK-8776 is a recently described inhibitor that is highly selective for checkpoint kinase 1 (Chk1), which can weaken the DNA repair capacity in cancer cells to achieve chemo-sensitization.	MK-8776	0-7	checkpoint kinase 1	Homo sapiens	71-90
28042876-1	2017	MK-8776 is a recently described inhibitor that is highly selective for checkpoint kinase 1 (Chk1), which can weaken the DNA repair capacity in cancer cells to achieve chemo-sensitization.	MK-8776	0-7	checkpoint kinase 1	Homo sapiens	92-96
28401005-6	2017	Secondly, we tested the anticancer effects of Chk1 chemical inhibitor LY2606368, which is a novel Chk1/2 targeted drug undergoing clinical trials in many malignant diseases.	prexasertib	70-79	checkpoint kinase 1	Homo sapiens	46-50
28401005-6	2017	Secondly, we tested the anticancer effects of Chk1 chemical inhibitor LY2606368, which is a novel Chk1/2 targeted drug undergoing clinical trials in many malignant diseases.	prexasertib	70-79	checkpoint kinase 1	Homo sapiens	98-102
28131548-0	2017	An orally bioavailable Chk1 inhibitor, CCT244747, sensitizes bladder and head and neck cancer cell lines to radiation.	3-((1-(dimethylamino)propan-2-yl)oxy)-5-((4-methoxy-5-(1-methyl-1H-pyrazol-4-yl)pyridin-2-yl)amino)pyrazine-2-carbonitrile	39-48	checkpoint kinase 1	Homo sapiens	23-27
28262781-3	2017	We demonstrated that cisplatin activates ATR, CHK1 and WEE1, which shut down DNA replication and attenuate cisplatin induced-lethality.	Cisplatin	21-30	checkpoint kinase 1	Homo sapiens	46-50
28262781-3	2017	We demonstrated that cisplatin activates ATR, CHK1 and WEE1, which shut down DNA replication and attenuate cisplatin induced-lethality.	Cisplatin	107-116	checkpoint kinase 1	Homo sapiens	46-50
28098859-6	2017	An impaired hydroxyurea-induced phosphorylation of CHK1 was observed in the WBS cells.	Hydroxyurea	12-23	checkpoint kinase 1	Homo sapiens	51-55
28376202-9	2017	Results: CPS1 knockdown reduced cell growth, decreased metabolite levels associated with nucleic acid biosynthesis pathway, and contributed an additive effect when combined with gemcitabine, pemetrexed, or CHK1 inhibitor AZD7762.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	221-228	checkpoint kinase 1	Homo sapiens	206-210
27996348-5	2017	Compared with FZD alone group, curcumin pretreatment significantly reduced the expression of phospho (p)-p38, cyclin D1, p-checkpoint kinase 1 (ChK1) and breast cancer associated gene 1 (BRCA1) protein, followed to attenuate S phase arrest.	Curcumin	31-39	checkpoint kinase 1	Homo sapiens	121-142
27996348-5	2017	Compared with FZD alone group, curcumin pretreatment significantly reduced the expression of phospho (p)-p38, cyclin D1, p-checkpoint kinase 1 (ChK1) and breast cancer associated gene 1 (BRCA1) protein, followed to attenuate S phase arrest.	Curcumin	31-39	checkpoint kinase 1	Homo sapiens	144-148
27501113-10	2017	Sensitive SK-BR-3 but not the less sensitive BT-474 breast cancer cells showed increased level of apoptosis and S phase arrest and reduced expression levels of phosphorylated check-point kinase 1 (CHK1) and other repair markers.	sk-br-3	10-17	checkpoint kinase 1	Homo sapiens	175-195
28228262-3	2017	AR or CDC6 knockdown, together with AZD7762, a Chk1/2 inhibitor, results in decreased TopBP1-ATR-Chk1 signaling and markedly increased ataxia-telangiectasia-mutated (ATM) phosphorylation, a biomarker of DNA damage, and synergistically increases treatment efficacy.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	36-43	checkpoint kinase 1	Homo sapiens	47-53
28228262-3	2017	AR or CDC6 knockdown, together with AZD7762, a Chk1/2 inhibitor, results in decreased TopBP1-ATR-Chk1 signaling and markedly increased ataxia-telangiectasia-mutated (ATM) phosphorylation, a biomarker of DNA damage, and synergistically increases treatment efficacy.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	36-43	checkpoint kinase 1	Homo sapiens	47-51
28228262-4	2017	Combination treatment with the AR signaling inhibitor enzalutamide (ENZ) and the Chk1/2 inhibitor AZD7762 demonstrates synergy with regard to inhibition of AR-CDC6-ATR-Chk1 signaling, ATM phosphorylation induction, and apoptosis in VCaP (mutant p53) and LNCaP-C4-2b (wild-type p53) cells.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	98-105	checkpoint kinase 1	Homo sapiens	81-87
28228262-4	2017	Combination treatment with the AR signaling inhibitor enzalutamide (ENZ) and the Chk1/2 inhibitor AZD7762 demonstrates synergy with regard to inhibition of AR-CDC6-ATR-Chk1 signaling, ATM phosphorylation induction, and apoptosis in VCaP (mutant p53) and LNCaP-C4-2b (wild-type p53) cells.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	98-105	checkpoint kinase 1	Homo sapiens	81-85
28035370-4	2017	Furthermore, baicalein induced phosphorylation of CHK1, as a marker of DNA damage response to S-to-G2/M phase arrest.	baicalein	13-22	checkpoint kinase 1	Homo sapiens	50-54
27939202-6	2017	Wee-inhibition by AZD1775 resulted in the activation of Chk1.	adavosertib	18-25	checkpoint kinase 1	Homo sapiens	56-60
28106079-1	2017	Chk1 kinase inhibitors are currently under clinical investigation as potentiators of cytotoxic chemotherapy and demonstrate potent activity in combination with anti-metabolite drugs that increase replication stress through the inhibition of nucleotide or deoxyribonucleotide biosynthesis.	Deoxyribonucleotides	255-274	checkpoint kinase 1	Homo sapiens	0-4
28106079-3	2017	A screen of small molecule metabolism modulators identified combinatorial activity between a Chk1 inhibitor and chloroquine or the LDHA/LDHB inhibitor GSK 2837808A.	Chloroquine	112-123	checkpoint kinase 1	Homo sapiens	93-97
28106079-4	2017	Compounds, such as 2-deoxyglucose or 6-aminonicotinamide, that reduced the fraction of cells undergoing active replication rendered tumour cells more resistant to Chk1 inhibitor-induced DNA damage.	Deoxyglucose	19-33	checkpoint kinase 1	Homo sapiens	163-167
28106079-4	2017	Compounds, such as 2-deoxyglucose or 6-aminonicotinamide, that reduced the fraction of cells undergoing active replication rendered tumour cells more resistant to Chk1 inhibitor-induced DNA damage.	6-Aminonicotinamide	37-56	checkpoint kinase 1	Homo sapiens	163-167
28106079-5	2017	Withdrawal of glucose or glutamine induced G1 and G2/M arrest without increasing DNA damage and reduced Chk1 expression and activation through autophosphorylation.	Glutamine	25-34	checkpoint kinase 1	Homo sapiens	104-108
28106079-7	2017	Glutamine starvation rendered tumour cells more resistant to Chk1 inhibitor-induced DNA damage and reversal of the glutamine starvation restored the sensitivity of tumour cells to Chk1 inhibitor-induced DNA damage.	Glutamine	0-9	checkpoint kinase 1	Homo sapiens	61-65
28106079-7	2017	Glutamine starvation rendered tumour cells more resistant to Chk1 inhibitor-induced DNA damage and reversal of the glutamine starvation restored the sensitivity of tumour cells to Chk1 inhibitor-induced DNA damage.	Glutamine	115-124	checkpoint kinase 1	Homo sapiens	180-184
28049532-2	2017	We therefore explored the efficacy of the combination of gemcitabine and AZD7762, a checkpoint kinase 1/2 (CHK1/2) inhibitor, for bladder cancer.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	73-80	checkpoint kinase 1	Homo sapiens	84-105
28049532-2	2017	We therefore explored the efficacy of the combination of gemcitabine and AZD7762, a checkpoint kinase 1/2 (CHK1/2) inhibitor, for bladder cancer.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	73-80	checkpoint kinase 1	Homo sapiens	107-113
28049532-10	2017	Mechanistic investigations showed that AZD7762 treatment inhibited the repair of gemcitabine-induced double strand breaks by interference with CHK1, since siRNA-mediated depletion of CHK1 but not of CHK2 mimicked the effects of AZD7762.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	39-46	checkpoint kinase 1	Homo sapiens	143-147
28049532-10	2017	Mechanistic investigations showed that AZD7762 treatment inhibited the repair of gemcitabine-induced double strand breaks by interference with CHK1, since siRNA-mediated depletion of CHK1 but not of CHK2 mimicked the effects of AZD7762.	gemcitabine	81-92	checkpoint kinase 1	Homo sapiens	143-147
28049532-10	2017	Mechanistic investigations showed that AZD7762 treatment inhibited the repair of gemcitabine-induced double strand breaks by interference with CHK1, since siRNA-mediated depletion of CHK1 but not of CHK2 mimicked the effects of AZD7762.	gemcitabine	81-92	checkpoint kinase 1	Homo sapiens	183-187
28391269-10	2017	The rebeccamycin-mediated reduction in MLCK production and protection of epithelial barrier function were alleviated by Chk1 inhibition.	rebeccamycin	4-16	checkpoint kinase 1	Homo sapiens	120-124
28391269-11	2017	CONCLUSION: Rebeccamycin attenuates TNF-alpha-induced disruption of intestinal epithelial barrier integrity by inducing claudin-5 expression and suppressing MLCK production via Chk1 activation.	rebeccamycin	12-24	checkpoint kinase 1	Homo sapiens	177-181
28030798-4	2017	Strikingly, the Chk1-inhibitors AZD7762 and LY2603618 were among the top candidate hits of 1664 tested compounds, suggesting that the synergistic cytotoxic effects are due to increased S-phase DNA damage.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	32-39	checkpoint kinase 1	Homo sapiens	16-20
28030798-4	2017	Strikingly, the Chk1-inhibitors AZD7762 and LY2603618 were among the top candidate hits of 1664 tested compounds, suggesting that the synergistic cytotoxic effects are due to increased S-phase DNA damage.	LY2603618	44-53	checkpoint kinase 1	Homo sapiens	16-20
28030834-7	2017	We found that inhibition of both HDAC1 and HDAC2 was necessary to decrease the expression of BRCA1, CHK1, and RAD51, enhance cytarabine- or daunorubicin-induced DNA damage and apoptosis, and abrogate cytarabine- or daunorubicin-induced cell cycle checkpoint activation in AML cells.	Cytarabine	200-210	checkpoint kinase 1	Homo sapiens	100-104
28030834-7	2017	We found that inhibition of both HDAC1 and HDAC2 was necessary to decrease the expression of BRCA1, CHK1, and RAD51, enhance cytarabine- or daunorubicin-induced DNA damage and apoptosis, and abrogate cytarabine- or daunorubicin-induced cell cycle checkpoint activation in AML cells.	Daunorubicin	215-227	checkpoint kinase 1	Homo sapiens	100-104
27926485-2	2017	Antiangiogenic strategies targeting VEGF based on tyrosine kinase inhibitors (TKIs) are currently undergoing extensive research for the treatment of glioma.Herein we demonstrated that the TKI axitinib induces DNA damage response (DDR) characterized by gamma-H2AX phosphorylation and Chk1 kinase activation leading to G2/M cell cycle arrest and mitotic catastrophe in U87, T98 and U251 glioma cell lines.	Axitinib	192-200	checkpoint kinase 1	Homo sapiens	283-287
26914363-0	2017	Sterigmatocystin-induced checkpoint adaptation depends on Chk1 in immortalized human gastric epithelial cells in vitro.	Sterigmatocystin	0-16	checkpoint kinase 1	Homo sapiens	58-62
27501113-10	2017	Sensitive SK-BR-3 but not the less sensitive BT-474 breast cancer cells showed increased level of apoptosis and S phase arrest and reduced expression levels of phosphorylated check-point kinase 1 (CHK1) and other repair markers.	sk-br-3	10-17	checkpoint kinase 1	Homo sapiens	197-201
27245274-0	2016	A supported liquid extraction LC-MS/MS method for determination of concentrations of GDC-0425, a small molecule Checkpoint kinase 1 inhibitor, in human plasma.	GDC-0425	85-93	checkpoint kinase 1	Homo sapiens	112-131
28123581-5	2017	To further investigate the effectiveness of selenium in radiotherapy, the present study examined the protective effects of sodium selenite supplementation administered prior to X-ray radiation treatment in CHEK-1 non-cancerous human esophageal cells.	Sodium Selenite	123-138	checkpoint kinase 1	Homo sapiens	206-212
28123581-8	2017	The half-maximal inhibitory concentration of sodium selenite in CHEK-1 cells was 3.6 microM.	Sodium Selenite	45-60	checkpoint kinase 1	Homo sapiens	64-70
28123581-13	2017	These results suggest that 50 nM sodium selenite supplementation administered for 72 h prior to irradiation may protect CHEK-1 cells from irradiation-induced damage by inhibiting irradiation-induced apoptosis.	Sodium Selenite	33-48	checkpoint kinase 1	Homo sapiens	120-126
28004747-0	2016	Corrigendum: A ruthenium polypyridyl intercalator stalls DNA replication forks, radiosensitizes human cancer cells and is enhanced by Chk1 inhibition.	Ruthenium	15-24	checkpoint kinase 1	Homo sapiens	134-138
27888802-6	2016	Co-treatment with TPL and araC or ADM upregulated pro-apoptotic caspase-9 protein, inhibited checkpoint kinase 1 (Chk1) and 2 (Chk2) phosphorylation, and induced gammaH2A.X (a DNA damage marker).	triptolide	18-21	checkpoint kinase 1	Homo sapiens	93-112
27888802-6	2016	Co-treatment with TPL and araC or ADM upregulated pro-apoptotic caspase-9 protein, inhibited checkpoint kinase 1 (Chk1) and 2 (Chk2) phosphorylation, and induced gammaH2A.X (a DNA damage marker).	triptolide	18-21	checkpoint kinase 1	Homo sapiens	114-118
27888802-6	2016	Co-treatment with TPL and araC or ADM upregulated pro-apoptotic caspase-9 protein, inhibited checkpoint kinase 1 (Chk1) and 2 (Chk2) phosphorylation, and induced gammaH2A.X (a DNA damage marker).	Cytarabine	26-30	checkpoint kinase 1	Homo sapiens	93-112
27888802-6	2016	Co-treatment with TPL and araC or ADM upregulated pro-apoptotic caspase-9 protein, inhibited checkpoint kinase 1 (Chk1) and 2 (Chk2) phosphorylation, and induced gammaH2A.X (a DNA damage marker).	Cytarabine	26-30	checkpoint kinase 1	Homo sapiens	114-118
27888802-6	2016	Co-treatment with TPL and araC or ADM upregulated pro-apoptotic caspase-9 protein, inhibited checkpoint kinase 1 (Chk1) and 2 (Chk2) phosphorylation, and induced gammaH2A.X (a DNA damage marker).	Doxorubicin	34-37	checkpoint kinase 1	Homo sapiens	93-112
27888802-6	2016	Co-treatment with TPL and araC or ADM upregulated pro-apoptotic caspase-9 protein, inhibited checkpoint kinase 1 (Chk1) and 2 (Chk2) phosphorylation, and induced gammaH2A.X (a DNA damage marker).	Doxorubicin	34-37	checkpoint kinase 1	Homo sapiens	114-118
28751935-0	2017	Chk1 Promotes DNA Damage Response Bypass following Oxidative Stress in a Model of Hydrogen Peroxide-Associated Ulcerative Colitis through JNK Inactivation and Chromatin Binding.	Hydrogen Peroxide	82-99	checkpoint kinase 1	Homo sapiens	0-4
27829224-0	2016	Inhibition of Chk1 with the small molecule inhibitor V158411 induces DNA damage and cell death in an unperturbed S-phase.	V158411	53-60	checkpoint kinase 1	Homo sapiens	14-18
27829224-4	2016	Here we characterize the mechanism by which the novel Chk1 inhibitor (V158411) increased DNA damage and cell death in models of human cancer.	V158411	70-77	checkpoint kinase 1	Homo sapiens	54-58
27829224-10	2016	We identified two distinct classes of Chk1 inhibitors: those that induced a strong increase in gammaH2AX, pChk1 (S317) and pRPA32 (S4/S8) (including V158411, LY2603618 and ARRY-1A) and those that did not (including MK-8776 and GNE-900).	LY2603618	158-167	checkpoint kinase 1	Homo sapiens	38-42
27829224-10	2016	We identified two distinct classes of Chk1 inhibitors: those that induced a strong increase in gammaH2AX, pChk1 (S317) and pRPA32 (S4/S8) (including V158411, LY2603618 and ARRY-1A) and those that did not (including MK-8776 and GNE-900).	MK-8776	215-222	checkpoint kinase 1	Homo sapiens	38-42
27358488-9	2016	Selinexor treatment of AML cells resulted in a c-MYC-dependent reduction of DNA damage repair genes (Rad51 and Chk1) mRNA and protein expression and subsequent inhibition of homologous recombination repair and increased sensitivity to Topo II inhibitors.	selinexor	0-9	checkpoint kinase 1	Homo sapiens	111-115
27740938-0	2016	7-Ketocholesterol induces ATM/ATR, Chk1/Chk2, PI3K/Akt signalings, cytotoxicity and IL-8 production in endothelial cells.	7-ketocholesterol	0-17	checkpoint kinase 1	Homo sapiens	35-39
27693461-3	2016	Chk1 inhibition with V158411 increases DNA damage and activates the ATR, ATM and DNA-PKcs dependent DNA damage response pathways.	V158411	21-28	checkpoint kinase 1	Homo sapiens	0-4
27693461-7	2016	gammaH2AX induction following Chk1 inhibition protected cells from caspase-dependent apoptosis.	gammah2ax	0-9	checkpoint kinase 1	Homo sapiens	30-34
27905519-3	2016	We here report the retrospective analysis of polymorphisms in 5 genes (ATM, ATR, Chk1, Chk2 and CDK12) involved in the cellular response to platinum in a cohort of 240 cancer patients with late stage ovarian cancer.	Platinum	140-148	checkpoint kinase 1	Homo sapiens	81-85
27690219-0	2016	MK-8776, a novel chk1 kinase inhibitor, radiosensitizes p53-defective human tumor cells.	MK-8776	0-7	checkpoint kinase 1	Homo sapiens	17-21
28025997-6	2016	Of note, the polyarginine-mediated internalization of Chk1-NP redistributed nuclear Chk1 with a prominent decrease in the nucleus in the absence of DNA damage.	polyarginine	13-25	checkpoint kinase 1	Homo sapiens	54-58
28025997-6	2016	Of note, the polyarginine-mediated internalization of Chk1-NP redistributed nuclear Chk1 with a prominent decrease in the nucleus in the absence of DNA damage.	polyarginine	13-25	checkpoint kinase 1	Homo sapiens	84-88
27664008-5	2016	We found that dietary flavonoids could inhibit Chk1 phosphorylation and decrease clonogenic cell growth once breast cancer cells receive ultraviolet irradiation, cisplatin, or etoposide treatment.	Flavonoids	22-32	checkpoint kinase 1	Homo sapiens	47-51
27664008-5	2016	We found that dietary flavonoids could inhibit Chk1 phosphorylation and decrease clonogenic cell growth once breast cancer cells receive ultraviolet irradiation, cisplatin, or etoposide treatment.	Cisplatin	162-171	checkpoint kinase 1	Homo sapiens	47-51
27664008-5	2016	We found that dietary flavonoids could inhibit Chk1 phosphorylation and decrease clonogenic cell growth once breast cancer cells receive ultraviolet irradiation, cisplatin, or etoposide treatment.	Etoposide	176-185	checkpoint kinase 1	Homo sapiens	47-51
27664008-6	2016	Since the ATR-Chk1 pathway mainly involves response to DNA replication stress, we propose that flavonoid derivatives reduce the side effect of chemotherapy by improving the sensitivity of cycling cells.	Flavonoids	95-104	checkpoint kinase 1	Homo sapiens	14-18
27690730-0	2016	Chk1 and DNA-PK mediate TPEN-induced DNA damage in a ROS dependent manner in human colon cancer cells.	N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine	24-28	checkpoint kinase 1	Homo sapiens	0-4
27690730-0	2016	Chk1 and DNA-PK mediate TPEN-induced DNA damage in a ROS dependent manner in human colon cancer cells.	Reactive Oxygen Species	53-56	checkpoint kinase 1	Homo sapiens	0-4
27690730-10	2016	In addition, siRNA silencing of Chk1, DNA-PK and ATM abrogated the expression of gamma-H2AX and reversed cell death, suggesting that Chk1 and DNA-PK mediate TPEN-induced cytotoxicity in colon cancer cells.	N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine	157-161	checkpoint kinase 1	Homo sapiens	32-36
27690730-10	2016	In addition, siRNA silencing of Chk1, DNA-PK and ATM abrogated the expression of gamma-H2AX and reversed cell death, suggesting that Chk1 and DNA-PK mediate TPEN-induced cytotoxicity in colon cancer cells.	N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine	157-161	checkpoint kinase 1	Homo sapiens	133-137
27690730-11	2016	This study shows for the first time the involvement of Chk1, DNA-PK and ATM in TPEN-induced DNA damage and confirms our previous findings that ROS generation and the redox cycling of copper in response to TPEN are the main mechanisms by which this compound induces cell death in human colon cancer cells.	N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine	79-83	checkpoint kinase 1	Homo sapiens	55-59
27690730-11	2016	This study shows for the first time the involvement of Chk1, DNA-PK and ATM in TPEN-induced DNA damage and confirms our previous findings that ROS generation and the redox cycling of copper in response to TPEN are the main mechanisms by which this compound induces cell death in human colon cancer cells.	Reactive Oxygen Species	143-146	checkpoint kinase 1	Homo sapiens	55-59
27690730-11	2016	This study shows for the first time the involvement of Chk1, DNA-PK and ATM in TPEN-induced DNA damage and confirms our previous findings that ROS generation and the redox cycling of copper in response to TPEN are the main mechanisms by which this compound induces cell death in human colon cancer cells.	Copper	183-189	checkpoint kinase 1	Homo sapiens	55-59
27690219-2	2016	The aim of this study was to assess the Chk1 kinase inhibitor, MK-8776, for its ability to radiosensitize human tumor cells.	MK-8776	63-70	checkpoint kinase 1	Homo sapiens	40-44
27523643-0	2016	Retraction notice to "Identification of novel aminothiazole and aminothiadiazole conjugated cyanopyridines as selective CHK1 inhibitors" [Eur.	cyanopyridines	92-106	checkpoint kinase 1	Homo sapiens	120-124
27743378-4	2016	To gain the mechanistic insights, firstly, in the presence of 3-methyladenine (3MA), an autophagy inhibitor, we found that the reduction of CHK1 and the inhibition of cell growth in RAD51-deficient EC109 cells were strikingly restored.	3-methyladenine	62-77	checkpoint kinase 1	Homo sapiens	140-144
27743378-4	2016	To gain the mechanistic insights, firstly, in the presence of 3-methyladenine (3MA), an autophagy inhibitor, we found that the reduction of CHK1 and the inhibition of cell growth in RAD51-deficient EC109 cells were strikingly restored.	3-methyladenine	79-82	checkpoint kinase 1	Homo sapiens	140-144
27350064-0	2016	Phase II evaluation of LY2603618, a first-generation CHK1 inhibitor, in combination with pemetrexed in patients with advanced or metastatic non-small cell lung cancer.	LY2603618	23-32	checkpoint kinase 1	Homo sapiens	53-57
27350064-1	2016	Introduction LY2603618 is a selective inhibitor of checkpoint kinase 1 (CHK1) protein kinase, a key regulator of the DNA damage checkpoint, and is predicted to enhance the effects of antimetabolites, such as pemetrexed.	LY2603618	13-22	checkpoint kinase 1	Homo sapiens	51-70
27350064-1	2016	Introduction LY2603618 is a selective inhibitor of checkpoint kinase 1 (CHK1) protein kinase, a key regulator of the DNA damage checkpoint, and is predicted to enhance the effects of antimetabolites, such as pemetrexed.	LY2603618	13-22	checkpoint kinase 1	Homo sapiens	72-76
27350064-1	2016	Introduction LY2603618 is a selective inhibitor of checkpoint kinase 1 (CHK1) protein kinase, a key regulator of the DNA damage checkpoint, and is predicted to enhance the effects of antimetabolites, such as pemetrexed.	Pemetrexed	208-218	checkpoint kinase 1	Homo sapiens	51-70
27350064-1	2016	Introduction LY2603618 is a selective inhibitor of checkpoint kinase 1 (CHK1) protein kinase, a key regulator of the DNA damage checkpoint, and is predicted to enhance the effects of antimetabolites, such as pemetrexed.	Pemetrexed	208-218	checkpoint kinase 1	Homo sapiens	72-76
27556692-4	2016	In p53-proficient NALM-6 cells, SCH900776 added to NAs enhanced signaling towards Chk1 (pSer317/pSer345), effectively blocked Chk1 activation (Ser296 autophosphorylation), increased replication stress (p53 and gamma-H2AX accumulation) and temporarily potentiated apoptosis.	MK-8776	32-41	checkpoint kinase 1	Homo sapiens	82-86
27634334-6	2016	Chemical and cytotoxic induction of replication stress, through aphidicolin, gemcitabine, camptothecin or hydroxyurea exposure, activates transcription of APOBEC3B via an ATR/Chk1-dependent pathway in vitro.	Aphidicolin	64-75	checkpoint kinase 1	Homo sapiens	175-179
27634334-6	2016	Chemical and cytotoxic induction of replication stress, through aphidicolin, gemcitabine, camptothecin or hydroxyurea exposure, activates transcription of APOBEC3B via an ATR/Chk1-dependent pathway in vitro.	gemcitabine	77-88	checkpoint kinase 1	Homo sapiens	175-179
27634334-6	2016	Chemical and cytotoxic induction of replication stress, through aphidicolin, gemcitabine, camptothecin or hydroxyurea exposure, activates transcription of APOBEC3B via an ATR/Chk1-dependent pathway in vitro.	Camptothecin	90-102	checkpoint kinase 1	Homo sapiens	175-179
27634334-6	2016	Chemical and cytotoxic induction of replication stress, through aphidicolin, gemcitabine, camptothecin or hydroxyurea exposure, activates transcription of APOBEC3B via an ATR/Chk1-dependent pathway in vitro.	Hydroxyurea	106-117	checkpoint kinase 1	Homo sapiens	175-179
27625304-5	2016	High abundance of CHK1 in AML patient cells correlated with higher clonogenic ability and more efficient DNA replication fork progression upon cytarabine treatment.	Cytarabine	143-153	checkpoint kinase 1	Homo sapiens	18-22
27625304-6	2016	Exposing the patient cells with the high abundance of CHK1 to SCH900776, an inhibitor of the kinase activity of CHK1, reduced clonogenic ability and progression of DNA replication in the presence of cytarabine.	MK-8776	62-71	checkpoint kinase 1	Homo sapiens	54-58
27625304-6	2016	Exposing the patient cells with the high abundance of CHK1 to SCH900776, an inhibitor of the kinase activity of CHK1, reduced clonogenic ability and progression of DNA replication in the presence of cytarabine.	MK-8776	62-71	checkpoint kinase 1	Homo sapiens	112-116
27625304-6	2016	Exposing the patient cells with the high abundance of CHK1 to SCH900776, an inhibitor of the kinase activity of CHK1, reduced clonogenic ability and progression of DNA replication in the presence of cytarabine.	Cytarabine	199-209	checkpoint kinase 1	Homo sapiens	54-58
27625304-6	2016	Exposing the patient cells with the high abundance of CHK1 to SCH900776, an inhibitor of the kinase activity of CHK1, reduced clonogenic ability and progression of DNA replication in the presence of cytarabine.	Cytarabine	199-209	checkpoint kinase 1	Homo sapiens	112-116
27625304-7	2016	These results indicated that some AML cells rely on an efficient CHK1-mediated replication stress response for viability and that therapeutic strategies that inhibit CHK1 could extend current cytarabine-based treatments and overcome drug resistance.	Cytarabine	192-202	checkpoint kinase 1	Homo sapiens	166-170
27612029-7	2016	Pterostilbene also activated ATM and CHK1/2, which are upstream of p53, in both cell lines, though pterostilbene-induced senescence was dependent on the presence of p53.	pterostilbene	0-13	checkpoint kinase 1	Homo sapiens	37-43
27556692-4	2016	In p53-proficient NALM-6 cells, SCH900776 added to NAs enhanced signaling towards Chk1 (pSer317/pSer345), effectively blocked Chk1 activation (Ser296 autophosphorylation), increased replication stress (p53 and gamma-H2AX accumulation) and temporarily potentiated apoptosis.	MK-8776	32-41	checkpoint kinase 1	Homo sapiens	126-130
27556692-4	2016	In p53-proficient NALM-6 cells, SCH900776 added to NAs enhanced signaling towards Chk1 (pSer317/pSer345), effectively blocked Chk1 activation (Ser296 autophosphorylation), increased replication stress (p53 and gamma-H2AX accumulation) and temporarily potentiated apoptosis.	pser317	88-95	checkpoint kinase 1	Homo sapiens	82-86
27422809-0	2016	CHK1 Inhibition Radiosensitizes Head and Neck Cancers to Paclitaxel-Based Chemoradiotherapy.	Paclitaxel	57-67	checkpoint kinase 1	Homo sapiens	0-4
27422809-11	2016	CHK1 may serve as a biomarker for identifying tumors likely to recur and, therefore, patients who may benefit from concomitant treatment with a CHK1 inhibitor and paclitaxel during radiotherapy.	Paclitaxel	163-173	checkpoint kinase 1	Homo sapiens	0-4
27449089-2	2016	Previous work has demonstrated the effectiveness of inhibiting CHK1 with small-molecule inhibitors, but the role of CHK1 mediated DDR in medulloblastoma is unknown.	ddr	130-133	checkpoint kinase 1	Homo sapiens	116-120
27558808-0	2016	A ruthenium polypyridyl intercalator stalls DNA replication forks, radiosensitizes human cancer cells and is enhanced by Chk1 inhibition.	Ruthenium	2-11	checkpoint kinase 1	Homo sapiens	121-125
27438145-0	2016	Prexasertib, a Chk1/Chk2 inhibitor, increases the effectiveness of conventional therapy in B-/T- cell progenitor acute lymphoblastic leukemia.	prexasertib	0-11	checkpoint kinase 1	Homo sapiens	15-19
27449089-4	2016	CHK1 inhibition with the small-molecule drug AZD7762, results in decreased cell growth, increased DNA damage and cell apoptosis.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	45-52	checkpoint kinase 1	Homo sapiens	0-4
27443255-3	2016	In this study, we found that Chk1 and ERK1/2 were activated to promote cell survival upon addition of excess thymidine.	Thymidine	109-118	checkpoint kinase 1	Homo sapiens	29-33
27438145-2	2016	In this study we evaluated the efficacy of the Chk 1/2 inhibitor prexasertib mesylate monohydrate in B-/T- cell progenitor acute lymphoblastic leukemia (ALL) as single agent and in combination with other drugs.	Prexasertib mesylate monohydrate	65-97	checkpoint kinase 1	Homo sapiens	47-54
27383768-0	2016	A balanced pyrimidine pool is required for optimal Chk1 activation to prevent ultrafine anaphase bridge formation.	pyrimidine	11-21	checkpoint kinase 1	Homo sapiens	51-55
27443255-6	2016	Our findings suggested that Chk1 and ERK1/2 were activated to promote cell survival upon addition of excess thymidine, but prolonged activation of ERK1/2 led to cellular senescence.	Thymidine	108-117	checkpoint kinase 1	Homo sapiens	28-32
27303922-5	2016	Mechanistically, pyrvinium pamoate promoted nuclear import of HuR by activating the AMP-activated kinase/importin alpha1 cascade and blocked HuR nucleo-cytoplasmic translocation by inhibiting the checkpoint kinase1/cyclin-dependent kinase 1 pathway.	pyrvinium	17-34	checkpoint kinase 1	Homo sapiens	196-240
27383768-5	2016	Chemical inhibition of the ATR-Chk1 pathway leads to UFB accumulation, and we found that this pathway was compromised in CDA-deficient cells.	ufb	53-56	checkpoint kinase 1	Homo sapiens	31-35
27383768-6	2016	Our data demonstrate that ATR-Chk1 acts downstream from PARP-1, preventing the accumulation of unreplicated DNA in mitosis, and, thus, UFB formation.	ufb	135-138	checkpoint kinase 1	Homo sapiens	30-34
27098276-4	2016	Melflufen induces gamma-H2AX, ATR, and CHK1 as early as after 2 h exposure in both melphalan-sensitive and -resistant cells.	melflufen	0-9	checkpoint kinase 1	Homo sapiens	39-43
27286453-7	2016	Combination of LY2603618, a specific Chk1/2 inhibitor, with irinotecan resulted in a significant reduction of CRC-SC growth in vivo, confirming that irinotecan treatment coupled to inhibition of Chk1 represents a potentially effective therapeutic approach for CRC treatment.	LY2603618	15-24	checkpoint kinase 1	Homo sapiens	37-43
27286453-7	2016	Combination of LY2603618, a specific Chk1/2 inhibitor, with irinotecan resulted in a significant reduction of CRC-SC growth in vivo, confirming that irinotecan treatment coupled to inhibition of Chk1 represents a potentially effective therapeutic approach for CRC treatment.	LY2603618	15-24	checkpoint kinase 1	Homo sapiens	37-41
27286453-7	2016	Combination of LY2603618, a specific Chk1/2 inhibitor, with irinotecan resulted in a significant reduction of CRC-SC growth in vivo, confirming that irinotecan treatment coupled to inhibition of Chk1 represents a potentially effective therapeutic approach for CRC treatment.	Irinotecan	149-159	checkpoint kinase 1	Homo sapiens	37-43
27286453-7	2016	Combination of LY2603618, a specific Chk1/2 inhibitor, with irinotecan resulted in a significant reduction of CRC-SC growth in vivo, confirming that irinotecan treatment coupled to inhibition of Chk1 represents a potentially effective therapeutic approach for CRC treatment.	Irinotecan	149-159	checkpoint kinase 1	Homo sapiens	37-41
27166183-0	2016	Inhibition of CHK1 enhances cell death induced by the Bcl-2-selective inhibitor ABT-199 in acute myeloid leukemia cells.	venetoclax	80-87	checkpoint kinase 1	Homo sapiens	14-18
27167172-0	2016	Multiparameter Lead Optimization to Give an Oral Checkpoint Kinase 1 (CHK1) Inhibitor Clinical Candidate: (R)-5-((4-((Morpholin-2-ylmethyl)amino)-5-(trifluoromethyl)pyridin-2-yl)amino)pyrazine-2-carbonitrile (CCT245737).	CCT245737	209-218	checkpoint kinase 1	Homo sapiens	49-68
27167172-0	2016	Multiparameter Lead Optimization to Give an Oral Checkpoint Kinase 1 (CHK1) Inhibitor Clinical Candidate: (R)-5-((4-((Morpholin-2-ylmethyl)amino)-5-(trifluoromethyl)pyridin-2-yl)amino)pyrazine-2-carbonitrile (CCT245737).	CCT245737	209-218	checkpoint kinase 1	Homo sapiens	70-74
27167172-1	2016	Multiparameter optimization of a series of 5-((4-aminopyridin-2-yl)amino)pyrazine-2-carbonitriles resulted in the identification of a potent and selective oral CHK1 preclinical development candidate with in vivo efficacy as a potentiator of deoxyribonucleic acid (DNA) damaging chemotherapy and as a single agent.	5-((4-aminopyridin-2-yl)amino)pyrazine-2-carbonitriles	43-97	checkpoint kinase 1	Homo sapiens	160-164
27167172-2	2016	Cellular mechanism of action assays were used to give an integrated assessment of compound selectivity during optimization resulting in a highly CHK1 selective adenosine triphosphate (ATP) competitive inhibitor.	Adenosine Triphosphate	160-182	checkpoint kinase 1	Homo sapiens	145-149
27167172-2	2016	Cellular mechanism of action assays were used to give an integrated assessment of compound selectivity during optimization resulting in a highly CHK1 selective adenosine triphosphate (ATP) competitive inhibitor.	Adenosine Triphosphate	184-187	checkpoint kinase 1	Homo sapiens	145-149
27191498-10	2016	J-82R cells showed an enhanced sensitivity to pharmacological inhibition of checkpoint kinase 1 (Chk1) and, moreover, could be re-sensitized to CisPt upon Chk1 inhibition.	Cisplatin	144-149	checkpoint kinase 1	Homo sapiens	155-159
27196780-5	2016	Platinum resistance is shown to be associated with activating phosphorylation of AKT and CHK1, inactivating phosphorylation of 4E-BP1, the negative regulator of eIF4E, which promotes increased cap-dependent mRNA translation and increased levels of CHK1 and BRCA1 proteins.	Platinum	0-8	checkpoint kinase 1	Homo sapiens	89-93
27196780-5	2016	Platinum resistance is shown to be associated with activating phosphorylation of AKT and CHK1, inactivating phosphorylation of 4E-BP1, the negative regulator of eIF4E, which promotes increased cap-dependent mRNA translation and increased levels of CHK1 and BRCA1 proteins.	Platinum	0-8	checkpoint kinase 1	Homo sapiens	248-252
27246979-0	2016	Cdc6 contributes to cisplatin-resistance by activation of ATR-Chk1 pathway in bladder cancer cells.	Cisplatin	20-29	checkpoint kinase 1	Homo sapiens	62-66
27246979-7	2016	Cdc6 depletion abrogates S phase arrest caused by CDDP, leading to aberrant mitosis by inactivating ATR-Chk1-Cdc25C pathway.	Cisplatin	50-54	checkpoint kinase 1	Homo sapiens	104-108
27167194-3	2016	Here, we demonstrate that CHK1 inhibitor AZD7762 alone significantly inhibited the growth of radioresistant breast cancer cells (RBCC).	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	41-48	checkpoint kinase 1	Homo sapiens	26-30
27166183-4	2016	In this study, we utilized a CHK1 inhibitor, LY2603618, to decrease Mcl-1 and enhance ABT-199 efficacy.	LY2603618	45-54	checkpoint kinase 1	Homo sapiens	29-33
27166183-4	2016	In this study, we utilized a CHK1 inhibitor, LY2603618, to decrease Mcl-1 and enhance ABT-199 efficacy.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	86-89	checkpoint kinase 1	Homo sapiens	29-33
27163202-4	2016	Cisplatin however caused a significant accumulation of the resistant cells in S and G2/M phases, which was associated with a rapid and sustained checkpoint kinase 1 (Chk1) activation.	Cisplatin	0-9	checkpoint kinase 1	Homo sapiens	145-164
26876155-5	2016	Lovastatin selectively blocked the activation of Chk1 and ATR kinases following treatment with IR, Doxo and the ribonucleotide reductase inhibitor hydroxyurea, indicating that the statin antagonizes ATR/Chk1-regulated replicative stress responses.	Lovastatin	0-10	checkpoint kinase 1	Homo sapiens	49-53
26876155-5	2016	Lovastatin selectively blocked the activation of Chk1 and ATR kinases following treatment with IR, Doxo and the ribonucleotide reductase inhibitor hydroxyurea, indicating that the statin antagonizes ATR/Chk1-regulated replicative stress responses.	Lovastatin	0-10	checkpoint kinase 1	Homo sapiens	203-207
26876155-5	2016	Lovastatin selectively blocked the activation of Chk1 and ATR kinases following treatment with IR, Doxo and the ribonucleotide reductase inhibitor hydroxyurea, indicating that the statin antagonizes ATR/Chk1-regulated replicative stress responses.	Doxorubicin	99-103	checkpoint kinase 1	Homo sapiens	49-53
26876155-5	2016	Lovastatin selectively blocked the activation of Chk1 and ATR kinases following treatment with IR, Doxo and the ribonucleotide reductase inhibitor hydroxyurea, indicating that the statin antagonizes ATR/Chk1-regulated replicative stress responses.	Hydroxyurea	147-158	checkpoint kinase 1	Homo sapiens	49-53
26876155-5	2016	Lovastatin selectively blocked the activation of Chk1 and ATR kinases following treatment with IR, Doxo and the ribonucleotide reductase inhibitor hydroxyurea, indicating that the statin antagonizes ATR/Chk1-regulated replicative stress responses.	Hydroxyurea	147-158	checkpoint kinase 1	Homo sapiens	203-207
27272773-2	2016	Our previous work demonstrated a therapeutic synergism with gemcitabine (GEM) and the CHK1 inhibitor (AZD7762) combination treatment in a TNBC cell line.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	102-109	checkpoint kinase 1	Homo sapiens	86-90
27272773-5	2016	RESULTS: TNBC cell lines harboring low levels of endogenous CHK1, cIAP1 and cIAP2 were responsive to GEM alone, whereas cell lines demonstrating a minimal increase in phospho-S345 CHK1 after treatment were responsive to GEM/AZD7762 or GEM/AZD7762/TL32711 combination.	gemcitabine	101-104	checkpoint kinase 1	Homo sapiens	60-64
26988986-0	2016	Proteasomal Inhibition by Ixazomib Induces CHK1 and MYC-Dependent Cell Death in T-cell and Hodgkin Lymphoma.	ixazomib	26-34	checkpoint kinase 1	Homo sapiens	43-47
26988986-7	2016	The predicted activity for tumor suppressors and oncogenes, the impact on "hallmarks of cancer," and the analysis of key significant genes from global transcriptome analysis for ixazomib strongly favored tumor inhibition via downregulation of MYC and CHK1, its target genes.	ixazomib	178-186	checkpoint kinase 1	Homo sapiens	251-255
26988986-8	2016	Furthermore, in ixazomib-treated lymphoma cells, we identified that CHK1 was involved in the regulation of MYC expression through chromatin modification involving histone H3 acetylation via chromatin immunoprecipitation.	ixazomib	16-24	checkpoint kinase 1	Homo sapiens	68-72
26988986-10	2016	Altogether, ixazomib significantly downregulates MYC and induces potent cell death in T-cell lymphoma and Hodgkin lymphoma, and we identified that combinatorial therapy with anti-CHK1 treatment represents a rational and novel therapeutic approach.	ixazomib	12-20	checkpoint kinase 1	Homo sapiens	179-183
27163202-4	2016	Cisplatin however caused a significant accumulation of the resistant cells in S and G2/M phases, which was associated with a rapid and sustained checkpoint kinase 1 (Chk1) activation.	Cisplatin	0-9	checkpoint kinase 1	Homo sapiens	166-170
27163202-5	2016	In contrast, while cisplatin also elicited a rapid activation of Chk1 in sensitive cells, it markedly decreased total ChK1 and phospho-Chk1 contents over 12 h. Over-expression of dominant negative (DN)-AKT alone increased phospho-Chk1 content, and induced G2/M arrest and apoptosis.	Cisplatin	19-28	checkpoint kinase 1	Homo sapiens	65-69
27163202-5	2016	In contrast, while cisplatin also elicited a rapid activation of Chk1 in sensitive cells, it markedly decreased total ChK1 and phospho-Chk1 contents over 12 h. Over-expression of dominant negative (DN)-AKT alone increased phospho-Chk1 content, and induced G2/M arrest and apoptosis.	Cisplatin	19-28	checkpoint kinase 1	Homo sapiens	118-122
27163202-5	2016	In contrast, while cisplatin also elicited a rapid activation of Chk1 in sensitive cells, it markedly decreased total ChK1 and phospho-Chk1 contents over 12 h. Over-expression of dominant negative (DN)-AKT alone increased phospho-Chk1 content, and induced G2/M arrest and apoptosis.	Cisplatin	19-28	checkpoint kinase 1	Homo sapiens	135-139
27163202-5	2016	In contrast, while cisplatin also elicited a rapid activation of Chk1 in sensitive cells, it markedly decreased total ChK1 and phospho-Chk1 contents over 12 h. Over-expression of dominant negative (DN)-AKT alone increased phospho-Chk1 content, and induced G2/M arrest and apoptosis.	Cisplatin	19-28	checkpoint kinase 1	Homo sapiens	135-139
27163202-8	2016	Chk1 knock-down also facilitated cisplatin-induced apoptosis in chemoresistant cells.	Cisplatin	33-42	checkpoint kinase 1	Homo sapiens	0-4