ライフサイエンスコーパス: ataxia telangiectasia

1 r the pathogenic dissection and treatment of ataxia telangiectasia.

2 f disease states, including malignancies and ataxia telangiectasia.

3 n the pleiotropic neurodegeneration disorder ataxia-telangiectasia.

4 ding to genetic instability in patients with ataxia-telangiectasia.

5 marker of brain function, in 10 adults with ataxia-telangiectasia, 19 non-affected adult relatives (

6 Ataxia telangiectasia (A-T) is a pleiotropic disease, wi

7 Ataxia telangiectasia (A-T) is a syndrome associated wit

8 The hereditary autosomal recessive disease ataxia telangiectasia (A-T) is caused by mutation in the

9 Ataxia telangiectasia (A-T) mutated (ATM) is a key deoxy

10 Ataxia telangiectasia (A-T) mutated (ATM) kinase orchest

11 Ataxia telangiectasia (A-T) results from inactivation of

12 Ataxia telangiectasia (A-T), a rare autosomal recessive

13 The human genomic instability syndrome ataxia telangiectasia (A-T), caused by mutations in the

14 ein kinase mutated in the rare human disease ataxia telangiectasia (A-T), has been the focus of inten

15 ponsible for the autosomal recessive disease ataxia- telangiectasia (A-T) was localized to 11q22.3-23

16 The symptoms of ataxia-telangiectasia (A-T) include a progressive neurod

17 Ataxia-telangiectasia (A-T) is a cerebellar neurodegener

18 Ataxia-telangiectasia (A-T) is a rare multi-system disor

19 Ataxia-telangiectasia (A-T) is a rare neurodegenerative

20 Ataxia-telangiectasia (A-T) is an autosomal recessive ne

21 Ataxia-telangiectasia (A-T) is associated with insuffici

22 Germline ATM inactivation causes ataxia-telangiectasia (A-T) syndrome with severe lymphoc

23 eneration is a hallmark of the human disease ataxia-telangiectasia (A-T) that is caused by mutation o

24 ystem (CNS) neurodegeneration in the disease ataxia-telangiectasia (A-T), we analyzed flies mutant fo

25 Participants with ataxia-telangiectasia also had higher metabolism in glob

26 uced the expression of genes involved in ATM/ataxia telangiectasia and Rad-3-related (ATR) signaling,

27 ATR (ataxia telangiectasia and Rad-3-related) is a protein ki

28 mutants for the cell cycle checkpoint genes ATAXIA TELANGIECTASIA AND RAD3 RELATED (ATR) and ALUMINU

29 rotein A (RPA), which triggers activation of ataxia telangiectasia and Rad3 related (ATR) and phospho

30 s in a manner that is partially dependent on ataxia telangiectasia and Rad3 related (ATR) but not cyc

31 bserved positive correlation between ERH and ataxia telangiectasia and Rad3 related (ATR) expression

32 ataxia telangiectasia mutated (ATM)- and the ataxia telangiectasia and Rad3 related (ATR)-mediated de

33 -S and G2-M checkpoints mediated by the ATR (ataxia telangiectasia and Rad3 related) and Chk1 kinases

34 ATR (ataxia telangiectasia and Rad3 related) is an essential

35 on hinders homology-directed repair and ATR (ataxia telangiectasia and Rad3 related)-dependent checkp

36 gase is important for activation of the ATR (ataxia telangiectasia and Rad3 related)-regulated DNA da

37 ing promotes PKA-mediated phosphorylation of ataxia telangiectasia and rad3-related (ATR) at Ser435 (

38 The DNA damage response kinase ataxia telangiectasia and Rad3-related (ATR) coordinates

39 Both exposures induce ataxia telangiectasia and Rad3-related (ATR) kinase and

40 on relies on phosphorylation of FANCI by the ataxia telangiectasia and Rad3-related (ATR) kinase, fol

41 d by the ataxia telangiectasia mutated (ATM)/ataxia telangiectasia and Rad3-related (ATR) kinases.

42 Ataxia telangiectasia and Rad3-related (ATR) mediates re

43 terations creates a selective sensitivity to ataxia telangiectasia and Rad3-related (ATR) pathway inh

44 marily involves a pathway hierarchy in which ataxia telangiectasia and Rad3-related (ATR) signals to

45 he single-stranded telomeric DNA and prevent ataxia telangiectasia and Rad3-related kinase activation

46 ed PH domains, which inhibits recruitment of Ataxia telangiectasia and Rad3-related protein (ATR) and

47 PKA directly phosphorylates ataxia telangiectasia and Rad3-related protein (ATR) at

48 pendence of UV-induced XPA nuclear import on ataxia telangiectasia and Rad3-related protein (ATR) in

49 ion of the replication stress sensing kinase ataxia telangiectasia and Rad3-related protein (ATR) red

50 he action of a G2 checkpoint mediated by the ataxia telangiectasia and Rad3-related protein (ATR)-che

51 licative stress leading to activation of the ataxia telangiectasia and Rad3-related protein (ATR)-med

52 of Cdc25C was regulated by activation of the ataxia telangiectasia and Rad3-related protein (ATR)/che

53 Further analysis of ataxia telangiectasia and Rad3-related protein (ATR)/Chk

54 silencing of ataxia telangiectasia mutated, ataxia telangiectasia and Rad3-related protein, and DNA-

55 Mutations in ATR(ataxia telangiectasia and RAD3-related) cause Seckel syn

56 vator of the DNA damage response kinase ATR (ataxia telangiectasia and rad3-related) is critical for

57 Both compounds also lead to ataxia telangiectasia and Rad3-related- (ATR-) dependent

58 vage complexes (Top1ccs) in murine models of ataxia telangiectasia and spinocerebellar ataxia with ax

59 n neurons, is substantially reduced in human ataxia-telangiectasia and Atm(-/-) mouse cerebellar Purk

60 rtantly, this pathogenesis appears common to ataxia-telangiectasia and Cockayne syndrome, two other D

61 Ataxia-telangiectasia and RAD3-related (ATR) signals the

62 ic promoter region of DNA repair kinase ATR (ataxia-telangiectasia and Rad3-related protein) and acts

63 ion in other brain areas in individuals with ataxia-telangiectasia and tested for brain changes in as

64 erlie other neurodegenerative disorders (eg, ataxia-telangiectasia), and DNA double-strand breaks are

65 pendent protein kinase catalytic subunit and ataxia telangiectasia- and Rad3-related kinase.

66 the ataxia-telangiectasia mutated (ATM) and ataxia-telangiectasia- and rad3-related (ATR) kinases.

67 sponse kinases ataxia-telangiectasia mutated/ataxia-telangiectasia- and Rad3-related effectively bloc

68 Cells isolated from patients with ataxia telangiectasia are exquisitely sensitive to ioniz

69 alyses were used to compare individuals with ataxia-telangiectasia, asymptomatic relatives, and unrel

70 of unknown etiology are commonly observed in ataxia telangiectasia (AT) and Artemis deficiency.

71 Ataxia telangiectasia (AT) is a multisystem DNA-repair d

72 Ataxia telangiectasia (AT) is a progressive multisystem

73 Ataxia-telangiectasia (AT) is a pleiotropic multisystem

74 Biallelic mutations in ATM cause ataxia-telangiectasia (AT), a rare inherited disease wit

75 sponse, cause the neurodegenerative disorder ataxia-telangiectasia (AT).

76 inase inhibitors of ATM, the gene mutated in ataxia telangiectasia, can sensitize tumor cells to radi

77 The ataxia telangiectasia group D complementing gene (ATDC,

78 e we describe a novel mouse model expressing ataxia telangiectasia group D complementing gene (ATDC,

79 Ataxia-telangiectasia group D-associated gene (ATDC) med

80 We found that participants with ataxia-telangiectasia had lower metabolism in cerebellar

81 in cerebellar metabolism, participants with ataxia-telangiectasia had widespread changes in metaboli

82 So far, murine models of ataxia telangiectasia have failed to accurately recapitu

83 and post-mortem studies in individuals with ataxia-telangiectasia have reported cerebellar atrophy;

84 opyridine has been extended to patients with ataxia-telangiectasia in whom it seems to reduce slow-ph

85 subtype that showed increased sensitivity to ataxia telangiectasia inhibition, and a neuroendocrine-a

86 Ataxia telangiectasia is a devastating neurodegenerative

87 Ataxia-telangiectasia is a genetic disorder associated w

88 Ataxia-telangiectasia is a recessive genetic disorder (A

89 A long-standing mystery surrounding ataxia-telangiectasia is why it is mainly cerebellar neu

90 W248R differs from other ataxia telangiectasia-like disorder analog alleles by th

91 two pediatric cancer patients with enhanced ataxia telangiectasia-like disorder.

92 Mutations throughout MRE11 cause ataxia-telangiectasia-like disorder (ATLD) featuring cer

93 the hereditary cancer-susceptibility disease ataxia-telangiectasia-like disorder (ATLD).

94 Nuclear protein, ataxia-telangiectasia locus (NPAT) and FLICE-associated

95 nal SANT/Myb-like domain of nuclear protein, ataxia-telangiectasia locus (NPAT), a transcriptional co

96 Using an ataxia-telangiectasia mouse model, we compared lymphoma

97 Ataxia telangiectasia mutant (ATM) is an S/T-Q-directed

98 DR) defects, particularly TP53 and biallelic ataxia telangiectasia mutated (ATM) aberrations, are ass

99 CLY) is phosphorylated at S455 downstream of ataxia telangiectasia mutated (ATM) and AKT following DN

100 and phospho-modification of proteins in the ataxia telangiectasia mutated (ATM) and ATM and Rad3-rel

101 strated by the DNA damage checkpoint kinases ATAXIA TELANGIECTASIA MUTATED (ATM) and ATM AND RAD3-REL

102 artnering with DNA-damage checkpoint kinases ataxia telangiectasia mutated (ATM) and ATM- and Rad3-re

103 ytic subunit (DNA-PKcs) [a kinase related to ataxia telangiectasia mutated (ATM) and ATR] has well ch

104 tor of p300) is activated upon DNA damage by ataxia telangiectasia mutated (ATM) and Chk2 kinases and

105 ease during V(D)J recombination activate the Ataxia Telangiectasia mutated (ATM) and DNA-dependent pr

106 resentative DDR-associated proteins, such as ataxia telangiectasia mutated (ATM) and H2AX, was induce

107 , HU-induced SMR5/SMR7 expression depends on ATAXIA TELANGIECTASIA MUTATED (ATM) and SUPPRESSOR OF GA

108 tate resulted in increased levels of phospho-ataxia telangiectasia mutated (ATM) and the ATM substrat

109 , by negatively regulating the expression of ataxia telangiectasia mutated (ATM) and the subsequent D

110 d cytokine signaling pathways, including the ataxia telangiectasia mutated (ATM) and transforming gro

111 iation suppresses miR-205 expression through ataxia telangiectasia mutated (ATM) and zinc finger E-bo

112 At low dose, doxorubicin activated ataxia telangiectasia mutated (ATM) but not ATM and Rad3

113 The ataxia telangiectasia mutated (ATM) checkpoint is the ce

114 TP53 and ataxia telangiectasia mutated (ATM) defects are associat

115 Here we report that ataxia telangiectasia mutated (ATM) deficiency causes nu

116 epithelial cell as well as activation of the ataxia telangiectasia mutated (ATM) DNA repair pathway t

117 Mutations in the ataxia telangiectasia mutated (ATM) gene, which encodes

118 A-repair disorder caused by mutations in the ataxia telangiectasia mutated (ATM) gene.

119 ymptoms, is caused by a defective or missing ataxia telangiectasia mutated (ATM) gene.

120 Involvement of tumor suppressor ataxia telangiectasia mutated (ATM) in the TGF-beta1 pat

121 Ataxia telangiectasia mutated (ATM) is a protein kinase

122 Ataxia telangiectasia mutated (ATM) is activated upon DN

123 The protein kinase ataxia telangiectasia mutated (ATM) is an important prox

124 Ataxia telangiectasia mutated (ATM) is an important sign

125 ince demonstrated that in replicating cells, ataxia telangiectasia mutated (ATM) is predominantly a n

126 e-like kinases (PI3KKs) involved in the DDR: ataxia telangiectasia mutated (ATM) kinase and ATM and R

127 The ataxia telangiectasia mutated (ATM) kinase and H2AX hist

128 Inhibitors of ataxia telangiectasia mutated (ATM) kinase decreased man

129 The ataxia telangiectasia mutated (ATM) kinase is involved i

130 ther the DNA damage response mediated by the Ataxia Telangiectasia Mutated (ATM) kinase may affect th

131 Strikingly, we found that the ataxia telangiectasia mutated (ATM) kinase regulates the

132 ced at one Igkappa allele signal through the ataxia telangiectasia mutated (ATM) kinase to feedback-i

133 viously, we reported that the absence of the ataxia telangiectasia mutated (ATM) kinase, a critical D

134 and optimized as selective inhibitors of the ataxia telangiectasia mutated (ATM) kinase.

135 vated in human cancers, is phosphorylated by ataxia telangiectasia mutated (ATM) on Ser131 upon DNA d

136 trated that DNA damage signaling through the ataxia telangiectasia mutated (ATM) pathway induces the

137 w for first time, to our knowledge, that the ataxia telangiectasia mutated (ATM) pathway, involved in

138 The ataxia telangiectasia mutated (ATM) protein kinase regul

139 MV) infection of multiple cell lines lacking ataxia telangiectasia mutated (ATM) protein produced wil

140 ant intermediate state activate differential ataxia telangiectasia mutated (ATM) signaling where CHK2

141 on DNA-dependent protein kinase (DNA-PK) and Ataxia telangiectasia mutated (ATM) signaling.

142 on-associated feedback loop between DDB2 and ataxia telangiectasia mutated (ATM) was observed in infe

143 break repair factors histone H2AX (H2AX) and ataxia telangiectasia mutated (ATM) were examined in pan

144 80, ARTEMIS, DNA-PKcs, DNA ligase IV (LIG4), Ataxia telangiectasia mutated (ATM), and ATM- and Rad3-r

145 recruitment is independent of the DDR sensor ataxia telangiectasia mutated (ATM), but dependent on po

146 mediated by the DNA damage response protein, ataxia telangiectasia mutated (ATM), in cytokine-induced

147 nd non-TIP damage sites, DDR factors such as ataxia telangiectasia mutated (ATM), MDC1, WRN, and FANC

148 d by up-regulation and/or phosphorylation of ataxia telangiectasia mutated (ATM), phosphorylated H2AX

149 s acetylation of the major DNA damage kinase Ataxia telangiectasia mutated (ATM), thereby triggering

150 f gamma-H2AX foci and activation of both the ataxia telangiectasia mutated (ATM)- and the ataxia tela

151 Ataxia telangiectasia mutated (ATM)-Chk2 and ATM- and Ra

152 d impaired DSB-induced checkpoint integrity, Ataxia Telangiectasia Mutated (ATM)-deficient mice harbo

153 These 3 responses are ataxia telangiectasia mutated (ATM)-dependent and promot

154 Human papillomaviruses (HPV) activate the ataxia telangiectasia mutated (ATM)-dependent DNA damage

155 hatase that dephosphorylates proteins in the ataxia telangiectasia mutated (ATM)-initiated DNA damage

156 The ataxia telangiectasia mutated (ATM)-interacting protein

157 double strand breaks (DSBs), as indicated by ataxia telangiectasia mutated (ATM)-mediated H2AX phosph

158 chronic lymphocytic leukemia (CLL) where the ataxia telangiectasia mutated (ATM)-p53 pathway is inact

159 absence of the DNA damage response mediator ataxia telangiectasia mutated (ATM).

160 re it showed a synergistic relationship with ataxia telangiectasia mutated (ATM).

161 A damage in the bone marrow regulated by the ataxia telangiectasia mutated (ATM)/ataxia telangiectasi

162 served an up-regulation of components of the ataxia telangiectasia mutated (ATM)/Chek1/p53 pathway in

163 rks (replication stress), which activate the ataxia telangiectasia mutated (ATM)/p53-dependent tumor

164 d DNA damage response marker, phosphorylated ataxia telangiectasia mutated (pATM), were quantified in

165 Here we show that CST and ATR (ataxia telangiectasia mutated [ATM] and Rad3-related) ac

166 n of single strand DNA, the key platform for ataxia telangiectasia mutated and Rad3-related (ATR) act

167 rticipant in PKA-mediated phosphorylation of ataxia telangiectasia mutated and Rad3-related (ATR) at

168 ing for immediate phosphorylation of Chk1 by ataxia telangiectasia mutated and Rad3-related (ATR) in

169 tion of ATRIP, the regulatory partner of the ataxia telangiectasia mutated and Rad3-related (ATR) kin

170 The ataxia telangiectasia mutated and Rad3-related (ATR) kin

171 The ataxia telangiectasia mutated and Rad3-related (ATR)-che

172 re to UV also produced maximal activation of ataxia telangiectasia mutated and Rad3-related (Atr)-med

173 s damage is mediated by additive activity of ATAXIA TELANGIECTASIA MUTATED AND RAD3-RELATED and ATAXI

174 phosphorylation of human Chk1 kinase by ATR (ataxia telangiectasia mutated and Rad3-related) is depen

175 ence of chromosomal anomalies (trisomy-12 or ataxia telangiectasia mutated anomaly + del13q14) and ne

176 Inhibition of ataxia telangiectasia mutated decreased the induction of

177 ease in the number of nuclear phosphorylated ataxia telangiectasia mutated foci in the post-LVAD hear

178 se (PARP), replication factor c2-5 (Rfc2-5), ataxia telangiectasia mutated gene 1 (ATM), meiotic reco

179 ficiency disorder caused by mutations in the ataxia telangiectasia mutated gene.

180 mulate angiogenesis through the silencing of ataxia telangiectasia mutated in neighboring target cell

181 ntaining miR-214 repressed the expression of ataxia telangiectasia mutated in recipient cells, thereb

182 state cancer cells, comparable to effects of Ataxia Telangiectasia Mutated inhibition.

183 anscription factor that is phosphorylated by ataxia telangiectasia mutated kinase (ATM) in response t

184 n alveolar epithelial cells, as indicated by ataxia telangiectasia mutated kinase (ATM)-dependent pho

185 Upon IR, CHK2 is activated by ataxia telangiectasia mutated kinase and regulates the S

186 joins because of functional redundancy with ataxia telangiectasia mutated kinase, a protein that als

187 TELANGIECTASIA MUTATED AND RAD3-RELATED and ATAXIA TELANGIECTASIA MUTATED kinases, which cause postr

188 To further investigate this, ataxia telangiectasia mutated KO (Atm(-/-)) mice, which

189 The association of Tcl1 and Ataxia Telangiectasia Mutated leads to activation of the

190 cardiomyocyte nuclear foci of phosphorylated ataxia telangiectasia mutated protein, an upstream regul

191 ec1, the yeast Ataxia telangiectasia mutated/Ataxia telangiectasia mutated Rad3-related checkpoint re

192 Knock down of ataxia telangiectasia mutated suppressed gammaH2AX and C

193 Ataxia telangiectasia mutated was activated but not its

194 this methylation conferred compromised ATM (ataxia telangiectasia mutated) activation, decreased eff

195 orylation of proteins (H2AX, protein 53, and ataxia telangiectasia mutated) after SPECT.

196 is induced selectively by DSBs through ATM (ataxia telangiectasia mutated) as a unique mechanism to

197 nce (RNAi)-based screen that identified ATM (ataxia telangiectasia mutated) as being synthetic lethal

198 e that pTyr(267)-AR is recruited to the ATM (ataxia telangiectasia mutated) enhancer in an Ack1-depen

199 The DNA damage-responsive kinase ATM (ataxia telangiectasia mutated) is indispensable for UV-i

200 tor of the DNA damage response pathway, ATM (ataxia telangiectasia mutated) kinase.

201 , we show that absence of the essential ATM (ataxia telangiectasia mutated) substrate Chk2-interactin

202 amage is provided by the protein kinase ATM (ataxia telangiectasia mutated) that is capable of comman

203 lained by the consecutive activation of ATM (ataxia telangiectasia mutated), Chk2, and p53.

204 age control (poly(ADP)-ribose polymerase and ataxia telangiectasia mutated), those within the cell me

205 n in other systems is known to activate ATM (ataxia telangiectasia mutated)-mediated DNA damage respo

206 and breaks, as well as in activation of ATM (ataxia telangiectasia mutated).

207 T3 induces a rapid activation of ATM (ataxia telangiectasia mutated)/PRKAA (adenosine monophos

208 However, silencing of ataxia telangiectasia mutated, ataxia telangiectasia and

209 quired the master DNA damage response kinase Ataxia telangiectasia mutated, revealing potential mecha

210 gulated genes requires ATR and ALT2, but not ATAXIA TELANGIECTASIA MUTATED, thus demonstrating that i

211 Both 1 and 3 induce ataxia telangiectasia mutated- (ATM-) and DNA-dependent

212 tial mechanistic links between PALB2 and the Ataxia telangiectasia mutated-dependent DNA damage respo

213 ter DNA damage, and this dissociation may be ataxia telangiectasia mutated-dependent.

214 antly elevated levels of both phosphorylated ataxia telangiectasia mutated-Ser(1980) and phospho-H2AX

215 entify a novel interaction between Tcl1 with Ataxia Telangiectasia Mutated.

216 -dependent kinase (CDK), and Mec1, the yeast Ataxia telangiectasia mutated/Ataxia telangiectasia muta

217 the classical DNA damage signaling proteins, ataxia-telangiectasia mutated (ATM) (Ser-1981), Chk.2 (T

218 Nuclear PKR antagonizes ataxia-telangiectasia mutated (ATM) activation by a mech

219 ced signaling cascades via activation of the ataxia-telangiectasia mutated (ATM) and ataxia-telangiec

220 nhibitors of Chk1 and siRNA directed against ataxia-telangiectasia mutated (ATM) and ataxia-telangiec

221 mplex is critical for activating the kinases ataxia-telangiectasia mutated (ATM) and ATM and Rad3-rel

222 phorylations of the key DNA repair molecules ataxia-telangiectasia mutated (ATM) and checkpoint kinas

223 s that coordinate recognition of DNA damage, ataxia-telangiectasia mutated (ATM) and PARP-1, were ind

224 t kinase 1 (Chk1) phosphorylation in an ATR [ataxia-telangiectasia mutated (ATM) and Rad3-related]-de

225 A-T is caused by biallelic mutations in the ataxia-telangiectasia mutated (ATM) gene, but heterozygo

226 The protein ataxia-telangiectasia mutated (ATM) is activated by DNA

227 regulation occurred in a manner dependent on ataxia-telangiectasia mutated (ATM) kinase and the DNA-d

228 Here we identify ataxia-telangiectasia mutated (ATM) kinase as a modulato

229 previously reported a novel inhibitor of the ataxia-telangiectasia mutated (ATM) kinase, which is a t

230 responsible for the efficient activation of ataxia-telangiectasia mutated (ATM) kinase.

231 Upon DNA damage, the protein kinase ataxia-telangiectasia mutated (ATM) phosphorylates 53BP1

232 Ataxia-telangiectasia mutated (ATM) plays a unique yet i

233 The ataxia-telangiectasia mutated (ATM) protein is an apical

234 The ataxia-telangiectasia mutated (ATM) protein kinase is a

235 Ataxia-telangiectasia mutated (ATM) protein kinase regul

236 Ataxia-telangiectasia mutated (ATM) regulates the DNA da

237 ia (A-T) is associated with insufficiency of ataxia-telangiectasia mutated (ATM), a critical DNA dama

238 Ataxia-telangiectasia mutated (ATM), a member of the pho

239 ue mechanism: DIM caused rapid activation of ataxia-telangiectasia mutated (ATM), a nuclear kinase th

240 romic CIDs, autosomal recessive mutations in ataxia-telangiectasia mutated (ATM), autosomal dominant

241 JADE, that is induced after DNA damage in an ataxia-telangiectasia mutated (ATM)-dependent manner.

242 is observed effect on 53BP1 foci is p53- and ataxia-telangiectasia mutated (ATM)-independent and can

243 duced NBS1 expression and epirubicin-induced ataxia-telangiectasia mutated (ATM)phosphorylation in br

244 Under these conditions, ataxia-telangiectasia mutated activation and accumulatio

245 s IFN-beta and ISG induction is dependent on ataxia-telangiectasia mutated and Rad3-related (ATR) kin

246 on 5, which led to the downregulation of the ataxia-telangiectasia mutated DNA damage pathway and the

247 DDR kinases DNA-dependent protein kinase or ataxia-telangiectasia mutated enhanced GDC-0973/GDC-0941

248 Here we report that ataxia-telangiectasia mutated kinase (ATM) plays a major

249 ) polymerase activity, but is independent of ataxia-telangiectasia mutated kinase function.

250 cell-cycle checkpoints via activation of the ataxia-telangiectasia mutated kinase.

251 a-C is mediated in part by activation of the ataxia-telangiectasia mutated pathway, which is prelimin

252 ced gastric cancer, especially in those with ataxia-telangiectasia mutated protein (ATM)-negative tum

253 tein kinase catalytic subunit (DNA-PKcs) and ataxia-telangiectasia mutated respond primarily to DNA d

254 le-strand break repair is the recruitment of ataxia-telangiectasia mutated serine/threonine kinase (A

255 ATM (ataxia-telangiectasia mutated) and ATR (ATM and Rad3-rel

256 leus where it interacted with activated ATM (ataxia-telangiectasia mutated) at sites of DNA repair.

257 Rap1-interacting factor 1 (Rif1) as an ATM (ataxia-telangiectasia mutated) phosphorylation-dependent

258 Cytokine array analysis identified several ataxia-telangiectasia mutated-dependent senescence-assoc

259 depletion of the DNA damage response kinases ataxia-telangiectasia mutated/ataxia-telangiectasia- and

260 NA-dependent kinase, encoded by PRKDC), ATM (ataxia telangiectasia, mutated), and ATR (ATM and Rad3-r

261 tes in the DNA damage response downstream of ataxia telangiectasia-mutated (ATM) and p38/MK2 and prom

262 a degeneration process critically involving ataxia telangiectasia-mutated (ATM) and p53.

263 ng to replication stress in malignant cells (ataxia telangiectasia-mutated (ATM) and Rad3-related-che

264 iciency results in reduced activation of the ataxia telangiectasia-mutated (ATM) checkpoint kinase, i

265 -locus translocations that are a hallmark of ataxia telangiectasia-mutated (ATM) deficiency.

266 ubly mutant for Chaos3 and components of the ataxia telangiectasia-mutated (ATM) double-strand break

267 for this process in cells deficient for the ataxia telangiectasia-mutated (ATM) DSB response factor.

268 Mutations in the XLF C-NHEJ factor or ataxia telangiectasia-mutated (ATM) DSB response protein

269 pair of cyclobutane pyrimidine dimers in the ataxia telangiectasia-mutated (ATM) gene in human fibrob

270 By contrast, loss of the DSB signaling ataxia telangiectasia-mutated (ATM) kinase did not signi

271 The Ataxia Telangiectasia-Mutated (ATM) protein kinase is re

272 genitor colony formation required NF-kappaB, ataxia telangiectasia-mutated (ATM), and the inhibitor o

273 Decreased levels of p53, but not Hdm2 or ataxia telangiectasia-mutated (ATM), were seen after exp

274 le of the DNA damage response protein kinase ataxia telangiectasia-mutated (ATM)- and Rad-3-related (

275 gM(+) B-cell lymphomas that arise in certain ataxia telangiectasia-mutated (ATM)-deficient compound m

276 checkpoint activation involves activation of ataxia telangiectasia-mutated (ATM)/ATM- and rad3-relate

277 of the replication damage checkpoint kinase ataxia telangiectasia-mutated and rad3-related homolog.

278 r of which affects the cell cycle checkpoint ATAXIA TELANGIECTASIA-MUTATED AND RAD3-RELATED, are seve

279 n increases p53 stability as demonstrated by ataxia telangiectasia-mutated kinase activation, increas

280 Ataxia telangiectasia-mutated kinase activity can compen

281 ive replication even in the presence of ATM (ataxia telangiectasia-mutated kinase) and Chk2 phosphory

282 he intra-S-phase arrest is regulated by ATM (ataxia telangiectasia-mutated kinase) signaling in a p53

283 Activation of the ATM (ataxia telangiectasia-mutated kinase)-dependent DNA dama

284 vated protein kinase, nuclear factor-kappaB, ataxia telangiectasia-mutated kinase, or reactive oxygen

285 , DNA-PKcs also acts in concert with MRN and ataxia telangiectasia-mutated to regulate resection and

286 phosphoinositide 3-kinase-like kinases ATM (ataxia telangiectasia-mutated) and ATR (ATM and Rad3-rel

287 Following UV irradiation, ataxia telangiectasia-mutated- and Rad3-related protein

288 The ATR (ATM [ataxia telangiectasia-mutated]- and Rad3-related) checkp

289 enetic interference with HER3 but not by the ataxia-telangiectasia-mutated (ATM) and ATM and Rad3-rel

290 ) by the DNA damage-activated protein kinase ataxia-telangiectasia-mutated (ATM) and casein kinase1 (

291 to DNA damage by the coordinated actions of ataxia-telangiectasia-mutated (ATM) and casein kinases (

292 osphorylation of KAP1-Serine 824 (Ser824) by ataxia-telangiectasia-mutated (ATM) kinase is necessary

293 lls, and this was abrogated by inhibition of ataxia-telangiectasia-mutated signaling, suggesting that

294 M (encoding the DNA-damage signaling kinase, ataxia-telangiectasia-mutated) increase Familial Pancrea

295 calization of HDAC4 in the events leading to ataxia telangiectasia neurodegeneration.

296 ards from patients diagnosed with SCID, XLA, ataxia-telangiectasia, Nijmegen-breakage-syndrome, commo

297 HDAC4 in the cytoplasm, suggesting that the ataxia telangiectasia phenotype results both from a loss

298 inst ataxia-telangiectasia mutated (ATM) and ataxia-telangiectasia Rad3-related (ATR) pathways signif

299 Thus, ataxia-telangiectasia should be considered, at least in

300 Here we present a model of human ataxia telangiectasia using induced pluripotent stem cel