PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
33663221-9	2021	Low LARP7 levels in failing hearts was linked to elevated reactive oxygen species (ROS), which activated the ATM-mediated DNA damage response pathway and promoted LARP7 ubiquitination and degradation.	Reactive Oxygen Species	58-81	ataxia telangiectasia mutated	Mus musculus	109-112
465681-1	1979	A rise of hemoglobin concentration accompanied by an increase of the total iron in the blood serum of white mice was found under oxygen pressure of 4 atm for an hour (preconvulsive state) and 6 atm (convulsive state).	Iron	75-79	ataxia telangiectasia mutated	Mus musculus	150-153
465681-1	1979	A rise of hemoglobin concentration accompanied by an increase of the total iron in the blood serum of white mice was found under oxygen pressure of 4 atm for an hour (preconvulsive state) and 6 atm (convulsive state).	Iron	75-79	ataxia telangiectasia mutated	Mus musculus	194-197
465681-1	1979	A rise of hemoglobin concentration accompanied by an increase of the total iron in the blood serum of white mice was found under oxygen pressure of 4 atm for an hour (preconvulsive state) and 6 atm (convulsive state).	Oxygen	129-135	ataxia telangiectasia mutated	Mus musculus	150-153
212990-0	1977	Effect of a novel adenosine deaminase inhibitor (co-vidarabine, co-V) upon the antiviral activity in vitro and in vivo of vidarabine (Vira-Atm) for DNA virus replication.	Pentostatin	49-62	ataxia telangiectasia mutated	Mus musculus	139-142
212990-0	1977	Effect of a novel adenosine deaminase inhibitor (co-vidarabine, co-V) upon the antiviral activity in vitro and in vivo of vidarabine (Vira-Atm) for DNA virus replication.	Pentostatin	64-68	ataxia telangiectasia mutated	Mus musculus	139-142
212990-0	1977	Effect of a novel adenosine deaminase inhibitor (co-vidarabine, co-V) upon the antiviral activity in vitro and in vivo of vidarabine (Vira-Atm) for DNA virus replication.	Vidarabine	52-62	ataxia telangiectasia mutated	Mus musculus	139-142
212990-1	1977	A new potent inhibitor of adenosine deaminase (co-vidarabine) was used in combination studies with adenine arabinoside (vidarabine, Vira-ATM) to protect this purine nucleoside from enzymatic deamination to the more weakly active metabolite, hypoxanthine arabinoside.	Pentostatin	47-60	ataxia telangiectasia mutated	Mus musculus	137-140
212990-1	1977	A new potent inhibitor of adenosine deaminase (co-vidarabine) was used in combination studies with adenine arabinoside (vidarabine, Vira-ATM) to protect this purine nucleoside from enzymatic deamination to the more weakly active metabolite, hypoxanthine arabinoside.	Purine Nucleosides	158-175	ataxia telangiectasia mutated	Mus musculus	137-140
857355-4	1977	4(1):1-8.-Adult and baby mice were subjected to helium pressures up to 120 atm.	Helium	48-54	ataxia telangiectasia mutated	Mus musculus	75-78
860978-4	1977	Earlier studies (8) showed that exposure to 13.8 atm nitrogen under normoxic conditions reduced running activity by 10%.	Nitrogen	53-61	ataxia telangiectasia mutated	Mus musculus	49-52
860978-6	1977	Visual observations of social behavior and respiratory distress suggest that a nitrogen tension of 13.8 atm does not provide protection against oxygen toxicity.	Nitrogen	79-87	ataxia telangiectasia mutated	Mus musculus	104-107
33663221-9	2021	Low LARP7 levels in failing hearts was linked to elevated reactive oxygen species (ROS), which activated the ATM-mediated DNA damage response pathway and promoted LARP7 ubiquitination and degradation.	Reactive Oxygen Species	83-86	ataxia telangiectasia mutated	Mus musculus	109-112
33715230-0	2021	ATM inhibitor KU-55933 induces apoptosis and inhibits motility by blocking GLUT1-mediated glucose uptake in aggressive cancer cells with sustained activation of Akt.	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	14-22	ataxia telangiectasia mutated	Mus musculus	0-3
33892746-0	2021	A dual-targeting ruthenium nanodrug that inhibits primary tumor growth and lung metastasis via the PARP/ATM pathway.	Ruthenium	17-26	ataxia telangiectasia mutated	Mus musculus	104-107
33734555-6	2021	NR treatment also prevents neurodegeneration, suppresses senescence and neuroinflammation, and improves motor function in Atm-/- mice.	nicotinamide-beta-riboside	0-2	ataxia telangiectasia mutated	Mus musculus	122-125
33715230-4	2021	In the present study, we found that aggressive breast and prostate cancer cell lines with overactivated Akt activity exhibit enhanced glucose uptake and GLUT1 translocation upon insulin treatment, and KU-55933, a specific inhibitor of ATM, inhibits insulin-mediated glucose uptake by blocking translocation of GLUT1 to the cell surface.	Glucose	266-273	ataxia telangiectasia mutated	Mus musculus	235-238
34055781-12	2021	DL-Norvaline increased the expression levels of ATM, JNK, and AMBRA1 in A549 cells.	DL-NORVALINE	0-12	ataxia telangiectasia mutated	Mus musculus	48-51
33683737-0	2021	Transplanted hepatocytes rescue mice in acetaminophen-induced acute liver failure through paracrine signals for hepatic ATM and STAT3 pathways.	Acetaminophen	40-53	ataxia telangiectasia mutated	Mus musculus	120-123
33683737-6	2021	Significantly, recapitulating hepatotoxicity-related DNA damage response in cultured cells identified impairments in ATM and JAK/STAT3 intersections since replacing cytokines produced less from injured hepatocytes restored these pathways to avoid acetaminophen hepatotoxicity.	Acetaminophen	247-260	ataxia telangiectasia mutated	Mus musculus	117-120
33715230-8	2021	The roles of ATM in stimulating glucose uptake, glycolysis, motility, and proliferation of cancer cells were demonstrated by knocking-down ATM in these cells.	Glucose	32-39	ataxia telangiectasia mutated	Mus musculus	13-16
33715230-0	2021	ATM inhibitor KU-55933 induces apoptosis and inhibits motility by blocking GLUT1-mediated glucose uptake in aggressive cancer cells with sustained activation of Akt.	Glucose	90-97	ataxia telangiectasia mutated	Mus musculus	0-3
33715230-10	2021	These results suggest that ATM acts as a promoter of tumorigenesis in cancer cells with overactivated Akt, and KU-55933 induces apoptosis and inhibits motility by blocking GLUT1-mediated glucose uptake and glycolysis in these cancer cells, which may lead to the use of KU-55933 and its analogs as new preventive or therapeutic agents against cancer.	Glucose	187-194	ataxia telangiectasia mutated	Mus musculus	27-30
33715230-2	2021	We previously discovered that ATM, a protein kinase deficient in Ataxia-telangiectasia (A-T) disease, is an insulin-responsive protein that participates in insulin-mediated glucose uptake in muscle cells by stimulating glucose transporter 4 (GLUT4) translocation.	Glucose	173-180	ataxia telangiectasia mutated	Mus musculus	30-33
33715230-10	2021	These results suggest that ATM acts as a promoter of tumorigenesis in cancer cells with overactivated Akt, and KU-55933 induces apoptosis and inhibits motility by blocking GLUT1-mediated glucose uptake and glycolysis in these cancer cells, which may lead to the use of KU-55933 and its analogs as new preventive or therapeutic agents against cancer.	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	269-277	ataxia telangiectasia mutated	Mus musculus	27-30
33715230-3	2021	However, the role of ATM in glucose uptake and tumorigenesis of cancer cells is unclear.	Glucose	28-35	ataxia telangiectasia mutated	Mus musculus	21-24
33715230-4	2021	In the present study, we found that aggressive breast and prostate cancer cell lines with overactivated Akt activity exhibit enhanced glucose uptake and GLUT1 translocation upon insulin treatment, and KU-55933, a specific inhibitor of ATM, inhibits insulin-mediated glucose uptake by blocking translocation of GLUT1 to the cell surface.	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	201-209	ataxia telangiectasia mutated	Mus musculus	235-238
33619545-6	2021	Firstly, by activating the DNA damage response (DDR) kinase ATM, DSBs restrict pre-DSB recombinosome numbers without affecting IHO1.	dsbs	65-69	ataxia telangiectasia mutated	Mus musculus	60-63
33342076-7	2021	Notably, TB treatment led to a significant reduction in ATM accumulation and a shift of the activation state of ATMs from the proinflammatory M1-like to the anti-inflammatory M2-like phenotype.	talabostat	9-11	ataxia telangiectasia mutated	Mus musculus	56-59
33536256-3	2021	Truncation mutation in the FATC domain (R3047X) selectively compromised reactive oxygen species-induced ATM activation in cell-free assays.	Oxygen	81-87	ataxia telangiectasia mutated	Mus musculus	104-107
33373327-4	2021	We exploit two different animal models of autism, the Mecp2y/- mouse model of Rett syndrome, and mice prenatally exposed to valproic acid, and found increased ATM levels.	Valproic Acid	124-137	ataxia telangiectasia mutated	Mus musculus	159-162
33373327-5	2021	Accordingly, the treatment with the specific ATM kinase inhibitor KU55933 (KU) normalises molecular, functional and behavioural defects in these mouse models such as the i) delayed GABAergic development, ii) hippocampal hyper-excitability, iii) low cognitive performances, iv) social impairments.	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	66-73	ataxia telangiectasia mutated	Mus musculus	45-48
33608602-4	2021	In response to acute lung injury, ATM-deficiency causes decreased survival, reduced blood oxygen saturation, elevated neutrophil recruitment, exaggerated and prolonged inflammatory responses and excessive lung injury compared to controls.	Oxygen	90-96	ataxia telangiectasia mutated	Mus musculus	34-37
33608602-6	2021	Moreover, we demonstrated that activated ATM-deficient macrophages exhibit significantly elevated production of harmful reactive oxygen and nitrogen species and pro-inflammatory cytokines.	Nitrogen	140-148	ataxia telangiectasia mutated	Mus musculus	41-44
33608602-7	2021	These findings indicate that ATM-deficient immune cells play major roles in causing the lung pathologies in A-T. Based on these results, we examined the impact of inhibiting the aberrant inflammatory responses caused by ATM-deficiency with reparixin, a CXCR1/CXCR2 chemokine receptor antagonist.	reparixin	240-249	ataxia telangiectasia mutated	Mus musculus	220-223
33608602-8	2021	We demonstrated that reparixin treatment reduces neutrophil recruitment, edema and tissue damage in ATM mutant lungs.	reparixin	21-30	ataxia telangiectasia mutated	Mus musculus	100-103
32029507-5	2021	Here, we provide evidence that FCCP-induced mitophagy in MCL and other cancer cell lines is dependent on ATM but independent of its kinase function.	Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone	31-35	ataxia telangiectasia mutated	Mus musculus	105-108
33342076-9	2021	CONCLUSIONS: Our study demonstrates that TB at a low dose could increase energy expenditure and control ATM-mediated adipose inflammation in obese mice, thereby alleviating obesity and its associated metabolic dysfunction.	talabostat	41-43	ataxia telangiectasia mutated	Mus musculus	104-107
33239428-5	2021	R3008H abrogated DNA damage- and oxidative stress-induced activation of ATM without consistently affecting ATM protein stability and recruitment.	r3008h	0-6	ataxia telangiectasia mutated	Mus musculus	72-75
32990677-8	2021	These results suggest that tumor genotype may determine whether inhibition of ATM during radiotherapy will be an effective clinical approach to treat DIPGs.	dipinacoline glutamate	150-155	ataxia telangiectasia mutated	Mus musculus	78-81
33097595-4	2020	Using biochemical approaches and mass spectrometry analysis, we show that upon the onset of the DNA-damage response, SMURF2 becomes phosphorylated at S384 by ataxia telangiectasia mutated (ATM) serine/threonine kinase and this phosphorylation is required for its interaction with RNF20.	Serine	194-200	ataxia telangiectasia mutated	Mus musculus	189-192
32462882-9	2020	Production of 2-hydroxy glutarate by Isocitrate Dehydrogenase1/2 neomorphic oncogenic mutants interferes with the function of alpha-ketoglutarate-dependent enzymes and modulates ATM signaling and glutathione pools.	alpha-hydroxyglutarate	14-33	ataxia telangiectasia mutated	Mus musculus	178-181
33180744-9	2020	Thus, caspase-3-induced ATM/p53/Cox-2/PGE2 signaling pathway could provide potential therapeutic targets to reduce NSCLC recurrence after radiotherapy.	Dinoprostone	38-42	ataxia telangiectasia mutated	Mus musculus	24-27
33021950-3	2020	Phosphorylated ATM at serine 1981 was greater (P < 0.05) in large relative to small follicles with no additional impact of obesity.	Serine	22-28	ataxia telangiectasia mutated	Mus musculus	15-18
32201398-6	2020	In addition, treatment of Ercc1-/  mice with the ATM inhibitor KU-55933 suppressed markers of senescence and SASP.	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	63-71	ataxia telangiectasia mutated	Mus musculus	49-52
32649882-5	2020	Here we report that, in response to DPC induction, the deubiquitinase VCPIP1/VCIP135 is phosphorylated and activated by ATM/ATR.	dpc	36-39	ataxia telangiectasia mutated	Mus musculus	120-123
32708903-9	2020	Concomitant use of TP5 and either temozolomide or irradiation reduced the phosphorylation of ATM, increased DNA damage, and inhibited the G2/M arrest induced by temozolomide or irradiation.	Temozolomide	34-46	ataxia telangiectasia mutated	Mus musculus	93-96
31845160-4	2020	In this study, mice cortical neurons preconditioned with sublethal exposure to oxygen glucose deprivation (OGD) exhibited ATM/glucose-6-phosphate dehydrogenase pathway activation.	Oxygen	79-85	ataxia telangiectasia mutated	Mus musculus	122-125
31845160-4	2020	In this study, mice cortical neurons preconditioned with sublethal exposure to oxygen glucose deprivation (OGD) exhibited ATM/glucose-6-phosphate dehydrogenase pathway activation.	Glucose-6-Phosphate	126-145	ataxia telangiectasia mutated	Mus musculus	122-125
31845160-6	2020	Meanwhile, we found that ATM/P53 pro-apoptosis pathway was driven by lethal OGD injury, and pharmacological inhibition of ATM during fatal oxygen-glucose deprivation/reperfusion injury promoted neuronal survival.	Oxygen	139-145	ataxia telangiectasia mutated	Mus musculus	122-125
32402277-5	2020	We discover a feedback mechanism involving key downstream effectors of DDR, ATM, ATR, and CHK1/2 that regulates OGT stability to promote O-GlcNAcylation and elevate DDR.	o-glcnacylation	137-152	ataxia telangiectasia mutated	Mus musculus	76-79
32741974-7	2020	ATRi/gem caused growth delay in ATM-WT xenografts in NSG mice and induced regression in ATM-KO xenografts.	A-trisaccharide	0-4	ataxia telangiectasia mutated	Mus musculus	32-35
32741974-7	2020	ATRi/gem caused growth delay in ATM-WT xenografts in NSG mice and induced regression in ATM-KO xenografts.	A-trisaccharide	0-4	ataxia telangiectasia mutated	Mus musculus	88-91
32741974-8	2020	CONCLUSIONS: ATM loss augments replication catastrophe-mediated cell death induced by ATRi/gem and may predict clinical responsiveness to this combination.	A-trisaccharide	86-90	ataxia telangiectasia mutated	Mus musculus	13-16
32427532-7	2020	However, the EGCG-treated group required less time to achieve 50% cleavage rate of one-cell embryos, and the EGCG-treated zygotes showed enhanced expression of ATM (pSer-1981) than the untreated group.	epigallocatechin gallate	13-17	ataxia telangiectasia mutated	Mus musculus	160-163
32427532-7	2020	However, the EGCG-treated group required less time to achieve 50% cleavage rate of one-cell embryos, and the EGCG-treated zygotes showed enhanced expression of ATM (pSer-1981) than the untreated group.	epigallocatechin gallate	109-113	ataxia telangiectasia mutated	Mus musculus	160-163
32427532-8	2020	EGCG at optimum concentrations may exert beneficial effects by modulating the ATM activation and moving up the time to enter into mitotic (M) phase.Abbreviations: ROS: reactive oxygen species; EGCG: epigallocatechin-3-gallate; ATM: ataxia telangiectasia mutated; M: mitotic.	epigallocatechin gallate	0-4	ataxia telangiectasia mutated	Mus musculus	78-81
32444694-4	2020	Here, we show that olaparib combines synergistically with the ATR-inhibitor AZD6738 (ceralasertib), in vitro, leading to selective cell death in ATM-deficient cells.	olaparib	19-27	ataxia telangiectasia mutated	Mus musculus	145-148
32444694-4	2020	Here, we show that olaparib combines synergistically with the ATR-inhibitor AZD6738 (ceralasertib), in vitro, leading to selective cell death in ATM-deficient cells.	ceralasertib	76-83	ataxia telangiectasia mutated	Mus musculus	145-148
32444694-4	2020	Here, we show that olaparib combines synergistically with the ATR-inhibitor AZD6738 (ceralasertib), in vitro, leading to selective cell death in ATM-deficient cells.	ceralasertib	85-97	ataxia telangiectasia mutated	Mus musculus	145-148
32444694-6	2020	Selectively in ATM-knockout cells, we show that combined olaparib/AZD6738 treatment induces more chromosomal aberrations and achieves this at lower concentrations and earlier treatment time-points than either monotherapy.	olaparib	57-65	ataxia telangiectasia mutated	Mus musculus	15-18
32444694-6	2020	Selectively in ATM-knockout cells, we show that combined olaparib/AZD6738 treatment induces more chromosomal aberrations and achieves this at lower concentrations and earlier treatment time-points than either monotherapy.	ceralasertib	66-73	ataxia telangiectasia mutated	Mus musculus	15-18
32444694-8	2020	Here, we demonstrate in several ATM-deficient cell lines that the olaparib and AZD6738 combination induces cell death within 1-2 cell divisions, suggesting that combined treatment could circumvent the need for prolonged drug exposure.	olaparib	66-74	ataxia telangiectasia mutated	Mus musculus	32-35
32444694-8	2020	Here, we demonstrate in several ATM-deficient cell lines that the olaparib and AZD6738 combination induces cell death within 1-2 cell divisions, suggesting that combined treatment could circumvent the need for prolonged drug exposure.	ceralasertib	79-86	ataxia telangiectasia mutated	Mus musculus	32-35
32444694-9	2020	Finally, we demonstrate in vivo combination activity of olaparib and AZD6738 in xenograft and PDX mouse models with complete ATM loss.	olaparib	56-64	ataxia telangiectasia mutated	Mus musculus	125-128
32444694-9	2020	Finally, we demonstrate in vivo combination activity of olaparib and AZD6738 in xenograft and PDX mouse models with complete ATM loss.	ceralasertib	69-76	ataxia telangiectasia mutated	Mus musculus	125-128
32187724-0	2020	ATM-CHK2-Beclin 1 axis promotes autophagy to maintain ROS homeostasis under oxidative stress.	Reactive Oxygen Species	54-57	ataxia telangiectasia mutated	Mus musculus	0-3
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	ataxia telangiectasia mutated	Mus musculus	113-142
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	ataxia telangiectasia mutated	Mus musculus	144-147
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	ataxia telangiectasia mutated	Mus musculus	113-142
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	ataxia telangiectasia mutated	Mus musculus	144-147
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	ataxia telangiectasia mutated	Mus musculus	52-55
32244177-4	2020	Here we review ROS responses related to ATM function, recent evidence for ATM roles in mitochondrial maintenance and turnover, and the relationship between ATM and regulation of protein homeostasis.	Reactive Oxygen Species	15-18	ataxia telangiectasia mutated	Mus musculus	40-43
31859574-3	2020	Based on our recent observation that ATM inhibitor (ATMi) efficiently inhibited ionizing radiation (IR)-induced EGFR activation in mouse embryo fibroblasts (MEF), the main purpose of this study is to determine whether ATMi could inhibit IR-induced EGFR activation in human tumor cell lines and explore its potential in EGFRi-alternative therapies.Materials and methods: We compared the effects of ATMi, EGFRi individually or in combination on IR-induced EGFR phosphorylation, cell growth and radio-sensitization in nine human tumor cell lines including lung adenocarcinoma (A549 and H358), glioblastoma (LN229), cervical cancer (HeLa), colorectal carcinoma (SW480 and HCT116) and nasopharygeal carcinoma (5-8F, 6-10B and HK1) cell lines.	phenylalanyl-leucyl-phenylalanyl-glutaminyl-prolyl-glutaminyl-arginyl-phenylalaninamide	705-709	ataxia telangiectasia mutated	Mus musculus	37-40
32052028-1	2020	Wortmannin, a fungal metabolite, is a specific inhibitor of the phosphatidylinositol 3-kinase (PI3K) family, which includes double-stranded DNA dependent protein kinase (DNA-PK) and ataxia telangiectasia mutated kinase (ATM).	wortmannin	0-10	ataxia telangiectasia mutated	Mus musculus	182-218
32052028-1	2020	Wortmannin, a fungal metabolite, is a specific inhibitor of the phosphatidylinositol 3-kinase (PI3K) family, which includes double-stranded DNA dependent protein kinase (DNA-PK) and ataxia telangiectasia mutated kinase (ATM).	wortmannin	0-10	ataxia telangiectasia mutated	Mus musculus	220-223
32052028-1	2020	Wortmannin, a fungal metabolite, is a specific inhibitor of the phosphatidylinositol 3-kinase (PI3K) family, which includes double-stranded DNA dependent protein kinase (DNA-PK) and ataxia telangiectasia mutated kinase (ATM).	Phosphatidylinositols	64-84	ataxia telangiectasia mutated	Mus musculus	182-218
32052028-1	2020	Wortmannin, a fungal metabolite, is a specific inhibitor of the phosphatidylinositol 3-kinase (PI3K) family, which includes double-stranded DNA dependent protein kinase (DNA-PK) and ataxia telangiectasia mutated kinase (ATM).	Phosphatidylinositols	64-84	ataxia telangiectasia mutated	Mus musculus	220-223
32052028-9	2020	These results suggest that wortmannin induces cellular toxicity by accumulation of spontaneous DSBs through inhibition of ATM.	wortmannin	27-37	ataxia telangiectasia mutated	Mus musculus	122-125
32148392-13	2020	Conclusion: KRG suppressed ATM-mediated DDRs and apoptosis by reducing ROS in H. pylori-infected gastric epithelial cells.	Reactive Oxygen Species	71-74	ataxia telangiectasia mutated	Mus musculus	27-30
31291716-9	2020	In Capan-1 mouse xenograft model, AZD1775 plus AZD0156 (ATM inhibitor) treatment reduced tumor growth and downregulated tumor expression of PD-L1, CMTM6, CD163, and CXCR2, all of which contribute to tumor immune evasion.	adavosertib	34-41	ataxia telangiectasia mutated	Mus musculus	56-59
31291716-9	2020	In Capan-1 mouse xenograft model, AZD1775 plus AZD0156 (ATM inhibitor) treatment reduced tumor growth and downregulated tumor expression of PD-L1, CMTM6, CD163, and CXCR2, all of which contribute to tumor immune evasion.	T0156	47-54	ataxia telangiectasia mutated	Mus musculus	56-59
32157166-3	2020	Pharmacological ATM inhibition by KU55933 in cisplatin-treated mice did not ameliorate, but instead exacerbated cisplatin-induced DNA damage and tubular injury, thereby increasing mortality.	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	34-41	ataxia telangiectasia mutated	Mus musculus	16-19
32157166-3	2020	Pharmacological ATM inhibition by KU55933 in cisplatin-treated mice did not ameliorate, but instead exacerbated cisplatin-induced DNA damage and tubular injury, thereby increasing mortality.	Cisplatin	45-54	ataxia telangiectasia mutated	Mus musculus	16-19
32157166-3	2020	Pharmacological ATM inhibition by KU55933 in cisplatin-treated mice did not ameliorate, but instead exacerbated cisplatin-induced DNA damage and tubular injury, thereby increasing mortality.	Cisplatin	112-121	ataxia telangiectasia mutated	Mus musculus	16-19
31435664-0	2020	Ataxia Telangiectasia Mutated coordinates the ovarian DNA repair and atresia-initiating response to phosphoramide mustard.	phosphoramide mustard	100-121	ataxia telangiectasia mutated	Mus musculus	0-29
31435664-3	2020	Phosphoramide mustard (PM) induces ovarian DNA damage and destroys primordial follicles, and pharmacological ATM inhibition prevents PM-induced follicular depletion.	phosphoramide mustard	133-135	ataxia telangiectasia mutated	Mus musculus	109-112
31766690-2	2019	Here, we report that all-trans retinoic acid (tRA) can directly induce the expression of a newly identified potent anti-angiogenic factor, seryl tRNA synthetase (SerRS), whose angiostatic role can, however, be inhibited by UV-activated ataxia telangiectasia mutated (ATM) kinase.	Tretinoin	21-44	ataxia telangiectasia mutated	Mus musculus	267-270
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	ataxia telangiectasia mutated	Mus musculus	158-161
31766690-2	2019	Here, we report that all-trans retinoic acid (tRA) can directly induce the expression of a newly identified potent anti-angiogenic factor, seryl tRNA synthetase (SerRS), whose angiostatic role can, however, be inhibited by UV-activated ataxia telangiectasia mutated (ATM) kinase.	Tretinoin	46-49	ataxia telangiectasia mutated	Mus musculus	267-270
31766690-4	2019	However, UV irradiation induced activation of ATM-phosphorylated SerRS, leading to the inactivation of SerRS as a transcriptional repressor of vascular endothelial growth factor A (VEGFA), which dampened the effect of tRA.	Tretinoin	218-221	ataxia telangiectasia mutated	Mus musculus	46-49
31766690-5	2019	When combined with ATM inhibitor KU-55933, tRA showed a greatly enhanced efficiency in inhibiting VEGFA expression and a much better protection of mouse skin from photo damage.	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	33-41	ataxia telangiectasia mutated	Mus musculus	19-22
31766690-5	2019	When combined with ATM inhibitor KU-55933, tRA showed a greatly enhanced efficiency in inhibiting VEGFA expression and a much better protection of mouse skin from photo damage.	Tretinoin	43-46	ataxia telangiectasia mutated	Mus musculus	19-22
31766690-7	2019	Taken together, tRA combined with an ATM inhibitor can greatly enhance the anti-angiogenic activity of SerRS under UV irradiation and could be a better strategy in protecting skin from angiogenesis-associated skin damage and melanoma caused by UV radiation.	Tretinoin	16-19	ataxia telangiectasia mutated	Mus musculus	37-40
31419512-0	2019	BIBR1532, a selective telomerase inhibitor, enhances radiosensitivity of non-small cell lung cancer through increasing telomere dysfunction and ATM/CHK1 inhibition.	BIBR 1532	0-8	ataxia telangiectasia mutated	Mus musculus	144-147
31419512-9	2019	Mechanistically, lower concentrations BIBR1532 effectively inhibited telomerase activity and increased IR-induced telomere dysfunction, resulting in disruption of chromosomal stability and inhibition of the ATM/CHK1 pathway, which impaired DNA damage repair.	BIBR 1532	38-46	ataxia telangiectasia mutated	Mus musculus	207-210
31722724-7	2019	Surprisingly, we found that Mdm2 is required for MTX-induced H2A ubiquitination and is recruited to the sites of DSB, which is dependent on DNA damage signaling kinase ATM.	methotrexate-alpha-phenylalanine	49-52	ataxia telangiectasia mutated	Mus musculus	168-171
31696503-0	2019	Resveratrol ameliorates high-fat diet-induced insulin resistance and fatty acid oxidation via ATM-AMPK axis in skeletal muscle.	resveratrol	0-11	ataxia telangiectasia mutated	Mus musculus	94-97
31370106-9	2019	Although activated ATM levels were decreased by melatonin treatment, the effect of melatonin on DNA damage response was not a direct consequence of ATM inhibition.	Melatonin	48-57	ataxia telangiectasia mutated	Mus musculus	19-22
31591327-7	2019	Bleomycin-treated chimeric CD44KO-mice had decreased EMT markers, ATM, and mesenchymal cells (alpha-SMA+) accumulation in lung, increased surfactant-b, diminished lung mesenchymal cell motility, and increased lung tissue regenerative capacity following bleomycin injury, as indicated by lung collagen content and semiquantitave morphological index scoring.	Bleomycin	0-9	ataxia telangiectasia mutated	Mus musculus	66-69
31376482-5	2019	In the present study, the downregulation of IDH2 expression resulted in an increase in cell apoptosis in mouse skin through ROS-dependent ATM-mediated p53 signaling.	Reactive Oxygen Species	124-127	ataxia telangiectasia mutated	Mus musculus	138-141
31229705-10	2019	In addition, inhibiting JNK and ATM/ATR signaling pathways partially rescued the decrease in cell viability, indicating that abamectin-induced ROS overproduction and DNA damage might finally lead to cytotoxicity through JNK and ATM/ATR signaling pathways.	abamectin	125-134	ataxia telangiectasia mutated	Mus musculus	32-35
31229705-10	2019	In addition, inhibiting JNK and ATM/ATR signaling pathways partially rescued the decrease in cell viability, indicating that abamectin-induced ROS overproduction and DNA damage might finally lead to cytotoxicity through JNK and ATM/ATR signaling pathways.	abamectin	125-134	ataxia telangiectasia mutated	Mus musculus	228-231
31229705-10	2019	In addition, inhibiting JNK and ATM/ATR signaling pathways partially rescued the decrease in cell viability, indicating that abamectin-induced ROS overproduction and DNA damage might finally lead to cytotoxicity through JNK and ATM/ATR signaling pathways.	ros	143-146	ataxia telangiectasia mutated	Mus musculus	228-231
31696503-15	2019	The effects of RSV on ameliorating HFD-induced abnormal lipid metabolism and insulin resistance mediated through ATM-AMPK pathway may due to its improvement in fatty acid oxidation efficiency and sequential reduction in ROS production in skeletal muscle.	resveratrol	15-18	ataxia telangiectasia mutated	Mus musculus	113-116
31696503-15	2019	The effects of RSV on ameliorating HFD-induced abnormal lipid metabolism and insulin resistance mediated through ATM-AMPK pathway may due to its improvement in fatty acid oxidation efficiency and sequential reduction in ROS production in skeletal muscle.	Fatty Acids	160-170	ataxia telangiectasia mutated	Mus musculus	113-116
30940905-6	2019	Furthermore, we found that both pharmacological and genetic perturbation of ATM and p65 significantly decreased the residual ALL cells after Ara-C treatment in ALL xenograft mouse models.	Cytarabine	141-146	ataxia telangiectasia mutated	Mus musculus	76-79
30664664-8	2019	Furthermore, ATM loss severely impairs phosphorylation of 53BP1 following co-treatment with CB-5083 and ACY-1215 in response to gamma irradiation.	CB-5083	92-99	ataxia telangiectasia mutated	Mus musculus	13-16
31534549-12	2019	Using genome-wide 450K methylation array, we identified chromosomal genes (POT1, ATM and HIST1H2AA) were preferentially methylated by PGE2.	Dinoprostone	134-138	ataxia telangiectasia mutated	Mus musculus	81-84
31384309-3	2019	The antimalarial drug chloroquine activates the kinase ataxia telangiectasia mutated (ATM), improves metabolic syndrome and reduces atherosclerosis in mice.	Chloroquine	22-33	ataxia telangiectasia mutated	Mus musculus	86-89
31384309-19	2019	Conclusions: These findings suggest that low dose chloroquine, which improves the metabolic syndrome through ATM-dependent mechanisms in mice, modestly improves components of the metabolic syndrome in humans but is unlikely to be clinically useful in this setting.Trial registration ClinicalTrials.gov (NCT00455325, NCT00455403), both posted 03 April 2007.	Chloroquine	50-61	ataxia telangiectasia mutated	Mus musculus	109-112
31337415-9	2019	ATM also increased the expression of iron metabolism-related genes (FABP4, Hmox1, Ferroportin, CD163, TfR1, Ceruloplasmin, FtL1, FtH1) associated with a reduction in iron storage and increased turnover.	Iron	37-41	ataxia telangiectasia mutated	Mus musculus	0-3
31337415-9	2019	ATM also increased the expression of iron metabolism-related genes (FABP4, Hmox1, Ferroportin, CD163, TfR1, Ceruloplasmin, FtL1, FtH1) associated with a reduction in iron storage and increased turnover.	Iron	166-170	ataxia telangiectasia mutated	Mus musculus	0-3
30664664-8	2019	Furthermore, ATM loss severely impairs phosphorylation of 53BP1 following co-treatment with CB-5083 and ACY-1215 in response to gamma irradiation.	ricolinostat	104-112	ataxia telangiectasia mutated	Mus musculus	13-16
30735837-8	2019	We also found that hydrogen decreased the expression of the DNA damage-related protein ATM, cyclinD1 and NF-kappaB but increased the expression of the DNA repair-related protein HMGB1, suggesting that hydrogen inhibits senescence in retinas of NaIO3 mice.	Hydrogen	19-27	ataxia telangiectasia mutated	Mus musculus	87-90
31211693-6	2019	Treatment with the ATM DNA damage repair pathway inhibitor KU55933 (KU) during activation reduced NCE by improving expression of activation markers and genes involved in cell survival, by sustaining NKG2D expression and by preserving cell functionality.	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	59-66	ataxia telangiectasia mutated	Mus musculus	19-22
31211693-6	2019	Treatment with the ATM DNA damage repair pathway inhibitor KU55933 (KU) during activation reduced NCE by improving expression of activation markers and genes involved in cell survival, by sustaining NKG2D expression and by preserving cell functionality.	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	59-61	ataxia telangiectasia mutated	Mus musculus	19-22
30986493-6	2019	We further revealed that melatonin rescues spermatogonia from apoptosis by neutralizing reactive oxidative species (ROS) induced by busulfan and recovered the phosphorylation of ATM and p53 to normal levels, and as a result apoptosis in spermatogonial progenitor cells was avoided.	Melatonin	25-34	ataxia telangiectasia mutated	Mus musculus	178-181
30735837-8	2019	We also found that hydrogen decreased the expression of the DNA damage-related protein ATM, cyclinD1 and NF-kappaB but increased the expression of the DNA repair-related protein HMGB1, suggesting that hydrogen inhibits senescence in retinas of NaIO3 mice.	Hydrogen	201-209	ataxia telangiectasia mutated	Mus musculus	87-90
30735837-8	2019	We also found that hydrogen decreased the expression of the DNA damage-related protein ATM, cyclinD1 and NF-kappaB but increased the expression of the DNA repair-related protein HMGB1, suggesting that hydrogen inhibits senescence in retinas of NaIO3 mice.	sodium iodate	244-249	ataxia telangiectasia mutated	Mus musculus	87-90
30961670-16	2019	Importantly, inhibition of ATM suppressed EMT and tumor metastasis in cisplatin-resistant lung cancer cells in an orthotopic xenograft mouse model.	Cisplatin	70-79	ataxia telangiectasia mutated	Mus musculus	27-30
30850480-11	2019	In conclusion, loss of either ATM or adipocyte APC function, but not both, improves systemic glucose metabolism because of maintenance of AT regulatory T cells.	Glucose	93-100	ataxia telangiectasia mutated	Mus musculus	30-33
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	ataxia telangiectasia mutated	Mus musculus	115-118
30710454-11	2019	The transfection of TIGAR siRNA into SMMC7721 cells and xenografts in nude mice further confirmed that the potent activity of dioscin against HCC is evoked by adjusting TIGAR-mediated inhibition of p53, Akt/mTOR, and CDK5/ATM pathways.	dioscin	126-133	ataxia telangiectasia mutated	Mus musculus	222-225
30850587-0	2019	Intracellular citrate accumulation by oxidized ATM-mediated metabolism reprogramming via PFKP and CS enhances hypoxic breast cancer cell invasion and metastasis.	Citric Acid	14-21	ataxia telangiectasia mutated	Mus musculus	47-50
30850587-3	2019	Here we find that hypoxia (1% O2) induces DNA damage-independent ATM activation (oxidized ATM) and suppression of oxidized ATM reduces intracellular citrate via decreasing the levels of phosphofructokinase (PFKP) and citrate synthase (CS), two key glucose metabolism-associated enzymes.	Oxygen	30-32	ataxia telangiectasia mutated	Mus musculus	65-68
30850587-3	2019	Here we find that hypoxia (1% O2) induces DNA damage-independent ATM activation (oxidized ATM) and suppression of oxidized ATM reduces intracellular citrate via decreasing the levels of phosphofructokinase (PFKP) and citrate synthase (CS), two key glucose metabolism-associated enzymes.	Oxygen	30-32	ataxia telangiectasia mutated	Mus musculus	90-93
30850587-3	2019	Here we find that hypoxia (1% O2) induces DNA damage-independent ATM activation (oxidized ATM) and suppression of oxidized ATM reduces intracellular citrate via decreasing the levels of phosphofructokinase (PFKP) and citrate synthase (CS), two key glucose metabolism-associated enzymes.	Oxygen	30-32	ataxia telangiectasia mutated	Mus musculus	90-93
30805937-6	2019	Furthermore, WISP1 increased cell survival rates, diminished cell death rates, and suppressed ataxia-telangiectasia-mutated (ATM)-mediated DNA damage response pathway in cancer cells treated with cisplatin through GLUT1.	Cisplatin	196-205	ataxia telangiectasia mutated	Mus musculus	94-123
30805937-6	2019	Furthermore, WISP1 increased cell survival rates, diminished cell death rates, and suppressed ataxia-telangiectasia-mutated (ATM)-mediated DNA damage response pathway in cancer cells treated with cisplatin through GLUT1.	Cisplatin	196-205	ataxia telangiectasia mutated	Mus musculus	125-128
30522863-5	2019	In addition, we investigated the role of NPRL2 expression and silencing in cell proliferation and in the regulation of ataxia telangiectasia mutated (ATM), which can mediate DNA repair and sensitivity to Olaparib.	olaparib	204-212	ataxia telangiectasia mutated	Mus musculus	119-148
30522863-5	2019	In addition, we investigated the role of NPRL2 expression and silencing in cell proliferation and in the regulation of ataxia telangiectasia mutated (ATM), which can mediate DNA repair and sensitivity to Olaparib.	olaparib	204-212	ataxia telangiectasia mutated	Mus musculus	150-153
30522863-9	2019	In addition, the Olaparib-induced growth delay in NPRL2-silenced PC3 tumors in mice correlated with ATM signaling downregulation, an apoptosis increase and migration/invasion suppression.	olaparib	17-25	ataxia telangiectasia mutated	Mus musculus	100-103
30400801-0	2018	Ibuprofen prevents progression of ataxia telangiectasia symptoms in ATM-deficient mice.	Ibuprofen	0-9	ataxia telangiectasia mutated	Mus musculus	68-71
30400801-12	2018	In vivo administration of ibuprofen to Atm-/- animals before a systemic LPS immune challenge suppressed cytological damage.	Ibuprofen	26-35	ataxia telangiectasia mutated	Mus musculus	39-42
29800228-12	2018	Other studies revealed activation of ROS-ATM-LKB1-AMPK axis as a possible mechanism of PCSK-induced autophagy.	ros	37-40	ataxia telangiectasia mutated	Mus musculus	41-44
30150306-6	2018	beta-Cell-specific inactivation of the master DNA repair gene ataxia telangiectasia mutated (ATM) in STZ-treated mice decreases the expression of proinflammatory cytokines in islets and attenuates the development of hyperglycemia.	Streptozocin	101-104	ataxia telangiectasia mutated	Mus musculus	93-96
29172151-7	2018	ATM (ataxia telangiectasia mutated) deficiency resulted in reduced cell viability, a delay in the resolution of gammaH2AX expression and a significant increase in intracellular ROS in pulmonary epithelial cells after BLM treatment.	Reactive Oxygen Species	177-180	ataxia telangiectasia mutated	Mus musculus	0-34
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	ataxia telangiectasia mutated	Mus musculus	166-195
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	ataxia telangiectasia mutated	Mus musculus	197-200
29769307-0	2018	Orally Bioavailable and Blood-Brain Barrier-Penetrating ATM Inhibitor (AZ32) Radiosensitizes Intracranial Gliomas in Mice.	AZ32	71-75	ataxia telangiectasia mutated	Mus musculus	56-59
29660504-9	2018	Downregulation of IDH2 expression resulted in an increase in oxidative DNA damage in mice skin through ROS-dependent ATM-mediated p53 signaling.	Reactive Oxygen Species	103-106	ataxia telangiectasia mutated	Mus musculus	117-120
29930336-8	2018	Furthermore, naringin counteracted fructose-induced cardiomyocyte apoptosis, and this function of naringin was linked to its ability to inhibit ROS-dependent ATM-mediated p53 signaling.	ros	144-147	ataxia telangiectasia mutated	Mus musculus	158-161
29683659-4	2018	These efforts resulted in the discovery of 64 (AZD0156), an exceptionally potent and selective inhibitor of ATM based on an imidazo[4,5- c]quinolin-2-one core.	T0156	47-54	ataxia telangiectasia mutated	Mus musculus	108-111
29683659-4	2018	These efforts resulted in the discovery of 64 (AZD0156), an exceptionally potent and selective inhibitor of ATM based on an imidazo[4,5- c]quinolin-2-one core.	imidazo(4,5-c)quinolin-2-one	124-153	ataxia telangiectasia mutated	Mus musculus	108-111
29717979-3	2018	Here, we demonstrate that ATM-centered DNA damage response (DDR) progressively declines with senescence and age, while low dose of chloroquine (CQ) activates ATM, promotes DNA damage clearance, rescues age-related metabolic shift, and prolongs replicative lifespan.	Chloroquine	131-142	ataxia telangiectasia mutated	Mus musculus	158-161
29717979-3	2018	Here, we demonstrate that ATM-centered DNA damage response (DDR) progressively declines with senescence and age, while low dose of chloroquine (CQ) activates ATM, promotes DNA damage clearance, rescues age-related metabolic shift, and prolongs replicative lifespan.	Chloroquine	144-146	ataxia telangiectasia mutated	Mus musculus	158-161
29768045-9	2018	This acute model of iron overload was associated with increased numbers of MFehi ATMs; 17% could be attributed to monocyte recruitment and 83% to MFelo ATM incorporation into the MFehi pool.	Iron	20-24	ataxia telangiectasia mutated	Mus musculus	81-84
29768045-10	2018	The MFehi ATM population maintained its low inflammatory profile and iron-cycling expression profile.	Iron	69-73	ataxia telangiectasia mutated	Mus musculus	10-13
29855474-8	2018	Results indicated that (S)-crizotinib decreased GC cell viability, induced growth arrest and apoptosis, and increased levels of gammaH2AX and Ser1981-phosphorylated ATM, which were inhibited by NAC.	Crizotinib	23-37	ataxia telangiectasia mutated	Mus musculus	165-168
29855474-10	2018	Moreover, ATM-activated Akt, a pro-survival signal, whose inhibition further enhanced (S)-crizotinib-induced inhibition of GC cell growth and tumor growth in xenograft mice, and re-sensitized resistant GC cells to (S)-crizotinib.	Crizotinib	86-100	ataxia telangiectasia mutated	Mus musculus	10-13
29855474-10	2018	Moreover, ATM-activated Akt, a pro-survival signal, whose inhibition further enhanced (S)-crizotinib-induced inhibition of GC cell growth and tumor growth in xenograft mice, and re-sensitized resistant GC cells to (S)-crizotinib.	Crizotinib	214-228	ataxia telangiectasia mutated	Mus musculus	10-13
29172151-8	2018	This was confirmed in the human epithelial cell line A549 treated with the ATM-kinase inhibitor KU55933.	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	96-103	ataxia telangiectasia mutated	Mus musculus	75-78
29172151-9	2018	Our results demonstrate high bronchoalveolar sensitivity to ROS and ROS-induced DNA damage in the Atm-deficient mouse model and support the hypothesis that ATM plays a pivotal role in the control of oxidative stress-driven lung inflammation and fibrosis.	Reactive Oxygen Species	60-63	ataxia telangiectasia mutated	Mus musculus	98-101
29172151-9	2018	Our results demonstrate high bronchoalveolar sensitivity to ROS and ROS-induced DNA damage in the Atm-deficient mouse model and support the hypothesis that ATM plays a pivotal role in the control of oxidative stress-driven lung inflammation and fibrosis.	Reactive Oxygen Species	60-63	ataxia telangiectasia mutated	Mus musculus	156-159
29172151-9	2018	Our results demonstrate high bronchoalveolar sensitivity to ROS and ROS-induced DNA damage in the Atm-deficient mouse model and support the hypothesis that ATM plays a pivotal role in the control of oxidative stress-driven lung inflammation and fibrosis.	Reactive Oxygen Species	68-71	ataxia telangiectasia mutated	Mus musculus	98-101
29172151-9	2018	Our results demonstrate high bronchoalveolar sensitivity to ROS and ROS-induced DNA damage in the Atm-deficient mouse model and support the hypothesis that ATM plays a pivotal role in the control of oxidative stress-driven lung inflammation and fibrosis.	Reactive Oxygen Species	68-71	ataxia telangiectasia mutated	Mus musculus	156-159
28964605-0	2017	ATM signals to AMPK to promote autophagy and positively regulate DNA damage in response to cadmium-induced ROS in mouse spermatocytes.	Reactive Oxygen Species	107-110	ataxia telangiectasia mutated	Mus musculus	0-3
29472706-4	2018	Atm tamoxifen-inducible mouse models were generated to explore whether Atm reconstitution is able to restore Atm function in an Atm-deficient background.	Tamoxifen	4-13	ataxia telangiectasia mutated	Mus musculus	0-3
29151191-6	2018	The protein expressions of ATM, CHK-2, P53, E2F1, P73, BAX, Caspase-9, and Caspase-3 were significantly increased, while expressions of RAD51 were down-regulated after SiNP exposure by days 15.	sinp	168-172	ataxia telangiectasia mutated	Mus musculus	27-30
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	ataxia telangiectasia mutated	Mus musculus	78-81
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	ataxia telangiectasia mutated	Mus musculus	117-120
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	ataxia telangiectasia mutated	Mus musculus	18-21
28780388-3	2018	This suggested an alternative signaling system redundant with ATM kinase for activating p53 in this cell line- one that was altered by KU55933 at these higher concentrations (i.e. mTORC1, DNApk, PI3K).	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	135-142	ataxia telangiectasia mutated	Mus musculus	62-65
28964605-0	2017	ATM signals to AMPK to promote autophagy and positively regulate DNA damage in response to cadmium-induced ROS in mouse spermatocytes.	Cadmium	91-98	ataxia telangiectasia mutated	Mus musculus	0-3
28898446-7	2018	In diethylnitrosamine (DEN)-treated primary hepatocytes, NAC and Trolox alleviated DNA damage by activating ataxia-telangiectasia mutated (ATM)/ATM and Rad3-related (ATR) for DNA repair whereas SS-31 and Mito-Q aggravated damage by inactivating them.	Diethylnitrosamine	3-21	ataxia telangiectasia mutated	Mus musculus	139-142
28898446-7	2018	In diethylnitrosamine (DEN)-treated primary hepatocytes, NAC and Trolox alleviated DNA damage by activating ataxia-telangiectasia mutated (ATM)/ATM and Rad3-related (ATR) for DNA repair whereas SS-31 and Mito-Q aggravated damage by inactivating them.	Diethylnitrosamine	3-21	ataxia telangiectasia mutated	Mus musculus	144-147
28898446-7	2018	In diethylnitrosamine (DEN)-treated primary hepatocytes, NAC and Trolox alleviated DNA damage by activating ataxia-telangiectasia mutated (ATM)/ATM and Rad3-related (ATR) for DNA repair whereas SS-31 and Mito-Q aggravated damage by inactivating them.	Diethylnitrosamine	23-26	ataxia telangiectasia mutated	Mus musculus	139-142
28898446-7	2018	In diethylnitrosamine (DEN)-treated primary hepatocytes, NAC and Trolox alleviated DNA damage by activating ataxia-telangiectasia mutated (ATM)/ATM and Rad3-related (ATR) for DNA repair whereas SS-31 and Mito-Q aggravated damage by inactivating them.	Diethylnitrosamine	23-26	ataxia telangiectasia mutated	Mus musculus	144-147
28898446-7	2018	In diethylnitrosamine (DEN)-treated primary hepatocytes, NAC and Trolox alleviated DNA damage by activating ataxia-telangiectasia mutated (ATM)/ATM and Rad3-related (ATR) for DNA repair whereas SS-31 and Mito-Q aggravated damage by inactivating them.	Acetylcysteine	57-60	ataxia telangiectasia mutated	Mus musculus	139-142
28898446-7	2018	In diethylnitrosamine (DEN)-treated primary hepatocytes, NAC and Trolox alleviated DNA damage by activating ataxia-telangiectasia mutated (ATM)/ATM and Rad3-related (ATR) for DNA repair whereas SS-31 and Mito-Q aggravated damage by inactivating them.	Acetylcysteine	57-60	ataxia telangiectasia mutated	Mus musculus	144-147
28898446-7	2018	In diethylnitrosamine (DEN)-treated primary hepatocytes, NAC and Trolox alleviated DNA damage by activating ataxia-telangiectasia mutated (ATM)/ATM and Rad3-related (ATR) for DNA repair whereas SS-31 and Mito-Q aggravated damage by inactivating them.	6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid	65-71	ataxia telangiectasia mutated	Mus musculus	139-142
28898446-7	2018	In diethylnitrosamine (DEN)-treated primary hepatocytes, NAC and Trolox alleviated DNA damage by activating ataxia-telangiectasia mutated (ATM)/ATM and Rad3-related (ATR) for DNA repair whereas SS-31 and Mito-Q aggravated damage by inactivating them.	6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid	65-71	ataxia telangiectasia mutated	Mus musculus	144-147
28898446-9	2018	Localization of ATM between mitochondria and nuclei was altered after NAC and SS-31 treatment.	Acetylcysteine	70-73	ataxia telangiectasia mutated	Mus musculus	16-19
28898446-9	2018	Localization of ATM between mitochondria and nuclei was altered after NAC and SS-31 treatment.	arginyl-2,'6'-dimethyltyrosyl-lysyl-phenylalaninamide	78-83	ataxia telangiectasia mutated	Mus musculus	16-19
28964605-6	2017	The results showed that Cd induced autophagy and DNA damage in GC-2 cells via ROS generation, and the autophagy signal pathway AMPK/mTOR was activated by ATM which is a DNA damage sensor.	Cadmium	24-26	ataxia telangiectasia mutated	Mus musculus	154-157
28964605-9	2017	These findings demonstrated the protective role of autophagy in DNA damage and suggested that the mechanism of autophagy induced by Cd was through the ATM/AMPK/mTOR signal pathway in spermatozoa cells.	Cadmium	132-134	ataxia telangiectasia mutated	Mus musculus	151-154
28833137-7	2017	Coherent with in vitro findings, pharmacological inhibition of TERT by costunolide decreased lipid accumulation and elevated ATM expression in heterotypic xenograft glioma mouse model.	costunolide	71-82	ataxia telangiectasia mutated	Mus musculus	125-128
28648892-3	2017	In contrast, we show here that ATM activation, and phosphorylation of its substrates KAP1, p53 and H2AX in response to the replication blocking agent aphidicolin was unaffected in both immortalized and primary ASCIZ/ATMIN-deficient murine embryonic fibroblasts compared to control cells.	Aphidicolin	150-161	ataxia telangiectasia mutated	Mus musculus	31-34
28797171-8	2017	PDMP + radiotherapy treatment was most effective in inhibiting tumor growth, prolonging survival time, decreasing expression of CD31, CD133, and aldehyde dehydrogenase 1 (ALDH1), inducing G2/M phase arrest, apoptosis, and expression of Ataxia telangiectasia mutated (ATM) and histone H2AX phosphorylation (gamma-H2AX).	RV 538	0-6	ataxia telangiectasia mutated	Mus musculus	236-265
28797171-8	2017	PDMP + radiotherapy treatment was most effective in inhibiting tumor growth, prolonging survival time, decreasing expression of CD31, CD133, and aldehyde dehydrogenase 1 (ALDH1), inducing G2/M phase arrest, apoptosis, and expression of Ataxia telangiectasia mutated (ATM) and histone H2AX phosphorylation (gamma-H2AX).	RV 538	0-6	ataxia telangiectasia mutated	Mus musculus	267-270
28652249-10	2017	Our data suggest that lack of phosphorylation of LKB1 by ATM was involved in AZD1775-mediated cytotoxicity.	adavosertib	77-84	ataxia telangiectasia mutated	Mus musculus	57-60
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	ataxia telangiectasia mutated	Mus musculus	173-176
28714954-5	2017	Virus-mediated expression of C9orf72-related RNA and dipeptide repeats in the mouse central nervous system increases double strand breaks and ATM defects and triggers neurodegeneration.	Dipeptides	53-62	ataxia telangiectasia mutated	Mus musculus	142-145
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	ataxia telangiectasia mutated	Mus musculus	173-176
28341201-0	2017	The ATM kinase inhibitor KU-55933 provides neuroprotection against hydrogen peroxide-induced cell damage via a gammaH2AX/p-p53/caspase-3-independent mechanism: Inhibition of calpain and cathepsin D.	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	25-33	ataxia telangiectasia mutated	Mus musculus	4-7
28341201-4	2017	Furthermore, this ATM inhibitor attenuated the Dox- but not H2O2-induced caspase-3 activity in both UN- and RA-SH-SY5Y cells.	Doxorubicin	47-50	ataxia telangiectasia mutated	Mus musculus	18-21
28341201-0	2017	The ATM kinase inhibitor KU-55933 provides neuroprotection against hydrogen peroxide-induced cell damage via a gammaH2AX/p-p53/caspase-3-independent mechanism: Inhibition of calpain and cathepsin D.	Hydrogen Peroxide	67-84	ataxia telangiectasia mutated	Mus musculus	4-7
28341201-5	2017	Although KU-55933 inhibited the H2O2- and Dox-induced activation of ATM, it attenuated the toxin-induced phosphorylation of the proteins H2AX and p53 only in the latter model of cell damage.	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	9-17	ataxia telangiectasia mutated	Mus musculus	68-71
28487983-0	2017	Role of ataxia-telangiectasia mutated in hydrogen peroxide preconditioning against oxidative stress in Neuro-2a cells.	Hydrogen Peroxide	41-58	ataxia telangiectasia mutated	Mus musculus	8-37
28341201-5	2017	Although KU-55933 inhibited the H2O2- and Dox-induced activation of ATM, it attenuated the toxin-induced phosphorylation of the proteins H2AX and p53 only in the latter model of cell damage.	Hydrogen Peroxide	32-36	ataxia telangiectasia mutated	Mus musculus	68-71
28341201-5	2017	Although KU-55933 inhibited the H2O2- and Dox-induced activation of ATM, it attenuated the toxin-induced phosphorylation of the proteins H2AX and p53 only in the latter model of cell damage.	Doxorubicin	42-45	ataxia telangiectasia mutated	Mus musculus	68-71
28341201-6	2017	Moreover, the ATM inhibitor prevented the H2O2-evoked increases in calpain and cathepsin D activity and attenuated cell damage to a similar degree as inhibitors of calpain (MDL28170) and cathepsin D (pepstatin A).	Hydrogen Peroxide	42-46	ataxia telangiectasia mutated	Mus musculus	14-17
28341201-6	2017	Moreover, the ATM inhibitor prevented the H2O2-evoked increases in calpain and cathepsin D activity and attenuated cell damage to a similar degree as inhibitors of calpain (MDL28170) and cathepsin D (pepstatin A).	pepstatin	200-211	ataxia telangiectasia mutated	Mus musculus	14-17
28487983-8	2017	In conclusion, these findings suggested that ATM is involved in H2O2 preconditioning-mediated protection against oxidative stress-induced injury in N2a cells.	Hydrogen Peroxide	64-68	ataxia telangiectasia mutated	Mus musculus	45-48
28487983-9	2017	To the best of our knowledge, the present study demonstrated, for the first time, that the ATM protein is a key mediator of H2O2 preconditioning.	Hydrogen Peroxide	124-128	ataxia telangiectasia mutated	Mus musculus	91-94
28487983-4	2017	The aim of the present study was therefore to investigate whether ATM mediates H2O2 preconditioning.	Hydrogen Peroxide	79-83	ataxia telangiectasia mutated	Mus musculus	66-69
28487983-6	2017	In addition, preconditioning with 100 microM H2O2 activated ATM and increased ATM mRNA and protein expression levels in N2a cells.	Hydrogen Peroxide	45-49	ataxia telangiectasia mutated	Mus musculus	60-63
28487983-6	2017	In addition, preconditioning with 100 microM H2O2 activated ATM and increased ATM mRNA and protein expression levels in N2a cells.	Hydrogen Peroxide	45-49	ataxia telangiectasia mutated	Mus musculus	78-81
28487983-7	2017	Furthermore, the protective effects induced by H2O2 preconditioning were attenuated by pretreatment with the ATM inhibitor, Ku55933, or ATM small interfering RNA.	Hydrogen Peroxide	47-51	ataxia telangiectasia mutated	Mus musculus	109-112
28487983-7	2017	Furthermore, the protective effects induced by H2O2 preconditioning were attenuated by pretreatment with the ATM inhibitor, Ku55933, or ATM small interfering RNA.	Hydrogen Peroxide	47-51	ataxia telangiectasia mutated	Mus musculus	136-139
28213176-0	2017	LC-MS/MS assay for the simultaneous quantitation of the ATM inhibitor AZ31 and the ATR inhibitor AZD6738 in mouse plasma.	AZ31	70-74	ataxia telangiectasia mutated	Mus musculus	56-59
28213176-1	2017	The ATM kinase inhibitor AZ31 and ATR kinase inhibitor AZD6738 are in various phases of preclinical and clinical evaluation for their ability to potentiate chemoradiation.	AZ31	25-29	ataxia telangiectasia mutated	Mus musculus	4-7
28138034-6	2017	Furthermore, in an in vivo tumor xenograft mouse model, AZD6738 significantly suppressed tumor growth and increased apoptosis.These findings suggest synthetic lethality between ATR inhibition and ATM deficiency in gastric cancer cells.	ceralasertib	56-63	ataxia telangiectasia mutated	Mus musculus	196-199
28565765-10	2017	Pravastatin reduced the intestinal expression of ataxia-telangiectasia mutated and gamma-H2AX after irradiation.	Pravastatin	0-11	ataxia telangiectasia mutated	Mus musculus	49-78
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	ataxia telangiectasia mutated	Mus musculus	257-260
28074659-5	2017	ROS enhanced nuclear translocation of p53, activated ATM (ataxia telangiectasia-mutated protein), increased expression of GADD45a (growth arrest and DNA-damage-inducible protein) gene and inactivated Non homologous end joining (NHEJ) repair pathway.	Reactive Oxygen Species	0-3	ataxia telangiectasia mutated	Mus musculus	53-95
27929719-3	2017	In a cross-species study, using primary rat neurons, the roundworm C. elegans, and a mouse model of A-T, we showed that loss of ATM induces mitochondrial dysfunction and compromised mitophagy due to NAD+ insufficiency.	NAD	199-203	ataxia telangiectasia mutated	Mus musculus	128-131
27929719-4	2017	Remarkably, NAD+ repletion mitigates both the DNA repair defect and mitochondrial dysfunction in ATM-deficient neurons.	NAD	12-16	ataxia telangiectasia mutated	Mus musculus	97-100
28081255-4	2017	NM administration had the following DNA methylation effects: AuNP 60 nm induced CpG hypermethylation in Atm, Cdk and Gsr genes and hypomethylation in Gpx; Gsr and Trp53 showed changes in methylation between low- and high-dose AuNP, 60 and 250 nm respectively, and AuNP had size effects on methylation for Trp53.	aunp	61-65	ataxia telangiectasia mutated	Mus musculus	104-107
28477114-7	2017	Phosphorylation of the serine residue within the target sequence by ATM would lead to its interaction with the phospho-serine-binding domain, thereby preventing complementation of the split luciferase pair and loss of reporter activity.	Serine	23-29	ataxia telangiectasia mutated	Mus musculus	68-71
28477114-7	2017	Phosphorylation of the serine residue within the target sequence by ATM would lead to its interaction with the phospho-serine-binding domain, thereby preventing complementation of the split luciferase pair and loss of reporter activity.	Serine	119-125	ataxia telangiectasia mutated	Mus musculus	68-71
27940962-6	2016	A knock-in mutation of the ATM phosphorylation site on E2F1 (S29A) prevents the interaction between E2F1 and TopBP1 and recruitment of RB, E2F1, and BRG1 to DSBs.	dsbs	157-161	ataxia telangiectasia mutated	Mus musculus	27-30
28293885-7	2017	Phosphorylation of the serine residue within the target sequence by ATM would lead to its interaction with the phospho-serine-binding domain, thereby preventing complementation of the split luciferase pair and loss of reporter activity.	Serine	23-29	ataxia telangiectasia mutated	Mus musculus	68-71
28293885-7	2017	Phosphorylation of the serine residue within the target sequence by ATM would lead to its interaction with the phospho-serine-binding domain, thereby preventing complementation of the split luciferase pair and loss of reporter activity.	Serine	119-125	ataxia telangiectasia mutated	Mus musculus	68-71
27974220-0	2016	Histone H3 Lysine 9 Acetylation Obstructs ATM Activation and Promotes Ionizing Radiation Sensitivity in Normal Stem Cells.	Lysine	11-17	ataxia telangiectasia mutated	Mus musculus	42-45
30542240-0	2017	A role for ataxia telangiectasia mutated in insulin-independent stimulation of glucose transport.	Glucose	79-86	ataxia telangiectasia mutated	Mus musculus	11-40
30542240-1	2017	Literature reports suggest that ataxia telangiectasia mutated (ATM) can activate the AMP-activated protein kinase (AMPK), a protein that can stimulate glucose transport in skeletal muscle.	Glucose	151-158	ataxia telangiectasia mutated	Mus musculus	32-61
30542240-1	2017	Literature reports suggest that ataxia telangiectasia mutated (ATM) can activate the AMP-activated protein kinase (AMPK), a protein that can stimulate glucose transport in skeletal muscle.	Glucose	151-158	ataxia telangiectasia mutated	Mus musculus	63-66
30542240-2	2017	We hypothesized that 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR), an AMPK activator, would increase glucose transport in mouse extensor digitorum longus (EDL) muscles in an ATM-dependent manner.	AICA ribonucleotide	21-66	ataxia telangiectasia mutated	Mus musculus	183-186
30542240-2	2017	We hypothesized that 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR), an AMPK activator, would increase glucose transport in mouse extensor digitorum longus (EDL) muscles in an ATM-dependent manner.	AICA ribonucleotide	68-73	ataxia telangiectasia mutated	Mus musculus	183-186
30542240-3	2017	AICAR-stimulated glucose transport was prevented by the ATM inhibitor KU-55933 despite normal stimulation of AMPK phosphorylation.	Glucose	17-24	ataxia telangiectasia mutated	Mus musculus	56-59
30542240-3	2017	AICAR-stimulated glucose transport was prevented by the ATM inhibitor KU-55933 despite normal stimulation of AMPK phosphorylation.	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	70-78	ataxia telangiectasia mutated	Mus musculus	56-59
30542240-5	2017	S231 of TBC1D1 matches the sequence motif of ATM substrates, and phosphorylation of this site is known to inhibit TBC1D1 and lead to increased glucose transport.	Glucose	143-150	ataxia telangiectasia mutated	Mus musculus	45-48
30542240-8	2017	The data suggest that ATM plays a role in AICAR-stimulated glucose transport downstream of AMPK.	Glucose	59-66	ataxia telangiectasia mutated	Mus musculus	22-25
27431323-2	2016	Here we show that phosphorylation of CREB on a conserved cluster of Ser residues (the ATM/CK cluster) by the DNA damage-activated protein kinase ataxia-telangiectasia-mutated (ATM) and casein kinase1 (CK1) and casein kinase2 (CK2) positively and negatively regulates CREB-mediated transcription in a signal dependent manner.	Serine	68-71	ataxia telangiectasia mutated	Mus musculus	86-89
27431323-2	2016	Here we show that phosphorylation of CREB on a conserved cluster of Ser residues (the ATM/CK cluster) by the DNA damage-activated protein kinase ataxia-telangiectasia-mutated (ATM) and casein kinase1 (CK1) and casein kinase2 (CK2) positively and negatively regulates CREB-mediated transcription in a signal dependent manner.	Serine	68-71	ataxia telangiectasia mutated	Mus musculus	176-179
27431323-3	2016	In response to genotoxic stress, phosphorylation of the ATM/CK cluster inhibited CREB-mediated gene expression, DNA binding activity and chromatin occupancy proportional to the number of modified Ser residues.	Serine	196-199	ataxia telangiectasia mutated	Mus musculus	56-59
27431323-4	2016	Paradoxically, substoichiometric, ATM-independent, phosphorylation of the ATM/CK cluster potentiated bursts in CREB-mediated transcription by promoting recruitment of the CREB coactivator, cAMP-regulated transcriptional coactivators (CRTC2).	Cyclic AMP	189-193	ataxia telangiectasia mutated	Mus musculus	34-37
27431323-4	2016	Paradoxically, substoichiometric, ATM-independent, phosphorylation of the ATM/CK cluster potentiated bursts in CREB-mediated transcription by promoting recruitment of the CREB coactivator, cAMP-regulated transcriptional coactivators (CRTC2).	Cyclic AMP	189-193	ataxia telangiectasia mutated	Mus musculus	74-77
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	ataxia telangiectasia mutated	Mus musculus	100-103
27199493-8	2016	In repair-deficient ATM-/- neurons, large persisting damage foci reflect multiple unrepaired DSBs concentrated at the boundary of heterochromatin due to disturbed KAP1 phosphorylation.	dsbs	93-97	ataxia telangiectasia mutated	Mus musculus	20-23
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	ataxia telangiectasia mutated	Mus musculus	112-115
26862121-0	2016	Ataxia telangiectasia mutated in cardiac fibroblasts regulates doxorubicin-induced cardiotoxicity.	Doxorubicin	63-74	ataxia telangiectasia mutated	Mus musculus	0-29
27732834-2	2016	(2016) show that both the DNA repair defect and mitochondrial dysfunction in ATM-/- cells or mice are mitigated by the anti-aging compound nicotinamide riboside or a SIRT1 activator.	nicotinamide-beta-riboside	139-160	ataxia telangiectasia mutated	Mus musculus	77-80
27538496-5	2016	In ATM mutants, glutamine supplementation restored serum glutamine and glucose levels and reduced body weight loss.	Glutamine	16-25	ataxia telangiectasia mutated	Mus musculus	3-6
27538496-8	2016	In vitro assays revealed that ATM-deficient cells are more sensitive to glutamine deprivation, while supra-molar glutamine (8 mM) partially rescued the reduction of BDNF expression and HDAC4 nuclear translocation of genetically mutant Atm(-/-) neurons.	Glutamine	72-81	ataxia telangiectasia mutated	Mus musculus	30-33
27538496-8	2016	In vitro assays revealed that ATM-deficient cells are more sensitive to glutamine deprivation, while supra-molar glutamine (8 mM) partially rescued the reduction of BDNF expression and HDAC4 nuclear translocation of genetically mutant Atm(-/-) neurons.	Glutamine	113-122	ataxia telangiectasia mutated	Mus musculus	235-238
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	ataxia telangiectasia mutated	Mus musculus	146-175
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	ataxia telangiectasia mutated	Mus musculus	177-180
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	ataxia telangiectasia mutated	Mus musculus	213-216
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	ataxia telangiectasia mutated	Mus musculus	146-175
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	ataxia telangiectasia mutated	Mus musculus	177-180
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	ataxia telangiectasia mutated	Mus musculus	213-216
27318254-8	2016	These data indicate that defective Atm reduces the redox homeostasis of the testis and genetic integrity of sperm by regulating glutathione levels independently from G6PDH activity.	Glutathione	128-139	ataxia telangiectasia mutated	Mus musculus	35-38
26862121-3	2016	Here, we show that ATM in cardiac fibroblasts is essential for Dox-induced cardiotoxicity.	Doxorubicin	63-66	ataxia telangiectasia mutated	Mus musculus	19-22
26862121-4	2016	METHODS AND RESULTS: ATM knockout mice showed attenuated Dox-induced cardiotoxic effects (e.g. cardiac dysfunction, apoptosis, and mortality).	Doxorubicin	57-60	ataxia telangiectasia mutated	Mus musculus	21-24
26862121-7	2016	Therapeutically, a potent and selective inhibitor of ATM, KU55933, when administered systemically was able to prevent Dox-induced cardiotoxicity.	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	58-65	ataxia telangiectasia mutated	Mus musculus	53-56
26862121-7	2016	Therapeutically, a potent and selective inhibitor of ATM, KU55933, when administered systemically was able to prevent Dox-induced cardiotoxicity.	Doxorubicin	118-121	ataxia telangiectasia mutated	Mus musculus	53-56
26862121-8	2016	CONCLUSION: ATM-regulated effects within cardiac fibroblasts are pivotal in Dox-induced cardiotoxicity, and antagonism of ATM and its functions may have potential therapeutic implications.	Doxorubicin	76-79	ataxia telangiectasia mutated	Mus musculus	12-15
26822034-4	2016	Here we show that phosphorylation of GSK3beta on Ser(389) by p38 MAPK (mitogen-activated protein kinase) is induced selectively by DSBs through ATM (ataxia telangiectasia mutated) as a unique mechanism to attenuate the activity of nuclear GSK3beta and promote survival of cells undergoing DSBs.	Serine	49-52	ataxia telangiectasia mutated	Mus musculus	144-178
26912395-9	2016	Collectively, our data show that adipocyte-originated PGE2with inflammation suppressive properties plays a significant role in mediating ATM accumulation during lipolysis.	pge2with	54-62	ataxia telangiectasia mutated	Mus musculus	137-140
25915840-9	2016	Whereas Hus1(neo/neo) and Atm(-/-) single mutant mice survived low-dose MMC similar to wild-type controls, Hus1(neo/neo)Atm(-/-) double mutants showed striking MMC hypersensitivity, consistent with a model in which MMC exposure in the context of Hus1 dysfunction results in DSBs to which the ATM pathway normally responds.	Mitomycin	160-163	ataxia telangiectasia mutated	Mus musculus	120-123
25915840-9	2016	Whereas Hus1(neo/neo) and Atm(-/-) single mutant mice survived low-dose MMC similar to wild-type controls, Hus1(neo/neo)Atm(-/-) double mutants showed striking MMC hypersensitivity, consistent with a model in which MMC exposure in the context of Hus1 dysfunction results in DSBs to which the ATM pathway normally responds.	Mitomycin	160-163	ataxia telangiectasia mutated	Mus musculus	120-123
26822034-4	2016	Here we show that phosphorylation of GSK3beta on Ser(389) by p38 MAPK (mitogen-activated protein kinase) is induced selectively by DSBs through ATM (ataxia telangiectasia mutated) as a unique mechanism to attenuate the activity of nuclear GSK3beta and promote survival of cells undergoing DSBs.	dsbs	131-135	ataxia telangiectasia mutated	Mus musculus	144-178
26822034-4	2016	Here we show that phosphorylation of GSK3beta on Ser(389) by p38 MAPK (mitogen-activated protein kinase) is induced selectively by DSBs through ATM (ataxia telangiectasia mutated) as a unique mechanism to attenuate the activity of nuclear GSK3beta and promote survival of cells undergoing DSBs.	dsbs	289-293	ataxia telangiectasia mutated	Mus musculus	144-178
26280532-3	2015	Using mouse cells containing targeted mutant alleles of Mre11 (Mre11a) and/or Ku70 (Xrcc6), together with pharmacologic kinase inhibition, we demonstrate that ATM can be activated by DSBs in the absence of MRN.	dsbs	183-187	ataxia telangiectasia mutated	Mus musculus	159-162
26489644-9	2015	Overall, ABCG1 modulates ATM cholesterol content in obesity and weight loss regimes leading to an alteration in M1 to M2 ratio that we suggest is due to the extent of macrophage egress from adipose tissue.	Cholesterol	29-40	ataxia telangiectasia mutated	Mus musculus	25-28
26632965-4	2016	We performed extensive structure-activity and structure-property relationship studies on this quinazoline ATM kinase inhibitor in order to identify structural variants with enhanced selectivity and metabolic stability.	Quinazolines	94-105	ataxia telangiectasia mutated	Mus musculus	106-109
26625310-5	2016	Furthermore, recruited mast cells could also increase the phosphorylation of ATM at ser-1981 site, and inhibition of ATM activity could reverse mast cell-induced radiotherapy resistance.	Serine	84-87	ataxia telangiectasia mutated	Mus musculus	77-80
26510954-0	2015	Alteration in 5-hydroxymethylcytosine-mediated epigenetic regulation leads to Purkinje cell vulnerability in ATM deficiency.	5-hydroxymethylcytosine	14-37	ataxia telangiectasia mutated	Mus musculus	109-112
26510954-3	2015	We further show that TET1, an enzyme that converts 5-methylcytosine (5mC) to 5hmC, responds to DNA damage and manipulation of TET1 activity directly affects the DNA damage signalling and ATM-deficient neuronal cell cycle re-entry and death.	5-Methylcytosine	51-67	ataxia telangiectasia mutated	Mus musculus	187-190
26510954-3	2015	We further show that TET1, an enzyme that converts 5-methylcytosine (5mC) to 5hmC, responds to DNA damage and manipulation of TET1 activity directly affects the DNA damage signalling and ATM-deficient neuronal cell cycle re-entry and death.	5-Methylcytosine	69-72	ataxia telangiectasia mutated	Mus musculus	187-190
26510954-3	2015	We further show that TET1, an enzyme that converts 5-methylcytosine (5mC) to 5hmC, responds to DNA damage and manipulation of TET1 activity directly affects the DNA damage signalling and ATM-deficient neuronal cell cycle re-entry and death.	5-hydroxymethylcytosine	77-81	ataxia telangiectasia mutated	Mus musculus	187-190
26510954-5	2015	Finally, we verify that TET1-mediated 5hmC production is linked to the degenerative process of Purkinje cells and behavioural deficits in Atm(-/-) mice.	5-hydroxymethylcytosine	38-42	ataxia telangiectasia mutated	Mus musculus	138-141
26205951-10	2015	At this time, radiation-induces activation of ATM-dependent p53 apoptotic proteins-ATM, p53, p21, Bax, cytochrome C, active caspase-3 and caspases-9 expression, which were significantly reversed in melatonin pre-treated mice.	Melatonin	198-207	ataxia telangiectasia mutated	Mus musculus	46-49
26205951-14	2015	The detailed study will benefit in understanding the role of melatonin in modulation of radiation-induced ATM-dependent p53-mediated pro-vs.-anti apoptotic proteins in testicular injury.	Melatonin	61-70	ataxia telangiectasia mutated	Mus musculus	106-109
25489053-9	2015	To determine if this phenotype contributes to the deficit in manganese-dependent ATM activation, we used pharmacological manipulation to equalize manganese levels between HD and control mouse striatal cells and rescued the ATM-p53 signaling deficit.	Manganese	61-70	ataxia telangiectasia mutated	Mus musculus	81-84
25489053-10	2015	Collectively, our data demonstrate selective alterations in manganese biology in cellular models of HD manifest in ATM-p53 signaling.	Manganese	60-69	ataxia telangiectasia mutated	Mus musculus	115-118
25091220-1	2015	We have recently reported that glioblastoma (GB)-initiating cells (GIC) with low expression and/or mutation of TP53 and high expression of PI3K ("responder" genetic profile) can be effectively and safely radiosensitized by the ATM inhibitor KU60019.	2-(2,6-dimethylmorpholin-4-yl)-N-(5-(6-morpholin-4-yl-4-oxo-4H-pyran-2-yl)-9H-thioxanthen-2-yl)acetamide	241-248	ataxia telangiectasia mutated	Mus musculus	227-230
25397632-5	2015	In the present study, we identified Fe65 Ser(228) as a novel target of the ATM (ataxia telangiectasia mutated) and ATR (ataxia-telangiectasia- and Rad3-related protein) protein kinases, in a reaction that occurred independently of APP.	Serine	41-44	ataxia telangiectasia mutated	Mus musculus	75-109
25768017-0	2015	The ATM signaling cascade promotes recombination-dependent pachytene arrest in mouse spermatocytes.	pachytene	59-68	ataxia telangiectasia mutated	Mus musculus	4-7
25646414-2	2015	The ATM protein has roles in DNA repair and in the regulation of reactive oxygen species (ROS).	Reactive Oxygen Species	65-88	ataxia telangiectasia mutated	Mus musculus	4-7
25646414-2	2015	The ATM protein has roles in DNA repair and in the regulation of reactive oxygen species (ROS).	Reactive Oxygen Species	90-93	ataxia telangiectasia mutated	Mus musculus	4-7
24366691-3	2014	Our laboratory previously demonstrated that the dual phosphoinositide 3-kinase/mTOR inhibitor NVP-BEZ235 can potently inhibit the two central DDR kinases, DNA-dependent protein kinase catalytic subunit (DNA-PKcs) and ataxia-telangiectasia mutated (ATM), in vitro.	dactolisib	94-104	ataxia telangiectasia mutated	Mus musculus	217-246
25448685-7	2014	Ovarian ATM, XRCC6, PRKDC, RAD51 and PARP1 proteins were increased (P&lt;0.05) by DMBA exposure in lean mice.	9,10-Dimethyl-1,2-benzanthracene	82-86	ataxia telangiectasia mutated	Mus musculus	8-11
24913718-9	2014	Our findings indicate that ATM deficiency allows IgH V(D)J recombination DSBs in developing B cells to generate dicentric translocations that, via BFB cycles, lead to c-myc-activating oncogenic translocations and amplifications in mature B cells.	1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione	73-77	ataxia telangiectasia mutated	Mus musculus	27-30
24913718-9	2014	Our findings indicate that ATM deficiency allows IgH V(D)J recombination DSBs in developing B cells to generate dicentric translocations that, via BFB cycles, lead to c-myc-activating oncogenic translocations and amplifications in mature B cells.	bfb	147-150	ataxia telangiectasia mutated	Mus musculus	27-30
25101980-2	2014	We show that ataxia telangiectasia mutated (ATM) integrates the DNA damage response with DNA metabolism by regulating the salvage of deoxyribonucleosides.	Deoxyribonucleosides	133-153	ataxia telangiectasia mutated	Mus musculus	13-42
25101980-2	2014	We show that ataxia telangiectasia mutated (ATM) integrates the DNA damage response with DNA metabolism by regulating the salvage of deoxyribonucleosides.	Deoxyribonucleosides	133-153	ataxia telangiectasia mutated	Mus musculus	44-47
25101980-3	2014	Specifically, ATM phosphorylates and activates deoxycytidine kinase (dCK) at serine 74 in response to ionizing radiation (IR).	Serine	77-83	ataxia telangiectasia mutated	Mus musculus	14-17
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	ataxia telangiectasia mutated	Mus musculus	74-77
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	ataxia telangiectasia mutated	Mus musculus	74-77
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	ataxia telangiectasia mutated	Mus musculus	12-15
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	ataxia telangiectasia mutated	Mus musculus	35-38
24817034-8	2014	Moreover, TVX induced activation of the DNA damage sensor kinases, ataxia telangiectasia mutated (ATM) and Rad3-related (ATR).	trovafloxacin	10-13	ataxia telangiectasia mutated	Mus musculus	67-102
24817034-9	2014	The ATR inhibitor NU6027 [6-(cyclohexylmethoxy)-5-nitrosopyrimidine-2,4-diamine] prevented the TVX-mediated increases in LPS-induced TNF mRNA and protein release, whereas a selective ATM inhibitor [2-(4-morpholinyl)-6-(1-thianthrenyl)-4H-pyran-4-one (KU55933)] was without effect.	4-cyclohexylmethoxy-5-nitrosopyrimidine-2,6-diamine	18-24	ataxia telangiectasia mutated	Mus musculus	183-186
24817034-9	2014	The ATR inhibitor NU6027 [6-(cyclohexylmethoxy)-5-nitrosopyrimidine-2,4-diamine] prevented the TVX-mediated increases in LPS-induced TNF mRNA and protein release, whereas a selective ATM inhibitor [2-(4-morpholinyl)-6-(1-thianthrenyl)-4H-pyran-4-one (KU55933)] was without effect.	trovafloxacin	95-98	ataxia telangiectasia mutated	Mus musculus	183-186
24810048-0	2014	Chaetocin-induced ROS-mediated apoptosis involves ATM-YAP1 axis and JNK-dependent inhibition of glucose metabolism.	chaetocin	0-9	ataxia telangiectasia mutated	Mus musculus	50-53
24810048-0	2014	Chaetocin-induced ROS-mediated apoptosis involves ATM-YAP1 axis and JNK-dependent inhibition of glucose metabolism.	ros	18-21	ataxia telangiectasia mutated	Mus musculus	50-53
24810048-5	2014	Increased intracellular ROS induced (i) Yes-associated protein 1 (YAP1) expression independent of the canonical Hippo pathway as well as (ii) ATM and JNK activation.	ros	24-27	ataxia telangiectasia mutated	Mus musculus	142-145
24810048-11	2014	Our study highlights the coordinated control of glioma cell proliferation and metabolism by ROS through (i) ATM-YAP1-driven apoptotic pathway and (ii) JNK-regulated metabolic adaptation.	ros	92-95	ataxia telangiectasia mutated	Mus musculus	108-111
24741006-1	2014	In response to DNA damage, the E2F1 transcription factor is phosphorylated at serine 31 (serine 29 in mouse) by the ATM or ATR kinases, which promotes E2F1 protein stabilization.	Serine	78-84	ataxia telangiectasia mutated	Mus musculus	116-119
24741006-1	2014	In response to DNA damage, the E2F1 transcription factor is phosphorylated at serine 31 (serine 29 in mouse) by the ATM or ATR kinases, which promotes E2F1 protein stabilization.	Serine	89-95	ataxia telangiectasia mutated	Mus musculus	116-119
24411679-0	2014	2-Hydroxyethyl methacrylate-induced apoptosis through the ATM- and p53-dependent intrinsic mitochondrial pathway.	hydroxyethyl methacrylate	0-27	ataxia telangiectasia mutated	Mus musculus	58-61
24411679-11	2014	However, ATM, a protein kinase which responds to DNA double-strand breaks, and the signaling pathway downstream were activated in HEMA-exposed cells.	hydroxyethyl methacrylate	130-134	ataxia telangiectasia mutated	Mus musculus	9-12
24411679-12	2014	Likewise, expression and phosphorylation of the ATM targets H2AX and p53 was reduced in the presence of KU55399.	ku55399	104-111	ataxia telangiectasia mutated	Mus musculus	48-51
24366691-3	2014	Our laboratory previously demonstrated that the dual phosphoinositide 3-kinase/mTOR inhibitor NVP-BEZ235 can potently inhibit the two central DDR kinases, DNA-dependent protein kinase catalytic subunit (DNA-PKcs) and ataxia-telangiectasia mutated (ATM), in vitro.	dactolisib	94-104	ataxia telangiectasia mutated	Mus musculus	248-251
24366691-4	2014	Here, we tested whether NVP-BEZ235 could also inhibit ATM and DNA-PKcs in tumors in vivo and assessed its potential as a radio- and chemosensitizer in preclinical mouse glioblastoma models.	dactolisib	28-34	ataxia telangiectasia mutated	Mus musculus	54-57
24366691-8	2014	RESULTS: NVP-BEZ235 potently inhibited both DNA-PKcs and ATM kinases and attenuated the repair of ionizing radiation-induced DNA damage in tumors.	dactolisib	13-19	ataxia telangiectasia mutated	Mus musculus	57-60
24276232-1	2014	Individuals carrying mutations at both ataxia telangiectasia mutated (ATM) gene alleles reportedly have increased plasma cholesterol and triglyceride levels.	Cholesterol	121-132	ataxia telangiectasia mutated	Mus musculus	39-68
24568192-13	2014	Pretreatment of BALB/c mice with forskolin stimulated phosphorylation of PP2A B56delta, inhibited the activation of ATM and NF-kappaB, and augmented radiation-induced apoptosis in the lung tissue.	Colforsin	33-42	ataxia telangiectasia mutated	Mus musculus	116-119
24276232-1	2014	Individuals carrying mutations at both ataxia telangiectasia mutated (ATM) gene alleles reportedly have increased plasma cholesterol and triglyceride levels.	Cholesterol	121-132	ataxia telangiectasia mutated	Mus musculus	70-73
24276232-1	2014	Individuals carrying mutations at both ataxia telangiectasia mutated (ATM) gene alleles reportedly have increased plasma cholesterol and triglyceride levels.	Triglycerides	137-149	ataxia telangiectasia mutated	Mus musculus	39-68
24276232-1	2014	Individuals carrying mutations at both ataxia telangiectasia mutated (ATM) gene alleles reportedly have increased plasma cholesterol and triglyceride levels.	Triglycerides	137-149	ataxia telangiectasia mutated	Mus musculus	70-73
24276232-7	2014	In addition, following treatment with the ATM activator, chloroquine, and E(-)/B(48) lipoproteins, ATM interacted with class III phosphatidylinositol-3-kinases (PI3Ks) and the activated ATM protein enhanced class III PI3K activity.	Chloroquine	57-68	ataxia telangiectasia mutated	Mus musculus	99-102
24276232-7	2014	In addition, following treatment with the ATM activator, chloroquine, and E(-)/B(48) lipoproteins, ATM interacted with class III phosphatidylinositol-3-kinases (PI3Ks) and the activated ATM protein enhanced class III PI3K activity.	Chloroquine	57-68	ataxia telangiectasia mutated	Mus musculus	99-102
24276232-8	2014	Furthermore, treatment with a class III PI3K inhibitor (LY290042 and 3-MA) attenuated the intracellular total cholesterol accumulation induced by ATM activation.	LY 290042	56-64	ataxia telangiectasia mutated	Mus musculus	146-149
24276232-8	2014	Furthermore, treatment with a class III PI3K inhibitor (LY290042 and 3-MA) attenuated the intracellular total cholesterol accumulation induced by ATM activation.	3-methyladenine	69-73	ataxia telangiectasia mutated	Mus musculus	146-149
24276232-8	2014	Furthermore, treatment with a class III PI3K inhibitor (LY290042 and 3-MA) attenuated the intracellular total cholesterol accumulation induced by ATM activation.	Cholesterol	110-121	ataxia telangiectasia mutated	Mus musculus	146-149
23688655-7	2013	The DSBs were associated with phosphorylation of ATM/ATR, a central signal transducer mediating the DNA damage response, and upregulation of the cyclin-dependent kinase inhibitor p21(CIP1).	dsbs	4-8	ataxia telangiectasia mutated	Mus musculus	49-52
24457965-0	2014	ROS-PIASgamma cross talk channelizes ATM signaling from resistance to apoptosis during chemosensitization of resistant tumors.	Reactive Oxygen Species	0-3	ataxia telangiectasia mutated	Mus musculus	37-40
24457965-3	2014	At a low reactive oxygen species (ROS) condition during genotoxic insult, the ATM/sumoylated-IKKgamma interaction induced NFkappaB activation that resisted JNK-mediated apoptosis, whereas increasing cellular ROS restored ATM/JNK apoptotic signaling.	Reactive Oxygen Species	9-32	ataxia telangiectasia mutated	Mus musculus	78-81
24457965-3	2014	At a low reactive oxygen species (ROS) condition during genotoxic insult, the ATM/sumoylated-IKKgamma interaction induced NFkappaB activation that resisted JNK-mediated apoptosis, whereas increasing cellular ROS restored ATM/JNK apoptotic signaling.	Reactive Oxygen Species	34-37	ataxia telangiectasia mutated	Mus musculus	78-81
24457965-3	2014	At a low reactive oxygen species (ROS) condition during genotoxic insult, the ATM/sumoylated-IKKgamma interaction induced NFkappaB activation that resisted JNK-mediated apoptosis, whereas increasing cellular ROS restored ATM/JNK apoptotic signaling.	Reactive Oxygen Species	34-37	ataxia telangiectasia mutated	Mus musculus	221-224
24457965-3	2014	At a low reactive oxygen species (ROS) condition during genotoxic insult, the ATM/sumoylated-IKKgamma interaction induced NFkappaB activation that resisted JNK-mediated apoptosis, whereas increasing cellular ROS restored ATM/JNK apoptotic signaling.	Reactive Oxygen Species	208-211	ataxia telangiectasia mutated	Mus musculus	78-81
24457965-7	2014	Cumulatively, our findings identified an unappreciated yet critical combinatorial function of cellular ROS and PIASgamma in regulating ATM-mediated chemosensitization of resistant tumors.	Reactive Oxygen Species	103-106	ataxia telangiectasia mutated	Mus musculus	135-138
24412381-7	2014	Gene expression analyses from mouse tissues showed significantly decreased expression of ATM and Xrcc6 in BaP-treated liver and lung.	Benzo(a)pyrene	106-109	ataxia telangiectasia mutated	Mus musculus	89-92
23829351-0	2013	Silibinin protects murine fibroblast L929 cells from UVB-induced apoptosis through the simultaneous inhibition of ATM-p53 pathway and autophagy.	Silybin	0-9	ataxia telangiectasia mutated	Mus musculus	114-117
24156442-5	2013	It is concluded that ROS results in the apoptosis of BMHSC through inhibiting the expression of ATM gene and activating P21 protein.	Reactive Oxygen Species	21-24	ataxia telangiectasia mutated	Mus musculus	96-99
24040138-0	2013	Zygotic G2/M cell cycle arrest induced by ATM/Chk1 activation and DNA repair in mouse embryos fertilized with hydrogen peroxide-treated epididymal mouse sperm.	Hydrogen Peroxide	110-127	ataxia telangiectasia mutated	Mus musculus	42-45
24040138-10	2013	In conclusions, ATM (pSer-1981)-Chk1 (pSer-345) cascade might have mediated G2/M cell cycle arrest and allowed time to facilitate sperm-derived DNA-damage repair in mouse zygotes fertilized with oxygen-stressed sperm, and the DNA-damage repair might be effective.	Oxygen	195-201	ataxia telangiectasia mutated	Mus musculus	16-19
23829351-10	2013	Silibinin treatment simultaneously repressed the activation of ATM-p53 and autophagy and thereby protected UVB-irradiated L929 cells from apoptotic death.	Silybin	0-9	ataxia telangiectasia mutated	Mus musculus	63-66
23824039-14	2013	Collectively, MPTQ-induced neuro 2a cell death is mediated by ATM and p53 activation, and Bax-mediated activation of caspase-dependent and caspase-independent mitochondrial apoptosis pathways.	8-methoxypyrimido(4',5'-4,5)thieno(2,3-b)quinoline-4(3H)-one	14-18	ataxia telangiectasia mutated	Mus musculus	62-65
23598467-6	2013	MECs isolated from RGS6(-/-) mice also showed a deficit in DMBA-induced ATM/p53 activation, reactive oxygen species generation and apoptosis confirming that RGS6 is required for effective activation of the DNA damage response in these cells, a critical countermeasure against carcinogen-mediated genotoxic stress.	6,11-dimethylbenzo(b)naphtho(2,3-d)thiophene	59-63	ataxia telangiectasia mutated	Mus musculus	72-75
23935957-6	2013	Genetic inactivation of Atm in the central nervous system of Nbn-deficient mice led to reduced life span and increased DSBs, resulting in increased apoptosis during neural development.	1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione	119-123	ataxia telangiectasia mutated	Mus musculus	24-27
23852118-3	2013	We found that SIRT1 was rapidly recruited to DSBs in postmitotic neurons, where it showed a synergistic relationship with ataxia telangiectasia mutated (ATM).	dsbs	45-49	ataxia telangiectasia mutated	Mus musculus	122-151
23852118-3	2013	We found that SIRT1 was rapidly recruited to DSBs in postmitotic neurons, where it showed a synergistic relationship with ataxia telangiectasia mutated (ATM).	dsbs	45-49	ataxia telangiectasia mutated	Mus musculus	153-156
23824039-9	2013	MPTQ-mediated apoptosis is associated with increased phosphorylation of p53 at Ser15 and Ser20 which correlates with the hyperphosphorylation of Ataxia-Telangiectasia mutated protein (ATM).	8-methoxypyrimido(4',5'-4,5)thieno(2,3-b)quinoline-4(3H)-one	0-4	ataxia telangiectasia mutated	Mus musculus	145-182
23824039-9	2013	MPTQ-mediated apoptosis is associated with increased phosphorylation of p53 at Ser15 and Ser20 which correlates with the hyperphosphorylation of Ataxia-Telangiectasia mutated protein (ATM).	8-methoxypyrimido(4',5'-4,5)thieno(2,3-b)quinoline-4(3H)-one	0-4	ataxia telangiectasia mutated	Mus musculus	184-187
23724874-8	2013	Together, the findings suggest that ATM plays a role in insulin-stimulated glucose transport at the level of AS160 in muscle comprised of slow and fast oxidative-glycolytic fibers (soleus) and at the level of Akt in muscle containing fast glycolytic fibers (EDL).	Glucose	75-82	ataxia telangiectasia mutated	Mus musculus	36-39
23776597-1	2013	OBJECTIVE: The glucose and dehydroascorbic acid (DHA) transporter GLUT1 contains a phosphorylation site, S490, for ataxia telangiectasia mutated (ATM).	Glucose	15-22	ataxia telangiectasia mutated	Mus musculus	115-144
23776597-1	2013	OBJECTIVE: The glucose and dehydroascorbic acid (DHA) transporter GLUT1 contains a phosphorylation site, S490, for ataxia telangiectasia mutated (ATM).	Glucose	15-22	ataxia telangiectasia mutated	Mus musculus	146-149
23776597-4	2013	RESULTS: In myoblasts, inhibition of ATM significantly diminished cell surface GLUT1, glucose and DHA transport, GLUT1 externalization, and association of GLUT1 with Galpha-interacting protein-interacting protein, C-terminus (GIPC1), which has been implicated in recycling of endosomal proteins.	Glucose	86-93	ataxia telangiectasia mutated	Mus musculus	37-40
23776597-4	2013	RESULTS: In myoblasts, inhibition of ATM significantly diminished cell surface GLUT1, glucose and DHA transport, GLUT1 externalization, and association of GLUT1 with Galpha-interacting protein-interacting protein, C-terminus (GIPC1), which has been implicated in recycling of endosomal proteins.	Dehydroascorbic Acid	98-101	ataxia telangiectasia mutated	Mus musculus	37-40
23776597-5	2013	In contrast, ATM activation by doxorubicin (DXR) increased DHA transport, cell surface GLUT1, and the GLUT1/GIPC1 association.	Doxorubicin	31-42	ataxia telangiectasia mutated	Mus musculus	13-16
23776597-5	2013	In contrast, ATM activation by doxorubicin (DXR) increased DHA transport, cell surface GLUT1, and the GLUT1/GIPC1 association.	Dehydroascorbic Acid	59-62	ataxia telangiectasia mutated	Mus musculus	13-16
23776597-7	2013	ATM dysfunction or ATM inhibition reduced DHA transport in extensor digitorum longus (EDL) muscles and decreased glucose transport in EDL and soleus.	Dehydroascorbic Acid	42-45	ataxia telangiectasia mutated	Mus musculus	0-3
23776597-7	2013	ATM dysfunction or ATM inhibition reduced DHA transport in extensor digitorum longus (EDL) muscles and decreased glucose transport in EDL and soleus.	Dehydroascorbic Acid	42-45	ataxia telangiectasia mutated	Mus musculus	19-22
23776597-7	2013	ATM dysfunction or ATM inhibition reduced DHA transport in extensor digitorum longus (EDL) muscles and decreased glucose transport in EDL and soleus.	Glucose	113-120	ataxia telangiectasia mutated	Mus musculus	0-3
23776597-7	2013	ATM dysfunction or ATM inhibition reduced DHA transport in extensor digitorum longus (EDL) muscles and decreased glucose transport in EDL and soleus.	Glucose	113-120	ataxia telangiectasia mutated	Mus musculus	19-22
23724874-0	2013	Impaired insulin-stimulated glucose transport in ATM-deficient mouse skeletal muscle.	Glucose	28-35	ataxia telangiectasia mutated	Mus musculus	49-52
23602475-6	2013	Interestingly, enhancement occurs both in wild-type cells and in cells lacking either the p53 tumor suppressor gene or the master regulator of the DNA damage response, ATM, suggesting that doxorubicin action on nucleosome dynamics is independent of the DNA damage checkpoint.	Doxorubicin	189-200	ataxia telangiectasia mutated	Mus musculus	168-171
23293085-2	2013	The strategy presented here to target ATM for breast cancer therapy involves the use of liposomal-encapsulated, gene-specific ATM siRNA delivered with a well-characterized porous silicon-based multistage vector (MSV) delivery system (MSV/ATM).	Silicon	179-186	ataxia telangiectasia mutated	Mus musculus	38-41
23241668-1	2013	The histone variant 2AX (H2AX) is phosphorylated at Serine 139 by the PI3K-like kinase family members ATM, ATR and DNA-PK.	Serine	52-58	ataxia telangiectasia mutated	Mus musculus	102-105
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	ataxia telangiectasia mutated	Mus musculus	157-160
23338613-7	2013	Activation of ATM/p53 apoptosis signaling by doxorubicin in ventricles of WT mice was also absent in their RGS6(-/-) counterparts.	Doxorubicin	45-56	ataxia telangiectasia mutated	Mus musculus	14-17
22941977-6	2013	The ATM inhibitor KU55933 prevented stimulation of S6K phosphorylation in C2C12 myotubes exposed to IGF-1, suggesting that decreased IGF-1 action is not limited to chronic conditions of decreased ATM function.	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	18-25	ataxia telangiectasia mutated	Mus musculus	4-7
23338613-3	2013	The tripartite G-protein inactivating protein RGS6 has been implicated in reactive oxygen species (ROS) generation, ATM/p53 activation, and apoptosis in doxorubicin-treated cells.	Doxorubicin	153-164	ataxia telangiectasia mutated	Mus musculus	116-119
23355489-1	2013	Ataxia telangiectasia mutated (ATM) is activated upon DNA double strand breaks (DSBs) and phosphorylates numerous DSB response proteins, including histone H2AX on serine 139 (Ser-139) to form gamma-H2AX.	Serine	163-169	ataxia telangiectasia mutated	Mus musculus	0-29
23355489-1	2013	Ataxia telangiectasia mutated (ATM) is activated upon DNA double strand breaks (DSBs) and phosphorylates numerous DSB response proteins, including histone H2AX on serine 139 (Ser-139) to form gamma-H2AX.	Serine	163-169	ataxia telangiectasia mutated	Mus musculus	31-34
23355489-1	2013	Ataxia telangiectasia mutated (ATM) is activated upon DNA double strand breaks (DSBs) and phosphorylates numerous DSB response proteins, including histone H2AX on serine 139 (Ser-139) to form gamma-H2AX.	Serine	175-178	ataxia telangiectasia mutated	Mus musculus	0-29
23355489-1	2013	Ataxia telangiectasia mutated (ATM) is activated upon DNA double strand breaks (DSBs) and phosphorylates numerous DSB response proteins, including histone H2AX on serine 139 (Ser-139) to form gamma-H2AX.	Serine	175-178	ataxia telangiectasia mutated	Mus musculus	31-34
23355489-7	2013	The ATM-independent HR function of H2AX requires both Ser-139 phosphorylation and gamma-H2AX/MDC1 interaction.	Serine	54-57	ataxia telangiectasia mutated	Mus musculus	4-7
22941977-6	2013	The ATM inhibitor KU55933 prevented stimulation of S6K phosphorylation in C2C12 myotubes exposed to IGF-1, suggesting that decreased IGF-1 action is not limited to chronic conditions of decreased ATM function.	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	18-25	ataxia telangiectasia mutated	Mus musculus	196-199
22977252-8	2012	Up-regulation of SHP by metformin-mediated activation of the ATM-AMP-activated protein kinase pathway led to inhibition of GH-mediated induction of hepatic gluconeogenesis, which was abolished by an ATM inhibitor, KU-55933.	Metformin	24-33	ataxia telangiectasia mutated	Mus musculus	61-64
23042680-2	2012	We discovered that ATM-dependent phosphorylation of PNKP at serines 114 and 126 in response to oxidative DNA damage inhibits ubiquitylation-dependent proteasomal degradation of PNKP, and consequently increases PNKP stability that is required for DNA repair.	Serine	60-67	ataxia telangiectasia mutated	Mus musculus	19-22
23370278-11	2013	As a proof of principle, ATM inhibition in bulk cells increased their cisplatin resistance, as demonstrated by reduced PARP cleavage.	Cisplatin	70-79	ataxia telangiectasia mutated	Mus musculus	25-28
23211021-0	2012	Starvation-induced activation of ATM/Chk2/p53 signaling sensitizes cancer cells to cisplatin.	Cisplatin	83-92	ataxia telangiectasia mutated	Mus musculus	33-36
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	ataxia telangiectasia mutated	Mus musculus	79-82
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	ataxia telangiectasia mutated	Mus musculus	79-82
22445004-1	2012	PURPOSE: We have previously shown that the antimalarial agent chloroquine can abrogate the lethal cellular effects of low-dose-rate (LDR) radiation in vitro, most likely by activating the ataxia-telangiectasia mutated (ATM) protein.	Chloroquine	62-73	ataxia telangiectasia mutated	Mus musculus	188-217
22445004-1	2012	PURPOSE: We have previously shown that the antimalarial agent chloroquine can abrogate the lethal cellular effects of low-dose-rate (LDR) radiation in vitro, most likely by activating the ataxia-telangiectasia mutated (ATM) protein.	Chloroquine	62-73	ataxia telangiectasia mutated	Mus musculus	219-222
22445004-12	2012	CONCLUSION: Chloroquine administration before radiation had a significant effect on the survival of normal but not ATM null mice, strongly suggesting that the in vivo effect, like the in vitro effect, is also ATM dependent.	Chloroquine	12-23	ataxia telangiectasia mutated	Mus musculus	209-212
22977252-8	2012	Up-regulation of SHP by metformin-mediated activation of the ATM-AMP-activated protein kinase pathway led to inhibition of GH-mediated induction of hepatic gluconeogenesis, which was abolished by an ATM inhibitor, KU-55933.	Metformin	24-33	ataxia telangiectasia mutated	Mus musculus	199-202
22895013-5	2012	This process is controlled by the ATM-MTOR pathway and depends on the activation of selective autophagy to regulate cholesterol efflux from macrophage foam cells.	Cholesterol	116-127	ataxia telangiectasia mutated	Mus musculus	34-37
22263785-3	2012	NAMI-A pre-mitotic stop to cell proliferation was due to the maintenance of the phosphorylated, inactive, form of Cdk1, caused by the activation of the ATM/ATR checkpoint, as confirmed by the up-regulation and phosphorylation of Chk1.	imidazolium-bis(imidazole)dimethylsulfoxideimidazotetrachlororuthenate(III)	0-6	ataxia telangiectasia mutated	Mus musculus	152-155
22263785-6	2012	The ex-vivo data confirm the interaction of the ruthenium compound NAMI-A with the ATM/ATR pathway, leading to the modulation of cell cycle regulating proteins, that can break the metastases cell cycle progression off.	ruthenium compound nami-a	48-73	ataxia telangiectasia mutated	Mus musculus	83-86
22515193-6	2012	Moreover, near-infrared treatment increased the phosphorylation of ataxia-telangiectasia mutated (ATM) at Ser(1981), H2AX at Ser(139), Chk1 at Ser(317), structural maintenance of chromosome (SMC) 1 at Ser(966), and p53 at Ser(15) in A549 cells compared with control.	Serine	106-109	ataxia telangiectasia mutated	Mus musculus	67-96
22515193-6	2012	Moreover, near-infrared treatment increased the phosphorylation of ataxia-telangiectasia mutated (ATM) at Ser(1981), H2AX at Ser(139), Chk1 at Ser(317), structural maintenance of chromosome (SMC) 1 at Ser(966), and p53 at Ser(15) in A549 cells compared with control.	Serine	106-109	ataxia telangiectasia mutated	Mus musculus	98-101
22210379-0	2012	The mitochondria-targeted antioxidant MitoQ decreases features of the metabolic syndrome in ATM+/-/ApoE-/- mice.	mitoquinone	38-43	ataxia telangiectasia mutated	Mus musculus	92-95
23197859-6	2012	However, after a 2-month treatment with the p38MAPK inhibitor SB203580, starting at 1 month old, Atm(-/-) mice showed restoration of normal levels of Bmi-1 and p21 with the rescue of NSC population in the SVZ.	SB 203580	62-70	ataxia telangiectasia mutated	Mus musculus	97-100
22561209-0	2012	Berberine, a genotoxic alkaloid, induces ATM-Chk1 mediated G2 arrest in prostate cancer cells.	Berberine	0-9	ataxia telangiectasia mutated	Mus musculus	41-44
22561209-8	2012	Pharmacological inhibition of ATM by KU55933, or Chk1 by UCN-01, could efficiently abrogate the G2/M arrest in berberine-treated cells.	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	37-44	ataxia telangiectasia mutated	Mus musculus	30-33
22561209-8	2012	Pharmacological inhibition of ATM by KU55933, or Chk1 by UCN-01, could efficiently abrogate the G2/M arrest in berberine-treated cells.	Berberine	111-120	ataxia telangiectasia mutated	Mus musculus	30-33
22561209-10	2012	Abrogation of G2/M arrest by ATM inhibition forced more cells to undergo apoptosis in response to berberine treatment.	Berberine	98-107	ataxia telangiectasia mutated	Mus musculus	29-32
22624716-3	2012	We have utilized mice bearing altered Mdm2 alleles to demonstrate that ATM phosphorylation of Mdm2 serine 394 is required for robust p53 stabilization and activation after DNA damage.	Serine	99-105	ataxia telangiectasia mutated	Mus musculus	71-74
22797809-3	2012	Here we show that Atm in mice is activated specifically in immature vessels in response to the accumulation of reactive oxygen species (ROS).	Reactive Oxygen Species	111-134	ataxia telangiectasia mutated	Mus musculus	18-21
22797809-3	2012	Here we show that Atm in mice is activated specifically in immature vessels in response to the accumulation of reactive oxygen species (ROS).	Reactive Oxygen Species	136-139	ataxia telangiectasia mutated	Mus musculus	18-21
22260947-0	2012	Activation of AMP-activated protein kinase in cerebella of Atm-/- mice is attributable to accumulation of reactive oxygen species.	Reactive Oxygen Species	106-129	ataxia telangiectasia mutated	Mus musculus	59-62
21922345-5	2012	Earlier reports show that Atm-deficient mice exhibit severe degeneration of tyrosine hydroxylase (TH)-positive dopaminergic nigro-striatal neurons and their terminals in the striatum.	Tyrosine	76-84	ataxia telangiectasia mutated	Mus musculus	26-29
22207345-0	2012	A positive feedback signaling loop between ATM and the vitamin D receptor is critical for cancer chemoprevention by vitamin D.	Vitamin D	55-64	ataxia telangiectasia mutated	Mus musculus	43-46
22207345-9	2012	Together, our findings identify a novel vitamin D-mediated chemopreventive mechanism involving a positive feedback loop between the DNA repair proteins ATM and VDR.	Vitamin D	40-49	ataxia telangiectasia mutated	Mus musculus	152-155
22173583-8	2012	Activated ATM relocalized to HSV DNA replication compartments where it likely enhanced oHSV replication and could not participate in repairing TMZ-induced DNA damage.	ohsv	87-91	ataxia telangiectasia mutated	Mus musculus	10-13
22144182-2	2012	Here, we show that ATM loss also leads to intrinsic mitochondrial abnormalities in thymocytes, including elevated reactive oxygen species, increased aberrant mitochondria, high cellular respiratory capacity, and decreased mitophagy.	Reactive Oxygen Species	114-137	ataxia telangiectasia mutated	Mus musculus	19-22
22144182-6	2012	These data support a model in which ATM plays direct roles in modulating mitochondrial homeostasis and suggest that mitochondrial dysfunction and associated increases in mitochondrial reactive oxygen species contribute to the cancer-prone phenotype observed in organisms lacking ATM.	Reactive Oxygen Species	184-207	ataxia telangiectasia mutated	Mus musculus	36-39
22144182-6	2012	These data support a model in which ATM plays direct roles in modulating mitochondrial homeostasis and suggest that mitochondrial dysfunction and associated increases in mitochondrial reactive oxygen species contribute to the cancer-prone phenotype observed in organisms lacking ATM.	Reactive Oxygen Species	184-207	ataxia telangiectasia mutated	Mus musculus	279-282
22413000-10	2012	Further, a 10-day course of dietary glutamine supplementation reduced inflammation-induced neuronal cell cycle activation, tau phosphorylation and ATM-activation in two different mouse models of familial AD while raising the levels of two synaptic proteins, VAMP2 and synaptophysin.	Glutamine	36-45	ataxia telangiectasia mutated	Mus musculus	147-150
22355272-0	2012	The dual PI3K/mTOR inhibitor NVP-BEZ235 is a potent inhibitor of ATM- and DNA-PKCs-mediated DNA damage responses.	dactolisib	33-39	ataxia telangiectasia mutated	Mus musculus	65-68
22355272-3	2012	Here, we show that NVP-BEZ235 also potently inhibits ATM and DNA-PKcs, the two major kinases responding to ionizing radiation (IR)-induced DNA double-strand breaks (DSBs).	dactolisib	23-29	ataxia telangiectasia mutated	Mus musculus	53-56
22355272-8	2012	Our results, showing that NVP-BEZ235 is a potent and novel inhibitor of ATM and DNA-PKcs, have important implications for the informed and rational design of clinical trials involving this drug and also reveal the potential utility of NVP-BEZ235 as an effective radiosensitizer for GBMs in the clinic.	dactolisib	30-36	ataxia telangiectasia mutated	Mus musculus	72-75
21900239-9	2011	The surprising function of ATM in TNF signaling was confirmed where reduced NF-kappaB/RelA translocation and Ser-276 phosphorylation were seen in ATM(-/-) mouse embryo fibroblasts.	Serine	109-112	ataxia telangiectasia mutated	Mus musculus	27-30
22055193-6	2011	p53 phosphorylation on Ser18 in response to low glucose is ROS and ATM dependent.	Glucose	48-55	ataxia telangiectasia mutated	Mus musculus	67-70
21900239-9	2011	The surprising function of ATM in TNF signaling was confirmed where reduced NF-kappaB/RelA translocation and Ser-276 phosphorylation were seen in ATM(-/-) mouse embryo fibroblasts.	Serine	109-112	ataxia telangiectasia mutated	Mus musculus	146-149
22002603-5	2011	Here we report that the number of meiotic DSBs in mouse is controlled by ATM, a kinase activated by DNA damage to trigger checkpoint signalling and promote DSB repair.	dsbs	42-46	ataxia telangiectasia mutated	Mus musculus	73-76
21292994-0	2011	Iron loading and oxidative stress in the Atm-/- mouse liver.	Iron	0-4	ataxia telangiectasia mutated	Mus musculus	41-44
21297001-0	2011	Telomerase reverse transcriptase protects ATM-deficient hematopoietic stem cells from ROS-induced apoptosis through a telomere-independent mechanism.	Reactive Oxygen Species	86-89	ataxia telangiectasia mutated	Mus musculus	42-45
21593482-8	2011	Caffeine (inhibits both ATM and ATR), but not KU55933 (ATM-selective inhibitor), reversed the G(2)-M block induced by UV, inferring a primary role for ATR in sensing this form of DNA damage.	Caffeine	0-8	ataxia telangiectasia mutated	Mus musculus	24-27
21593482-9	2011	Caffeine and KU55933 were equally effective in reversing the cisplatin-induced G(1)-S block, implicating ATM as the primary sensing enzyme.	Caffeine	0-8	ataxia telangiectasia mutated	Mus musculus	105-108
21593482-9	2011	Caffeine and KU55933 were equally effective in reversing the cisplatin-induced G(1)-S block, implicating ATM as the primary sensing enzyme.	Cisplatin	61-70	ataxia telangiectasia mutated	Mus musculus	105-108
21596788-4	2011	Strikingly, DSBs accumulate in ATM(-/-) mouse embryo fibroblasts (MEFs) and in ATM or Artemis-defective human primary fibroblasts maintained for prolonged periods under confluence arrest.	dsbs	12-16	ataxia telangiectasia mutated	Mus musculus	31-34
21596788-4	2011	Strikingly, DSBs accumulate in ATM(-/-) mouse embryo fibroblasts (MEFs) and in ATM or Artemis-defective human primary fibroblasts maintained for prolonged periods under confluence arrest.	dsbs	12-16	ataxia telangiectasia mutated	Mus musculus	79-82
21849621-0	2011	Heme oxygenase-1 and carbon monoxide modulate DNA repair through ataxia-telangiectasia mutated (ATM) protein.	Carbon Monoxide	21-36	ataxia telangiectasia mutated	Mus musculus	65-94
21849621-0	2011	Heme oxygenase-1 and carbon monoxide modulate DNA repair through ataxia-telangiectasia mutated (ATM) protein.	Carbon Monoxide	21-36	ataxia telangiectasia mutated	Mus musculus	96-99
21496344-0	2011	Antisense oligodeoxynucleotides targeting ATM strengthen apoptosis of laryngeal squamous cell carcinoma grown in nude mice.	Oligodeoxyribonucleotides	10-31	ataxia telangiectasia mutated	Mus musculus	42-45
21292994-6	2011	Atm(-/-) mice had increased serum iron, hepatic iron, and ferritin and significantly higher Hepcidin compared with wild-type mice.	Iron	34-38	ataxia telangiectasia mutated	Mus musculus	0-3
21292994-6	2011	Atm(-/-) mice had increased serum iron, hepatic iron, and ferritin and significantly higher Hepcidin compared with wild-type mice.	Iron	48-52	ataxia telangiectasia mutated	Mus musculus	0-3
21292994-8	2011	Atm(-/-) mice had increased protein tyrosine nitration and significantly higher Heme Oxygenase (decycling) 1 levels that were substantially increased by a high-iron diet.	Tyrosine	36-44	ataxia telangiectasia mutated	Mus musculus	0-3
21292994-8	2011	Atm(-/-) mice had increased protein tyrosine nitration and significantly higher Heme Oxygenase (decycling) 1 levels that were substantially increased by a high-iron diet.	Iron	160-164	ataxia telangiectasia mutated	Mus musculus	0-3
21292994-10	2011	We demonstrate that Atm(-/-) mice have a propensity to accumulate iron that is associated with a significant increase in hepatic OS.	Iron	66-70	ataxia telangiectasia mutated	Mus musculus	20-23
21144805-4	2011	We investigated the role of ATM in the NF-kappaB signalling cascade induced by ionising radiation (IR) in breast cancer cell lines using KU55933, a novel and specific inhibitor of ATM.	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	137-144	ataxia telangiectasia mutated	Mus musculus	180-183
21266166-6	2011	Incubation of wild-type extensor digitorum longus muscles for 1h with the ATM inhibitor KU55933 caused a ~50% reduction (P&lt;0.05, n = 5/group) in COX activity compared to muscles incubated with vehicle alone.	Hydrogen	62-64	ataxia telangiectasia mutated	Mus musculus	74-77
21266166-6	2011	Incubation of wild-type extensor digitorum longus muscles for 1h with the ATM inhibitor KU55933 caused a ~50% reduction (P&lt;0.05, n = 5/group) in COX activity compared to muscles incubated with vehicle alone.	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	88-95	ataxia telangiectasia mutated	Mus musculus	74-77
21266166-7	2011	Among the control muscles and muscles treated with the ATM inhibitor, COX activity was correlated (r = 0.61, P&lt;0.05) with activity of glucose 6-phosphate dehydrogenase, a key determinant of antioxidant defense through production of NADPH.	NADP	235-240	ataxia telangiectasia mutated	Mus musculus	55-58
21177254-3	2011	We hypothesize that a deficient DSB repair, as a result of an Atm mutation, may reinforce the clastogenic effect of dietary flavonoids and increase the frequency of Mll rearrangements.	Flavonoids	124-134	ataxia telangiectasia mutated	Mus musculus	62-65
21177254-5	2011	In vitro exposure to genistein/quercetin induced higher numbers of Mll rearrangements in bone marrow cells of Atm-DeltaSRI mutant mice compared with wt mice.	Genistein	21-30	ataxia telangiectasia mutated	Mus musculus	110-113
21177254-5	2011	In vitro exposure to genistein/quercetin induced higher numbers of Mll rearrangements in bone marrow cells of Atm-DeltaSRI mutant mice compared with wt mice.	Quercetin	31-40	ataxia telangiectasia mutated	Mus musculus	110-113
19544430-4	2009	We found that cultured subventricular zone neurosphere cells from Atm(-/-) mice show impaired proliferation, as well as intrinsic elevation of reactive oxygen species (ROS) levels, compared with those from Atm(+/+) mice.	Reactive Oxygen Species	168-171	ataxia telangiectasia mutated	Mus musculus	66-69
21315248-6	2010	Although the ATM and DNA-PKcs mRNA and protein expressions in wortmannin + D1 + D2 groups were much lower than those in the D1 + D2 groups, there were no significant changes in the apoptosis and cell cycle progression between the wortmannin + D1 + D2 and the D1 + D2 groups.	Wortmannin	62-72	ataxia telangiectasia mutated	Mus musculus	13-16
20208057-3	2010	The antimalarial drug chloroquine activates ATM signaling and improves metabolic phenotypes in mice.	Chloroquine	22-33	ataxia telangiectasia mutated	Mus musculus	44-47
20206019-6	2010	RESULTS: In repair-deficient SCID(-/-) and ATM(-/-)homozygous mice, large proportions of radiation-induced DSBs remained unrepaired after each fraction, leading to the pronounced accumulation of residual DNA damage after fractionated irradiation, similarly visible in early- and late-responding tissues.	dsbs	107-111	ataxia telangiectasia mutated	Mus musculus	43-46
20151649-0	2010	Gallic acid induces apoptosis of lung fibroblasts via a reactive oxygen species-dependent ataxia telangiectasia mutated-p53 activation pathway.	Gallic Acid	0-11	ataxia telangiectasia mutated	Mus musculus	90-119
20151649-0	2010	Gallic acid induces apoptosis of lung fibroblasts via a reactive oxygen species-dependent ataxia telangiectasia mutated-p53 activation pathway.	Reactive Oxygen Species	56-79	ataxia telangiectasia mutated	Mus musculus	90-119
20151649-9	2010	Mechanistic studies showed that gallic acid induces early phosphorylation of p53(Ser18) and histone 2AX(Ser139) (H2AX) via ataxia telangiectasia mutated (ATM) activation in response to ROS-provoked DNA damage.	Gallic Acid	32-43	ataxia telangiectasia mutated	Mus musculus	123-152
20151649-9	2010	Mechanistic studies showed that gallic acid induces early phosphorylation of p53(Ser18) and histone 2AX(Ser139) (H2AX) via ataxia telangiectasia mutated (ATM) activation in response to ROS-provoked DNA damage.	Gallic Acid	32-43	ataxia telangiectasia mutated	Mus musculus	154-157
20151649-9	2010	Mechanistic studies showed that gallic acid induces early phosphorylation of p53(Ser18) and histone 2AX(Ser139) (H2AX) via ataxia telangiectasia mutated (ATM) activation in response to ROS-provoked DNA damage.	Reactive Oxygen Species	185-188	ataxia telangiectasia mutated	Mus musculus	123-152
20151649-9	2010	Mechanistic studies showed that gallic acid induces early phosphorylation of p53(Ser18) and histone 2AX(Ser139) (H2AX) via ataxia telangiectasia mutated (ATM) activation in response to ROS-provoked DNA damage.	Reactive Oxygen Species	185-188	ataxia telangiectasia mutated	Mus musculus	154-157
20151649-10	2010	When mouse lung fibroblasts were treated with caffeine, an ATM kinase inhibitor, the levels of p53, phosphorylated p53(Ser18), and cell death induced by gallic acid were significantly attenuated.	Caffeine	46-54	ataxia telangiectasia mutated	Mus musculus	59-62
20151649-10	2010	When mouse lung fibroblasts were treated with caffeine, an ATM kinase inhibitor, the levels of p53, phosphorylated p53(Ser18), and cell death induced by gallic acid were significantly attenuated.	Gallic Acid	153-164	ataxia telangiectasia mutated	Mus musculus	59-62
20151649-11	2010	Additionally, pretreatment with antioxidants drastically inhibited the gallic acid-induced 8-hydroxy-2"-deoxyguanosine (8-OH-dG) formation and phosphorylation of p53(Ser18) and ATM(Ser1981), as well as apoptosis.	Gallic Acid	71-82	ataxia telangiectasia mutated	Mus musculus	177-180
20151649-12	2010	Our results provide the first evidence of the activation of ROS-dependent ATM/p53 signaling as a critical mechanism of gallic acid-induced cell death in primary cultured mouse lung fibroblasts.	Reactive Oxygen Species	60-63	ataxia telangiectasia mutated	Mus musculus	74-77
20151649-12	2010	Our results provide the first evidence of the activation of ROS-dependent ATM/p53 signaling as a critical mechanism of gallic acid-induced cell death in primary cultured mouse lung fibroblasts.	Gallic Acid	119-130	ataxia telangiectasia mutated	Mus musculus	74-77
19660469-9	2009	Pitavastatin attenuated doxorubicin-induced oxidative stress, DNA damage, ATM activation, p53 accumulation, and apoptosis in vitro.	pitavastatin	0-12	ataxia telangiectasia mutated	Mus musculus	74-77
19660469-9	2009	Pitavastatin attenuated doxorubicin-induced oxidative stress, DNA damage, ATM activation, p53 accumulation, and apoptosis in vitro.	Doxorubicin	24-35	ataxia telangiectasia mutated	Mus musculus	74-77
19660469-12	2009	These data collectively suggest that doxorubicin-induced cardiotoxicity is mediated by oxidative DNA damage-ATM-p53-apoptosis pathway, and is attenuated by pitavastatin through its antioxidant effect involving Rac1 inhibition.	Doxorubicin	37-48	ataxia telangiectasia mutated	Mus musculus	108-111
21167867-4	2011	In this study, we show that one of the clinically used compounds of ATR and ataxia telangiectasia-mutated (ATM) kinases inhibitor, theophylline (Tp), significantly reduced the yield of HBV DNA, HBsAg and HBeAg in HepG2215 cell culture system, furthermore, Tp could also suppress serum HBV DNA and HBsAg levels in the HBV-transgenic mice.	Theophylline	131-143	ataxia telangiectasia mutated	Mus musculus	76-105
21167867-4	2011	In this study, we show that one of the clinically used compounds of ATR and ataxia telangiectasia-mutated (ATM) kinases inhibitor, theophylline (Tp), significantly reduced the yield of HBV DNA, HBsAg and HBeAg in HepG2215 cell culture system, furthermore, Tp could also suppress serum HBV DNA and HBsAg levels in the HBV-transgenic mice.	Theophylline	131-143	ataxia telangiectasia mutated	Mus musculus	107-110
21167867-4	2011	In this study, we show that one of the clinically used compounds of ATR and ataxia telangiectasia-mutated (ATM) kinases inhibitor, theophylline (Tp), significantly reduced the yield of HBV DNA, HBsAg and HBeAg in HepG2215 cell culture system, furthermore, Tp could also suppress serum HBV DNA and HBsAg levels in the HBV-transgenic mice.	Theophylline	145-147	ataxia telangiectasia mutated	Mus musculus	76-105
21167867-4	2011	In this study, we show that one of the clinically used compounds of ATR and ataxia telangiectasia-mutated (ATM) kinases inhibitor, theophylline (Tp), significantly reduced the yield of HBV DNA, HBsAg and HBeAg in HepG2215 cell culture system, furthermore, Tp could also suppress serum HBV DNA and HBsAg levels in the HBV-transgenic mice.	Theophylline	145-147	ataxia telangiectasia mutated	Mus musculus	107-110
20739657-1	2010	The Ataxia Telangiectasia Mutated (ATM) gene is frequently inactivated in lymphoid malignancies such as chronic lymphocytic leukemia (CLL), T-prolymphocytic leukemia (T-PLL), and mantle cell lymphoma (MCL) and is associated with defective apoptosis in response to alkylating agents and purine analogues.	purine	286-292	ataxia telangiectasia mutated	Mus musculus	4-33
20739657-1	2010	The Ataxia Telangiectasia Mutated (ATM) gene is frequently inactivated in lymphoid malignancies such as chronic lymphocytic leukemia (CLL), T-prolymphocytic leukemia (T-PLL), and mantle cell lymphoma (MCL) and is associated with defective apoptosis in response to alkylating agents and purine analogues.	purine	286-292	ataxia telangiectasia mutated	Mus musculus	35-38
20739657-4	2010	We investigated in vitro sensitivity to the poly (ADP-ribose) polymerase inhibitor olaparib (AZD2281) of 5 ATM mutant lymphoblastoid cell lines (LCL), an ATM mutant MCL cell line, an ATM knockdown PGA CLL cell line, and 9 ATM-deficient primary CLLs induced to cycle and observed differential killing compared with ATM wildtype counterparts.	olaparib	83-91	ataxia telangiectasia mutated	Mus musculus	107-110
20739657-4	2010	We investigated in vitro sensitivity to the poly (ADP-ribose) polymerase inhibitor olaparib (AZD2281) of 5 ATM mutant lymphoblastoid cell lines (LCL), an ATM mutant MCL cell line, an ATM knockdown PGA CLL cell line, and 9 ATM-deficient primary CLLs induced to cycle and observed differential killing compared with ATM wildtype counterparts.	olaparib	93-100	ataxia telangiectasia mutated	Mus musculus	107-110
20739657-6	2010	A nonobese diabetic/severe combined immunodeficient (NOD/SCID) murine xenograft model of an ATM mutant MCL cell line demonstrated significantly reduced tumor load and an increased survival of animals after olaparib treatment in vivo.	olaparib	206-214	ataxia telangiectasia mutated	Mus musculus	92-95
20739657-7	2010	Addition of olaparib sensitized ATM null tumor cells to DNA-damaging agents.	olaparib	12-20	ataxia telangiectasia mutated	Mus musculus	32-35
20739657-8	2010	We suggest that olaparib would be an appropriate agent for treating refractory ATM mutant lymphoid tumors.	olaparib	16-24	ataxia telangiectasia mutated	Mus musculus	79-82
20183801-0	2010	Etoposide induces G2/M arrest and apoptosis in neural progenitor cells via DNA damage and an ATM/p53-related pathway.	Etoposide	0-9	ataxia telangiectasia mutated	Mus musculus	93-96
20183801-6	2010	Phosphorylation of ataxia telangiectasia-mutated kinase (ATM) at Ser1981 and gammaH2AX after VP-16 treatment showed DNA damage.	Etoposide	93-98	ataxia telangiectasia mutated	Mus musculus	19-55
20183801-6	2010	Phosphorylation of ataxia telangiectasia-mutated kinase (ATM) at Ser1981 and gammaH2AX after VP-16 treatment showed DNA damage.	Etoposide	93-98	ataxia telangiectasia mutated	Mus musculus	57-60
20160076-0	2010	ATM signals to TSC2 in the cytoplasm to regulate mTORC1 in response to ROS.	Reactive Oxygen Species	71-74	ataxia telangiectasia mutated	Mus musculus	0-3
20160076-2	2010	However, ATM also has been implicated in metabolic regulation, and ATM deficiency is associated with elevated reactive oxygen species (ROS).	Reactive Oxygen Species	110-133	ataxia telangiectasia mutated	Mus musculus	67-70
20160076-2	2010	However, ATM also has been implicated in metabolic regulation, and ATM deficiency is associated with elevated reactive oxygen species (ROS).	Reactive Oxygen Species	135-138	ataxia telangiectasia mutated	Mus musculus	67-70
20160076-4	2010	We have identified a cytoplasmic function for ATM that participates in the cellular damage response to ROS.	Reactive Oxygen Species	103-106	ataxia telangiectasia mutated	Mus musculus	46-49
20160076-5	2010	We show that in response to elevated ROS, ATM activates the TSC2 tumor suppressor via the LKB1/AMPK metabolic pathway in the cytoplasm to repress mTORC1 and induce autophagy.	Reactive Oxygen Species	37-40	ataxia telangiectasia mutated	Mus musculus	42-45
20160076-6	2010	Importantly, elevated ROS and dysregulation of mTORC1 in ATM-deficient cells is inhibited by rapamycin, which also rescues lymphomagenesis in Atm-deficient mice.	Reactive Oxygen Species	22-25	ataxia telangiectasia mutated	Mus musculus	57-60
20160076-6	2010	Importantly, elevated ROS and dysregulation of mTORC1 in ATM-deficient cells is inhibited by rapamycin, which also rescues lymphomagenesis in Atm-deficient mice.	Reactive Oxygen Species	22-25	ataxia telangiectasia mutated	Mus musculus	142-145
20160076-6	2010	Importantly, elevated ROS and dysregulation of mTORC1 in ATM-deficient cells is inhibited by rapamycin, which also rescues lymphomagenesis in Atm-deficient mice.	Sirolimus	93-102	ataxia telangiectasia mutated	Mus musculus	57-60
20160076-6	2010	Importantly, elevated ROS and dysregulation of mTORC1 in ATM-deficient cells is inhibited by rapamycin, which also rescues lymphomagenesis in Atm-deficient mice.	Sirolimus	93-102	ataxia telangiectasia mutated	Mus musculus	142-145
20160076-7	2010	Our results identify a cytoplasmic pathway for ROS-induced ATM activation of TSC2 to regulate mTORC1 signaling and autophagy, identifying an integration node for the cellular damage response with key pathways involved in metabolism, protein synthesis, and cell survival.	Reactive Oxygen Species	47-50	ataxia telangiectasia mutated	Mus musculus	59-62
20179206-0	2010	Atm-deficient mice exhibit increased sensitivity to dextran sulfate sodium-induced colitis characterized by elevated DNA damage and persistent immune activation.	Dextran Sulfate	52-74	ataxia telangiectasia mutated	Mus musculus	0-3
20179206-7	2010	Markers of reactive oxygen and nitrogen species-mediated damage, including 8-oxoguanine and nitrotyrosine, were present both in the distal colon and in peripheral leukocytes, with Atm(-/-) mice manifesting more 8-oxoguanine formation than wild-type mice.	reactive oxygen and nitrogen species	11-47	ataxia telangiectasia mutated	Mus musculus	180-183
20179206-9	2010	ATM, therefore, may be a critical immunoregulatory factor dampening the deleterious effects of chronic DSS-induced inflammation, necessary for systemic genomic stability and homeostasis of the gut epithelial barrier.	Dextran Sulfate	103-106	ataxia telangiectasia mutated	Mus musculus	0-3
19919837-3	2010	Our aims were to establish whether ATM deficiency alters the carcinogenic response of hepatocytes to diethylnitrosamine (DEN).	Diethylnitrosamine	101-119	ataxia telangiectasia mutated	Mus musculus	35-38
19919837-3	2010	Our aims were to establish whether ATM deficiency alters the carcinogenic response of hepatocytes to diethylnitrosamine (DEN).	Diethylnitrosamine	121-124	ataxia telangiectasia mutated	Mus musculus	35-38
19919837-7	2010	Whereas livers of DEN-treated ATM(-/-) mice showed markers of senescence (beta-galactosidase, Cxcl-1), up-regulation of telomerase occurred concurrently.	Diethylnitrosamine	18-21	ataxia telangiectasia mutated	Mus musculus	30-33
19919837-8	2010	The possibility that such balanced senescence could result in immortalization was demonstrated in hepatocytes prepared at 9 months from DEN-treated ATM(-/-) liver.	Diethylnitrosamine	136-139	ataxia telangiectasia mutated	Mus musculus	148-151
19919837-10	2010	Resultant cell cycle arrest and apoptosis of DNA-damaged cells are possible mechanisms that underlie this unique "refractoriness" to malignant transformation in DEN-initiated ATM(-/-) hepatocytes.	Diethylnitrosamine	161-164	ataxia telangiectasia mutated	Mus musculus	175-178
20124459-7	2010	Furthermore, the PARP-1 inhibitor olaparib (known previously as AZD2281/KU-0059436) significantly decreased tumor growth and increased overall survival in mice bearing s.c. xenografts of ATM-deficient Granta-519 cells while producing only a modest effect on overall survival of mice bearing xenografts of the ATM-proficient cell line, Z138.	olaparib	34-42	ataxia telangiectasia mutated	Mus musculus	187-190
20124459-7	2010	Furthermore, the PARP-1 inhibitor olaparib (known previously as AZD2281/KU-0059436) significantly decreased tumor growth and increased overall survival in mice bearing s.c. xenografts of ATM-deficient Granta-519 cells while producing only a modest effect on overall survival of mice bearing xenografts of the ATM-proficient cell line, Z138.	olaparib	34-42	ataxia telangiectasia mutated	Mus musculus	309-312
20124459-7	2010	Furthermore, the PARP-1 inhibitor olaparib (known previously as AZD2281/KU-0059436) significantly decreased tumor growth and increased overall survival in mice bearing s.c. xenografts of ATM-deficient Granta-519 cells while producing only a modest effect on overall survival of mice bearing xenografts of the ATM-proficient cell line, Z138.	olaparib	64-71	ataxia telangiectasia mutated	Mus musculus	187-190
20124459-7	2010	Furthermore, the PARP-1 inhibitor olaparib (known previously as AZD2281/KU-0059436) significantly decreased tumor growth and increased overall survival in mice bearing s.c. xenografts of ATM-deficient Granta-519 cells while producing only a modest effect on overall survival of mice bearing xenografts of the ATM-proficient cell line, Z138.	olaparib	64-71	ataxia telangiectasia mutated	Mus musculus	309-312
20124459-7	2010	Furthermore, the PARP-1 inhibitor olaparib (known previously as AZD2281/KU-0059436) significantly decreased tumor growth and increased overall survival in mice bearing s.c. xenografts of ATM-deficient Granta-519 cells while producing only a modest effect on overall survival of mice bearing xenografts of the ATM-proficient cell line, Z138.	olaparib	72-82	ataxia telangiectasia mutated	Mus musculus	187-190
20145032-2	2010	In cells undergoing ionizing radiation, ATM is activated by double-strand DNA breaks and phosphorylates the NH(2) terminus of p53 at serine residue 18.	Serine	133-139	ataxia telangiectasia mutated	Mus musculus	40-43
20574919-0	2010	Reactive oxygen species abrogate the anticarcinogenic effect of eicosapentaenoic acid in Atm-deficient mice.	Reactive Oxygen Species	0-23	ataxia telangiectasia mutated	Mus musculus	89-92
20574919-0	2010	Reactive oxygen species abrogate the anticarcinogenic effect of eicosapentaenoic acid in Atm-deficient mice.	Eicosapentaenoic Acid	64-85	ataxia telangiectasia mutated	Mus musculus	89-92
20574919-2	2010	The objective of our study was to investigate the influence of a high dose EPA on the development of the tumor phenotype in ataxia-telangiectasia mutated (Atm)-deficient mice, a genetic cancer model that is associated with increased levels of oxidative stress.	Eicosapentaenoic Acid	75-78	ataxia telangiectasia mutated	Mus musculus	124-153
20574919-2	2010	The objective of our study was to investigate the influence of a high dose EPA on the development of the tumor phenotype in ataxia-telangiectasia mutated (Atm)-deficient mice, a genetic cancer model that is associated with increased levels of oxidative stress.	Eicosapentaenoic Acid	75-78	ataxia telangiectasia mutated	Mus musculus	155-158
20574919-9	2010	On the other hand, EPA treatment of Atm-deficient mice led to the formation of ROS and accumulation of ODD that might have abrogated the anticarcinogenic effect caused by EPA.	Eicosapentaenoic Acid	19-22	ataxia telangiectasia mutated	Mus musculus	36-39
20574919-9	2010	On the other hand, EPA treatment of Atm-deficient mice led to the formation of ROS and accumulation of ODD that might have abrogated the anticarcinogenic effect caused by EPA.	Reactive Oxygen Species	79-82	ataxia telangiectasia mutated	Mus musculus	36-39
20574919-9	2010	On the other hand, EPA treatment of Atm-deficient mice led to the formation of ROS and accumulation of ODD that might have abrogated the anticarcinogenic effect caused by EPA.	Eicosapentaenoic Acid	171-174	ataxia telangiectasia mutated	Mus musculus	36-39
19660469-0	2009	Chronic doxorubicin cardiotoxicity is mediated by oxidative DNA damage-ATM-p53-apoptosis pathway and attenuated by pitavastatin through the inhibition of Rac1 activity.	Doxorubicin	8-19	ataxia telangiectasia mutated	Mus musculus	71-74
19660469-3	2009	In cultured cardiac myocytes, doxorubicin induced oxidative stress, DNA damage, ATM activation, and p53 induction.	Doxorubicin	30-41	ataxia telangiectasia mutated	Mus musculus	80-83
19660469-4	2009	A free radical scavenger NAC attenuated all of these events, whereas an ATM kinase inhibitor wortmannin attenuated doxorubicin-induced ATM activation and p53 induction but not oxidative stress.	Wortmannin	93-103	ataxia telangiectasia mutated	Mus musculus	72-75
19660469-4	2009	A free radical scavenger NAC attenuated all of these events, whereas an ATM kinase inhibitor wortmannin attenuated doxorubicin-induced ATM activation and p53 induction but not oxidative stress.	Wortmannin	93-103	ataxia telangiectasia mutated	Mus musculus	135-138
19660469-4	2009	A free radical scavenger NAC attenuated all of these events, whereas an ATM kinase inhibitor wortmannin attenuated doxorubicin-induced ATM activation and p53 induction but not oxidative stress.	Doxorubicin	115-126	ataxia telangiectasia mutated	Mus musculus	72-75
19660469-4	2009	A free radical scavenger NAC attenuated all of these events, whereas an ATM kinase inhibitor wortmannin attenuated doxorubicin-induced ATM activation and p53 induction but not oxidative stress.	Doxorubicin	115-126	ataxia telangiectasia mutated	Mus musculus	135-138
19660469-5	2009	Doxorubicin treatment in vivo also induced oxidative stress, DNA damage, ATM activation, and p53 accumulation.	Doxorubicin	0-11	ataxia telangiectasia mutated	Mus musculus	73-76
19660469-6	2009	These observations suggest that p53 induction by doxorubicin is mediated by oxidative DNA damage-ATM pathway.	Doxorubicin	49-60	ataxia telangiectasia mutated	Mus musculus	97-100
19557426-7	2009	Interestingly, DIDO3 is missing from the synaptonemal complex in Atm mutant spermatocytes, which form synapses but show persistent trimethylation of histone H3 lysine 4.	dido3	15-20	ataxia telangiectasia mutated	Mus musculus	65-68
19557426-7	2009	Interestingly, DIDO3 is missing from the synaptonemal complex in Atm mutant spermatocytes, which form synapses but show persistent trimethylation of histone H3 lysine 4.	HS 3	157-159	ataxia telangiectasia mutated	Mus musculus	65-68
19557426-7	2009	Interestingly, DIDO3 is missing from the synaptonemal complex in Atm mutant spermatocytes, which form synapses but show persistent trimethylation of histone H3 lysine 4.	Lysine	160-166	ataxia telangiectasia mutated	Mus musculus	65-68
19705844-4	2009	Activation of ATM by tricetin phosphorylated p53 at serine 15, resulting in increased stability of p53 by decreasing p53 and murine double minute-2 (MDM2) interaction.	tricetin	21-29	ataxia telangiectasia mutated	Mus musculus	14-17
19705844-4	2009	Activation of ATM by tricetin phosphorylated p53 at serine 15, resulting in increased stability of p53 by decreasing p53 and murine double minute-2 (MDM2) interaction.	Serine	52-58	ataxia telangiectasia mutated	Mus musculus	14-17
19544430-4	2009	We found that cultured subventricular zone neurosphere cells from Atm(-/-) mice show impaired proliferation, as well as intrinsic elevation of reactive oxygen species (ROS) levels, compared with those from Atm(+/+) mice.	Reactive Oxygen Species	143-166	ataxia telangiectasia mutated	Mus musculus	66-69
19544430-5	2009	We also show that increasing the levels of ROS by H(2)O(2) treatment significantly reduces Atm(+/+) neurosphere formation and proliferation.	Reactive Oxygen Species	43-46	ataxia telangiectasia mutated	Mus musculus	91-94
19544430-7	2009	Treatment of these cells with the antioxidant N-acetyl-L-cysteine (NAC) or with a p38 MAPK inhibitor restores normal proliferation and reduced expression of p21(cip1) and p27(kip1) in the Atm(-/-) NSCs.	Acetylcysteine	46-65	ataxia telangiectasia mutated	Mus musculus	188-191
19544430-7	2009	Treatment of these cells with the antioxidant N-acetyl-L-cysteine (NAC) or with a p38 MAPK inhibitor restores normal proliferation and reduced expression of p21(cip1) and p27(kip1) in the Atm(-/-) NSCs.	Acetylcysteine	67-70	ataxia telangiectasia mutated	Mus musculus	188-191
19544430-8	2009	These observations indicate that ATM plays a crucial role in NSC proliferation, by activating Akt and Erk1/2 pathways and by suppressing ROS-p38 MAPK signaling.	Reactive Oxygen Species	137-140	ataxia telangiectasia mutated	Mus musculus	33-36
19536869-4	2009	Activation of ATM by ISL phosphorylated p53 at Serine15, resulting in increased stability of p53 by decreasing p53 and murine double minute-2 (MDM2) interaction.	serine15	47-55	ataxia telangiectasia mutated	Mus musculus	14-17
19061978-9	2009	Interestingly, Atm-/- animals also exhibited hypersensitivity to the crosslinking agent mitomycin C, which was increased by deficiency of either one of the Rad54 paralogs.	Mitomycin	88-99	ataxia telangiectasia mutated	Mus musculus	15-18
19364503-4	2009	Here, we show that inhibition of mTOR signaling with its specific inhibitor, rapamycin, suppresses normal thymocyte DNA synthesis by downregulating 4EBP1, but not S6K, and that 4EBP1 phosphorylation and cyclin D1 expression are coordinately increased in Atm-/- thymocytes.	Sirolimus	77-86	ataxia telangiectasia mutated	Mus musculus	254-257
19364503-5	2009	Administration of rapamycin to Atm-/- mice attenuates elevated phospho-4EBP1, c-Myc and cyclin D1 in their thymocytes, and delays thymic lymphoma development.	Sirolimus	18-27	ataxia telangiectasia mutated	Mus musculus	31-34
18671277-3	2009	Using microarray technology, a screening analysis of genes responding to DHT in the uterus of ovariectomized mice, has allowed us to highlight multiple genes of the ATM/Gadd45g pathway that are modulated following exposure to DHT.	Dihydrotestosterone	73-76	ataxia telangiectasia mutated	Mus musculus	165-168
18671277-8	2009	Profile determination of temporal uterine gene expression at the transcriptional level enables us to suggest that the DHT modulation of genes involved in ATM/Gadd45g signaling in an ATM- or p53-independent manner, could play an important role in the cyclical changes of uterine cells in the mouse uterus.	Dihydrotestosterone	118-121	ataxia telangiectasia mutated	Mus musculus	154-157
18671277-8	2009	Profile determination of temporal uterine gene expression at the transcriptional level enables us to suggest that the DHT modulation of genes involved in ATM/Gadd45g signaling in an ATM- or p53-independent manner, could play an important role in the cyclical changes of uterine cells in the mouse uterus.	Dihydrotestosterone	118-121	ataxia telangiectasia mutated	Mus musculus	182-185
19435407-0	2009	Inhibition of ataxia-telangiectasia mutated by antisense oligonucleotide nanoparticles induces radiosensitization of head and neck squamous-cell carcinoma in mice.	Oligonucleotides	57-72	ataxia telangiectasia mutated	Mus musculus	14-43
19435407-2	2009	In the present study, we investigated the efficacy of poly(D,L-lactide-co-glycolide) (PLGA) nanoparticles containing ATM antisense oligonucleotides (ASOs) for the radiosensitization of head and neck squamous-cell carcinoma in mice, using the SCCVII cell line.	Polylactic Acid-Polyglycolic Acid Copolymer	54-83	ataxia telangiectasia mutated	Mus musculus	117-120
19435407-2	2009	In the present study, we investigated the efficacy of poly(D,L-lactide-co-glycolide) (PLGA) nanoparticles containing ATM antisense oligonucleotides (ASOs) for the radiosensitization of head and neck squamous-cell carcinoma in mice, using the SCCVII cell line.	Oligonucleotides	131-147	ataxia telangiectasia mutated	Mus musculus	117-120
19435407-4	2009	The results showed that the nanoparticles were suitable for intracellular uptake, and ATM ASOs inhibited ATM expression when delivered by using nanoparticles or lipofectin, but not in their free form.	1,2-dielaidoylphosphatidylethanolamine	161-171	ataxia telangiectasia mutated	Mus musculus	86-89
19435407-4	2009	The results showed that the nanoparticles were suitable for intracellular uptake, and ATM ASOs inhibited ATM expression when delivered by using nanoparticles or lipofectin, but not in their free form.	1,2-dielaidoylphosphatidylethanolamine	161-171	ataxia telangiectasia mutated	Mus musculus	105-108
19321450-5	2009	We show here that intrinsic elevated intracellular levels of reactive oxygen species (ROS) are associated with the senescence-like growth defect of Atm(-/-) astrocytes.	Reactive Oxygen Species	61-84	ataxia telangiectasia mutated	Mus musculus	148-151
19321450-5	2009	We show here that intrinsic elevated intracellular levels of reactive oxygen species (ROS) are associated with the senescence-like growth defect of Atm(-/-) astrocytes.	Reactive Oxygen Species	86-89	ataxia telangiectasia mutated	Mus musculus	148-151
19321450-8	2009	Furthermore, both mitogen-activated protein kinase (MAPK)/ERK inhibitor PD98059 and antioxidant N-acetyl-l-cysteine restored normal proliferation of Atm(-/-) astrocytes.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	72-79	ataxia telangiectasia mutated	Mus musculus	149-152
19321450-8	2009	Furthermore, both mitogen-activated protein kinase (MAPK)/ERK inhibitor PD98059 and antioxidant N-acetyl-l-cysteine restored normal proliferation of Atm(-/-) astrocytes.	Acetylcysteine	96-115	ataxia telangiectasia mutated	Mus musculus	149-152
18671277-3	2009	Using microarray technology, a screening analysis of genes responding to DHT in the uterus of ovariectomized mice, has allowed us to highlight multiple genes of the ATM/Gadd45g pathway that are modulated following exposure to DHT.	Dihydrotestosterone	226-229	ataxia telangiectasia mutated	Mus musculus	165-168
19234633-16	2009	Atm mRNA was detected in most cell bodies of the adult mouse eye by in situ hybridization of ocular tissue sections with specific digoxigenin-labeled PCR-amplified cDNA probes.	Digoxigenin	130-141	ataxia telangiectasia mutated	Mus musculus	0-3
19047460-5	2008	In this study, we show that ATM-dependent responses at both cellular and organismal levels are functional in mice that express a triple serine mutant form of ATM as their sole ATM species.	Serine	136-142	ataxia telangiectasia mutated	Mus musculus	28-31
19047460-5	2008	In this study, we show that ATM-dependent responses at both cellular and organismal levels are functional in mice that express a triple serine mutant form of ATM as their sole ATM species.	Serine	136-142	ataxia telangiectasia mutated	Mus musculus	158-161
19047460-5	2008	In this study, we show that ATM-dependent responses at both cellular and organismal levels are functional in mice that express a triple serine mutant form of ATM as their sole ATM species.	Serine	136-142	ataxia telangiectasia mutated	Mus musculus	158-161
18950535-2	2008	Our objective is to sensitize SCCVII cells to ionizing radiation in vitro and in vivo through inhibiting ATM expression using antisense oligodeoxynucleotides (AS-ODNs), and investigate the potential mechanism of radiosensitization.	Oligodeoxyribonucleotides	136-157	ataxia telangiectasia mutated	Mus musculus	105-108
18620545-6	2008	DSB-induced FUS phosphorylation in vivo at Ser(42) requires ATM and not DNA-PK.	Serine	43-46	ataxia telangiectasia mutated	Mus musculus	60-63
18469863-7	2008	The absence of ATM impaired apoptosis induced by E2F3a and treating K5 E2F3a transgenic mice with caffeine, an inhibitor of ATM and Rad3-related (ATR), promoted skin tumor development.	Caffeine	98-106	ataxia telangiectasia mutated	Mus musculus	124-127
18602349-7	2008	Similar results were obtained for ATM(-/-) mES cells.	2-(N-morpholino)ethanesulfonic acid	43-46	ataxia telangiectasia mutated	Mus musculus	34-37
18534819-9	2008	In addition, insulin-mediated Akt phosphorylation in mouse L6 muscle cells was greatly reduced by KU-55933, a specific inhibitor of ATM.	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	98-106	ataxia telangiectasia mutated	Mus musculus	132-135
18413980-3	2008	Although ataxia telangiectasia mutated (ATM) kinase phosphorylates Ser-139 of H2AX in vitro, the post-translational modification pattern and the modifier of H2AX in organs in vivo are not yet well understood.	Serine	67-70	ataxia telangiectasia mutated	Mus musculus	9-38
18511169-4	2008	Activation of ATM by KTA phosphorylated p53 at Serine15, resulting in increased stability of p53 by decreasing p53 and murine double minute-2 (MDM2) interaction.	kotomolide A	21-24	ataxia telangiectasia mutated	Mus musculus	14-17
18511169-4	2008	Activation of ATM by KTA phosphorylated p53 at Serine15, resulting in increased stability of p53 by decreasing p53 and murine double minute-2 (MDM2) interaction.	serine15	47-55	ataxia telangiectasia mutated	Mus musculus	14-17
18413980-3	2008	Although ataxia telangiectasia mutated (ATM) kinase phosphorylates Ser-139 of H2AX in vitro, the post-translational modification pattern and the modifier of H2AX in organs in vivo are not yet well understood.	Serine	67-70	ataxia telangiectasia mutated	Mus musculus	40-43
18381427-5	2008	ATM activation is polyamine dependent because alpha-difluoromethylornithine, a specific inhibitor of ODC activity, blocks its phosphorylation.	Polyamines	18-27	ataxia telangiectasia mutated	Mus musculus	0-3
18381427-5	2008	ATM activation is polyamine dependent because alpha-difluoromethylornithine, a specific inhibitor of ODC activity, blocks its phosphorylation.	Eflornithine	46-75	ataxia telangiectasia mutated	Mus musculus	0-3
18381462-3	2008	A single irradiation of mouse skin with UVB activated the ataxia-telangiectasia mutated- and Rad3-related (ATR) pathway, causing a severalfold increase in keratinocytes with phospho-Chk1 (Ser(345)) and a marked decrease in mitotic keratinocytes with cyclin B1 compared with baseline.	Serine	188-191	ataxia telangiectasia mutated	Mus musculus	58-111
18089834-0	2007	Ataxia telangiectasia-mutated and p53 are potential mediators of chloroquine-induced resistance to mammary carcinogenesis.	Chloroquine	65-76	ataxia telangiectasia mutated	Mus musculus	0-29
18097482-2	2008	Here we show that chloroquine, a drug that activates the stress-responsive Atm-p53 tumor-suppressor pathway, preferentially enhances the death of Myc oncogene-overexpressing primary mouse B cells and mouse embryonic fibroblasts (MEFs) and impairs Myc-induced lymphomagenesis in a transgenic mouse model of human Burkitt lymphoma.	Chloroquine	18-29	ataxia telangiectasia mutated	Mus musculus	75-78
18097482-4	2008	Accordingly, chloroquine impaired spontaneous lymphoma development in Atm-deficient mice, a mouse model of ataxia telangiectasia, but not in p53-deficient mice.	Chloroquine	13-24	ataxia telangiectasia mutated	Mus musculus	70-73
17925458-0	2008	p53 and ATM/ATR regulate 7,12-dimethylbenz[a]anthracene-induced immunosuppression.	7,12-dimethylbenz[a	25-44	ataxia telangiectasia mutated	Mus musculus	8-11
17925458-0	2008	p53 and ATM/ATR regulate 7,12-dimethylbenz[a]anthracene-induced immunosuppression.	anthracene	45-55	ataxia telangiectasia mutated	Mus musculus	8-11
17925458-9	2008	Increased ATM, phospho-ATM (Ser(1987)), and ATR levels were observed after DMBA treatment in WT, p53-null, and AhR-null mice but not in CYP1B1-null or mEH-null mice.	9,10-Dimethyl-1,2-benzanthracene	75-79	ataxia telangiectasia mutated	Mus musculus	10-13
17925458-9	2008	Increased ATM, phospho-ATM (Ser(1987)), and ATR levels were observed after DMBA treatment in WT, p53-null, and AhR-null mice but not in CYP1B1-null or mEH-null mice.	9,10-Dimethyl-1,2-benzanthracene	75-79	ataxia telangiectasia mutated	Mus musculus	23-26
18089799-2	2007	One of these phosphorylation sites (mouse Ser(18) and human Ser(15)) is a substrate for the ataxia telangiectasia-mutated (ATM) and ATM-related (ATR) protein kinases.	Serine	42-45	ataxia telangiectasia mutated	Mus musculus	132-135
18089799-2	2007	One of these phosphorylation sites (mouse Ser(18) and human Ser(15)) is a substrate for the ataxia telangiectasia-mutated (ATM) and ATM-related (ATR) protein kinases.	Serine	60-63	ataxia telangiectasia mutated	Mus musculus	132-135
18089799-3	2007	Studies of p53(S18A) mice (with a germ-line mutation that replaces Ser(18) with Ala) have indicated that ATM/ATR phosphorylation of p53 Ser(18) is required for normal DNA damage-induced PUMA expression and apoptosis but not for DNA damage-induced cell cycle arrest.	Serine	67-70	ataxia telangiectasia mutated	Mus musculus	105-108
18089799-10	2007	Together, these data indicate that the ATM/ATR phosphorylation site Ser(18) on p53 contributes to tumor suppression in vivo.	Serine	68-71	ataxia telangiectasia mutated	Mus musculus	39-42
18070599-7	2008	Furthermore, we determined Ser 148 of p32 as an ATM phosphorylation site.	Serine	27-30	ataxia telangiectasia mutated	Mus musculus	48-51
18283338-7	2008	Notably, treatment with hydrogen peroxide duplicated the effects of ATM deficiency in cultured thymocytes, and treatment with the novel cell-permeable thiol antioxidant N-acetylcysteine amide (AD4) reduced elevated p-eIF2alpha levels in thymocytes of Atm-/- mice.	Sulfhydryl Compounds	151-156	ataxia telangiectasia mutated	Mus musculus	251-254
18283338-7	2008	Notably, treatment with hydrogen peroxide duplicated the effects of ATM deficiency in cultured thymocytes, and treatment with the novel cell-permeable thiol antioxidant N-acetylcysteine amide (AD4) reduced elevated p-eIF2alpha levels in thymocytes of Atm-/- mice.	N-Acetylcysteinamide	169-191	ataxia telangiectasia mutated	Mus musculus	251-254
18283338-7	2008	Notably, treatment with hydrogen peroxide duplicated the effects of ATM deficiency in cultured thymocytes, and treatment with the novel cell-permeable thiol antioxidant N-acetylcysteine amide (AD4) reduced elevated p-eIF2alpha levels in thymocytes of Atm-/- mice.	N-Acetylcysteinamide	193-196	ataxia telangiectasia mutated	Mus musculus	251-254
17455238-9	2007	Inhibitor of the PI3K-family, LY294002 and the ATM/ATR inhibitor, caffeine, blocked vitamin C-induced growth arrest in B16F10 melanoma cells.	Caffeine	66-74	ataxia telangiectasia mutated	Mus musculus	47-50
17786544-11	2007	Our results demonstrate that AICAR treatment could lead to phosphorylation of AMPK in an ATM-dependent and LKB1-independent manner.	acadesine	29-34	ataxia telangiectasia mutated	Mus musculus	89-92
17455238-9	2007	Inhibitor of the PI3K-family, LY294002 and the ATM/ATR inhibitor, caffeine, blocked vitamin C-induced growth arrest in B16F10 melanoma cells.	Ascorbic Acid	84-93	ataxia telangiectasia mutated	Mus musculus	47-50
17418878-1	2007	We have previously demonstrated that spontaneous DNA synthesis in immature thymocytes of Atm-/- mice is elevated, and that treatment with the glucocorticoid dexamethasone (Dex) attenuates this increased DNA synthesis and prevents the development of thymic lymphomas.	Dexamethasone	157-170	ataxia telangiectasia mutated	Mus musculus	89-92
17576777-8	2007	In ataxia telangiectasia mutated (Atm)-deficient (Atm(-/-)) mice, ROS levels were elevated in chondrocytes of growth plates, accompanied by a proliferation defect and stimulation of chondrocyte hypertrophy.	Reactive Oxygen Species	66-69	ataxia telangiectasia mutated	Mus musculus	34-37
17576777-8	2007	In ataxia telangiectasia mutated (Atm)-deficient (Atm(-/-)) mice, ROS levels were elevated in chondrocytes of growth plates, accompanied by a proliferation defect and stimulation of chondrocyte hypertrophy.	Reactive Oxygen Species	66-69	ataxia telangiectasia mutated	Mus musculus	50-53
17356010-5	2007	Here we show that young Atm-deficient mice show normal fasting glucose levels and normal insulin sensitivity.	Glucose	63-70	ataxia telangiectasia mutated	Mus musculus	24-27
17356010-7	2007	Aged Atm-/- mice show a pronounced increase in blood glucose levels and a decrease in insulin and C-peptide levels.	Glucose	53-60	ataxia telangiectasia mutated	Mus musculus	5-8
17525732-4	2007	ATMIN and ATM co-localised in response to ATM activation by chloroquine and hypotonic stress, but not after induction of double-strand breaks by ionising radiation (IR).	Chloroquine	60-71	ataxia telangiectasia mutated	Mus musculus	0-3
17525732-4	2007	ATMIN and ATM co-localised in response to ATM activation by chloroquine and hypotonic stress, but not after induction of double-strand breaks by ionising radiation (IR).	Chloroquine	60-71	ataxia telangiectasia mutated	Mus musculus	10-13
17418878-1	2007	We have previously demonstrated that spontaneous DNA synthesis in immature thymocytes of Atm-/- mice is elevated, and that treatment with the glucocorticoid dexamethasone (Dex) attenuates this increased DNA synthesis and prevents the development of thymic lymphomas.	Dexamethasone	172-175	ataxia telangiectasia mutated	Mus musculus	89-92
17418878-4	2007	In cultured Atm-/- thymic lymphoma cells treated with Dex, GR nuclear translocation occurs, resulting in suppression of DNA synthesis and c-myc expression at both the mRNA and protein levels.	Dexamethasone	54-57	ataxia telangiectasia mutated	Mus musculus	12-15
17418878-7	2007	Administration of Dex to Atm-/- mice decreases the elevated c-Myc protein levels in their thymocytes.	Dexamethasone	18-21	ataxia telangiectasia mutated	Mus musculus	25-28
17010969-7	2006	A low frequency of bouquet spermatocytes in Spo11(-/-)Atm(-/-) spermatogenesis suggests that DSBs contribute to the Atm(-/-)-correlated bouquet stage exit defect.	dsbs	93-97	ataxia telangiectasia mutated	Mus musculus	116-119
17182545-0	2007	Regulation of reactive oxygen species by Atm is essential for proper response to DNA double-strand breaks in lymphocytes.	Reactive Oxygen Species	14-37	ataxia telangiectasia mutated	Mus musculus	41-44
17182545-3	2007	In this study, we intensively investigated the roles of reactive oxygen species (ROS) in phenotypes of Atm(-/-) mice.	Reactive Oxygen Species	81-84	ataxia telangiectasia mutated	Mus musculus	103-106
17182545-4	2007	Reduction of ROS by the antioxidant N-acetyl-l-cysteine (NAC) prevented the emergence of senescent phenotypes in Atm(-/-) mouse embryonic fibroblasts, hypersensitivity to total body irradiation, and thymic lymphomagenesis in Atm(-/-) mice.	Reactive Oxygen Species	13-16	ataxia telangiectasia mutated	Mus musculus	113-116
17182545-4	2007	Reduction of ROS by the antioxidant N-acetyl-l-cysteine (NAC) prevented the emergence of senescent phenotypes in Atm(-/-) mouse embryonic fibroblasts, hypersensitivity to total body irradiation, and thymic lymphomagenesis in Atm(-/-) mice.	Reactive Oxygen Species	13-16	ataxia telangiectasia mutated	Mus musculus	225-228
17182545-4	2007	Reduction of ROS by the antioxidant N-acetyl-l-cysteine (NAC) prevented the emergence of senescent phenotypes in Atm(-/-) mouse embryonic fibroblasts, hypersensitivity to total body irradiation, and thymic lymphomagenesis in Atm(-/-) mice.	Acetylcysteine	36-55	ataxia telangiectasia mutated	Mus musculus	113-116
17182545-4	2007	Reduction of ROS by the antioxidant N-acetyl-l-cysteine (NAC) prevented the emergence of senescent phenotypes in Atm(-/-) mouse embryonic fibroblasts, hypersensitivity to total body irradiation, and thymic lymphomagenesis in Atm(-/-) mice.	Acetylcysteine	36-55	ataxia telangiectasia mutated	Mus musculus	225-228
17182545-4	2007	Reduction of ROS by the antioxidant N-acetyl-l-cysteine (NAC) prevented the emergence of senescent phenotypes in Atm(-/-) mouse embryonic fibroblasts, hypersensitivity to total body irradiation, and thymic lymphomagenesis in Atm(-/-) mice.	Acetylcysteine	57-60	ataxia telangiectasia mutated	Mus musculus	113-116
17182545-4	2007	Reduction of ROS by the antioxidant N-acetyl-l-cysteine (NAC) prevented the emergence of senescent phenotypes in Atm(-/-) mouse embryonic fibroblasts, hypersensitivity to total body irradiation, and thymic lymphomagenesis in Atm(-/-) mice.	Acetylcysteine	57-60	ataxia telangiectasia mutated	Mus musculus	225-228
17182545-6	2007	Impairment of Ig class switch recombination seen in Atm(-/-) mice was mitigated by NAC, indicating that ROS elevation leads to abnormal response to programmed double-strand breaks in vivo.	Acetylcysteine	83-86	ataxia telangiectasia mutated	Mus musculus	52-55
17182545-6	2007	Impairment of Ig class switch recombination seen in Atm(-/-) mice was mitigated by NAC, indicating that ROS elevation leads to abnormal response to programmed double-strand breaks in vivo.	Reactive Oxygen Species	104-107	ataxia telangiectasia mutated	Mus musculus	52-55
17182545-7	2007	Significantly, in vivo administration of NAC to Atm(-/-) mice restored normal T cell development and inhibited aberrant V(D)J recombination.	Acetylcysteine	41-44	ataxia telangiectasia mutated	Mus musculus	48-51
17182545-8	2007	We conclude that Atm-mediated ROS regulation is essential for proper DNA recombination, preventing immunodeficiency, and lymphomagenesis.	Reactive Oxygen Species	30-33	ataxia telangiectasia mutated	Mus musculus	17-20
17097049-5	2006	In Atm-null testicular cells, differing from bone marrow cells of Atm-null mice, reactive oxygen species-mediated p16(Ink4a) activation does not occur in Atm-null premeiotic germ cells, which suggests the involvement of different signaling pathways from bone marrow defects.	Reactive Oxygen Species	81-104	ataxia telangiectasia mutated	Mus musculus	3-6
17084711-8	2006	These results suggest that ATM-dependent stress pathways mediate susceptibility to the metabolic syndrome and that chloroquine or related agents promoting ATM activity could modulate insulin resistance and decrease vascular disease.	Chloroquine	115-126	ataxia telangiectasia mutated	Mus musculus	155-158
16934683-0	2006	Dramatic extension of tumor latency and correction of neurobehavioral phenotype in Atm-mutant mice with a nitroxide antioxidant.	Hydroxylamine	106-115	ataxia telangiectasia mutated	Mus musculus	83-86
17084711-5	2006	Treatment of ATM+/+apoE-/- mice with low-dose chloroquine, an ATM activator, decreased atherosclerosis.	Chloroquine	46-57	ataxia telangiectasia mutated	Mus musculus	13-16
17084711-5	2006	Treatment of ATM+/+apoE-/- mice with low-dose chloroquine, an ATM activator, decreased atherosclerosis.	Chloroquine	46-57	ataxia telangiectasia mutated	Mus musculus	62-65
17084711-6	2006	In an ATM-dependent manner, chloroquine decreased macrophage JNK activity, decreased macrophage lipoprotein lipase activity (a proatherogenic consequence of JNK activation), decreased blood pressure, and improved glucose tolerance.	Chloroquine	28-39	ataxia telangiectasia mutated	Mus musculus	6-9
17084711-6	2006	In an ATM-dependent manner, chloroquine decreased macrophage JNK activity, decreased macrophage lipoprotein lipase activity (a proatherogenic consequence of JNK activation), decreased blood pressure, and improved glucose tolerance.	Glucose	213-220	ataxia telangiectasia mutated	Mus musculus	6-9
16934683-4	2006	We demonstrate here that the antioxidant 5-carboxy-1,1,3,3-tetramethylisoindolin-2-yloxyl (CTMIO) dramatically delays the onset of thymic lymphomas in Atm(-/-) mice which is not due to an enhancement of apoptosis by CTMIO.	5-carboxy-1,1,3,3-tetramethylisoindolin-2-yloxyl	41-89	ataxia telangiectasia mutated	Mus musculus	151-154
16934683-4	2006	We demonstrate here that the antioxidant 5-carboxy-1,1,3,3-tetramethylisoindolin-2-yloxyl (CTMIO) dramatically delays the onset of thymic lymphomas in Atm(-/-) mice which is not due to an enhancement of apoptosis by CTMIO.	5-carboxy-1,1,3,3-tetramethylisoindolin-2-yloxyl	91-96	ataxia telangiectasia mutated	Mus musculus	151-154
16790486-0	2006	A developmental role for ataxia-telangiectasia mutated in protecting the embryo from spontaneous and phenytoin-enhanced embryopathies in culture.	Phenytoin	101-110	ataxia telangiectasia mutated	Mus musculus	25-54
16906133-6	2006	These results suggest an alternative mode for stimulation of Atm by DSBs in which Atm autophosphorylation at Ser 1987, like trans-phosphorylation of downstream substrates, is a consequence rather than a cause of Atm activation.	dsbs	68-72	ataxia telangiectasia mutated	Mus musculus	61-64
16906133-6	2006	These results suggest an alternative mode for stimulation of Atm by DSBs in which Atm autophosphorylation at Ser 1987, like trans-phosphorylation of downstream substrates, is a consequence rather than a cause of Atm activation.	dsbs	68-72	ataxia telangiectasia mutated	Mus musculus	82-85
16906133-6	2006	These results suggest an alternative mode for stimulation of Atm by DSBs in which Atm autophosphorylation at Ser 1987, like trans-phosphorylation of downstream substrates, is a consequence rather than a cause of Atm activation.	dsbs	68-72	ataxia telangiectasia mutated	Mus musculus	82-85
16906133-6	2006	These results suggest an alternative mode for stimulation of Atm by DSBs in which Atm autophosphorylation at Ser 1987, like trans-phosphorylation of downstream substrates, is a consequence rather than a cause of Atm activation.	Serine	109-112	ataxia telangiectasia mutated	Mus musculus	61-64
16906133-6	2006	These results suggest an alternative mode for stimulation of Atm by DSBs in which Atm autophosphorylation at Ser 1987, like trans-phosphorylation of downstream substrates, is a consequence rather than a cause of Atm activation.	Serine	109-112	ataxia telangiectasia mutated	Mus musculus	82-85
16906133-6	2006	These results suggest an alternative mode for stimulation of Atm by DSBs in which Atm autophosphorylation at Ser 1987, like trans-phosphorylation of downstream substrates, is a consequence rather than a cause of Atm activation.	Serine	109-112	ataxia telangiectasia mutated	Mus musculus	82-85
16714389-0	2006	Variable in vivo embryoprotective role for ataxia-telangiectasia-mutated against constitutive and phenytoin-enhanced oxidative stress in atm knockout mice.	Phenytoin	98-107	ataxia telangiectasia mutated	Mus musculus	43-72
16714389-3	2006	Wild-type (+/+) or heterozygous (+/-) Atm knockout dams were mated with +/- males, pregnant dams were treated with phenytoin (65 mg/kg ip) or its vehicle, and resorptions and fetuses were genotyped and characterized.	Phenytoin	115-124	ataxia telangiectasia mutated	Mus musculus	38-41
16714389-6	2006	Phenytoin enhanced this Atm-dependent embryopathic pattern (p &lt; 0.05).	Phenytoin	0-9	ataxia telangiectasia mutated	Mus musculus	24-27
16714389-11	2006	Despite variable actions in vivo, the embryoprotective effects of Atm suggest a role for reactive oxygen species and oxidative DNA damage in some spontaneous and phenytoin-enhanced embryopathies.	Reactive Oxygen Species	89-112	ataxia telangiectasia mutated	Mus musculus	66-69
16714389-11	2006	Despite variable actions in vivo, the embryoprotective effects of Atm suggest a role for reactive oxygen species and oxidative DNA damage in some spontaneous and phenytoin-enhanced embryopathies.	Phenytoin	162-171	ataxia telangiectasia mutated	Mus musculus	66-69
16952553-14	2006	CONCLUSIONS: ZBP-89 interacts with ATM in a butyrate-dependent manner and is essential for colonic homeostasis in the setting of acute mucosal injury.	Butyrates	44-52	ataxia telangiectasia mutated	Mus musculus	35-38
16790486-2	2006	We previously showed pregnant knockout mice lacking the A-T gene product ataxia-telangiectasia mutated (Atm) are highly susceptible to the embryopathic effects of IR, which damages DNA, possibly via generation of reactive oxygen species (ROS).	Reactive Oxygen Species	213-236	ataxia telangiectasia mutated	Mus musculus	73-102
16790486-2	2006	We previously showed pregnant knockout mice lacking the A-T gene product ataxia-telangiectasia mutated (Atm) are highly susceptible to the embryopathic effects of IR, which damages DNA, possibly via generation of reactive oxygen species (ROS).	Reactive Oxygen Species	213-236	ataxia telangiectasia mutated	Mus musculus	104-107
16790486-2	2006	We previously showed pregnant knockout mice lacking the A-T gene product ataxia-telangiectasia mutated (Atm) are highly susceptible to the embryopathic effects of IR, which damages DNA, possibly via generation of reactive oxygen species (ROS).	Reactive Oxygen Species	238-241	ataxia telangiectasia mutated	Mus musculus	73-102
16790486-2	2006	We previously showed pregnant knockout mice lacking the A-T gene product ataxia-telangiectasia mutated (Atm) are highly susceptible to the embryopathic effects of IR, which damages DNA, possibly via generation of reactive oxygen species (ROS).	Reactive Oxygen Species	238-241	ataxia telangiectasia mutated	Mus musculus	104-107
16790486-3	2006	Here we show that Atm more broadly protects against both spontaneous and phenytoin-enhanced embryopathies.	Phenytoin	73-82	ataxia telangiectasia mutated	Mus musculus	18-21
16790486-5	2006	A similar but significantly enhanced gene dose-dependent pattern of embryopathic susceptibility was evident in Atm knockout embryos exposed to the ROS-initiating teratogen phenytoin (p &lt; 0.05).	Reactive Oxygen Species	147-150	ataxia telangiectasia mutated	Mus musculus	111-114
16790486-7	2006	This developmental role of Atm further implicates DNA damage in ROS-mediated teratogenesis and DNA damage response and repair as risk factors for individual susceptibility.	Reactive Oxygen Species	64-67	ataxia telangiectasia mutated	Mus musculus	27-30
16918715-6	2006	The results in this study indicated that DHFR, MRP5, ATM, and P53 could play important roles in resistance to methotrexate and some of them would be new potential drug targets.	Methotrexate	110-122	ataxia telangiectasia mutated	Mus musculus	53-56
16863997-2	2006	We have demonstrated previously that spontaneous DNA synthesis in Atm(-/-) thymocytes is markedly increased over that of Atm(+/+) thymocytes and that glucocorticoid dexamethasone suppresses thymocyte DNA synthesis and prevents the ultimate development of thymic lymphoma in Atm(-/-) mice.	Dexamethasone	165-178	ataxia telangiectasia mutated	Mus musculus	66-69
16863997-5	2006	Here we also demonstrate that Atm(-/-) thymocytes exhibit increased levels of hydrogen peroxide, NF-E2-related factor (Nrf-2), peroxiredoxin-1, and intracellular glutathione relative to thymocytes from Atm(+/+) mice.	Hydrogen Peroxide	78-95	ataxia telangiectasia mutated	Mus musculus	30-33
16863997-5	2006	Here we also demonstrate that Atm(-/-) thymocytes exhibit increased levels of hydrogen peroxide, NF-E2-related factor (Nrf-2), peroxiredoxin-1, and intracellular glutathione relative to thymocytes from Atm(+/+) mice.	Glutathione	162-173	ataxia telangiectasia mutated	Mus musculus	30-33
16863997-6	2006	Importantly, reduction of hydrogen peroxide by administration of the antioxidant N-acetylcysteine to Atm(-/-) mice attenuates the elevation of Nrf-2, c-Myc, and DNA synthesis in their thymocytes, suggesting that ATM may control c-Myc and DNA synthesis during postnatal thymocyte development by preventing accumulation of reactive oxygen species.	Hydrogen Peroxide	26-43	ataxia telangiectasia mutated	Mus musculus	101-104
16863997-6	2006	Importantly, reduction of hydrogen peroxide by administration of the antioxidant N-acetylcysteine to Atm(-/-) mice attenuates the elevation of Nrf-2, c-Myc, and DNA synthesis in their thymocytes, suggesting that ATM may control c-Myc and DNA synthesis during postnatal thymocyte development by preventing accumulation of reactive oxygen species.	Hydrogen Peroxide	26-43	ataxia telangiectasia mutated	Mus musculus	212-215
16863997-6	2006	Importantly, reduction of hydrogen peroxide by administration of the antioxidant N-acetylcysteine to Atm(-/-) mice attenuates the elevation of Nrf-2, c-Myc, and DNA synthesis in their thymocytes, suggesting that ATM may control c-Myc and DNA synthesis during postnatal thymocyte development by preventing accumulation of reactive oxygen species.	Acetylcysteine	81-97	ataxia telangiectasia mutated	Mus musculus	101-104
16863997-6	2006	Importantly, reduction of hydrogen peroxide by administration of the antioxidant N-acetylcysteine to Atm(-/-) mice attenuates the elevation of Nrf-2, c-Myc, and DNA synthesis in their thymocytes, suggesting that ATM may control c-Myc and DNA synthesis during postnatal thymocyte development by preventing accumulation of reactive oxygen species.	Acetylcysteine	81-97	ataxia telangiectasia mutated	Mus musculus	212-215
16863997-6	2006	Importantly, reduction of hydrogen peroxide by administration of the antioxidant N-acetylcysteine to Atm(-/-) mice attenuates the elevation of Nrf-2, c-Myc, and DNA synthesis in their thymocytes, suggesting that ATM may control c-Myc and DNA synthesis during postnatal thymocyte development by preventing accumulation of reactive oxygen species.	Reactive Oxygen Species	321-344	ataxia telangiectasia mutated	Mus musculus	101-104
16918715-5	2006	Significant higher expressions of many genes especially dhfr, mrp5, atm and p53 were detected in methotrexate-resistant cells than in normal mouse cells by SuperArray analysis and corresponding excessive expressions of DHFR, MRP5, ATM, and P53 proteins in methotrexate-resistant cells were also confirmed by Western blot analysis.	Methotrexate	97-109	ataxia telangiectasia mutated	Mus musculus	68-71
16918715-5	2006	Significant higher expressions of many genes especially dhfr, mrp5, atm and p53 were detected in methotrexate-resistant cells than in normal mouse cells by SuperArray analysis and corresponding excessive expressions of DHFR, MRP5, ATM, and P53 proteins in methotrexate-resistant cells were also confirmed by Western blot analysis.	Methotrexate	97-109	ataxia telangiectasia mutated	Mus musculus	231-234
16781197-0	2006	Antioxidant N-acetyl cysteine reduces incidence and multiplicity of lymphoma in Atm deficient mice.	Acetylcysteine	12-29	ataxia telangiectasia mutated	Mus musculus	80-83
16781197-3	2006	We examined the effect of long-term dietary supplementation with the thiol-containing antioxidant, N-acetyl-L-cysteine (NAC), on survival and cancer formation in Atm (AT-mutated) deficient mice, used as an animal model of AT.	Sulfhydryl Compounds	69-74	ataxia telangiectasia mutated	Mus musculus	162-165
16781197-3	2006	We examined the effect of long-term dietary supplementation with the thiol-containing antioxidant, N-acetyl-L-cysteine (NAC), on survival and cancer formation in Atm (AT-mutated) deficient mice, used as an animal model of AT.	Sulfhydryl Compounds	69-74	ataxia telangiectasia mutated	Mus musculus	167-177
16138010-3	2005	We have found that inhibition of ATR and ATM kinases with caffeine or Chk1 with UCN-01, results in activation of a p38-dependent intra-S-phase checkpoint and activation of apoptosis in ES cells.	Caffeine	58-66	ataxia telangiectasia mutated	Mus musculus	41-44
16221684-2	2005	We recently showed that ATM phosphorylates the cyclic AMP response element-binding protein, CREB, following exposure to ionizing radiation (IR) and other DNA-damaging stimuli.	Cyclic AMP	47-57	ataxia telangiectasia mutated	Mus musculus	24-27
16221684-5	2005	IR strongly induced the phosphorylation of Ser-120 in an ATM-dependent manner in mouse embryo fibroblasts.	Serine	43-46	ataxia telangiectasia mutated	Mus musculus	57-60
16251211-7	2005	The nuclear localization of ATBF1 was suppressed by treatment with caffeine, an inhibitor of PI(3)K-related kinase activity of ataxa-telangiectasia mutated (ATM) gene product.	Caffeine	67-75	ataxia telangiectasia mutated	Mus musculus	127-155
16251211-7	2005	The nuclear localization of ATBF1 was suppressed by treatment with caffeine, an inhibitor of PI(3)K-related kinase activity of ataxa-telangiectasia mutated (ATM) gene product.	Caffeine	67-75	ataxia telangiectasia mutated	Mus musculus	157-160
16138010-4	2005	However, wortmannin at a concentration, that inhibits ATM kinase but not ATR kinase, did not affect cell cycle progression.	Wortmannin	9-19	ataxia telangiectasia mutated	Mus musculus	54-57
16799786-3	2006	We have also shown that mice haploinsufficient for ATM develop cataracts earlier than wild-type animals, when exposed to either low-LET X-rays or high-LET (56)Fe ions.	Iron	159-161	ataxia telangiectasia mutated	Mus musculus	51-54
16400190-4	2006	To test this hypothesis, we treated a congenic strain of Atm+/- mice with DMBA (7,12-dimethylbenz(alpha)anthracene), a mammary carcinogen, and observed mammary tumor incidence.	6,11-dimethylbenzo(b)naphtho(2,3-d)thiophene	74-78	ataxia telangiectasia mutated	Mus musculus	57-60
16141284-7	2005	P53 was transiently phosphorylated at serine 23 during liver regeneration in an Atm-dependent manner.	Serine	38-44	ataxia telangiectasia mutated	Mus musculus	80-83
15998665-5	2005	We found that DNA-PKcs can be ruled out as an essential kinase in this process, whereas ATM is strictly required for the chromatin-wide phosphorylation of H2AX occurring in leptotene spermatocytes in response to DSBs.	dsbs	212-216	ataxia telangiectasia mutated	Mus musculus	88-91
16189003-6	2005	The incubation of infected cells with caffeine, a known ATM inhibitor, did not block entry into S but reduced the rate of viral compared to cellular DNA synthesis.	Caffeine	38-46	ataxia telangiectasia mutated	Mus musculus	56-59
16081118-9	2005	Atm and p53 knockout mice deficient in DNA damage response/repair are more susceptible to xenobiotic or radiation embryopathies, suggesting a teratological role for DNA damage, consistent with enhanced susceptibility to methamphetamine in ogg1 knockout mice with deficient repair of oxidative DNA damage.	Methamphetamine	220-235	ataxia telangiectasia mutated	Mus musculus	0-3
15863839-4	2005	In contrast, the plasma cholesterol level was significantly higher in ATM(+)(/-)/ApoE(-)(/-) mice than in ATM(+)(/+)/ApoE(-)(/-) control mice.	Cholesterol	24-35	ataxia telangiectasia mutated	Mus musculus	70-73
15863839-4	2005	In contrast, the plasma cholesterol level was significantly higher in ATM(+)(/-)/ApoE(-)(/-) mice than in ATM(+)(/+)/ApoE(-)(/-) control mice.	Cholesterol	24-35	ataxia telangiectasia mutated	Mus musculus	106-109
15888486-1	2005	We previously demonstrated that the nitroxide antioxidant tempol (4-hydroxy-2,2,6,6-tetramethylpiperidine-N-oxyl) increased latency to tumorigenesis and doubled (100%) the lifespan of Atm-deficient mice, a mouse model of ataxia telangiectasia, which displays accelerated oxidative damage and stress.	tempol	66-113	ataxia telangiectasia mutated	Mus musculus	184-187
15735681-4	2005	The results indicate that ATM kinase is likely to be indispensable for the p53-dependent S-phase checkpoint since the suppression was abrogated by inhibitors such as caffeine and wortmannin.	Caffeine	166-174	ataxia telangiectasia mutated	Mus musculus	26-29
15888486-1	2005	We previously demonstrated that the nitroxide antioxidant tempol (4-hydroxy-2,2,6,6-tetramethylpiperidine-N-oxyl) increased latency to tumorigenesis and doubled (100%) the lifespan of Atm-deficient mice, a mouse model of ataxia telangiectasia, which displays accelerated oxidative damage and stress.	Hydroxylamine	36-45	ataxia telangiectasia mutated	Mus musculus	184-187
15888486-1	2005	We previously demonstrated that the nitroxide antioxidant tempol (4-hydroxy-2,2,6,6-tetramethylpiperidine-N-oxyl) increased latency to tumorigenesis and doubled (100%) the lifespan of Atm-deficient mice, a mouse model of ataxia telangiectasia, which displays accelerated oxidative damage and stress.	tempol	58-64	ataxia telangiectasia mutated	Mus musculus	184-187
15735681-4	2005	The results indicate that ATM kinase is likely to be indispensable for the p53-dependent S-phase checkpoint since the suppression was abrogated by inhibitors such as caffeine and wortmannin.	Wortmannin	179-189	ataxia telangiectasia mutated	Mus musculus	26-29
15864314-4	2005	Discovery of this intestinal radiosensitivity mechanism allowed design of an antisense Atm oligonucleotide treatment which phenocopied the Atm(-/-) mouse, reordering ceramide synthase-mediated stem cell death to become the first-line gastrointestinal response of wild-type littermates.	Oligonucleotides	91-106	ataxia telangiectasia mutated	Mus musculus	87-90
15864314-4	2005	Discovery of this intestinal radiosensitivity mechanism allowed design of an antisense Atm oligonucleotide treatment which phenocopied the Atm(-/-) mouse, reordering ceramide synthase-mediated stem cell death to become the first-line gastrointestinal response of wild-type littermates.	Oligonucleotides	91-106	ataxia telangiectasia mutated	Mus musculus	139-142
15570424-0	2005	Control of Atm-/- thymic lymphoma cell proliferation in vitro and in vivo by dexamethasone.	Dexamethasone	77-90	ataxia telangiectasia mutated	Mus musculus	11-14
15701627-7	2005	Caffeine, an inhibitor of the upstream checkpoint kinases ATM (ataxia telangiectasia-mutated) and ATR (ATM and Rad3-related), has no effect on the early inhibition of DNA synthesis, but cells are no longer able to maintain the block after 8 h. Instead, the addition of caffeine leads to arrest of cells in G(2)/M rather than S-phase after 24 h. Analysis of signaling pathways in cell extracts reveals an activation of Chk1 after treatment with MMS and 4-AN, which can be suppressed by caffeine.	Caffeine	0-8	ataxia telangiectasia mutated	Mus musculus	58-61
15570424-4	2005	The primary objectives of the present study were (1) to investigate possible mechanisms underlying the tumor-suppressing effect of Dex on Atm-/- thymic lymphoma cells, and (2) to determine whether Dex is an effective tumor-suppressing treatment in mice bearing transplanted Atm-/- thymic tumors.	Dexamethasone	131-134	ataxia telangiectasia mutated	Mus musculus	138-141
15570424-9	2005	In Atm+/+ mice transplanted subcutaneously with ATL-1 cells, tumor growth was either prevented completely or significantly suppressed by Dex treatment.	Dexamethasone	137-140	ataxia telangiectasia mutated	Mus musculus	3-6
15570424-10	2005	CONCLUSIONS: Our findings identify potential mechanisms by which Dex affects the proliferation and survival of ATL-1 cells in culture, and provide evidence that Dex can suppress the proliferation of Atm-/- thymic lymphoma cells growing in the body.	Dexamethasone	161-164	ataxia telangiectasia mutated	Mus musculus	199-202
15570424-7	2005	RESULTS: Atm-/- tumor cells were highly sensitive to Dex, both in culture and in vivo as ectopic tumors in mice.	Dexamethasone	53-56	ataxia telangiectasia mutated	Mus musculus	9-12
15735814-0	2005	The alkylating carcinogen N-methyl-N"-nitro-N-nitrosoguanidine activates the plasminogen activator inhibitor-1 gene through sequential phosphorylation of p53 by ATM and ATR kinases.	Methylnitronitrosoguanidine	26-62	ataxia telangiectasia mutated	Mus musculus	161-164
15735814-4	2005	Here, we show that ATM and ATR kinases, but not DNA-PK, which participate in DNA damage-activated checkpoints, regulate the phosphorylation of p53 at serine 15 in response to MNNG cell treatment.	Serine	150-156	ataxia telangiectasia mutated	Mus musculus	19-22
15922113-4	2005	Interestingly, flavonoids with chemopreventative effects, such as quercetin, genistein, and epigallocatechin gallate activate ATM.	Flavonoids	15-25	ataxia telangiectasia mutated	Mus musculus	126-129
15735814-5	2005	Using ATM-deficient cells, ATM was shown to be required for early phosphorylation of serine 15 in response to MNNG, whereas catalytically inactive ATR selectively interfered with late phase serine 15 phosphorylation.	Serine	85-91	ataxia telangiectasia mutated	Mus musculus	27-30
15546863-8	2005	Further supporting these results, we also observed that biological responses tightly regulated by Akt, such as transcription factor of the forkhead family activity after insulin treatment or gamma-radiation response, were altered in cell lines derived from AT patients and knockout mice for ATM in which phosphorylation in serine 473 was almost abolished.	Serine	323-329	ataxia telangiectasia mutated	Mus musculus	291-294
15922113-4	2005	Interestingly, flavonoids with chemopreventative effects, such as quercetin, genistein, and epigallocatechin gallate activate ATM.	Quercetin	66-75	ataxia telangiectasia mutated	Mus musculus	126-129
15922113-4	2005	Interestingly, flavonoids with chemopreventative effects, such as quercetin, genistein, and epigallocatechin gallate activate ATM.	Genistein	77-86	ataxia telangiectasia mutated	Mus musculus	126-129
15694690-5	2005	Recently, we found that the ATM gene product (mutated in ataxia-telangiectasia, A-T), is required for cell survival and genomic stability maintenance following exposure to low labile iron concentrations.	Iron	183-187	ataxia telangiectasia mutated	Mus musculus	28-31
15922113-4	2005	Interestingly, flavonoids with chemopreventative effects, such as quercetin, genistein, and epigallocatechin gallate activate ATM.	epigallocatechin gallate	92-116	ataxia telangiectasia mutated	Mus musculus	126-129
15694690-6	2005	Iron chelators (desferal, quercetin, and apoferritin) also increase A-T cell genomic stability and viability, and activate ATM-dependent cellular events in normal cells.	Iron	0-4	ataxia telangiectasia mutated	Mus musculus	123-126
15922113-5	2005	Since ATM activates pathways which increase genomic stability, oxidant resistance, and/or telomere stability, and since many diseases of old age (i.e., cancer, cardiovascular and neurodegenerative disease), result from attenuation of these pathways, pharmacologic manipulation of ATM activity via flavonoid intake may prove useful in slowing the appearance of age-associated disease.	Flavonoids	297-306	ataxia telangiectasia mutated	Mus musculus	6-9
15694690-6	2005	Iron chelators (desferal, quercetin, and apoferritin) also increase A-T cell genomic stability and viability, and activate ATM-dependent cellular events in normal cells.	Deferoxamine	16-24	ataxia telangiectasia mutated	Mus musculus	123-126
15213104-3	2004	We tested this hypothesis by determining whether the well-described nitroxide antioxidant, tempol (4-hydroxy-2,2,6,6-tetramethylpiperidine-N-oxyl), acts as a chemopreventative agent in Atm mutant mice, a model of the human cancer prone syndrome ataxia-telangiectasia.	Hydroxylamine	68-77	ataxia telangiectasia mutated	Mus musculus	185-188
15694690-6	2005	Iron chelators (desferal, quercetin, and apoferritin) also increase A-T cell genomic stability and viability, and activate ATM-dependent cellular events in normal cells.	Quercetin	26-35	ataxia telangiectasia mutated	Mus musculus	123-126
15694690-8	2005	Based on this, we propose that iron chelators protect the substantia nigra pars compacta not only by chelating labile iron and reducing oxyradical formation, but also by inducing ATM activity, leading to increased oxidative stress resistance and DNA repair.	Iron	31-35	ataxia telangiectasia mutated	Mus musculus	179-182
15694690-9	2005	Support for this hypothesis comes from the recent observation that the iron chelating flavonoid quercetin both directly activates ATM and protects neuronal cells from the toxic effects of the N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine.	Iron	71-75	ataxia telangiectasia mutated	Mus musculus	130-133
15694690-9	2005	Support for this hypothesis comes from the recent observation that the iron chelating flavonoid quercetin both directly activates ATM and protects neuronal cells from the toxic effects of the N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine.	Flavonoids	86-95	ataxia telangiectasia mutated	Mus musculus	130-133
15694690-9	2005	Support for this hypothesis comes from the recent observation that the iron chelating flavonoid quercetin both directly activates ATM and protects neuronal cells from the toxic effects of the N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine.	Quercetin	96-105	ataxia telangiectasia mutated	Mus musculus	130-133
15694690-10	2005	Therefore since; (1) ATM is required for iron toxicity resistance, (2) iron chelators such as quercetin, desferal, and apoferritin induce ATM activity and/or ATM-dependent events, and (3), Atm-deficient mice preferentially lose dopaminergic nigro-striatal neurons, we propose that ATM activity has an important function in PD.	Iron	41-45	ataxia telangiectasia mutated	Mus musculus	21-24
15694690-10	2005	Therefore since; (1) ATM is required for iron toxicity resistance, (2) iron chelators such as quercetin, desferal, and apoferritin induce ATM activity and/or ATM-dependent events, and (3), Atm-deficient mice preferentially lose dopaminergic nigro-striatal neurons, we propose that ATM activity has an important function in PD.	Iron	71-75	ataxia telangiectasia mutated	Mus musculus	138-141
15694690-10	2005	Therefore since; (1) ATM is required for iron toxicity resistance, (2) iron chelators such as quercetin, desferal, and apoferritin induce ATM activity and/or ATM-dependent events, and (3), Atm-deficient mice preferentially lose dopaminergic nigro-striatal neurons, we propose that ATM activity has an important function in PD.	Iron	71-75	ataxia telangiectasia mutated	Mus musculus	138-141
15694690-10	2005	Therefore since; (1) ATM is required for iron toxicity resistance, (2) iron chelators such as quercetin, desferal, and apoferritin induce ATM activity and/or ATM-dependent events, and (3), Atm-deficient mice preferentially lose dopaminergic nigro-striatal neurons, we propose that ATM activity has an important function in PD.	Iron	71-75	ataxia telangiectasia mutated	Mus musculus	138-141
15694690-10	2005	Therefore since; (1) ATM is required for iron toxicity resistance, (2) iron chelators such as quercetin, desferal, and apoferritin induce ATM activity and/or ATM-dependent events, and (3), Atm-deficient mice preferentially lose dopaminergic nigro-striatal neurons, we propose that ATM activity has an important function in PD.	Quercetin	94-103	ataxia telangiectasia mutated	Mus musculus	21-24
15694690-10	2005	Therefore since; (1) ATM is required for iron toxicity resistance, (2) iron chelators such as quercetin, desferal, and apoferritin induce ATM activity and/or ATM-dependent events, and (3), Atm-deficient mice preferentially lose dopaminergic nigro-striatal neurons, we propose that ATM activity has an important function in PD.	Quercetin	94-103	ataxia telangiectasia mutated	Mus musculus	138-141
15694690-10	2005	Therefore since; (1) ATM is required for iron toxicity resistance, (2) iron chelators such as quercetin, desferal, and apoferritin induce ATM activity and/or ATM-dependent events, and (3), Atm-deficient mice preferentially lose dopaminergic nigro-striatal neurons, we propose that ATM activity has an important function in PD.	Quercetin	94-103	ataxia telangiectasia mutated	Mus musculus	138-141
15694690-10	2005	Therefore since; (1) ATM is required for iron toxicity resistance, (2) iron chelators such as quercetin, desferal, and apoferritin induce ATM activity and/or ATM-dependent events, and (3), Atm-deficient mice preferentially lose dopaminergic nigro-striatal neurons, we propose that ATM activity has an important function in PD.	Quercetin	94-103	ataxia telangiectasia mutated	Mus musculus	189-192
15694690-10	2005	Therefore since; (1) ATM is required for iron toxicity resistance, (2) iron chelators such as quercetin, desferal, and apoferritin induce ATM activity and/or ATM-dependent events, and (3), Atm-deficient mice preferentially lose dopaminergic nigro-striatal neurons, we propose that ATM activity has an important function in PD.	Quercetin	94-103	ataxia telangiectasia mutated	Mus musculus	138-141
15694690-10	2005	Therefore since; (1) ATM is required for iron toxicity resistance, (2) iron chelators such as quercetin, desferal, and apoferritin induce ATM activity and/or ATM-dependent events, and (3), Atm-deficient mice preferentially lose dopaminergic nigro-striatal neurons, we propose that ATM activity has an important function in PD.	Deferoxamine	105-113	ataxia telangiectasia mutated	Mus musculus	138-141
15694690-10	2005	Therefore since; (1) ATM is required for iron toxicity resistance, (2) iron chelators such as quercetin, desferal, and apoferritin induce ATM activity and/or ATM-dependent events, and (3), Atm-deficient mice preferentially lose dopaminergic nigro-striatal neurons, we propose that ATM activity has an important function in PD.	Deferoxamine	105-113	ataxia telangiectasia mutated	Mus musculus	138-141
15694690-10	2005	Therefore since; (1) ATM is required for iron toxicity resistance, (2) iron chelators such as quercetin, desferal, and apoferritin induce ATM activity and/or ATM-dependent events, and (3), Atm-deficient mice preferentially lose dopaminergic nigro-striatal neurons, we propose that ATM activity has an important function in PD.	Deferoxamine	105-113	ataxia telangiectasia mutated	Mus musculus	189-192
15694690-10	2005	Therefore since; (1) ATM is required for iron toxicity resistance, (2) iron chelators such as quercetin, desferal, and apoferritin induce ATM activity and/or ATM-dependent events, and (3), Atm-deficient mice preferentially lose dopaminergic nigro-striatal neurons, we propose that ATM activity has an important function in PD.	Deferoxamine	105-113	ataxia telangiectasia mutated	Mus musculus	138-141
15694690-11	2005	Furthermore, pharmacological manipulation of ATM activity via iron chelation might have clinical efficacy in PD treatment.	Iron	62-66	ataxia telangiectasia mutated	Mus musculus	45-48
15496926-4	2004	Atm-/- mice older than 24 weeks showed progressive bone marrow failure resulting from a defect in HSC function that was associated with elevated reactive oxygen species.	Reactive Oxygen Species	145-168	ataxia telangiectasia mutated	Mus musculus	0-3
15336622-5	2004	We also show that labile iron levels are significantly elevated in Atm-deficient mouse sera compared to syngeniec wild type mice.	Iron	25-29	ataxia telangiectasia mutated	Mus musculus	67-70
15213104-3	2004	We tested this hypothesis by determining whether the well-described nitroxide antioxidant, tempol (4-hydroxy-2,2,6,6-tetramethylpiperidine-N-oxyl), acts as a chemopreventative agent in Atm mutant mice, a model of the human cancer prone syndrome ataxia-telangiectasia.	tempol	91-97	ataxia telangiectasia mutated	Mus musculus	185-188
15213104-3	2004	We tested this hypothesis by determining whether the well-described nitroxide antioxidant, tempol (4-hydroxy-2,2,6,6-tetramethylpiperidine-N-oxyl), acts as a chemopreventative agent in Atm mutant mice, a model of the human cancer prone syndrome ataxia-telangiectasia.	tempol	99-145	ataxia telangiectasia mutated	Mus musculus	185-188
15010311-0	2004	Loss of ATM sensitizes against O6-methylguanine triggered apoptosis, SCEs and chromosomal aberrations.	O-(6)-methylguanine	31-47	ataxia telangiectasia mutated	Mus musculus	8-11
15289318-4	2004	We examined the effect of dietary supplementation with the thiol-containing antioxidant N-acetyl-l-cysteine (NAC) on levels of oxidative DNA damage and the frequency of DNA deletions in Atm-deficient (AT-mutated) mice.	Sulfhydryl Compounds	59-64	ataxia telangiectasia mutated	Mus musculus	186-189
15289318-6	2004	Furthermore, we found that Atm-deficient mice have significantly increased levels of 8-OH deoxyguanosine, an indication of oxidative DNA damage.	8-oh deoxyguanosine	85-104	ataxia telangiectasia mutated	Mus musculus	27-30
15289318-7	2004	Dietary supplementation with NAC significantly reduced 8-OH deoxyguanosine level and the frequency of DNA deletions in Atm-deficient mice.	Acetylcysteine	29-32	ataxia telangiectasia mutated	Mus musculus	119-122
15289318-9	2004	Our findings demonstrate that NAC counteracts genetic instability and suggest that genetic instability may be a consequence of oxidative stress in Atm-deficient mice.	Acetylcysteine	30-33	ataxia telangiectasia mutated	Mus musculus	147-150
15178448-3	2004	It was shown by biochemical fractionation procedure that PARP-1 as well as ATM increases at chromatin level after induction of DSB with neocarzinostatin (NCS).	Zinostatin	136-152	ataxia telangiectasia mutated	Mus musculus	75-78
15178448-3	2004	It was shown by biochemical fractionation procedure that PARP-1 as well as ATM increases at chromatin level after induction of DSB with neocarzinostatin (NCS).	Zinostatin	154-157	ataxia telangiectasia mutated	Mus musculus	75-78
14681204-2	2004	Normally, ATM is present as inactive dimers; however, in response to DSBs, the ATM dimer partners cross-phosphorylate each other on serine 1981, and kinase active ATM monomers are subsequently released.	Serine	132-138	ataxia telangiectasia mutated	Mus musculus	10-13
14681204-2	2004	Normally, ATM is present as inactive dimers; however, in response to DSBs, the ATM dimer partners cross-phosphorylate each other on serine 1981, and kinase active ATM monomers are subsequently released.	Serine	132-138	ataxia telangiectasia mutated	Mus musculus	79-82
14681204-2	2004	Normally, ATM is present as inactive dimers; however, in response to DSBs, the ATM dimer partners cross-phosphorylate each other on serine 1981, and kinase active ATM monomers are subsequently released.	Serine	132-138	ataxia telangiectasia mutated	Mus musculus	79-82
15010311-8	2004	This was more pronounced in ATM-/- than in ATM+/+ cells, suggesting that O6MeG is responsible, at least in part, for increased MNNG sensitivity of ATM-/- cells.	O-(6)-methylguanine	73-78	ataxia telangiectasia mutated	Mus musculus	28-31
15010311-8	2004	This was more pronounced in ATM-/- than in ATM+/+ cells, suggesting that O6MeG is responsible, at least in part, for increased MNNG sensitivity of ATM-/- cells.	O-(6)-methylguanine	73-78	ataxia telangiectasia mutated	Mus musculus	43-46
15010311-8	2004	This was more pronounced in ATM-/- than in ATM+/+ cells, suggesting that O6MeG is responsible, at least in part, for increased MNNG sensitivity of ATM-/- cells.	O-(6)-methylguanine	73-78	ataxia telangiectasia mutated	Mus musculus	43-46
15010311-10	2004	Also, a significant higher frequency of MNNG-induced chromosomal aberrations was observed in ATM-/- than in ATM+/+ cells when analysed at a late recovery time, which is consistent with O6MeG being the inducing lesion.	O-(6)-methylguanine	185-190	ataxia telangiectasia mutated	Mus musculus	93-96
12644952-6	2003	In Atm(-/-) mice, abundant positively stained spermatocytes were present, indicating an accumulation of non-repaired DSBs, suggesting the involvement of ATM in repair of meiotic DSBs.	dsbs	117-121	ataxia telangiectasia mutated	Mus musculus	3-6
14729946-3	2004	Serine 18 in murine p53 has been implicated in mediating an ATM- and ataxia telangiectasia-related kinase-dependent growth arrest.	Serine	0-6	ataxia telangiectasia mutated	Mus musculus	60-63
14673010-5	2003	An antioxidant (isoindoline nitroxide) prevented Purkinje cell death in Atm-deficient mice and enhanced dendritogenesis to wild-type levels.	isoindoline nitroxide	16-37	ataxia telangiectasia mutated	Mus musculus	72-75
12766154-3	2003	We showed that selenite-induced apoptosis as evidenced by cleavage of poly(ADP-ribose) polymerase was reduced in NIH 3T3 cells treated with ATM small interfering RNA, suggesting the involvement of the DNA damage regulator ATM.	Selenious Acid	15-23	ataxia telangiectasia mutated	Mus musculus	140-143
12766154-3	2003	We showed that selenite-induced apoptosis as evidenced by cleavage of poly(ADP-ribose) polymerase was reduced in NIH 3T3 cells treated with ATM small interfering RNA, suggesting the involvement of the DNA damage regulator ATM.	Selenious Acid	15-23	ataxia telangiectasia mutated	Mus musculus	222-225
12796033-6	2003	Loss of ATM function did not result in increased apoptosis, but resulted in increased Trypan Blue staining in response to epirubicin, suggesting that processes other than apoptosis may mediate cytotoxicity.	Trypan Blue	86-97	ataxia telangiectasia mutated	Mus musculus	8-11
12796033-6	2003	Loss of ATM function did not result in increased apoptosis, but resulted in increased Trypan Blue staining in response to epirubicin, suggesting that processes other than apoptosis may mediate cytotoxicity.	Epirubicin	122-132	ataxia telangiectasia mutated	Mus musculus	8-11
12644952-6	2003	In Atm(-/-) mice, abundant positively stained spermatocytes were present, indicating an accumulation of non-repaired DSBs, suggesting the involvement of ATM in repair of meiotic DSBs.	dsbs	178-182	ataxia telangiectasia mutated	Mus musculus	3-6
12644952-6	2003	In Atm(-/-) mice, abundant positively stained spermatocytes were present, indicating an accumulation of non-repaired DSBs, suggesting the involvement of ATM in repair of meiotic DSBs.	dsbs	178-182	ataxia telangiectasia mutated	Mus musculus	153-156
12496286-8	2003	The ATM protein is a multifunctional protein kinase, which serves as a master regulator of cellular responses to DSBs.	dsbs	113-117	ataxia telangiectasia mutated	Mus musculus	4-7
12598732-0	2003	Reduced NMDA-induced apoptosis in neurons lacking ataxia telangiectasia mutated protein.	N-Methylaspartate	8-12	ataxia telangiectasia mutated	Mus musculus	50-87
12598732-3	2003	NMDA-induced apoptosis was reduced in cultures derived from mice with targeted deletions in the ATM gene.	N-Methylaspartate	0-4	ataxia telangiectasia mutated	Mus musculus	96-99
12598732-4	2003	In addition, NMDA-induced caspase-3 activity was abolished in cultures lacking two functioning copies of the ATM gene.	N-Methylaspartate	13-17	ataxia telangiectasia mutated	Mus musculus	109-112
12598732-5	2003	These data provide evidence to suggest that, in primary cortical culture, NMDA-induced apoptosis is partially mediated through ATM.	N-Methylaspartate	74-78	ataxia telangiectasia mutated	Mus musculus	127-130
12946702-8	2003	In addition, an age-dependent as well as topographic, medial-to-lateral loss of GAD, met-enkephaline and substance-P immunopositive cells was found in the striatum of the Atm-/- mice.	met-enkephaline	85-100	ataxia telangiectasia mutated	Mus musculus	171-174
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	ataxia telangiectasia mutated	Mus musculus	74-77
12234978-0	2002	Prevention of thymic lymphoma development in Atm-/- mice by dexamethasone.	Dexamethasone	60-73	ataxia telangiectasia mutated	Mus musculus	45-48
12364740-0	2002	ATM gene regulates oxygen-glucose deprivation-induced nuclear factor-kappaB DNA-binding activity and downstream apoptotic cascade in mouse cerebrovascular endothelial cells.	Oxygen	19-25	ataxia telangiectasia mutated	Mus musculus	0-3
12364740-0	2002	ATM gene regulates oxygen-glucose deprivation-induced nuclear factor-kappaB DNA-binding activity and downstream apoptotic cascade in mouse cerebrovascular endothelial cells.	Glucose	26-33	ataxia telangiectasia mutated	Mus musculus	0-3
12364740-3	2002	We investigated the potential interaction of ATM and NF-kappaB after oxygen-glucose deprivation (OGD) in cerebral endothelial cells (CECs).	oxygen-glucose	69-83	ataxia telangiectasia mutated	Mus musculus	45-48
12364740-9	2002	ATM gene knockdown with the use of an antisense oligonucleotide suppressed OGD-induced ATM protein expression, which was accompanied by an attenuation of NF-kappaB activation and the subsequent expression of downstream genes, including the antiapoptotic gene c-IAP2.	Oligonucleotides	48-63	ataxia telangiectasia mutated	Mus musculus	0-3
12364740-9	2002	ATM gene knockdown with the use of an antisense oligonucleotide suppressed OGD-induced ATM protein expression, which was accompanied by an attenuation of NF-kappaB activation and the subsequent expression of downstream genes, including the antiapoptotic gene c-IAP2.	Oligonucleotides	48-63	ataxia telangiectasia mutated	Mus musculus	87-90
12234978-3	2002	We show here that in Atm-/- mice: (a) increased DNA synthesis occurs, especially in the immature CD4(-) CD8(-) (dominant negative) and CD8(+) thymocyte populations; (b) the relative percentage of dominant negative cells increases significantly during postnatal development, with a sharp peak at 4 weeks of age; and (c) dexamethasone suppresses DNA synthesis in these thymocytes and prevents thymic lymphoma development.	Dexamethasone	319-332	ataxia telangiectasia mutated	Mus musculus	21-24
12234978-5	2002	The results also show that dexamethasone, like ATM, checks DNA synthesis in developing thymocytes.	Dexamethasone	27-40	ataxia telangiectasia mutated	Mus musculus	47-50
12234978-6	2002	Finally, the data document for the first time that dexamethasone prevents or slows thymic lymphoma development in Atm-/- mice.	Dexamethasone	51-64	ataxia telangiectasia mutated	Mus musculus	114-117
11344081-2	2001	Using freshly isolated thymocytes from Atm-/- mice that were under stress during postnatal differentiation, we noted that thiol redox activity, as indicated by reduction of the tetrazolium MTS, and DNA turnover activity, as indicated by incorporation of [(3)H]thymidine into DNA, were both greatly increased compared with activities in thymocytes from Atm+/+ mice.	Sulfhydryl Compounds	122-127	ataxia telangiectasia mutated	Mus musculus	39-42
11679583-0	2002	Accumulation of DNA damage and reduced levels of nicotine adenine dinucleotide in the brains of Atm-deficient mice.	nicotine adenine dinucleotide	49-78	ataxia telangiectasia mutated	Mus musculus	96-99
11679583-6	2002	There is a significant decrease in both the reduced and the oxidized forms of NAD and in the total levels of NADP(T) and NADP(+) in the brains of Atm(-/-) mice.	NADP	109-113	ataxia telangiectasia mutated	Mus musculus	146-149
11679583-6	2002	There is a significant decrease in both the reduced and the oxidized forms of NAD and in the total levels of NADP(T) and NADP(+) in the brains of Atm(-/-) mice.	NADP	121-125	ataxia telangiectasia mutated	Mus musculus	146-149
11679583-7	2002	The changes in NAD(T), NADH, NAD(+), NADP(T), and NADP(+) were progressive and observed primarily in the cerebellum of 4-month-old Atm(-/-) mice.	nad(t)	15-21	ataxia telangiectasia mutated	Mus musculus	131-134
11679583-7	2002	The changes in NAD(T), NADH, NAD(+), NADP(T), and NADP(+) were progressive and observed primarily in the cerebellum of 4-month-old Atm(-/-) mice.	NAD	23-27	ataxia telangiectasia mutated	Mus musculus	131-134
11484785-10	2001	The results are compatible with the assumption that inhibition of the Atm-dependent homologous recombination repair by caffeine, brings differential effects in LY sublines because of the defect of the alternative DNA repair system (NHEJ) in LY-S cells.	Caffeine	119-127	ataxia telangiectasia mutated	Mus musculus	70-73
11484785-10	2001	The results are compatible with the assumption that inhibition of the Atm-dependent homologous recombination repair by caffeine, brings differential effects in LY sublines because of the defect of the alternative DNA repair system (NHEJ) in LY-S cells.	ly-s	241-245	ataxia telangiectasia mutated	Mus musculus	70-73
11679583-7	2002	The changes in NAD(T), NADH, NAD(+), NADP(T), and NADP(+) were progressive and observed primarily in the cerebellum of 4-month-old Atm(-/-) mice.	N-acetyldemethylphosphinothricin	37-44	ataxia telangiectasia mutated	Mus musculus	131-134
11679583-7	2002	The changes in NAD(T), NADH, NAD(+), NADP(T), and NADP(+) were progressive and observed primarily in the cerebellum of 4-month-old Atm(-/-) mice.	NADP	50-57	ataxia telangiectasia mutated	Mus musculus	131-134
11357953-9	2001	These data are the first demonstration of elevated levels of ROS in neurons at risk in any genetic neurodegenerative disorder and, furthermore, suggest that ATM acts as a pro-survival signal in post-mitotic Purkinje cells and dopaminergic neurons by modifying superoxide radical handling in these selectively vulnerable neurons.	Reactive Oxygen Species	61-64	ataxia telangiectasia mutated	Mus musculus	157-160
11357953-9	2001	These data are the first demonstration of elevated levels of ROS in neurons at risk in any genetic neurodegenerative disorder and, furthermore, suggest that ATM acts as a pro-survival signal in post-mitotic Purkinje cells and dopaminergic neurons by modifying superoxide radical handling in these selectively vulnerable neurons.	Superoxides	260-270	ataxia telangiectasia mutated	Mus musculus	157-160
11344081-9	2001	ATM may suppress abnormal DNA turnover and the resultant oncogenesis by regulating cellular thiol redox pathways.	Sulfhydryl Compounds	92-97	ataxia telangiectasia mutated	Mus musculus	0-3
11280737-7	2001	These changes are indicative of increased levels of reactive oxygen species, which are seen primarily in the cerebellum of Atm-deficient mice.	Reactive Oxygen Species	52-75	ataxia telangiectasia mutated	Mus musculus	123-126
10373558-1	1999	A-T (ataxia telangiectasia) individuals frequently display gonadal atrophy, and Atm-/- mice show spermatogenic failure due to arrest at prophase of meiosis I. Chromosomal movements take place during meiotic prophase, with telomeres congregating on the nuclear envelope to transiently form a cluster during the leptotene/zygotene transition (bouquet arrangement).	leptotene	310-319	ataxia telangiectasia mutated	Mus musculus	80-83
11158303-3	2001	Here we report that wortmannin, an irreversible inhibitor of phosphatidylinositol 3-kinase (PI-3K)-related PKs, including the catalytic subunit of DNA-dependent protein kinase (DNA-PK(CS)) and ATM, sensitizes normal murine lymphocytes to retrovirus-mediated cell killing.	Wortmannin	20-30	ataxia telangiectasia mutated	Mus musculus	193-196
11003672-7	2000	Bouquet spermatocytes with clustered telomeres were generally void of H1t signals, while mid-late pachytene and diplotene Atm(-/-) p53(-/-) spermatocytes displayed expression of H1t and showed telomeres dispersed over the nuclear periphery.	diplotene	112-121	ataxia telangiectasia mutated	Mus musculus	122-125
10717437-0	2000	Atm-deficient mice Purkinje cells show age-dependent defects in calcium spike bursts and calcium currents.	Calcium	64-71	ataxia telangiectasia mutated	Mus musculus	0-3
10717437-0	2000	Atm-deficient mice Purkinje cells show age-dependent defects in calcium spike bursts and calcium currents.	Calcium	89-96	ataxia telangiectasia mutated	Mus musculus	0-3
10717437-10	2000	In other mutant mice, calcium current deficits have been shown to be related to cell death.Our experiments suggest that the electrophysiological defects displayed by Atm-deficient mice are early predegenerative lesions and may be a precursor of Purkinje cell degeneration displayed by ataxia telangiectasia patients.	Calcium	22-29	ataxia telangiectasia mutated	Mus musculus	166-169
11035798-1	2000	Ser-15 of human p53 (corresponding to Ser-18 of mouse p53) is phosphorylated by ataxia-telangiectasia mutated (ATM) family kinases in response to ionizing radiation (IR) and UV light.	Serine	0-3	ataxia telangiectasia mutated	Mus musculus	80-109
11035798-1	2000	Ser-15 of human p53 (corresponding to Ser-18 of mouse p53) is phosphorylated by ataxia-telangiectasia mutated (ATM) family kinases in response to ionizing radiation (IR) and UV light.	Serine	0-3	ataxia telangiectasia mutated	Mus musculus	111-114
11035798-1	2000	Ser-15 of human p53 (corresponding to Ser-18 of mouse p53) is phosphorylated by ataxia-telangiectasia mutated (ATM) family kinases in response to ionizing radiation (IR) and UV light.	Serine	38-41	ataxia telangiectasia mutated	Mus musculus	80-109
11035798-1	2000	Ser-15 of human p53 (corresponding to Ser-18 of mouse p53) is phosphorylated by ataxia-telangiectasia mutated (ATM) family kinases in response to ionizing radiation (IR) and UV light.	Serine	38-41	ataxia telangiectasia mutated	Mus musculus	111-114
10910365-7	2000	ATM phosphorylates CtIP at serine residues 664 and 745, and mutation of these sites to alanine abrogates the dissociation of BRCA1 from CtIP, resulting in persistent repression of BRCA1-dependent induction of GADD45 upon ionizing radiation.	Serine	27-33	ataxia telangiectasia mutated	Mus musculus	0-3
10910365-7	2000	ATM phosphorylates CtIP at serine residues 664 and 745, and mutation of these sites to alanine abrogates the dissociation of BRCA1 from CtIP, resulting in persistent repression of BRCA1-dependent induction of GADD45 upon ionizing radiation.	Alanine	87-94	ataxia telangiectasia mutated	Mus musculus	0-3
10801416-1	2000	Checkpoints of DNA integrity are conserved throughout evolution, as are the kinases ATM (Ataxia Telangiectasia mutated) and ATR (Ataxia- and Rad-related), which are related to phosphatidylinositol (PI) 3-kinase [1] [2] [3].	Phosphatidylinositols	176-196	ataxia telangiectasia mutated	Mus musculus	84-118
10373558-1	1999	A-T (ataxia telangiectasia) individuals frequently display gonadal atrophy, and Atm-/- mice show spermatogenic failure due to arrest at prophase of meiosis I. Chromosomal movements take place during meiotic prophase, with telomeres congregating on the nuclear envelope to transiently form a cluster during the leptotene/zygotene transition (bouquet arrangement).	zygotene	320-328	ataxia telangiectasia mutated	Mus musculus	80-83
9510011-6	1998	The Lp values in the presence of dimethylsulphoxide (DMSO) were 0.77, 0.81, 0.94, 0.86, and 1.10 microm/min/atm, and the PDMSO values were 1.85, 2.04, 2.41, 1.95, and 1.25x10(-3) cm/min for oocytes, zygotes, 2, 4, and 8-cell embryos respectively.	Dimethyl Sulfoxide	33-51	ataxia telangiectasia mutated	Mus musculus	108-111
9770541-9	1998	Behaviorally, Atm-deficient mice expressed locomotor abnormalities manifested as stride-length asymmetry, which could be corrected by peripheral application of the dopaminergic precursor L-dopa.	Levodopa	187-193	ataxia telangiectasia mutated	Mus musculus	14-17
9510011-6	1998	The Lp values in the presence of dimethylsulphoxide (DMSO) were 0.77, 0.81, 0.94, 0.86, and 1.10 microm/min/atm, and the PDMSO values were 1.85, 2.04, 2.41, 1.95, and 1.25x10(-3) cm/min for oocytes, zygotes, 2, 4, and 8-cell embryos respectively.	Dimethyl Sulfoxide	53-57	ataxia telangiectasia mutated	Mus musculus	108-111
8226839-6	1993	Under basal conditions, there was a 2-fold increase in the biliary excretion of bilirubin-IX alpha monoglucuronides and total glucuronides in the AT1 and ATM mutants compared to the normal controls.	bilirubin-ix alpha monoglucuronides	80-115	ataxia telangiectasia mutated	Mus musculus	154-157
8226839-6	1993	Under basal conditions, there was a 2-fold increase in the biliary excretion of bilirubin-IX alpha monoglucuronides and total glucuronides in the AT1 and ATM mutants compared to the normal controls.	Glucuronides	103-115	ataxia telangiectasia mutated	Mus musculus	154-157
34965965-8	2022	In contrast, the incidence of biallelic Igkappa expression is not elevated by inactivation of the SpiC transcriptional repressor, which is induced by RAG DSBs in an ATM-dependent manner and suppresses Igk accessibility.	rag dsbs	150-158	ataxia telangiectasia mutated	Mus musculus	165-168
34958116-6	2022	Furthermore, ACY-1215 displayed a synergistic effect with specific inhibitors of ATM, an activator of Akt, in inducing cancer cell apoptosis and inhibiting their motility.	ricolinostat	13-21	ataxia telangiectasia mutated	Mus musculus	81-84
34958116-8	2022	Collectively, our results demonstrated that ACY-1215 is a novel chemotherapeutic agent that could restore mutant p53 function in cancer cells with strong antitumor activity, either alone or in combination with inhibitors of the ATM protein kinase.	ricolinostat	44-52	ataxia telangiectasia mutated	Mus musculus	228-231
34715501-8	2021	Furthermore, pretreatment with the ATM inhibitor KU55933 could reduce the occurrence of autophagy and mitigate testicular toxicity of MC-LR through inhibiting the activation of the ATM/p53 pathway.	cyanoginosin LR	134-139	ataxia telangiectasia mutated	Mus musculus	35-38
34715501-0	2021	The activated ATM/p53 pathway promotes autophagy in response to oxidative stress-mediated DNA damage induced by Microcystin-LR in male germ cells.	cyanoginosin LR	112-126	ataxia telangiectasia mutated	Mus musculus	14-17
34715501-8	2021	Furthermore, pretreatment with the ATM inhibitor KU55933 could reduce the occurrence of autophagy and mitigate testicular toxicity of MC-LR through inhibiting the activation of the ATM/p53 pathway.	cyanoginosin LR	134-139	ataxia telangiectasia mutated	Mus musculus	181-184
34715501-8	2021	Furthermore, pretreatment with the ATM inhibitor KU55933 could reduce the occurrence of autophagy and mitigate testicular toxicity of MC-LR through inhibiting the activation of the ATM/p53 pathway.	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	49-56	ataxia telangiectasia mutated	Mus musculus	35-38
34715501-8	2021	Furthermore, pretreatment with the ATM inhibitor KU55933 could reduce the occurrence of autophagy and mitigate testicular toxicity of MC-LR through inhibiting the activation of the ATM/p53 pathway.	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	49-56	ataxia telangiectasia mutated	Mus musculus	181-184
34715501-9	2021	These results indicate that MC-LR-induced oxidative stress can activate the DNA damage-mediated ATM/p53 signalling pathway to induce autophagy in male germ cells.	cyanoginosin LR	28-33	ataxia telangiectasia mutated	Mus musculus	96-99
34680909-0	2021	Isorhamnetin Promotes 53BP1 Recruitment through the Enhancement of ATM Phosphorylation and Protects Mice from Radiation Gastrointestinal Syndrome.	3-methylquercetin	0-12	ataxia telangiectasia mutated	Mus musculus	67-70
34844627-12	2021	In addition, HCQ activated ATM to enhance HR repair, a high-fidelity repair for DNA double-strand breaks (DSBs) in cells, while BKM120 inhibited HR repair by blocking the phosphorylation of ATM and the expression of BRCA1/2 and Rad51.	Hydroxychloroquine	13-16	ataxia telangiectasia mutated	Mus musculus	27-30
34844627-12	2021	In addition, HCQ activated ATM to enhance HR repair, a high-fidelity repair for DNA double-strand breaks (DSBs) in cells, while BKM120 inhibited HR repair by blocking the phosphorylation of ATM and the expression of BRCA1/2 and Rad51.	Hydroxychloroquine	13-16	ataxia telangiectasia mutated	Mus musculus	190-193
34844627-12	2021	In addition, HCQ activated ATM to enhance HR repair, a high-fidelity repair for DNA double-strand breaks (DSBs) in cells, while BKM120 inhibited HR repair by blocking the phosphorylation of ATM and the expression of BRCA1/2 and Rad51.	NVP-BKM120	128-134	ataxia telangiectasia mutated	Mus musculus	190-193
34803506-6	2021	Additionally, KU-55933, a specific inhibitor of ataxia-telangiectasia mutated (ATM) was utilized in vivo and in vitro to explore the role of ATM in regulating MAD2B.	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	14-22	ataxia telangiectasia mutated	Mus musculus	48-77
34803506-6	2021	Additionally, KU-55933, a specific inhibitor of ataxia-telangiectasia mutated (ATM) was utilized in vivo and in vitro to explore the role of ATM in regulating MAD2B.	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	14-22	ataxia telangiectasia mutated	Mus musculus	79-82
33517789-10	2021	Real-time RT-PCR demonstrated that matrine could significantly reduce the expression of AKT1, TP53, TNF, IL6 and ATM in mice with liver injury or lung injury (P < 0.05), and increase the expression of BCL2L1 to a certain extent (P > 0.05).	matrine	35-42	ataxia telangiectasia mutated	Mus musculus	113-116
34680909-4	2021	Although isorhamnetin moderated p53 activity, it promoted phosphorylation of ataxia telangiectasia mutated (ATM) and enhanced 53BP1 recruitment in irradiated cells.	3-methylquercetin	9-21	ataxia telangiectasia mutated	Mus musculus	77-106
34680909-4	2021	Although isorhamnetin moderated p53 activity, it promoted phosphorylation of ataxia telangiectasia mutated (ATM) and enhanced 53BP1 recruitment in irradiated cells.	3-methylquercetin	9-21	ataxia telangiectasia mutated	Mus musculus	108-111
34680909-5	2021	The radioprotective effect of isorhamnetin was not observed in the presence of ATM inhibitor, indicating that its protective effect was dependent on ATM.	3-methylquercetin	30-42	ataxia telangiectasia mutated	Mus musculus	149-152
34680909-7	2021	These findings suggested that isorhamnetin enhances the ATM-dependent DNA repair process, which is presumably associated with the suppressive effect against GI syndrome.	3-methylquercetin	30-42	ataxia telangiectasia mutated	Mus musculus	56-59
34548492-0	2021	NAD+ augmentation with nicotinamide riboside improves lymphoid potential of Atm-/- and old mice HSCs.	NAD	0-4	ataxia telangiectasia mutated	Mus musculus	76-79
34685500-8	2021	We further show that class 1 HDAC activity promotes the hydroxyurea-induced activation of the checkpoint kinase ataxia-telangiectasia mutated (ATM).	Hydroxyurea	56-67	ataxia telangiectasia mutated	Mus musculus	143-146
34548492-0	2021	NAD+ augmentation with nicotinamide riboside improves lymphoid potential of Atm-/- and old mice HSCs.	nicotinamide-beta-riboside	23-44	ataxia telangiectasia mutated	Mus musculus	76-79
34408079-6	2021	We demonstrated that induction of telomere dysfunction resulted in ATM activation that, in turn, conferred resistance to temozolomide + SN-38 (4.2-fold change in IC50, P < 0.001).	Temozolomide	121-133	ataxia telangiectasia mutated	Mus musculus	67-70
34749877-14	2021	CONCLUSION: IL-17 antibody may reduce the secretion of ATM inflammatory factors by inhibiting the polarization of ATM to M1 type, thus improving the inflammation of adipose tissue in BPA-infected HFD-fed mice.	bisphenol A	183-186	ataxia telangiectasia mutated	Mus musculus	55-58
34749877-14	2021	CONCLUSION: IL-17 antibody may reduce the secretion of ATM inflammatory factors by inhibiting the polarization of ATM to M1 type, thus improving the inflammation of adipose tissue in BPA-infected HFD-fed mice.	bisphenol A	183-186	ataxia telangiectasia mutated	Mus musculus	114-117
34329458-9	2021	Overall, our work identifies novel biomarkers of ATRi efficacy in ATM-proficient and ATM-deficient cells, and highlights transcription-associated replication stress as a predominant driver of ATRi-induced cell death.	A-tri	49-53	ataxia telangiectasia mutated	Mus musculus	66-69
34329458-9	2021	Overall, our work identifies novel biomarkers of ATRi efficacy in ATM-proficient and ATM-deficient cells, and highlights transcription-associated replication stress as a predominant driver of ATRi-induced cell death.	A-tri	49-53	ataxia telangiectasia mutated	Mus musculus	85-88
34408079-6	2021	We demonstrated that induction of telomere dysfunction resulted in ATM activation that, in turn, conferred resistance to temozolomide + SN-38 (4.2-fold change in IC50, P < 0.001).	Irinotecan	136-141	ataxia telangiectasia mutated	Mus musculus	67-70
34408079-7	2021	ATM knockdown (shRNA) or inhibition using a clinical-stage small-molecule inhibitor (AZD0156) reversed resistance to temozolomide + irinotecan in ALT neuroblastoma cell lines in vitro (P < 0.001) and in four ALT xenografts in vivo (EFS, P < 0.0001).	Temozolomide	117-129	ataxia telangiectasia mutated	Mus musculus	0-3
34408079-7	2021	ATM knockdown (shRNA) or inhibition using a clinical-stage small-molecule inhibitor (AZD0156) reversed resistance to temozolomide + irinotecan in ALT neuroblastoma cell lines in vitro (P < 0.001) and in four ALT xenografts in vivo (EFS, P < 0.0001).	Irinotecan	132-142	ataxia telangiectasia mutated	Mus musculus	0-3
34376666-4	2021	Levels of R2TP substrates decreased, with strong effects on mTOR, ATM and ATR.	r2tp	10-14	ataxia telangiectasia mutated	Mus musculus	66-69
34180140-10	2021	These results indicated that ACY1215 exhibited hepatoprotective properties, which was associated with the inhibition of NLRP3 inflammasome, and this effect of ACY1215 was connected with upregulation of the ATM/F-actin mediated signalling pathways.	ricolinostat	29-36	ataxia telangiectasia mutated	Mus musculus	206-209
34180140-10	2021	These results indicated that ACY1215 exhibited hepatoprotective properties, which was associated with the inhibition of NLRP3 inflammasome, and this effect of ACY1215 was connected with upregulation of the ATM/F-actin mediated signalling pathways.	ricolinostat	159-166	ataxia telangiectasia mutated	Mus musculus	206-209
34180140-0	2021	HDAC6 inhibitor ACY1215 inhibits the activation of NLRP3 inflammasome in acute liver failure by regulating the ATM/F-actin signalling pathway.	ricolinostat	16-23	ataxia telangiectasia mutated	Mus musculus	111-114
34360715-6	2021	The ATM-mediated negative feedback control over SPO11 was lost and, consequently, the repair pathway of DSBs was highly affected in PRMT1 deficient male germ cells.	dsbs	104-108	ataxia telangiectasia mutated	Mus musculus	4-7
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	ataxia telangiectasia mutated	Mus musculus	57-60
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	ataxia telangiectasia mutated	Mus musculus	4-7
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	ataxia telangiectasia mutated	Mus musculus	54-57
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	ataxia telangiectasia mutated	Mus musculus	4-7
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	ataxia telangiectasia mutated	Mus musculus	54-57
34197485-3	2021	GWAS identified SNPs associated with metformin treatment success at a locus containing the NPAT (nuclear protein, ataxia-telangiectasia locus) and ATM (ataxia-telangiectasia mutated) genes.	Metformin	37-46	ataxia telangiectasia mutated	Mus musculus	147-181
34301812-0	2021	ATM/NEMO signaling modulates the expression of PD-L1 following docetaxel chemotherapy in prostate cancer.	Docetaxel	63-72	ataxia telangiectasia mutated	Mus musculus	0-3
34301812-12	2021	CONCLUSIONS: Our findings have revealed that a previously unrecognized ATM-NEMO signaling which induced by DTX is capable of suppressing tumor immunity by activating the expression of PD-L1, suggesting that the ATM-NEMO-NF-kappaB axis can be exploited to restore the immune balance and overcome cancer resistance triggered by DTX.Graphic Abstract: supplementary file 1.	Digitoxigenin	107-110	ataxia telangiectasia mutated	Mus musculus	71-74
34301812-12	2021	CONCLUSIONS: Our findings have revealed that a previously unrecognized ATM-NEMO signaling which induced by DTX is capable of suppressing tumor immunity by activating the expression of PD-L1, suggesting that the ATM-NEMO-NF-kappaB axis can be exploited to restore the immune balance and overcome cancer resistance triggered by DTX.Graphic Abstract: supplementary file 1.	Digitoxigenin	326-329	ataxia telangiectasia mutated	Mus musculus	71-74
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	ataxia telangiectasia mutated	Mus musculus	100-137
35608750-10	2022	5-fluorouracil induces the phosphorylation of KAP1, a target of the checkpoint kinase ataxia-telangiectasia mutated (ATM), stronger in HDAC2-negative cells than in their HDAC2-positive counterparts.	Fluorouracil	0-14	ataxia telangiectasia mutated	Mus musculus	117-120
35499079-10	2022	Therefore, these studies demonstrated that an ATM COX-2/PGE2/EP4 axis plays an important role in inhibiting adipose tissue dysfunction.	Dinoprostone	56-60	ataxia telangiectasia mutated	Mus musculus	46-49
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	ataxia telangiectasia mutated	Mus musculus	139-142
35218776-13	2022	In summary, moderate l-lactate administration suppresses ATM proinflammatory M1 polarization through activation of the GPR132-PKA-AMPKalpha1 signaling pathway to improve insulin resistance in HFD-fed mice, suggesting a new therapeutic and interventional approach to obesity-associated type 2 diabetes.	L-lactate	21-30	ataxia telangiectasia mutated	Mus musculus	57-60
35436937-9	2022	Correspondingly, the expressions of Nrf2, Atm, Atr, and Prkdc in IVM oocytes were markedly increased, following the inhibition of mTORC1 pathway by 10 nM rapamycin.	Sirolimus	154-163	ataxia telangiectasia mutated	Mus musculus	42-45
35530159-8	2022	These novel findings reveal shikonin as a pan DDR inhibitor and identify ATM as a primary factor in determining the chemo sensitizing effect of shikonin.	shikonin	144-152	ataxia telangiectasia mutated	Mus musculus	73-76
35530159-9	2022	Our data may facilitate the development of shikonin and its derivatives as potential chemotherapy sensitizers through inducing ATM degradation.	shikonin	43-51	ataxia telangiectasia mutated	Mus musculus	127-130
35530159-7	2022	Overexpression of ATM significantly mitigated DDR inhibition and cell death induced by shikonin and chemotherapeutic drugs.	shikonin	87-95	ataxia telangiectasia mutated	Mus musculus	18-21
35154904-1	2022	DNA damage by genotoxic drugs such as gemcitabine and 5-fluorouracil (5-FU) activates the ataxia telangiectasia, mutated (ATM)-Chk pathway and induces the expression of NKG2D ligands such as the MHC class I-related chain A and B (MICA/B).	gemcitabine	38-49	ataxia telangiectasia mutated	Mus musculus	122-125
35530159-0	2022	Chemical screen identifies shikonin as a broad DNA damage response inhibitor that enhances chemotherapy through inhibiting ATM and ATR.	shikonin	27-35	ataxia telangiectasia mutated	Mus musculus	123-126
35530159-7	2022	Overexpression of ATM significantly mitigated DDR inhibition and cell death induced by shikonin and chemotherapeutic drugs.	ddr	46-49	ataxia telangiectasia mutated	Mus musculus	18-21
35198439-9	2022	We performed immunoblotting of H2AX and ATM to assess DNA damage after treatment with DC10 and radiotherapy.	dc10	86-90	ataxia telangiectasia mutated	Mus musculus	40-43
35154904-1	2022	DNA damage by genotoxic drugs such as gemcitabine and 5-fluorouracil (5-FU) activates the ataxia telangiectasia, mutated (ATM)-Chk pathway and induces the expression of NKG2D ligands such as the MHC class I-related chain A and B (MICA/B).	Fluorouracil	54-68	ataxia telangiectasia mutated	Mus musculus	122-125
35154904-1	2022	DNA damage by genotoxic drugs such as gemcitabine and 5-fluorouracil (5-FU) activates the ataxia telangiectasia, mutated (ATM)-Chk pathway and induces the expression of NKG2D ligands such as the MHC class I-related chain A and B (MICA/B).	Fluorouracil	70-74	ataxia telangiectasia mutated	Mus musculus	122-125
35154904-1	2022	DNA damage by genotoxic drugs such as gemcitabine and 5-fluorouracil (5-FU) activates the ataxia telangiectasia, mutated (ATM)-Chk pathway and induces the expression of NKG2D ligands such as the MHC class I-related chain A and B (MICA/B).	mica	230-234	ataxia telangiectasia mutated	Mus musculus	122-125
35154904-4	2022	Inhibition of the ATM-Chk pathway blocks genotoxic drug-induced uric acid production, TGF-beta-activated kinase 1 (TAK1) activation, ERK phosphorylation, and MICA/B expression.	Uric Acid	64-73	ataxia telangiectasia mutated	Mus musculus	18-21