ライフサイエンスコーパス: ATM

1 ATM (ataxia-telangiectasia mutated) and ATR (ATM and Rad

2 ATM deficiency was associated with increased mitotic def

3 ATM inhibition also increased cell death in crypts at 4

4 ATM inhibition reduced upregulation of p21, an inhibitor

5 ATM is a unique host kinase that has both proviral and a

6 ATM mutations, clonal SF3B1, and both clonal and subclon

7 ATM phosphorylation of G9a on serine 569 is required for

8 ATM plus CA also detected an ESBL in 90.1% of isolates t

9 ATM results indicate that half-life (t1/2) and percent d

10 ATM was required for the efficient repair of all non-com

11 ATMs catabolize lipid in a lysosomal-dependent manner re

12 raditionally associated with CRC (3, ATM; 1, ATM/CHEK2; 2, BRCA1; 4, BRCA2; 1, CDKN2A; 2, PALB2); 10

13 n 16 genes, including BRCA2 (37 men [5.3%]), ATM (11 [1.6%]), CHEK2 (10 [1.9% of 534 men with data]),

14 es not traditionally associated with CRC (3, ATM; 1, ATM/CHEK2; 2, BRCA1; 4, BRCA2; 1, CDKN2A; 2, PAL

15 tion, we found that H. pylori might activate ATM through histone H3 and H4 hyperacetylation and DNA p

16 quires phosphorylated NBS1(S432) to activate ATM, while interaction of de-phosphorylated NBS1(S432) w

17 Once activated, ATM and DNA-PKcs regulate a genetic program with diverse

18 7p), affecting TP53, and del(11q), affecting ATM, are associated with resistance against genotoxic ch

19 y, we show that knockdown of SET also allows ATM to localize to incoming viral genomes bound by prote

20 th molecular maps of a rosemary plant and an ATM keypad after a PIN code was entered.

21 bilizes TRF1 at telomeres after damage in an ATM activation-dependent manner.

22 pic expression of Gene 33 triggers DDR in an ATM serine/threonine kinase (ATM)-dependent fashion and

23 tic gammaH2AX-labelled DNA damage foci in an ATM- and ATR-dependent manner.

24 odification occurs at DNA damage sites in an ATM-dependent manner, and ubiquitin-modifying enzymes, i

25 and cell death through the engagement of an ATM/Chk2- and gammaH2AX (phosphorylated H2A histone fami

26 Here, we report an ATM-kinase dependent, unforeseen function of the nuclear

27 tes in a manner dependent on MDC1, BRCA1 and ATM, down-regulation of And-1 impairs end resection by r

28 us system increases double strand breaks and ATM defects and triggers neurodegeneration.

29 The ATR-Chk1 and ATM-Chk2 pathways are central in DNA damage repair (DDR)

30 Herein we investigated the ATR-Chk1 and ATM-Chk2 signalings in male breast cancer (MBC).

31 motes binding to DNA, tethering DNA ends and ATM activation, but prevents nucleolytic processing of D

32 al status of TP53, SF3B1, BIRC3, NOTCH1, and ATM in 406 untreated CLL cases by ultra-deep next-genera

33 sponse through activation of ATM-p53-p21 and ATM-Chk2-Cdc25A pathways.

34 x and result in activation of the DNA-PK and ATM kinases, which play key roles in regulating the cell

35 e ends from double-stranded break repair and ATM signaling, whereas POT1 represses ATR signaling by e

36 ucocorticoid, B-cell receptor signaling, and ATM signaling.

37 nescence for the potent tumor suppressor and ATM substrate USP28.

38 Pancreatic Cancer (FPC) susceptibility, and ATM somatic mutations have been identified in resected h

39 d cells lacked ATM activation by Cr(VI), and ATM silencing produced no significant effects on p53 sta

40 the transcription factor p53 and the apical ATM and ATR kinases, were unaffected by immunoproteasome

41 found that H2AX shows a similar influence as ATM, whereas the influence of ATM on this rearrangement

42 affected by mutations in DNA repair, such as ATM and ATR.

43 Our findings show a mechanism associating ATM signaling induction with H. pylori infection.

44 ATM (ataxia telangiectasia-mutated) and ATR (ATM and Rad3-related) and by the cyclin-dependent kinase

45 ATM (ataxia-telangiectasia mutated) and ATR (ATM and Rad3-related) are large PI3 kinases whose human

46 M (ataxia telangiectasia, mutated), and ATR (ATM and Rad3-related) are related PI3K-like protein kina

47 ated the role of the apical DDR kinases ATR, ATM and DNA-PKcs in the cellular defense response.

48 Overall, the ATR/ATM-initiated molecular cascade seems to be active in a

49 of Gene 33 promotes the interaction between ATM and histone H2AX without triggering DNA damage.

50 nction of DNA-PKcs and the interplay between ATM and ATR during neurogenesis.

51 nd linked to t-loop formation, inhibits both ATM activation and NHEJ.

52 Whereas both ATM and BRCA1 promote end resection, which can be regula

53 Upon induction of DNA breaks, ATM activation leads to a cascade of local chromatin mod

54 -strand break (DSB) inducer and abolished by ATM/ATR inhibition.

55 ase UCHL3 is phosphorylated and activated by ATM.

56 gest that lack of phosphorylation of LKB1 by ATM was involved in AZD1775-mediated cytotoxicity.

57 Mechanistically, USP13 is phosphorylated by ATM following DNA damage which, in turn, facilitates its

58 is stabilized by phosphorylation of RAG2 by ATM.

59 moderately increased risks of breast cancer: ATM (OR, 2.78; 95% CI, 2.22-3.62), BARD1 (OR, 2.16; 95%

60 locking NMDA, but not GABA, receptors causes ATM levels to rise while ATR levels respond to GABA, but

61 Chronic [Ca2+]i dysregulation amplifies Cdk5-ATM signaling, possibly linking impaired glutamatergic s

62 Here we show that in human cells, ATM-dependent phosphorylation of CtIP and the epistatic

63 G2/M DNA damage checkpoint, ATM signaling, mitochondrial dysfunction, regulation of

64 of PARP inhibitors in ATM-affected human CLL.ATM and TP53 mutations are associated with poor prognosi

65 The yeast Tel1 and Mec1.Ddc2 complex (ATM and ATR-ATRIP in humans) play pivotal roles in DNA r

66 In contrast, ATM facilitates replication, reactivation, and latency e

67 Conversely, ATM Exos obtained from lean mice improve glucose toleran

68 Conversely, ATM is critical for controlling apoptosis in immature no

69 roteins play complementary roles in the DDR; ATM is engaged in the repair of double-strand breaks, wh

70 Expression of kinase-dead ATM (Atm(KD/-)) is more oncogenic than loss of ATM (Atm(

71 Kinase-dead ATM protein (Atm-KD), but not loss of ATM (Atm-null), pr

72 R-loops, double strand breaks and defective ATM-mediated repair as pathological consequences of C9or

73 We reveal that defective ATM-mediated DNA repair is a consequence of P62 accumula

74 ous DNA damage is concomitant with defective ATM-mediated DNA repair signaling and accumulation of pr

75 and gammaherpesvirus infection, we depleted ATM specifically in B cells, a cell type critical for ch

76 Different ATM signaling in response to chromium(VI) metabolism via

77 ionale to profile human tumors for disabling ATM mutations, particularly given their impact on PARP1

78 p53 through the DNA damage-response enzymes, ATM and ATR, and requires the phosphorylation of p53 at

79 We also examined ATM effectors and found that H2AX shows a similar influe

80 anslation indicates that this is an extended ATM-dependent mechanism to increase protein expression o

81 ot affect the ability of TIP60 to facilitate ATM activation.

82 sensitivities of the tests were as follows: ATM plus CA, 100%; CLSI plus BA, 93.3%; and CLSI, 60%.

83 of ESBL producers detected were as follows: ATM plus CA, 95.7%; CLSI plus BA, 88.6%; and CLSI, 78.6%

84 minate an important regulatory mechanism for ATM that also controls DNA repair pathway choice.

85 of both RAG1 and RAG2 are also required for ATM's capacity to limit signal (but not coding) joining.

86 the C terminus of RAG2 are also required for ATM's capacity to limit signal joining.

87 Consistent with a critical role for ATM in HDR in this background, loss of ATM leads to synt

88 al modulator protein, implicating a role for ATM-mediated activation of canonical NF-kappaB transcrip

89 duced localization of MDC1, a key target for ATM phosphorylation, which is a prerequisite for RNF8 re

90 ence and imply a common node downstream from ATM that links the TP53 and GATA4 branches of the senesc

91 these severe features, a lack of functional ATM is still compatible with early life, suggesting that

92 Furthermore, ATM suppresses rearrangement formation in an experimenta

93 Furthermore, ATM- and Rad3-related (ATR)-dependent signaling in respo

94 n is poorly controlled in a host with global ATM insufficiency, whether the host is a mouse or a huma

95 mmunological states, and consequently guides ATM polarization.

96 94 patients were determined to have ATM-negative tumours before unmasking for the primary an

97 f ATM kinase, which is an intact homodimeric ATM/Tel1 from Schizosaccharomyces pombe.

98 rstand the complex relationship between host ATM and gammaherpesvirus infection, we depleted ATM spec

99 of DNA damage signaling and repair, but how ATM participates in HDR and genetically interacts with B

100 To study how ATM deficiency affects genome integrity in this setting,

101 However, ATM deficiency markedly increases the proportion of chro

102 ignificantly inhibit ATM activity and impair ATM signaling upon DNA damage.

103 More importantly, ATM deficiency also renders murine pancreatic tumors hig

104 In ATM- or ATR-deficient neurons, spontaneous vesicle relea

105 This suggests an essential role for ATMIN in ATM regulation during hypoxia, which induces replication

106 us vesicle release is reduced, but a drop in ATM or ATR level also slows FM4-64 dye uptake.

107 .4-Mbp deletion rearrangement is enhanced in ATM-deficient cells.

108 l rational for the use of PARP inhibitors in ATM-affected human CLL.ATM and TP53 mutations are associ

109 impact on V(D)J recombination DSB joining in ATM-deficient pro-B lines.

110 Germline mutations in ATM (encoding the DNA-damage signaling kinase, ataxia-te

111 and frameshift variants in PALB2, but not in ATM or CHEK2, can also give rise to the same signature.

112 ense-mediated RNA decay switch exon (NSE) in ATM is repressed by U2AF, PUF60 and hnRNPA1.

113 haracterize several phosphorylation sites in ATM that are targets of DNA-PKcs and show that phospho-m

114 Modulating protein turnover in ATM-depleted cells also has an adverse effect on the DNA

115 R region of PLA2G6 and a missense variant in ATM were each seen in all three affected people in a sin

116 ypoxia promotes an inflammatory phenotype in ATMs.

117 High FA doses inactivated ATM via its covalent dimerization and formation of large

118 human kinases and kinase families, including ATM, CDKs, GSK-3, MAPKs, PKA, PKB, PKC, and SRC.

119 diet-fed (HFD) mice is sufficient to induce ATM accumulation, and to transfer metabolic disease in c

120 stimulated DNA damage, and therefore induced ATM in a virulence factor-dependent manner.

121 tudies we show that some of the inflammatory ATM inducing metabolic disease, originate from resident

122 e ratio of inflammatory to anti-inflammatory ATMs, and adoptive transfer of AT1-ILCs exacerbated meta

123 ions at these residues significantly inhibit ATM activity and impair ATM signaling upon DNA damage.

124 Other DNA repair pathways involving ATM and DNA-PKcs are unaffected by PPI sequestration.

125 mage signaling and repair response involving ATM.

126 hways, notably the DNA damage-induced kinase ATM, which regulated many IR-response genes, including i

127 tors downstream of the core responder kinase ATM/ATR.

128 mutations in the DNA damage response kinase ATM are common in lung adenocarcinoma but directly targe

129 The DNA damage response kinase ATM is frequently mutated in human cancer, but the signi

130 ons of the master DNA damage response kinase ATM, which has been shown to accelerate tumorigenesis an

131 ex chromosomes via the DSB-responsive kinase ATM, which also shapes the autosomal DSB landscape at mu

132 A analyses have shown that the stress kinase ATM and the transcription factor p53 are integral compon

133 angiectasia mutated serine/threonine kinase (ATM) to the damaged site, where it plays a key role in a

134 ggers DDR in an ATM serine/threonine kinase (ATM)-dependent fashion and through pathways dependent or

135 tivate the DNA damage response (DDR) kinases ATM and DNA-PKcs through the generation of double strand

136 y the phosphoinositide 3-kinase-like kinases ATM (ataxia telangiectasia-mutated) and ATR (ATM and Rad

137 not require the DNA damage response kinases ATM or ATR.

138 It is mainly coordinated by the kinases ATM, ATR, and DNA-PKcs, which control the repair of brok

139 sphorylation of the serine/threonine kinases ATM and Chk2 and of histone H2AX after IR treatment both

140 onse is controlled by three related kinases: ATM, ATR, and DNA-PK.

141 In contrast, fully Asc-restored cells lacked ATM activation by Cr(VI), and ATM silencing produced no

142 ity by stimulating M2 polarization and local ATM proliferation, presumably due to upregulation of the

143 cytokines, such as TNF-alpha, inhibit local ATM proliferation.

144 eems to be the underlying mechanism of local ATM proliferation in obesity.

145 dy the impact of cytokine treatment on local ATM proliferation, without the bias of early monocyte re

146 Up to now, AT macrophages (ATM) accumulation was considered to be due to blood infi

147 ssue (AT) and an increase of AT macrophages (ATMs) that is linked to the onset of type 2 diabetes.

148 Adipose tissue macrophages (ATMs) are key players orchestrating metabolic inflammati

149 re, we show that adipose tissue macrophages (ATMs) in obese mice secrete miRNA-containing exosomes (E

150 activity toward adipose tissue macrophages (ATMs).

151 esponsive kinase Tel1 (ortholog of mammalian ATM).

152 Mechanistically, ATM mediates crosstalk between the prosurvival MEK/ERK a

153 The age-trend model (ATM) described here uses a lake-specific age-contaminant

154 downstream of ataxia telangiectasia mutated (ATM) and AKT following DNA damage.

155 f DNA damage, ataxia-telangiectasia mutated (ATM) and PARP-1, were induced.

156 diated by the Ataxia Telangiectasia Mutated (ATM) kinase may affect the relative influence of C-NHEJ

157 l through the ataxia telangiectasia mutated (ATM) kinase to feedback-inhibit RAG expression and RAG c

158 rotein kinase ataxia-telangiectasia mutated (ATM) phosphorylates 53BP1 and recruits RAP1-interacting

159 Ataxia-telangiectasia mutated (ATM) plays a unique yet incompletely understood role in

160 Ataxia-telangiectasia mutated (ATM) regulates the DNA damage response as well as DNA do

161 (DNA-PK) and Ataxia telangiectasia mutated (ATM) signaling.

162 mutations in ataxia-telangiectasia mutated (ATM), autosomal dominant mutations in signal transducer

163 responses are ataxia telangiectasia mutated (ATM)-dependent and promote quiescent NSC (qNSC) activati

164 indicated by ataxia telangiectasia mutated (ATM)-mediated H2AX phosphorylation (gammaH2AX).

165 LL) where the ataxia telangiectasia mutated (ATM)-p53 pathway is inactivated with relatively high fre

166 cient for the ataxia telangiectasia-mutated (ATM) DSB response factor.

167 ed NF-kappaB, ataxia telangiectasia-mutated (ATM), and the inhibitor of kappaB kinase, IKKalpha.

168 t not Hdm2 or ataxia telangiectasia-mutated (ATM), were seen after expression of vIRF1, but not with

169 rotein kinase ataxia telangiectasia-mutated (ATM)- and Rad-3-related (ATR) in the cellular response t

170 Nevertheless, ATM inhibition reduced median time to moribund in Cdkn1a

171 Normally, ATM kinase is in an inactive, homodimer form and is tran

172 ells, APOBEC3A modestly elicited ATR but not ATM.

173 own adverse-prognostic impact (TP53, NOTCH1, ATM, SF3B1, NFKBIE, and BIRC3), a large proportion of ca

174 is one of the miRNAs overexpressed in obese ATM Exos, and earlier studies have shown that PPARgamma

175 maintaining cell survival in the absence of ATM function.

176 for replication stress-induced activation of ATM in response to aphidicolin and hydroxyurea.

177 ed DNA damage response through activation of ATM-p53-p21 and ATM-Chk2-Cdc25A pathways.

178 RD1 expression results in the attenuation of ATM/ATR signalling activities and further the hESC diffe

179 g DDR activation through genetic deletion of ATM, suggesting the causative role of SSB accumulation a

180 or inhibition of MRE11, but not depletion of ATM, abrogated IL-33 stimulation.

181 atency due to compromised differentiation of ATM-deficient B cells.

182 Pre-incubation of ATM protein with active DNA-PKcs also significantly redu

183 f phosphorylated MDC1 that is independent of ATM and DNA damage and is required for proper mitotic pr

184 oint in cortical progenitors, independent of ATM and DNA-PKcs.

185 nificant tumor-cell killing independently of ATM and p53 through the accumulation of genotoxic levels

186 r influence as ATM, whereas the influence of ATM on this rearrangement seems independent of 53BP1.

187 Targeted inhibition of ATM by siRNA attenuated the ability of XWL-1-48 on induc

188 non-canonical roles and how our knowledge of ATM, ATR, and DNA-PK is being translated to benefit huma

189 f human fibroblast adaptation to the lack of ATM.

190 The levels of ATM and ATR respond to each other; when ATM is deficient

191 M (Atm(KD/-)) is more oncogenic than loss of ATM (Atm(-/-)) in mouse models, leading to earlier and m

192 e-dead ATM protein (Atm-KD), but not loss of ATM (Atm-null), prevents replication-dependent removal o

193 mpse at the cellular consequences of loss of ATM and highlights a previously overlooked role for prot

194 ibition become highly sensitive upon loss of ATM both in vitro and in vivo.

195 stasis occurring very early on after loss of ATM in order to counter protein damage originating from

196 e for ATM in HDR in this background, loss of ATM leads to synthetic lethality of Brca1(S1598F) mice.

197 (A-T) is a syndrome associated with loss of ATM protein function.

198 nded to adenoviral DNA by phosphorylation of ATM and CHK2 and that depletion or inhibition of MRE11,

199 ates ATM activity through phosphorylation of ATM.

200 be attributed to the defective retention of ATM previously reported by us.

201 Thus, our study reveals a role of ATM as a host factor that promotes chronic gammaherpesvi

202 The proviral role of ATM is also evident in vivo, as myeloid-specific ATM exp

203 sts on the activation and functional role of ATM kinase, which controls DNA damage responses involvin

204 is at both sites, as does the stimulation of ATM kinase activity.

205 ere we report the first cryo-EM structure of ATM kinase, which is an intact homodimeric ATM/Tel1 from

206 P and ATR inhibitors to improve treatment of ATM-mutant PDAC.

207 also phosphorylates key factors upstream of ATM/ATR and regulates their DDR-related functions.

208 table amounts of DSB during the main wave of ATM activation, which did not require MRE11.

209 ing of how hypoxia modulates the response of ATMs to free fatty acids within obese adipose tissue is

210 t upon PARP1 activation and not dependent on ATM activation.

211 Downregulation of transcription depends on ATM kinase activity and on the distance from the DSB.

212 d in response to DNA damage by DNA-PK and/or ATM.

213 all survival with olaparib in the overall or ATM-negative population of Asian patients with advanced

214 In TP53- or ATM-defective CLL cells, inhibition of ATR signaling by

215 eatment of XWL-1-48 induced gamma-H2AX and p-ATM expression, and further triggered DNA damage respons

216 -dependent cell killing irrespective of p53, ATM, NOTCH1, or SF3B1 status.

217 r susceptibility genes: BRCA2 (12 patients), ATM (10 patients), BRCA1 (3 patients), PALB2 (2 patients

218 hich impairs H2A ubiquitylation and perturbs ATM signaling.

219 SBs to facilitate the interaction of phospho-ATM with MDC1 and phosphorylation of MDC1, which are req

220 own to be able to activate all three PI3KKs (ATM, ATR, and DNA-PKcs).

221 linositol 3-kinase-related kinases (PI3KKs): ATM, ATR, and DNA-PKcs.

222 ological roles for the DDR kinases DNA-PKcs, ATM, and ATR during neurogenesis.

223 Thus, our results illustrate how DNA-PKcs, ATM, and ATR have unique and essential roles during the

224 the DNA-dependent kinase, encoded by PRKDC), ATM (ataxia telangiectasia, mutated), and ATR (ATM and R

225 with ataxia-telangiectasia mutated protein (ATM)-negative tumours.

226 In response to ionizing radiation, ATM phosphorylates FBXW7 at serine 26 to recruit it to D

227 S-NaME by demonstrating enrichment of RARb2, ATM, MGMT and GSTP1 promoters in multiplexed MS-NaME rea

228 h active DNA-PKcs also significantly reduces ATM activity in vitro.

229 d joining pathway, thus negatively regulates ATM activity through phosphorylation of ATM.

230 ngs reveal a role for AT1-ILCs in regulating ATM homeostasis through cytotoxicity and suggest that th

231 r MRE11-RAD50-NBS1 (MRN), thereby repressing ATM-dependent DNA damage checkpoint responses.

232 (-/-) cells, but not Paxx(-/-) cells require ATM/DNA-PK kinase activity for end-ligation.

233 This upregulation requires ATM/ATR/Chk1 kinases.

234 g DNA synthesis (NPAT), DNA damage response (ATM), mitosis (PMF1, CENPN and MAD1L1) and apoptosis (TP

235 rom 21 genes (APEX1 rs1130409 and rs1760944, ATM rs664677, AXIN2 rs2240308, CHRNA3 rs6495309, CHRNA5

236 DH1 downregulates the DNA damage (DD) sensor ATM by altering histone methylation, leading to impaired

237 infection on the DNA damage response sensor, ATM, in gastric epithelial cells and in biopsy specimens

238 nd 6 months in preCGG brain, as is p-Ser1981-ATM.

239 B cell-specific ATM deficiency attenuated the establishment of viral lat

240 y defines a proviral role of B cell-specific ATM expression during chronic gammaherpesvirus infection

241 rus tropism for B-1 B cells, B cell-specific ATM expression was necessary to support viral reactivati

242 is also evident in vivo, as myeloid-specific ATM expression facilitates MHV68 reactivation during the

243 such as IL-4, IL-13, and GM-CSF, stimulates ATM proliferation, whereas Th1 cytokines, such as TNF-al

244 Paradoxically, substoichiometric, ATM-independent, phosphorylation of the ATM/CK cluster p

245 In support, the Cdk5 substrate, ATM, is upregulated by 1.5- to 2-fold at P0 and 6 months

246 ), which recruits the checkpoint kinase Tel1/ATM to DSBs.

247 test BRCA1/2 and moderate agreement to test ATM to inform prognosis and targeted therapy.

248 and an aztreonam plus clavulanate disk test (ATM plus CA).

249 that radioprotect intestinal crypts and that ATM inhibition promotes GI syndrome after TBI.

250 We conclude that ATM activity is essential for p21-dependent and p21-inde

251 and cell proliferation, and demonstrate that ATM deficiency leads to persistent DNA damage in both pr

252 These results demonstrate that ATM has a role in HDR independent of the BRCA1-53BP1 ant

253 ngs in our study conclusively establish that ATM activity poses a major barrier to oncogenic transfor

254 defect in adult somatic cells, we find that ATM inhibition leads to severely reduced HDR in Brca1(S1

255 oscopy and coimmunoprecipitation reveal that ATM associates exclusively with excitatory (VGLUT1(+)) v

256 We also reveal that ATM is activated in pancreatic precancerous lesions in t

257 Our results show that ATM and p53 regulate both RNA synthesis and stability as

258 We also show that ATM expression by peritoneal B cells is required to faci

259 In this study, we show that ATM expression by splenic B cells is required for effici

260 Here we show that ATM is hyperactive when the catalytic subunit of DNA-dep

261 We show that ATM kinase inhibition using AZ31 prior to 9 or 9.25 Gy t

262 ary tumors and liver metastases we show that ATM loss accelerates Kras-induced carcinogenesis without

263 Taken together, our data suggest that ATM and ATR are part of the cellular "infrastructure" th

264 gammaherpesviruses in vitro, suggesting that ATM is proviral in the context of infected cell cultures

265 Taken together, these studies show that ATMs secrete exosomes containing miRNA cargo.

266 The ATM kinase is involved in various aspects of DNA damage

267 To assess the interplay between the ATM and ATR pathways in responding to replication stress

268 ker of DNA replication stress induced by the ATM and ATR kinases.

269 checkpoint signaling cascade mediated by the ATM and Rad3-related (ATR) and checkpoint kinase 1 (CHK1

270 phorylated at Serine376 and Serine389 by the ATM kinase and is recruited to the site of DNA-DSBs via

271 .79 [97.5% CI 0.63-1.00]; p=0.026) or in the ATM-negative population (12.0 months [7.8-18.1] vs 10.0

272 geted therapies, CLL with alterations in the ATM/p53 pathway remains a clinical challenge.

273 pts encoding key DDR proteins, including the ATM kinase.

274 tenuation of ROS-dependent activation of the ATM and CaMKII proapoptotic signaling cascades.

275 mplex to viral genomes and activation of the ATM kinase can promote KSHV replication, proteins involv

276 We found that disruption of the ATM kinase causes an increase in the frequency of the re

277 gement frequency caused by inhibition of the ATM kinase.

278 A knock-in mutation of the ATM phosphorylation site on E2F1 (S29A) prevents the int

279 cross multiple cell types, activation of the ATM-CHK2 pathway during viral replication is a cell line

280 ric, ATM-independent, phosphorylation of the ATM/CK cluster potentiated bursts in CREB-mediated trans

281 Overall, the ATM plus CA test detected ESBLs more accurately than the

282 Recently, the ATM interactor (ATMIN) was identified as critical for re

283 lls play an important role in regulating the ATM mediated DNA damage response, for epithelial cell su

284 This transcriptional inhibition requires the ATM kinase and the NF-kappaB essential modulator protein

285 a sensor of DNA damage signaling through the ATM-Chk2 pathway, which induces it to migrate to the nuc

286 ing premature stop codons and related to the ATM and ATR kinases which are at the apex of DNA damage

287 ranslational modification coincides with the ATM-mediated DNA damage response that occurs on function

288 ting the DNA damage response pathway through ATM-mediated Ser15 phosphorylation of p53.

289 Thus, ATM activity is essential for p21-dependent arrest while

290 We show that partial or total ATM deficiency cooperates with Kras(G12D) to promote hig

291 ese results were validated further using two ATM small-molecule inhibitors that attenuated PARP cleav

292 However, whether ER stress pathways underlie ATM regulation of energy homeostasis remains unclear.

293 all patients and patients whose tumours were ATM-negative (identified after randomisation, before the

294 s of ATM and ATR respond to each other; when ATM is deficient, ATR levels rise, and vice versa.

295 logical malignancies with DDR defects, where ATM/p53-dependent apoptosis is compromised.

296 Whereas ATM loss leads to a mild HDR defect in adult somatic cel

297 tosis in cycling neural progenitors, whereas ATM regulated apoptosis in both proliferative and noncyc

298 While ATM expression did not affect gammaherpesvirus tropism f

299 The striking finding associated with ATM inhibition prior to TBI was increased crypt loss wit

300 TR signaling via Chk1 and did not occur with ATM inhibition.