PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
18167129-8	2008	Furthermore, Fhit-deficient mice demonstrated a decrease in the number of pChk2-positive cells not only in dysplastic lesions but also in N-nitrosobenzylamine-induced papilloma of the forestomach, suggesting that lack of Fhit expression and the resultant defects of the ataxia telangiectasia mutated-Chk2 pathway can cause a difference in the incidence of N-nitrosobenzylamine-induced forestomach lesions.	n-nitrosobenzylamine	138-158	checkpoint kinase 2	Mus musculus	75-79
18162465-0	2008	ATR-Chk2 signaling in p53 activation and DNA damage response during cisplatin-induced apoptosis.	Cisplatin	68-77	checkpoint kinase 2	Mus musculus	4-8
18162465-9	2008	Downstream of ATR, both Chk1 and Chk2 are phosphorylated during cisplatin treatment in an ATR-dependent manner.	Cisplatin	64-73	checkpoint kinase 2	Mus musculus	33-37
18162465-11	2008	Inhibition of Chk2 by a dominant-negative mutant or gene deficiency attenuates cisplatin-induced p53 activation and apoptosis.	Cisplatin	79-88	checkpoint kinase 2	Mus musculus	14-18
18162465-12	2008	In vivo in C57BL/6 mice, ATR and Chk2 are activated in renal tissues following cisplatin treatment.	Cisplatin	79-88	checkpoint kinase 2	Mus musculus	33-37
18162465-13	2008	Together, the results suggest an important role for the DNA damage response mediated by ATR-Chk2 in p53 activation and renal cell apoptosis during cisplatin nephrotoxicity.	Cisplatin	147-156	checkpoint kinase 2	Mus musculus	92-96
15632126-3	2005	We demonstrate that ubiquitination of histone H2B on lysine 123 by the Rad6-Bre1 complex, is necessary for activation of Rad53 kinase and cell cycle arrest.	Lysine	53-59	checkpoint kinase 2	Mus musculus	121-126
17455238-10	2007	These results suggest that vitamin C might be a potent agent to inhibit proliferative activity of melanoma cells via the regulation of Chk2-p53-p21Waf1/Cip1 pathway.	Ascorbic Acid	27-36	checkpoint kinase 2	Mus musculus	135-139
17431115-3	2007	Here, we show that apoptosis, induced synergistically by this combination treatment, was associated with accumulation of cells in early S phase, indicated by cell cycle analyses, increased proliferating cell nuclear antigen, and Chk2-Thr(68) phosphorylation in tumors xenografted in mice.	Threonine	234-237	checkpoint kinase 2	Mus musculus	229-233
15485917-2	2004	After DNA damage, BRCA1 is phosphorylated by CHK2 at serine 988, followed by a change in its intracellular location.	Serine	53-59	checkpoint kinase 2	Mus musculus	45-49
12356735-7	2002	Caffeine further reduced p53 accumulation, suggesting the existence of an ATM/ATR-dependent but Chk2-independent pathway for p53 stabilization.	Caffeine	0-8	checkpoint kinase 2	Mus musculus	96-100
14752107-5	2004	Using wortmannin, serine 15 mutants of p53, DNA-PK null cells and Chk2 null cells, we demonstrate that DNA-PK and Chk2 act independently and sequentially on p53.	Wortmannin	6-16	checkpoint kinase 2	Mus musculus	114-118
14752107-5	2004	Using wortmannin, serine 15 mutants of p53, DNA-PK null cells and Chk2 null cells, we demonstrate that DNA-PK and Chk2 act independently and sequentially on p53.	Serine	18-24	checkpoint kinase 2	Mus musculus	114-118
12192050-6	2002	Unlike ATM(-/-) and p53(-/-) mice, Chk2(-/-) mice do not spontaneously develop tumors, although Chk2 does suppress 7,12-dimethylbenzanthracene-induced skin tumors.	9,10-Dimethyl-1,2-benzanthracene	115-142	checkpoint kinase 2	Mus musculus	96-100
12192050-9	2002	IR-induced apoptosis was restored in Chk2(-/-) thymocytes by reintroduction of the wild-type Chk2 gene but not by a Chk2 gene in which the sites phosphorylated by ATM and ataxia telangiectasia and rad3(+) related (ATR) were mutated to alanine.	Alanine	235-242	checkpoint kinase 2	Mus musculus	37-41
34180140-4	2021	Furthermore, ACY1215 pretreatment increased the level of ATM, gamma-H2AX, Chk2, p53, p21, F-actin and vinculin in ALF.	ricolinostat	13-20	checkpoint kinase 2	Mus musculus	74-78
10710310-7	2000	Chk2 directly phosphorylated p53 on serine 20, which is known to interfere with Mdm2 binding.	Serine	36-42	checkpoint kinase 2	Mus musculus	0-4
34180140-6	2021	The ATM inhibitor KU55933 could decrease the level of ATM, gamma-H2AX, Chk2, p53, p21, F-actin and vinculin in ALF with ACY1215 pretreatment.	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	18-25	checkpoint kinase 2	Mus musculus	71-75
34180140-6	2021	The ATM inhibitor KU55933 could decrease the level of ATM, gamma-H2AX, Chk2, p53, p21, F-actin and vinculin in ALF with ACY1215 pretreatment.	ricolinostat	120-127	checkpoint kinase 2	Mus musculus	71-75
35504548-6	2022	This could be confirmed by the altered expression of CHK1 and CHK2 after zearalenone treatment.	Zearalenone	73-84	checkpoint kinase 2	Mus musculus	62-66
32578892-4	2020	Persistently stalled and unresolved DNA replication forks can "collapse" to generate DSBs that induce signaling via Chk2 and its upstream activator the ataxia telangiectasia-mutated (ATM) protein kinase.	1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione	85-89	checkpoint kinase 2	Mus musculus	116-120
35439335-6	2022	Furthermore, we confirmed that bendamustine activated DNA damage response (DDR) directly or through Ataxia Telangiectasia Mutated Protein (ATM)/Chk2 and ATR/Chk1 pathway and increased the intracellular reactive oxygen species (ROS) level in NKTCL cells, which caused G2/M phase arrest and apoptosis.	Bendamustine Hydrochloride	31-43	checkpoint kinase 2	Mus musculus	144-148
35075953-5	2022	C57BL/6J WT mice were intranasally infected with S. aureus to induce S. aureus-induced pneumonia, which was treated with BML-277, an inhibitor of Chek2.	BML-277	121-128	checkpoint kinase 2	Mus musculus	146-151
32993749-0	2020	FadA promotes DNA damage and progression of Fusobacterium nucleatum-induced colorectal cancer through up-regulation of chk2.	fada	0-4	checkpoint kinase 2	Mus musculus	119-123
35409089-10	2022	Inhibition of phospho-Chk2 phosphorylation of Brca1-S971 delays the end-resection; the delay of premature end-resection by combining Chk2 inhibition with ionizing radiation or carboplatin treatment restored ionizing radiation and platinum sensitivity in Wwox-deficient murine cells, as in human cells, supporting the use of murine in vitro and in vivo models in preclinical cancer treatment research.	Platinum	230-238	checkpoint kinase 2	Mus musculus	22-26
35409089-10	2022	Inhibition of phospho-Chk2 phosphorylation of Brca1-S971 delays the end-resection; the delay of premature end-resection by combining Chk2 inhibition with ionizing radiation or carboplatin treatment restored ionizing radiation and platinum sensitivity in Wwox-deficient murine cells, as in human cells, supporting the use of murine in vitro and in vivo models in preclinical cancer treatment research.	Platinum	230-238	checkpoint kinase 2	Mus musculus	133-137
33863812-4	2021	The screen revealed that sgRNAs targeting the serine/threonine kinase CHK2 were enriched following olaparib treatment.	Serine	46-52	checkpoint kinase 2	Mus musculus	70-74
33863812-4	2021	The screen revealed that sgRNAs targeting the serine/threonine kinase CHK2 were enriched following olaparib treatment.	olaparib	99-107	checkpoint kinase 2	Mus musculus	70-74
33863812-6	2021	Using a Cas9 base editor, we found that blocking CHK2-mediated phosphorylation of p53 also impaired olaparib response.	olaparib	100-108	checkpoint kinase 2	Mus musculus	49-53
33690219-8	2021	Notably, lower expression of PCK1 promoted CHK2 threonine 378 O-GlcNAcylation counteracting its stability and dimer formation, increasing CHK2-dependent Rb phosphorylation and HCC cell proliferation.	Threonine	48-57	checkpoint kinase 2	Mus musculus	43-47
31520908-5	2019	Moreover, BDE-209 could induce oxidative stress with decreased testosterone levels, result in DNA damage and activate DNA damage response signaling pathways (ATM/Chk2, ATR/Chk1 and DNA-PKcs/XRCC4/DNA ligase IV).	decabromobiphenyl ether	10-17	checkpoint kinase 2	Mus musculus	162-166
32187724-0	2020	ATM-CHK2-Beclin 1 axis promotes autophagy to maintain ROS homeostasis under oxidative stress.	Reactive Oxygen Species	54-57	checkpoint kinase 2	Mus musculus	4-8
32187724-3	2020	Here, we show that reactive oxygen species (ROS) function as signaling molecules that regulate autophagy through ataxia-telangiectasia mutated (ATM) and cell cycle checkpoint kinase 2 (CHK2), a DNA damage response (DDR) pathway activated during metabolic and hypoxic stress.	Reactive Oxygen Species	19-42	checkpoint kinase 2	Mus musculus	185-189
32187724-3	2020	Here, we show that reactive oxygen species (ROS) function as signaling molecules that regulate autophagy through ataxia-telangiectasia mutated (ATM) and cell cycle checkpoint kinase 2 (CHK2), a DNA damage response (DDR) pathway activated during metabolic and hypoxic stress.	Reactive Oxygen Species	44-47	checkpoint kinase 2	Mus musculus	185-189
32187724-4	2020	We report that CHK2 binds to and phosphorylates Beclin 1 at Ser90/Ser93, thereby impairing Beclin 1-Bcl-2 autophagy-regulatory complex formation in a ROS-dependent fashion.	Reactive Oxygen Species	150-153	checkpoint kinase 2	Mus musculus	15-19
32187724-5	2020	We further demonstrate that CHK2-mediated autophagy has an unexpected role in reducing ROS levels via the removal of damaged mitochondria, which is required for cell survival under stress conditions.	Reactive Oxygen Species	87-90	checkpoint kinase 2	Mus musculus	28-32
32187724-7	2020	Taken together, these results indicate that the ROS-ATM-CHK2-Beclin 1-autophagy axis serves as a physiological adaptation pathway that protects cells exposed to pathological conditions from stress-induced tissue damage.	Reactive Oxygen Species	48-51	checkpoint kinase 2	Mus musculus	56-60
31676238-2	2020	Wild-type p53-induced phosphatase 1 (Wip1) is a p53-inducible serine/threonine phosphatase that terminates DNA-damage responses via dephosphorylation of DNA-damage response proteins, namely ataxia-telangiectasia mutated (ATM) kinase, checkpoint kinase 2, and p53, thus enhancing cell proliferation.	Serine	62-68	checkpoint kinase 2	Mus musculus	234-253
31209362-4	2020	Specifically, SIRT1 interacts with CHK2 and deacetylates it at lysine 520 residue, which suppresses CHK2 phosphorylation, dimerization, and thus activation.	Lysine	63-69	checkpoint kinase 2	Mus musculus	35-39
31209362-4	2020	Specifically, SIRT1 interacts with CHK2 and deacetylates it at lysine 520 residue, which suppresses CHK2 phosphorylation, dimerization, and thus activation.	Lysine	63-69	checkpoint kinase 2	Mus musculus	100-104
31949138-6	2020	Remarkably, reverse transcriptase inhibitor AZT-treated Chk2 mutant oocytes that evade FOA initially accumulate, but subsequently resolve, L1-instigated genotoxic threats independent of piRNAs and differentiate, resulting in an increased functional ovarian reserve.	Zidovudine	44-47	checkpoint kinase 2	Mus musculus	56-60
31562295-6	2019	Cyclophosphamide exposure induced the activation of both DNAPK-gammaH2AX-checkpoint kinase 2 (CHK2)-p53/TAp63alpha isoform and protein kinase B (AKT)-forkhead box O3 (FOXO3a) signaling axes in the nucleus of oocytes.	Cyclophosphamide	0-16	checkpoint kinase 2	Mus musculus	57-92
31599189-5	2019	Further investigation revealed lovastatin sensitized GBC cells to cisplatin-induced apoptosis and suppressed the activation of CHK1, CHK2, and H2AX during DNA damage response.	Lovastatin	31-41	checkpoint kinase 2	Mus musculus	133-137
31562295-6	2019	Cyclophosphamide exposure induced the activation of both DNAPK-gammaH2AX-checkpoint kinase 2 (CHK2)-p53/TAp63alpha isoform and protein kinase B (AKT)-forkhead box O3 (FOXO3a) signaling axes in the nucleus of oocytes.	Cyclophosphamide	0-16	checkpoint kinase 2	Mus musculus	94-98
29725001-5	2018	Further studies discovered that CK2beta-deficient oocytes showed enhanced gammaH2AX signals, indicative of accumulative unrepaired DSBs, which activated CHK2-dependant p53 and p63 signaling.	1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione	131-135	checkpoint kinase 2	Mus musculus	153-157
29767555-8	2018	Mechanistically, JQ1 suppressed cisplatin-induced phosphorylation or activation of p53 and Chk2, key events in DNA damage response.	Cisplatin	32-41	checkpoint kinase 2	Mus musculus	91-95
30693443-4	2019	Our results revealed that sublethal concentrations of hydrogen peroxide (H2O2) exposure initiated a DNA damage response illustrated by increased gammaH2AX and 53BP1 expression and foci formation mainly in sensory hair cells, together with increased levels of p-Chk2 and p53.	Hydrogen Peroxide	54-71	checkpoint kinase 2	Mus musculus	261-265
30693443-4	2019	Our results revealed that sublethal concentrations of hydrogen peroxide (H2O2) exposure initiated a DNA damage response illustrated by increased gammaH2AX and 53BP1 expression and foci formation mainly in sensory hair cells, together with increased levels of p-Chk2 and p53.	Hydrogen Peroxide	73-77	checkpoint kinase 2	Mus musculus	261-265
29988075-1	2019	Platinum-based chemotherapies can result in ovarian insufficiency by reducing the ovarian reserve, a reduction believed to result from apoptosis of immature oocytes via activation/phosphorylation of TAp63alpha by multiple kinases including CHEK2, CK1, and ABL1.	Platinum	0-8	checkpoint kinase 2	Mus musculus	240-245
29988075-4	2019	Instead, CDDP activates TAp63alpha through the ATR > CHEK1 pathway independent of TAp63alpha hyper-phosphorylation, whereas X-irradiation activates the ATM > CHEK2 > TAp63alpha-hyper-phosphorylation pathway.	cddp	9-13	checkpoint kinase 2	Mus musculus	164-169
29988075-6	2019	Nevertheless, temporary repression of DNA damage response by a kinase inhibitor that attenuates phosphorylation of ATM, ATR, CHEK1, and CHEK2 fully preserves fertility in female mice against CDDP as well as X-ray.	cddp	191-195	checkpoint kinase 2	Mus musculus	136-141
30323964-5	2018	Molecular investigations demonstrated that atovaquone inhibits hepatoma cell proliferation by inducing double-stranded DNA breaks, leading to sustained activation of ataxia-telangiectasia mutated (ATM) and its downstream molecules such as cell cycle checkpoint kinase-2 (CHK2) and H2AX.	Atovaquone	43-53	checkpoint kinase 2	Mus musculus	271-275
30015873-6	2018	Western blotting indicated that the stimulating effect of AZD7762 on osteoblast development was associated with the inhibition of Chk2 and the downregulation of cellular tumor antigen p53.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	58-65	checkpoint kinase 2	Mus musculus	130-134
28498365-4	2017	In addition, ectopic Chk2, as well as its (Chk2) induction by natural podophyllotoxin analog, 4"-demethyl-deoxypodophyllotoxin glucoside (4DPG), strongly restrain Twist1 activity along with other mesenchymal markers, for example, ZEB-1, vimentin and Snail1, whereas the epithelial markers such as E-cadherin and TIMP-1 expression augmented robustly.	Podophyllotoxin	70-85	checkpoint kinase 2	Mus musculus	21-25
30537743-0	2018	Sodium Fluoride Arrests Renal G2/M Phase Cell-Cycle Progression by Activating ATM-Chk2-P53/Cdc25C Signaling Pathway in Mice.	Sodium Fluoride	0-15	checkpoint kinase 2	Mus musculus	82-86
30537743-8	2018	CONCLUSION: In this mouse model, NaF, at more than 12 mg/ kg, induced G2/M phase cell-cycle arrest by activating the ATM-Chk2-p53/Cdc25C signaling pathway, which inhibits the proliferation of renal cells and development of the kidney.	Sodium Fluoride	33-36	checkpoint kinase 2	Mus musculus	121-125
30537743-9	2018	Activation of the ATM-Chk2-p53/Cdc25C signaling pathway is the mechanism of NaF-induced renal G2/M phase cell-cycle arrest in this model.	Sodium Fluoride	76-79	checkpoint kinase 2	Mus musculus	22-26
29200877-12	2017	Exposure of glioma cells to MBZ resulted in a dose-dependent sequestration of Chk2 and Nbs1 in the cytoplasm.	Mebendazole	28-31	checkpoint kinase 2	Mus musculus	78-82
28498365-4	2017	In addition, ectopic Chk2, as well as its (Chk2) induction by natural podophyllotoxin analog, 4"-demethyl-deoxypodophyllotoxin glucoside (4DPG), strongly restrain Twist1 activity along with other mesenchymal markers, for example, ZEB-1, vimentin and Snail1, whereas the epithelial markers such as E-cadherin and TIMP-1 expression augmented robustly.	Podophyllotoxin	70-85	checkpoint kinase 2	Mus musculus	43-47
28498365-4	2017	In addition, ectopic Chk2, as well as its (Chk2) induction by natural podophyllotoxin analog, 4"-demethyl-deoxypodophyllotoxin glucoside (4DPG), strongly restrain Twist1 activity along with other mesenchymal markers, for example, ZEB-1, vimentin and Snail1, whereas the epithelial markers such as E-cadherin and TIMP-1 expression augmented robustly.	4"-demethyl	94-105	checkpoint kinase 2	Mus musculus	43-47
28498365-4	2017	In addition, ectopic Chk2, as well as its (Chk2) induction by natural podophyllotoxin analog, 4"-demethyl-deoxypodophyllotoxin glucoside (4DPG), strongly restrain Twist1 activity along with other mesenchymal markers, for example, ZEB-1, vimentin and Snail1, whereas the epithelial markers such as E-cadherin and TIMP-1 expression augmented robustly.	deoxypodophyllotoxin glucoside	106-136	checkpoint kinase 2	Mus musculus	21-25
28498365-4	2017	In addition, ectopic Chk2, as well as its (Chk2) induction by natural podophyllotoxin analog, 4"-demethyl-deoxypodophyllotoxin glucoside (4DPG), strongly restrain Twist1 activity along with other mesenchymal markers, for example, ZEB-1, vimentin and Snail1, whereas the epithelial markers such as E-cadherin and TIMP-1 expression augmented robustly.	deoxypodophyllotoxin glucoside	106-136	checkpoint kinase 2	Mus musculus	43-47
28498365-4	2017	In addition, ectopic Chk2, as well as its (Chk2) induction by natural podophyllotoxin analog, 4"-demethyl-deoxypodophyllotoxin glucoside (4DPG), strongly restrain Twist1 activity along with other mesenchymal markers, for example, ZEB-1, vimentin and Snail1, whereas the epithelial markers such as E-cadherin and TIMP-1 expression augmented robustly.	4dpg	138-142	checkpoint kinase 2	Mus musculus	43-47
28498365-5	2017	However, downregulation of endogenous Chk2 by siRNA as well as Chk2 selective inhibitor PV1019 implies that 4DPG-mediated inhibition of Twist1 is Chk2-dependent.	4dpg	108-112	checkpoint kinase 2	Mus musculus	38-42
28498365-5	2017	However, downregulation of endogenous Chk2 by siRNA as well as Chk2 selective inhibitor PV1019 implies that 4DPG-mediated inhibition of Twist1 is Chk2-dependent.	4dpg	108-112	checkpoint kinase 2	Mus musculus	63-67
28498365-5	2017	However, downregulation of endogenous Chk2 by siRNA as well as Chk2 selective inhibitor PV1019 implies that 4DPG-mediated inhibition of Twist1 is Chk2-dependent.	4dpg	108-112	checkpoint kinase 2	Mus musculus	63-67
28423495-6	2017	Furthermore, afatinib enhanced in vitro radiosensitivity of SCC1 and SCC10B cells by inducing mesenchymal to epithelial transition, G1 cell cycle arrest, and the attenuating ionizing radiation (IR)-induced activation of DNA double strand break repair (DSB) ATM/ATR/CHK2/BRCA1 pathway.	Afatinib	13-21	checkpoint kinase 2	Mus musculus	265-269
28617799-2	2017	In mammals, spermatocytes that display recombination defects experience a so-called recombination-dependent arrest at the pachytene stage, which relies on the MRE11 complex-ATM-CHK2 pathway responding to unrepaired DNA double-strand breaks (DSBs).	pachytene	122-131	checkpoint kinase 2	Mus musculus	177-181
28617799-2	2017	In mammals, spermatocytes that display recombination defects experience a so-called recombination-dependent arrest at the pachytene stage, which relies on the MRE11 complex-ATM-CHK2 pathway responding to unrepaired DNA double-strand breaks (DSBs).	dsbs	241-245	checkpoint kinase 2	Mus musculus	177-181
26427872-7	2015	Levels of p-Chk1, p-Chk2, and p53, were elevated under both maternal diabetic and high glucose conditions.	Glucose	87-94	checkpoint kinase 2	Mus musculus	20-24
27564101-3	2016	We show that Bisindolylmaleimide IX inhibits DNA topoisomerase, generates DNA breaks, activates the Atm-p53 and Atm-Chk2 pathways, and induces cell cycle arrest and cell death.	bisindolylmaleimide IX	13-35	checkpoint kinase 2	Mus musculus	116-120
26801745-8	2016	In these cells, phospho-ATM, phospho-CHK2, and phospho-gammaH2AX were increased by uridine.	Uridine	83-90	checkpoint kinase 2	Mus musculus	37-41
27991505-8	2016	More importantly, GSK2830371 significantly inhibited tumor growth in an orthotopic xenograft NB mouse model by inducing Chk2/p53-mediated apoptosis in vivo.	GSK2830371	18-28	checkpoint kinase 2	Mus musculus	120-124
26837068-9	2016	One possible mechanism underlying these effects is an increase in intracellular reactive oxygen species (ROS) levels leading to the activation of ataxia telangiectasia-mutated (ATM)/checkpoint kinase 2 (CHK2) and ATM/P53 pathways, thereby mediating cell cycle progression and apoptosis, respectively.	Reactive Oxygen Species	80-103	checkpoint kinase 2	Mus musculus	182-201
26837068-9	2016	One possible mechanism underlying these effects is an increase in intracellular reactive oxygen species (ROS) levels leading to the activation of ataxia telangiectasia-mutated (ATM)/checkpoint kinase 2 (CHK2) and ATM/P53 pathways, thereby mediating cell cycle progression and apoptosis, respectively.	Reactive Oxygen Species	80-103	checkpoint kinase 2	Mus musculus	203-207
26837068-9	2016	One possible mechanism underlying these effects is an increase in intracellular reactive oxygen species (ROS) levels leading to the activation of ataxia telangiectasia-mutated (ATM)/checkpoint kinase 2 (CHK2) and ATM/P53 pathways, thereby mediating cell cycle progression and apoptosis, respectively.	Reactive Oxygen Species	105-108	checkpoint kinase 2	Mus musculus	182-201
26837068-9	2016	One possible mechanism underlying these effects is an increase in intracellular reactive oxygen species (ROS) levels leading to the activation of ataxia telangiectasia-mutated (ATM)/checkpoint kinase 2 (CHK2) and ATM/P53 pathways, thereby mediating cell cycle progression and apoptosis, respectively.	Reactive Oxygen Species	105-108	checkpoint kinase 2	Mus musculus	203-207
27121056-5	2016	Furthermore, through combined in silico and functional screens of the Diversity Set II (NCI/NTP) chemical library we identified the carbanilide-derivative NSC105171, also known as ptu-23, as a novel Chk2 inhibitor (Chk2i).	Carbanilides	132-143	checkpoint kinase 2	Mus musculus	199-203
25319519-0	2015	Checkpoint kinase Chk2 controls renal Cyp27b1 expression, calcitriol formation, and calcium-phosphate metabolism.	Calcitriol	58-68	checkpoint kinase 2	Mus musculus	18-22
25319519-0	2015	Checkpoint kinase Chk2 controls renal Cyp27b1 expression, calcitriol formation, and calcium-phosphate metabolism.	calcium phosphate	84-101	checkpoint kinase 2	Mus musculus	18-22
25319519-4	2015	Since 25-hydroxyvitamin D 1alpha-hydroxylase expression is enhanced by IRF-1, the present study explored the role of Chk2 for calcitriol formation and mineral metabolism.	Calcitriol	126-136	checkpoint kinase 2	Mus musculus	117-121
25319519-9	2015	Renal calcium and phosphate excretion were significantly higher in chk2 (-/-) mice than in chk2 (+/+) mice despite hypophosphatemia and normocalcemia.	Calcium	6-13	checkpoint kinase 2	Mus musculus	67-71
25319519-9	2015	Renal calcium and phosphate excretion were significantly higher in chk2 (-/-) mice than in chk2 (+/+) mice despite hypophosphatemia and normocalcemia.	Phosphates	18-27	checkpoint kinase 2	Mus musculus	67-71
25319519-11	2015	We conclude that Chk2 regulates renal 25-hydroxyvitamin D 1alpha-hydroxylase expression thereby impacting on calcium and phosphate metabolism.	Calcium	109-116	checkpoint kinase 2	Mus musculus	17-21
25319519-11	2015	We conclude that Chk2 regulates renal 25-hydroxyvitamin D 1alpha-hydroxylase expression thereby impacting on calcium and phosphate metabolism.	Phosphates	121-130	checkpoint kinase 2	Mus musculus	17-21
25489053-6	2015	Likewise, analysis of ATM autophosphorylation and additional ATM kinase targets, H2AX and CHK2, support a role for ATM in the activation of p53 by manganese and that a defect in this process occurs in HD.	Manganese	147-156	checkpoint kinase 2	Mus musculus	90-94
24853623-6	2014	Therefore, the selective targeting of Chk1 and Chk2 by oncolytic adenovirus mutants was chosen to treat resistant tumor xenograft mice, and the maximum antitumoral efficacy was achieved with the combined co-abrogation of Chk1 and Chk2 in the presence of low-dose cisplatin.	Cisplatin	263-272	checkpoint kinase 2	Mus musculus	47-51
25520856-5	2014	The accumulated ROS induced DNA damage response (DDR), that mediated Chk1/Chk2 upregulation and activation which were essential factors for the G0/G1 arrest.	ros	16-19	checkpoint kinase 2	Mus musculus	74-78
24726884-8	2014	N-acetylcysteine (NAC), an antioxidant, suppressed the phosphorylation of ATM and p53 and, to a less extent, Chk2, but NAC increased the phosphorylation and nuclear foci formation of H2AX.	Acetylcysteine	0-16	checkpoint kinase 2	Mus musculus	109-113
24726884-8	2014	N-acetylcysteine (NAC), an antioxidant, suppressed the phosphorylation of ATM and p53 and, to a less extent, Chk2, but NAC increased the phosphorylation and nuclear foci formation of H2AX.	Acetylcysteine	18-21	checkpoint kinase 2	Mus musculus	109-113
24726884-10	2014	Ku55933, an ATM inhibitor, blocked ATM phosphorylation and ameliorated the phosphorylation of Chk2 and p53, but it increased H2AX phosphorylation and nuclear foci formation.	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	0-7	checkpoint kinase 2	Mus musculus	94-98
24853623-6	2014	Therefore, the selective targeting of Chk1 and Chk2 by oncolytic adenovirus mutants was chosen to treat resistant tumor xenograft mice, and the maximum antitumoral efficacy was achieved with the combined co-abrogation of Chk1 and Chk2 in the presence of low-dose cisplatin.	Cisplatin	263-272	checkpoint kinase 2	Mus musculus	230-234
24553354-5	2014	Moreover, Chel A-induced p53 protein accumulation and activation required ATR/Chk2 axis, which is distinct from the mechanism that we have most recently identified the Chk1/p53-dependent apoptotic response by Chel A in normal mouse epidermal Cl41 cells.	chel a	10-16	checkpoint kinase 2	Mus musculus	78-82
23667485-4	2013	We found that 5-Iodotubercidin could cause DNA damage, verified by induction of DNA breaks and nuclear foci positive for gammaH2AX and TopBP1, activation of Atm and Chk2, and S15 phosphorylation and up-regulation of p53.	5-iodotubercidin	14-30	checkpoint kinase 2	Mus musculus	165-169
23851027-10	2013	Furthermore, U0126 elevated the expression of cell cycle arrest-related proteins, p21 and phospholylated-chk2 in the post-ischemic kidney.	U 0126	13-18	checkpoint kinase 2	Mus musculus	105-109
23211021-0	2012	Starvation-induced activation of ATM/Chk2/p53 signaling sensitizes cancer cells to cisplatin.	Cisplatin	83-92	checkpoint kinase 2	Mus musculus	37-41
23211021-10	2012	Combination of CDDP with serum starvation in vitro increased the activation of ATM/Chk2/p53 signaling pathway compared to either treatment alone resulting in an enhanced sensitization of cancer cells to CDDP.	Cisplatin	15-19	checkpoint kinase 2	Mus musculus	83-87
23211021-10	2012	Combination of CDDP with serum starvation in vitro increased the activation of ATM/Chk2/p53 signaling pathway compared to either treatment alone resulting in an enhanced sensitization of cancer cells to CDDP.	Cisplatin	203-207	checkpoint kinase 2	Mus musculus	83-87
22732306-6	2012	Profiler  PCR array and RTqPCR analysis showed that either exogenous or endogenous 25HC3S generated by overexpression of oxysterol sulfotransferase (SULT2B1b) plus administration of 25HC significantly up-regulated the proliferation gene expression of Wt1, Pcna, cMyc, cyclin A, FoxM1b, and CDC25b in a dose-dependent manner in liver while substantially down-regulating the expression of cell cycle arrest gene Chek2 and apoptotic gene Apaf1.	25-hydroxycholesterol 3-sulfate	83-89	checkpoint kinase 2	Mus musculus	410-415
22159226-8	2012	Taken together, our study reveals a novel cross talk between Chk2 and TR3 and sheds light on the mechanism of cisplatin-induced apoptosis through TR3.	Cisplatin	110-119	checkpoint kinase 2	Mus musculus	61-65
22313396-6	2012	Recently, nonsense mutations in CHEK2, encoding the chk2 protein, were found to predict resistance to anthracycline therapy in some tumours harbouring wild-type TP53.	Anthracyclines	102-115	checkpoint kinase 2	Mus musculus	32-37
22313396-6	2012	Recently, nonsense mutations in CHEK2, encoding the chk2 protein, were found to predict resistance to anthracycline therapy in some tumours harbouring wild-type TP53.	Anthracyclines	102-115	checkpoint kinase 2	Mus musculus	52-56
22159226-0	2012	Orphan receptor TR3 participates in cisplatin-induced apoptosis via Chk2 phosphorylation to repress intestinal tumorigenesis.	Cisplatin	36-45	checkpoint kinase 2	Mus musculus	68-72
22159226-2	2012	Here, we demonstrate that cisplatin effectively induces orphan nuclear receptor TR3 phosphorylation by activating Chk2 kinase activity and promoting cross talk between these two proteins, thereby contributing to the repression of intestinal tumorigenesis via apoptosis.	Cisplatin	26-35	checkpoint kinase 2	Mus musculus	114-118
22030621-9	2011	Furthermore, inhibition of both Chk1/Chk2 with AZD7762 induces cell death and significantly delays disease progression of transplanted lymphoma cells in vivo.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	47-54	checkpoint kinase 2	Mus musculus	37-41
21745814-6	2011	Reduced HuR phosphorylation by Chk2 silencing or by reduction of Chk2 through polyamine depletion decreased HuR-binding to the occludin mRNA and repressed occludin translation, whereas Chk2 overexpression enhanced (HuR/occludin mRNA) association and stimulated occludin expression.	Polyamines	78-87	checkpoint kinase 2	Mus musculus	65-69
21745814-6	2011	Reduced HuR phosphorylation by Chk2 silencing or by reduction of Chk2 through polyamine depletion decreased HuR-binding to the occludin mRNA and repressed occludin translation, whereas Chk2 overexpression enhanced (HuR/occludin mRNA) association and stimulated occludin expression.	Polyamines	78-87	checkpoint kinase 2	Mus musculus	65-69
21664921-0	2011	Point mutation at the Nbs1 Threonine 278 site does not affect mouse development, but compromises the Chk2 and Smc1 phosphorylation after DNA damage.	Threonine	27-36	checkpoint kinase 2	Mus musculus	101-105
18936108-8	2009	Western blot analysis indicated that AZT treatment caused a decrease in checkpoint kinase 1 (Chk1) and checkpoint kinase 2 (Chk2) at all time points.	Zidovudine	37-40	checkpoint kinase 2	Mus musculus	103-122
18936108-8	2009	Western blot analysis indicated that AZT treatment caused a decrease in checkpoint kinase 1 (Chk1) and checkpoint kinase 2 (Chk2) at all time points.	Zidovudine	37-40	checkpoint kinase 2	Mus musculus	124-128
20820782-8	2011	Cryptotanshinone slightly increased the expression of p53, Chk1, and Chk2 in both B16 and B16BL6.	cryptotanshinone	0-16	checkpoint kinase 2	Mus musculus	69-73
20700484-5	2010	Moreover, this combination treatment results in higher Chk1 and Chk2 kinase activity than does treatment with cisplatin alone and can activate Chk2 in pleural metastases tumor xenograft in mice.	Cisplatin	110-119	checkpoint kinase 2	Mus musculus	64-68
20700484-5	2010	Moreover, this combination treatment results in higher Chk1 and Chk2 kinase activity than does treatment with cisplatin alone and can activate Chk2 in pleural metastases tumor xenograft in mice.	Cisplatin	110-119	checkpoint kinase 2	Mus musculus	143-147
20305300-7	2010	ICRF-193 treatment also causes phosphorylation of an effector kinase downstream of Rad9A in the DNA damage checkpoint pathway, Chk2, at Thr(68).	Threonine	136-139	checkpoint kinase 2	Mus musculus	127-131