ライフサイエンスコーパス: ataxia telangiectasia

1 f disease states, including malignancies and ataxia telangiectasia.

2 r the pathogenic dissection and treatment of ataxia telangiectasia.

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

4 n the pleiotropic neurodegeneration disorder 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 syndrome associated wit

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

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

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

10 Fanconi anaemia (FA), ataxia telangiectasia (A-T), Nijmegen breakage syndrome

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

12 People with ataxia-telangiectasia (A-T) display phenotypic variabili

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

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

15 Ataxia-telangiectasia (A-T) is an autosomal recessive di

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

17 entionally, the immune deficiencies found in ataxia-telangiectasia (A-T) patients are viewed as defec

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

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

20 the ATM gene result in a condition known as ataxia-telangiectasia (A-T) that is characterized by can

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

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

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

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

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

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

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

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

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

30 ed by the ataxia telangiectasia mutated- and ataxia telangiectasia and rad3 related-based DNA damage

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

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

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

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

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

36 cluding ataxia telangiectasia mutated (ATM), ataxia telangiectasia and Rad3-related (ATR), and the DN

37 inhibitors of ataxia telangiectasia mutated, ataxia telangiectasia and Rad3-related (ATR), DNA-depend

38 mide, unlike other alkylators, activated the ataxia telangiectasia and Rad3-related (ATR)-checkpoint

39 esponse to aberrant R loop accumulation, the ataxia telangiectasia and Rad3-related (ATR)-Chk1 pathwa

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

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

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

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

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

45 KKs) ataxia telangiectasia mutated (ATM) and ataxia telangiectasia and Rad3-related protein (ATR), an

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

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

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

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

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

51 response to perturbed DNA replication, ATR (ataxia telangiectasia and Rad3-related) kinase is activa

52 , PCAF activity is tightly regulated by ATR (ataxia telangiectasia and Rad3-related), which phosphory

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

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

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

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

57 tablished cohort of individuals with variant ataxia-telangiectasia and explore genotype-phenotype cor

58 bitors; inhibitors of the DNA damage kinases ataxia-telangiectasia and Rad3 related (ATR), CHK1, WEE1

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

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

61 Targeting ataxia-telangiectasia and Rad3-related/cell-cycle checkp

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

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

64 (hereditary nonpolyposis colorectal cancer), ataxia telangiectasia, and Li-Fraumeni syndrome, all of

65 vate ataxia telangiectasia mutated (ATM) and ataxia telangiectasia- and Rad3-related (ATR) DNA damage

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

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

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 Patients were classified as variant ataxia-telangiectasia based on retained ATM kinase activ

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

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

79 The ataxia telangiectasia group D complementing gene (ATDC,

80 Ataxia-telangiectasia group D complementing gene (ATDC,

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

82 Here we show that deletion of the ataxia-telangiectasia group D-complementing (Atdc) gene,

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

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

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

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

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

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

89 Ataxia telangiectasia is a devastating neurodegenerative

90 Ataxia-telangiectasia is a recessive genetic disorder (A

91 Variant ataxia-telangiectasia is caused by mutations that allow

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

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

94 Ataxia-telangiectasia-like disorder (ATLD) fibroblasts w

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

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

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

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

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

100 demonstrates that loss of ataxia telangiectasia mutated (ATM) activates microglia

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

102 illomaviruses (HPVs) constitutively activate ataxia telangiectasia mutated (ATM) and ataxia telangiec

103 ted under hypoxia through phosphorylation by ataxia telangiectasia mutated (ATM) and ataxia telangiec

104 ted by the PIP3-kinase-like kinases (PI3KKs) ataxia telangiectasia mutated (ATM) and ataxia telangiec

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

106 Two related kinases, ataxia telangiectasia mutated (ATM) and ATM and Rad3-rel

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

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

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

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

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

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

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

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

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

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

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

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

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

120 pharmacologic blockade or siRNA silencing of ataxia telangiectasia mutated (ATM) increases type I IFN

121 Ataxia telangiectasia mutated (ATM) is a protein kinase

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

123 Ataxia telangiectasia mutated (ATM) is an important sign

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

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

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

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

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

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

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

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

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

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

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

135 sing Hi-C experiments on wild type cells and ataxia telangiectasia mutated (ATM) patient cells.

136 The Ser/Thr protein kinase ataxia telangiectasia mutated (ATM) plays an important r

137 toxin-treated cells, largely mediated by the ATAXIA TELANGIECTASIA MUTATED (ATM) protein kinase, repr

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

139 se and highly specific nuclear expression of Ataxia Telangiectasia Mutated (ATM) protein within melan

140 SMURF2 becomes phosphorylated at Ser(384) by ataxia telangiectasia mutated (ATM) serine/threonine kin

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 ol 3-kinase-related kinase family, including ataxia telangiectasia mutated (ATM), ataxia telangiectas

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

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

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

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

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

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

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

153 The ataxia telangiectasia mutated (ATM)-interacting protein

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

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

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

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

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

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

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

161 Ataxia telangiectasia mutated and RAD3 related (ATR) pro

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

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

164 lly, LRRC31 interacts with Ku70/Ku80 and the ataxia telangiectasia mutated and RAD3-related (ATR) at

165 n by ataxia telangiectasia mutated (ATM) and ataxia telangiectasia mutated and RAD3-related (ATR) at

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

182 Knock down of ataxia telangiectasia mutated suppressed gammaH2AX and C

183 Ataxia telangiectasia mutated was activated but not its

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

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

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

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

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

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

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

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

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

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

194 by combining the MSLN-TTC with inhibitors of ataxia telangiectasia mutated, ataxia telangiectasia and

195 duced DNA double-strand breaks by activating Ataxia Telangiectasia Mutated, phosphorylating histone H

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

197 Conversely, KU-55933, a drug that inhibits ataxia telangiectasia mutated, thereby preventing p53 ph

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

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

200 aptation to the G(2) arrest triggered by the ataxia telangiectasia mutated- and ataxia telangiectasia

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

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

203 ubiquitination and degradation controlled by ataxia telangiectasia mutated-induced phosphorylation at

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

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

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

207 DNA damage response pathways mediated by the ataxia-telangiectasia mutated (ATM) and ataxia-telangiec

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

209 ng molecules that regulate autophagy through ataxia-telangiectasia mutated (ATM) and cell cycle check

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

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

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

213 Using this technology, we identify that ataxia-telangiectasia mutated (ATM) and RNF8 regulate ra

214 The ataxia-telangiectasia mutated (ATM) gene regulates DNA d

215 Inactivation of Ataxia-telangiectasia mutated (ATM) gene results in an i

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

217 Phosphorylation of ataxia-telangiectasia mutated (ATM) is the initial step

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

219 The ataxia-telangiectasia mutated (ATM) kinase, an upstream

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

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

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

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

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

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

226 The ataxia-telangiectasia mutated (ATM) protein kinase is wi

227 Ataxia-telangiectasia mutated (ATM) protein kinase regul

228 In silico analysis suggested that ataxia-telangiectasia mutated (ATM) protein, a protein k

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

230 Activation of ataxia-telangiectasia mutated (ATM), a kinase activated

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

232 diation sensitive, had reduced expression of ataxia-telangiectasia mutated (ATM), and exhibited multi

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

234 n of the DNA damage response factors phospho-ataxia-telangiectasia mutated (ATM), phospho-53BP1, gamm

235 ithelial-mesenchymal transitions (EMT) in an Ataxia-telangiectasia mutated (ATM)-dependent manner.

236 These telomere defects activated ataxia-telangiectasia mutated (ATM)-mediated DNA damage

237 asia and Rad3 related (ATR), CHK1, WEE1, and ataxia-telangiectasia mutated (ATM); and inhibitors of c

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

239 ATR (ataxia-telangiectasia mutated [ATM] and RAD3-related) is

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

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

242 the ataxia-telangiectasia mutated (ATM) and ataxia-telangiectasia mutated and Rad3-related (ATR) kin

243 We found that silencing of ataxia-telangiectasia mutated and RAD3-related (ATR), a

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

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

246 Lenti-Cre deleted one or two copies of ataxia-telangiectasia mutated gene (Atm; KPA(FL/+) or KP

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

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

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

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

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

252 The absence of Ataxia-Telangiectasia mutated protein kinase (ATM) is as

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

254 Loss of ATM (ataxia-telangiectasia mutated) activity leads to a slowi

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 ATM (ataxia-telangiectasia mutated) is a PI3K-like kinase bes

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

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

260 ng molecules (ataxia-telangiectasia mutated; ataxia-telangiectasia mutated-related and Rad3-related;

261 sensors (MLH1), damage signaling molecules (ataxia-telangiectasia mutated; ataxia-telangiectasia mut

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

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

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

265 A damage response Ser/Thr kinases, including ataxia telangiectasia-mutated (ATM) and Rad3-related (AT

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

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

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

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

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

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

272 cal evidence indicates that the reduction of ataxia telangiectasia-mutated (ATM) kinase activity can

273 caused by mutations that allow some retained ataxia telangiectasia-mutated (ATM) kinase activity.

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

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

276 d aberrant activation of DNA damage-response ataxia telangiectasia-mutated (ATM) signaling in HD tran

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

278 , Tel1 protein kinase, the ortholog of human ataxia telangiectasia-mutated (ATM), is activated in res

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

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

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

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

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

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

285 Ataxia telangiectasia-mutated kinase activity can compen

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

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

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

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

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

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

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

293 We have recently shown that ataxia-telangiectasia-mutated (ATM) deficiency in CD4 T

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

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

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

297 tion-defective primary immunodeficiencies or ataxia telangiectasia/Nijmegen breakage syndromes.

298 Individuals with variant ataxia-telangiectasia require malignancy surveillance an

299 reich ataxia, spinocerebellar ataxia type 2, ataxia telangiectasia, spastic paraplegia, giant axonal

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