ライフサイエンスコーパス: ATM

1 ATM is a central mediator of response for cellular DNA d

2 ATM is a DDR kinase that has a central role in coordinat

3 ATM is a serine/threonine protein kinase that is recruit

4 ATM is activated via the MRE11-RAD50-NBS1 (MRN) complex

5 ATM kinase is a tumor suppressor and a master regulator

6 ATM localizes to the nucleus and at the plasma membrane,

7 ATM loss altered DDR signaling, but did not directly imp

8 ATM loss occurs in a subset of prostate tumors.

9 ATM orchestrates the DDR by modulating the expression of

10 ATM phosphorylates multiple residues near the RING domai

11 ATM was inhibited through pharmacologic and genetic stra

12 ATM(-/-) DLBCL cells have decreased apoptosis in contras

13 ATM-deficient microglia adopt an active phenotype that i

14 , BRCA2 (3.1%), CHEK 2 (1.6%), PALB2 (1.0%), ATM (0.7%), and NBN (0.4%); in patients with ovarian can

15 most common (23%), followed by SF3B1 (16%), ATM (13%), and TP53 (10%).

16 tions affecting TP53 (n = 3), CHEK2 (n = 2), ATM (n = 2), and BRCA1, BRCA2, PALB2, MSH2, MSH6, NBN, F

17 en percent had mutations in PALB2, sBRCA1/2, ATM, or CHEK2.

18 A n = 2, POLG n = 1, FXN n = 4, ATXN2 n = 3, ATM n = 3, GAN n = 2, SPG7 n = 1, ZFYVE26 n = 1, FH n =

19 %) and DDR gene defects (BRCA2 7%; CDK12 5%; ATM 4%) were commonly detected.

20 These drugs commonly activate ATM, ATR and DNA-PKcs.

21 erates reactive oxygen species that activate ATM.

22 Activated ATM rapidly phosphorylates a vast number of substrates i

23 lation of DSBs mediated through Rv activates ATM-Chk2 pathway of DNA damage response (DDR) signaling,

24 vation of ATM without consistently affecting ATM protein stability and recruitment.

25 Tumor immunogenicity was evaluated after ATM inhibition alone and in combination with radiation b

26 loss of heterozygosity in lung tumors among ATM L2307F allele carriers.

27 Furthermore, an ATM kinase inhibitor increased C-NHEJ-mediated rearrange

28 We find a large-effect association with an ATM L2307F (rs56009889) mutation in adenocarcinoma for d

29 CHEK2 (1.4%), BRIP1 (0.9%), MSH2 (0.8%), and ATM (0.6%).

30 ses, ataxia telangiectasia mutated (ATM) and ATM and Rad3-related kinase (ATR), work together as apic

31 echanism that involved activation of ATR and ATM and induction of NF-kB recruitment to the HEXIM1 pro

32 BKPyV activates the DDR through the ATR and ATM pathways and how this prevents DNA damage and leads

33 y employed in the translation of the ATR and ATM Ser/Thr kinases, thereby establishing SLFN11 as a no

34 eprotection, regulated by TRF2, Aurora B and ATM.

35 68%, DNA damage repair genes (eg, BRCA2 and ATM) in 60%, and phosphatidylinositol 3-kinase/mitogen-a

36 monly identified in CHEK2, BRCA1, BRCA2, and ATM.

37 ell-cycle response following DNA damage, and ATM alterations are present in approximately 5% of advan

38 infection with Mtb led to sustained DSBs and ATM activation during chronic phase of tuberculosis.

39 anticancer agents, as functions of KAP1 and ATM are tightly linked to cancer.

40 We irradiate fibroblasts, lymphoblasts, and ATM-deficient fibroblasts with 5 Gy X-rays and perform H

41 he intricate interactions between miRNAs and ATM.

42 Three of the genes (MRE11, NBN and ATM) encode components of the MRN-ATM pathway, which lim

43 in protecting chromosome ends from NHEJ and ATM activation, but that other mechanisms are involved.

44 ifferences in the contribution of C-NHEJ and ATM kinase inhibition influence these rearrangements.

45 e, and mutations in BRCA1, BRCA2, PALB2, and ATM genes.

46 wns, we show that activation of DNA-PKcs and ATM by chemotherapeutic drugs promotes NF-kappaB activit

47 DNA-PKcs and ATM link now epistatically to resection and their inhibi

48 Consequently, recruitment of TIP60 and ATM, two key proximal HDR factors, is substantially impa

49 DNA repair pathway (deletion 17p, TP53, and ATM SNVs), and MYC (translocations or copy number variat

50 repair genes, with broader testing, such as ATM, for clinical trial eligibility.

51 ation of so-called crown-like structures, as ATMs accumulate around dying adipocytes, and the occurre

52 ific shRNAs, or chemical inhibitors for ATR, ATM, and/or DNA-PK.

53 gets within synthetic lethality, (PARP, ATR, ATM, DNA-PKcs, WEE1, CDK12, RAD51, RAD52, and PD-1) and

54 s from genomic DNA and the activation of ATR/ATM DNA damage kinase signaling.

55 lishing BRAF or IKKalpha activity attenuates ATM, Chk1, MDC1, Kap1, and 53BP1 phosphorylation, compro

56 Because ATM is an apical kinase in the radiation-induced DNA dam

57 point, because the difference in CSS between ATM/BRCA1/BRCA2/PALB2 carriers and noncarriers was not s

58 This suggests an interaction between ATM and the electron transfer chain in the mitochondria,

59 describe dose-dependent interactions between ATM, ATR and DNA-PKcs revealing unknown mechanistic unde

60 The relationship between ATM and redox stress sensing was further evidenced as we

61 nd validated an inverse relationship between ATM and SIRT3 expression.

62 in solely accelerates lymphomagenesis beyond ATM loss.

63 response to rDNA breaks is dependent on both ATM and ATR activity.

64 rriers, with consideration in HOXB13, BRCA1, ATM, and mismatch repair carriers.

65 POLB, BRCA2, EXO1, ERCC6, ATR, RBBP8, BRCA1, ATM, JAG1, XPC, and POLE in Caucasians.

66 us, in addition to governing SPO11 breakage, ATM and PRDM9 are critical local regulators of mammalian

67 ora B kinase- and kinetochore-dependent, but ATM/ATR-independent manner.

68 1/VCIP135 is phosphorylated and activated by ATM/ATR.

69 y of ICB in pancreatic cancer is enhanced by ATM inhibition and further potentiated by radiation as a

70 ts in DNA double-strand breaks, indicated by ATM kinase activation and 53BP1 foci induction.

71 Phosphorylation of MDM2 by ATM upon DNA damage is an important mechanism for deregu

72 l shuttle factor UBQLN4 is phosphorylated by ATM and interacts with ubiquitylated MRE11 to mediate ea

73 In addition, USP52 is phosphorylated by ATM at Ser-1003 after DNA damage, which enhances the cat

74 heckpoint that is epistatically regulated by ATM and ATR operating as an integrated module.

75 tain genomic stability, and are regulated by ATM/ATR-mediated signaling pathways that are conserved f

76 Causatively, ATM dysfunction results in the accumulation of DNA in th

77 Instead of the classical ATM-Chk2 DDR, Mtb gains survival advantage through ATM-A

78 Furthermore, combining ATM inhibition and radiotherapy amplifies type I IFN sig

79 y functionally characterizes the most common ATM missense mutation R3008H in cancer and identifies a

80 xenograft and PDX mouse models with complete ATM loss.

81 echanism of interaction of the lead compound ATM-3507 with Tpm3.1-containing actin filaments.

82 However, compromised ATM signaling is a common characteristic of tumor cells,

83 Conversely, ATM was required for efficient entry into S phase and to

84 damage foci, indicating that PRD coordinates ATM activation with its exchange at DNA-breaks.

85 by oxidative stress, but not by DNA damage, ATM phosphorylates NRF1.

86 This study shows that deleting ATM in prostate cancer models does not significantly inc

87 Strikingly, at low IR-doses, ATM and ATR epistatically regulate also resection, and i

88 s in tumour genes that can be evaluated (eg, ATM and DAXX) are limited to pancreatic NETs and are mos

89 ctors (CSF2, IL-6, TNF, HGF, VEGF, and EGF), ATM and p53 signaling pathways.

90 In conclusion, loss of either ATM or adipocyte APC function, but not both, improves sy

91 Compound 17 engages ATM kinase and shows robust dose-dependent inhibition of

92 Evaluating ATM phenotype and intracellular metabolism together may

93 ), an ufmylation E3 ligase, is important for ATM activation.

94 d weight cycling reveal additional roles for ATMs in systemic metabolism.

95 horylation of PRD-4 by a PI3KK distinct from ATM and ATR.

96 and oxidative phosphorylation, distinct from ATM from lean mice.

97 Furthermore, ATM loss did not significantly impact sensitivity to PAR

98 Furthermore, ATM phosphorylates UFL1 at serine 462, enhancing UFL1 E3

99 nts in 9 breast cancer predisposition genes (ATM, BRCA1, BRCA2, CDH1, CHEK2, NF1, PALB2, PTEN, and TP

100 air genes including direct DNA repair genes (ATM, ATR, BRCA1, BRCA2, FANCA, FANCD2, MLH1, MSH2, MSH6,

101 s that induce low DSB-numbers in the genome, ATM and ATR regulate epistatically the G(2)-checkpoint,

102 co-polymerization of Tpm3.1 with actin, (3)H-ATM-3507 is incorporated into the filaments and saturate

103 In contrast, (3)H-ATM-3507 is poorly incorporated into preformed Tpm3.1/ac

104 own that the C-terminal FATC domain of human ATM (hATMfatc) can interact with a range of membrane mim

105 Biochemical studies with human ATM and genetic studies in yeast suggest that recruitmen

106 ion occurred both in hypoxic and non-hypoxic ATM suggesting that both hypoxic and pseudohypoxic stimu

107 Increased activation of HIF-1alpha in ATM of obese visceral adipose tissue resulted in inducti

108 in vitro, leading to selective cell death in ATM-deficient cells.

109 ons in TRF2-depleted cells due to defects in ATM-dependent checkpoint signaling and that SMCHD1 media

110 with RAD50, fibroblast strains deficient in ATM or NBN did not show a significant slowing of mitotic

111 ique role of PI3-kinase regulatory domain in ATM activation.

112 activate HIF-1alpha and its target genes in ATM during diet-induced obesity.

113 nding of combined PARP and ATR inhibition in ATM-deficient models, and support the clinical developme

114 Notably, suppressor mutations in ATM-mutant backgrounds are different to those in BRCA1-m

115 thening after irradiation is not observed in ATM deficient fibroblasts and may indicate the presence

116 glutamate receptor and glutamine pathways in ATM deficient background compared to WT-ATM DLBCL cells.

117 Accordingly, suboptimal GC responses in ATM-deficient animals are characterized by decreased tit

118 resses miR-181c in hepatocytes, resulting in ATM activation and apoptosis inhibition for promotion of

119 Selectively in ATM-knockout cells, we show that combined olaparib/AZD67

120 several variants of unknown significance in ATM, BRCA1, MSH2, SLX4, ERCC, and various FANC genes wer

121 dings implicate germline genetic variants in ATM with lung cancer susceptibility and suggest KIAA0930

122 Radiation therapy should not be withheld in ATM carriers.

123 sulted in down-regulation of several miRs in ATMs, including the miR-466 family and miR-762.

124 r harboring molecular aberrations, including ATM loss and an ARID1A mutation, achieved RECISTv1.1 com

125 Exogenous expression of miR-181c inhibited ATM expression and activation of its downstream molecule

126 Expression of kinase-dead (KD) ATM protein solely accelerates lymphomagenesis beyond AT

127 phosphatidylinositol 3-kinase-related kinase ATM to cause phosphorylation of the heterochromatin enfo

128 Deletion of the DNA repair kinase ATM, on the other hand, stimulated HF-NHEJ and suppresse

129 ' exonuclease, but the DSB-responsive kinase ATM proved a key regulator of both initiation and extens

130 taxia-Telangiectasia mutated protein kinase (ATM) is associated with neurological, metabolic and card

131 ngly, the inactivation of checkpoint kinases ATM and CHK2 has no mutagenic consequences.

132 upon the infection, and basophilic kinases, ATM, and ATR engaging later.

133 While the role of adipose tissue macrophage (ATM) pro-inflammatory signalling in the development of i

134 hat characterize adipose tissue macrophages (ATM) in obesity are poorly defined.

135 d by an increasing number of AT macrophages (ATMs) and linked to type 2 diabetes.

136 upon systemic energy status, AT macrophages (ATMs) must adapt phenotypically and metabolically.

137 on of mRNA for DNA damage response mediators ATM, 53BP1, and MDC1.

138 r ampicillin, tobramycin, and metronidazole (ATM).

139 he homologous chromosome (at FH, NBN, MRE11, ATM, SH2B3 and TM2D3).

140 fructokinase), DNA repair molecules (MRE11A, ATM), regulators of protein trafficking (NMT1), and the

141 1, NBN and ATM) encode components of the MRN-ATM pathway, which limits cell division after DNA damage

142 Multiple ATM populations exist along the M2 to M1 continuum and a

143 horylation by ataxia telangiectasia mutated (ATM) and ataxia telangiectasia mutated and RAD3-related

144 diated by the ataxia-telangiectasia mutated (ATM) and ataxia-telangiectasia mutated and Rad3-related

145 ated kinases, ataxia telangiectasia mutated (ATM) and ATM and Rad3-related kinase (ATR), work togethe

146 phagy through ataxia-telangiectasia mutated (ATM) and cell cycle checkpoint kinase 2 (CHK2), a DNA da

147 identify that ataxia-telangiectasia mutated (ATM) and RNF8 regulate rapid chromatin decompaction at D

148 activation of Ataxia-telangiectasia mutated (ATM) gene results in an increased risk to develop cancer

149 horylation of ataxia-telangiectasia mutated (ATM) is the initial step in the DNA damage response and

150 ype cells and ataxia telangiectasia mutated (ATM) patient cells.

151 The ataxia-telangiectasia mutated (ATM) protein kinase is widely known for its function as

152 expression of Ataxia Telangiectasia Mutated (ATM) protein within melanocytes in anagen hair follicle

153 uggested that ataxia-telangiectasia mutated (ATM) protein, a protein kinase, is a direct target of mi

154 t Ser(384) by ataxia telangiectasia mutated (ATM) serine/threonine kinase, and this phosphorylation i

155 expression of ataxia-telangiectasia mutated (ATM), and exhibited multiple mitotic defects.

156 ctors phospho-ataxia-telangiectasia mutated (ATM), phospho-53BP1, gammaH2AX and neuronal apoptosis.

157 cts activated ataxia-telangiectasia mutated (ATM)-mediated DNA damage repair signaling.

158 K1, WEE1, and ataxia-telangiectasia mutated (ATM); and inhibitors of classical non-homologous end joi

159 es, including ataxia telangiectasia-mutated (ATM) and Rad3-related (ATR), control cell cycle progress

160 ly shown that ataxia-telangiectasia-mutated (ATM) deficiency in CD4 T cells accelerates DNA damage, t

161 tics such as ataxia-telangiesctasia-mutated (ATM) inhibitors.

162 We propose that in the absence of ATM, cerebellar Purkinje cells cannot respond adequately

163 and promoted inflammation and activation of ATM and the DNA damage response.

164 rovides survival niche through activation of ATM kinase.

165 ERbeta reduced expression and activation of ATM upon DNA damage.

166 - and oxidative stress-induced activation of ATM without consistently affecting ATM protein stability

167 us unwinding and inappropriate activation of ATM, but also counteracts replication conflicts at DNA s

168 ian of chromosome integrity and activator of ATM signaling, which promotes DNA double-strand break re

169 Addition of ATM inhibitor enhances isoniazid mediated Mtb clearance

170 es than nnMCL, with exclusive alterations of ATM in cMCL, whereas TP53 and TERT alterations were slig

171 re accurately illuminate the consequences of ATM accumulation in obese AT, lending further insight in

172 demonstrate that B cell-specific deletion of ATM in mice leads to reduction in germinal center (GC) f

173 Moreover, the FATC domain of ATM may function as a membrane-anchoring unit for other

174 age response, we investigated the effects of ATM inhibition and radiation on pancreatic tumor immunog

175 t cell cycle arrest; however, the effects of ATM inhibition on the injured kidney have not been explo

176 ically, R3008H rescued the tardy exchange of ATM-KD at DNA damage foci, indicating that PRD coordinat

177 ession, and a kinase-independent function of ATM is required for the induction.

178 owever, the precise location and function of ATM within mitochondria and its role in oxidative phosph

179 onse, centered on a noncanonical function of ATM, and demonstrates a role for the satellite RNA in tu

180 ression showed that SIRT3 promotes growth of ATM CRISPR knockout DLBCL xenografts compared to wild-ty

181 We show that hypersensitivity of ATM-mutant cells to topotecan or the poly-(ADP-ribose) p

182 state cancer models and tested the impact of ATM loss on DNA repair function and therapeutic sensitiv

183 The primary aim was to assess the impact of ATM/BRCA1/BRCA2/ PALB2 germline mutations on cause-speci

184 pidly activated by DNA damage independent of ATM-ATR, but dependent on BRAF-TAK1-p38-MAPK, and is req

185 Inhibition of ATM and ATR signaling contributes to the efficiency of v

186 denced as we observed that the inhibition of ATM expression by chemical inhibition promoted the loss

187 Chemical inhibition of ATM in rat cardiomyoblast cells (H9c2) significantly dec

188 Inhibition of ATM increased tumoral T1IFN expression in a cGAS/STING-i

189 Acute ex vivo inhibition of ATM protein kinase significantly decreased mitochondrial

190 epithelium or pharmacological inhibition of ATM, YAP1, or caspase-1 as well as antibiotic treatment,

191 The incidence and expression level of ATM correlated with pigmentary status in canities-affect

192 Loss of ATM following 20A treatment inhibits both autophagy and

193 We find that loss of ATM induces apoptosis of GC B cells, likely due to unres

194 ut sequencing analyses revealed that loss of ATM/ATR phosphorylation of CtIP at T855 or ATM kinase in

195 However, the mechanism of ATM activation is still not completely understood.

196 we introduce shelterin and the mechanisms of ATM activation and NHEJ at telomeres, before discussing

197 es and can be inhibited by overexpression of ATM from a clone lacking miR-181c binding sites.

198 mmunogenicity, underscoring the potential of ATM inhibition in combination with ICB and radiation as

199 ranslated region of ATM, and the presence of ATM in miR-181c-associated RNA-induced silencing complex

200 ctly targeting the 3'-untranslated region of ATM mRNA.

201 miR-181c with the 3' untranslated region of ATM, and the presence of ATM in miR-181c-associated RNA-

202 of miRNAs contribute to tight regulation of ATM by directly targeting the 3'-untranslated region of

203 ssessment of B cell-intrinsic requirement of ATM in humoral responses in vivo was confounded by the f

204 hese new findings illustrate the key role of ATM in the protection of human hair follicle melanocytes

205 To define the role of ATM loss in prostate tumor DDR function and sensitivity

206 mutants, establishing the functional role of ATM-mediated histone modification in plant growth under

207 DDR-directed agents, we created a series of ATM-deficient preclinical prostate cancer models and tes

208 ensuing growth arrest through suppression of ATM-FOXO3a association and downstream signaling cascade.

209 s DNA damage response activation upstream of ATM phosphorylation at uncapped telomeres.

210 AT inflammation and then representing ~3% of ATMs in mice.

211 turnover and pro-inflammatory activation of ATMs.

212 udies show that the phenotypic plasticity of ATMs is far more complicated, which is also reflected in

213 udies suggested differential polarization of ATMs, with M2-like macrophages predominant in lean AT an

214 sites does not affect formation of 53BP1 or ATM foci following DNA damage, but abolishes recruitment

215 Preterm infants received AT (32/44; 73%) or ATM (12/44; 27%) with median durations of 4 and 7 days,

216 hat inhibition of the protein kinase ACK1 or ATM contributes to the suppression of FOXO1 nuclear effl

217 at least one alteration in BRCA1, BRCA2, or ATM and whose disease had progressed during previous tre

218 at least one alteration in BRCA1, BRCA2, or ATM, and cohort B included 142 patients with at least on

219 at least one alteration in BRCA1, BRCA2, or ATM; cohort B (142 patients) had alterations in any of 1

220 f ATM/ATR phosphorylation of CtIP at T855 or ATM kinase inhibition suppresses resection without alter

221 Here, we report brain-penetrant ATM inhibitors that have robust pharmacodynamic (PD) eff

222 iants were found in the moderately penetrant ATM and CHEK2 genes, where only truncating variants from

223 Pharmacological ATM inhibition by KU55933 in cisplatin-treated mice did

224 As a result, the levels of phosphorylated ATM and P53 as well as other downstream proapoptotic pro

225 s or depletion via dysregulation of the PI3K/ATM pathways.

226 s or depletion via dysregulation of the PI3K/ATM pathways.

227 s and a gene signature consisting of PIK3CG, ATM, EPPK1, EP300, or KMT2C mutations were also associat

228 a different form of wiring between DNA-PKcs/ATM/ATR: The checkpoint activated in G(2)-phase is regul

229 of a mixed population of distinct polarized ATMs.

230 ERCC6, BRCA2, BRCA1, XPC, JAG1, RPA1, POLE, ATM, and LIG1 in African American men, and POLQ, NEIL3,

231 lts support recently identified PARP1, POT1, ATM, and MPHOSPH6 loci.

232 he mutation of SIM2s at one of the predicted ATM phosphorylation sites (S115) reduces HR efficiency t

233 Taken together, MRE11 UFMylation promotes ATM activation, DSB repair and genome stability, and pot

234 ancing UFL1 E3 ligase activity and promoting ATM activation in a positive feedback loop.

235 oss herpesviruses and two cellular proteins, ATM and KAP1, a lytic cycle amplification loop is establ

236 SMCHD1-deficient cells displayed reduced ATM S1981 phosphorylation and diminished formation of ga

237 alpha-derived from macrophages in regulating ATM accumulation, and local and systemic IL-1beta produc

238 es involved in DNA recombination and repair, ATM signaling and cell cycle check point control.

239 hand, introduction of anti-miR-181c restored ATM and phosphorylated Akt.

240 AF-TAK1-p38-MAPK, and is required for robust ATM activation and efficient DNA repair.

241 ogether, these results indicate that the ROS-ATM-CHK2-Beclin 1-autophagy axis serves as a physiologic

242 Here, we demonstrate in several ATM-deficient cell lines that the olaparib and AZD6738 c

243 on genes (PALB2, MLH1, MSH6, CHEK2, SMARCE1, ATM, BRCA1, and CTNNA1) in 9 patients, including 3 of 27

244 For specific ATM depletion of H2Ab1, GeRPs containing H2Ab1 siRNA wer

245 FR scores exhibited significantly suppressed ATM signaling and differential expression of a network p

246 ecognized as DSBs, thereby preventing a Tel1(ATM) checkpoint response.

247 Rif1, and Rif2, the Mre11 complex, and Tel1(ATM) promise to increase our insight into the coordinati

248 r the mechanisms by which Mec1(ATR) and Tel1(ATM) propagate histone modifications across chromatin.

249 gest that recruitment and activation of Tel1(ATM) depends on the heterotrimeric MRX(MRN) complex, com

250 phosphorylated, either by Mec1(ATR) or Tel1(ATM) checkpoint kinases.

251 subtelomere silencing by physiological Tel1(ATM) and Rpd3(HDAC) activities coveys tolerance to gluco

252 However, at very short telomeres, Tel1(ATM) can be recruited and activated by the MRX complex,

253 ontain candidate genes (TINF2, PARP1, TERF1, ATM and POT1) with potential roles in telomere biology a

254 the establishment of clinical trials testing ATM inhibitors in combination with highly conformal radi

255 Here, we demonstrate that ATM from obese mice exhibit metabolic profiles character

256 We further demonstrate that ATM- and NBS1-dependent recruitment of TOPBP1 in the nuc

257 Our results demonstrated that ATM expression is higher in HCV-infected hepatocytes and

258 Moreover, we found that ATM kinase promotes Alt-EJ-mediated CSR by suppressing i

259 Inhibitor studies indicated that ATM kinase activity might not grossly impact on mitotic

260 We show that ATM deficiency in diffuse large B-cell lymphoma (DLBCL)

261 lp hair follicle melanocytes, we showed that ATM expression increased after incubation with the pro-o

262 Our study suggested that ATM inhibition does not increase DNA repair after cispla

263 n the clinic, but the new work suggests that ATM-deficient cancers may be more vulnerable to ATR inhi

264 Recent evidence also suggests that ATMs of lean mice serve as a substrate buffer or reservo

265 The ATM/ATR module similarly regulates DNA end-resection at

266 rther show that ZIKV infection activates the ATM/Chk2 checkpoint but prevents the activation of anoth

267 ferase PRDM9 guides SPO11 targeting, and the ATM kinase controls meiotic DSB numbers.

268 sion and their repair is orchestrated by the ATM kinase.

269 Strikingly, at high IR-doses, the ATM/ATR coupling relaxes and each kinase exerts independ

270 Alterations in the ATM gene are the second most common defect after BRCA2,

271 Mutations in the ATM tumor suppressor gene confer hypersensitivity to DNA

272 he induction of DNA repair that involves the ATM kinase-signaling pathway.

273 recessive disease caused by mutation of the ATM gene and is characterized by loss of cerebellar Purk

274 lomere dysfunction-induced activation of the ATM-YAP1-pro-IL-18 pathway in epithelium is a key instig

275 sing under the regulatory supervision of the ATM/ATR module.

276 They further suggest the ATM-PIDDosome-caspase-2 signaling axis alerts the cell o

277 DNA-PKcs links to the ATM/ATR module and defects cause hyper-resection and hyp

278 DNA-PKcs integrates to the ATM/ATR module by regulating resection at all IR-doses,

279 In addition, this ATM increase was prevented by pre-incubation of cells wi

280 k2 DDR, Mtb gains survival advantage through ATM-Akt signaling cascade.

281 ed compensatory DNA damage responses through ATM loss) as monotherapy and combined with DNA-damaging

282 Most cancer-associated alterations to ATM are missense mutations at the PI3-kinase regulatory

283 specifically confer topotecan resistance to ATM-deficient cells.

284 TP53, ATM, ARID1A, AHR, and SMARCB1 mutations were more freque

285 ients with del(17p), del(11q), mutated TP53, ATM, and BIRC3, none of these parameters reduced complet

286 tream signaling for DSB repair by triggering ATM recruitment, H2AX phosphorylation and the recruitmen

287 trials and suggest that patients with tumor ATM alterations may be more likely to benefit from ATR i

288 ckout DLBCL xenografts compared to wild-type ATM control xenografts.

289 anomalies using this assay for the variants ATM c.3806A > G and BUB1 c.677C > T, whereas CHEK1 c.61G

290 Iso2 was hypoglycosylated and degraded, via ATM and GSK3beta-mediated phosphorylation and activation

291 drugs triggered a positive feedback loop via ATM/E2F1/STAT signaling, amplifying the TRIM37 network i

292 dney injury must be carefully monitored when ATM inhibitors become available in clinical practice in

293 We find that when ATM is activated by oxidative stress, but not by DNA dam

294 osomal DNA (rDNA) repeats is associated with ATM-dependent repression of ribosomal RNA synthesis and

295 pharmacodynamic (PD) effects consistent with ATM kinase inhibition in the mouse brain and an understa

296 atients, including 14 with BRCA2, eight with ATM, four with BRCA1, and none with PALB2 mutations.

297 No responses were observed with ATM or CHEK2 mutations alone.

298 t therapeutic target for DLBCL patients with ATM null phenotype.

299 d with DLBCL cells expressing wild type (WT)-ATM.

300 s in ATM deficient background compared to WT-ATM DLBCL cells.