ライフサイエンスコーパス: ataxia telangiectasia mutated

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

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

3 tein kinase catalytic subunit (DNA-PKcs) and ataxia telangiectasia mutated.

4 t lack or contain severely reduced levels of ataxia telangiectasia mutated, a serine/threonine kinase

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

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

7 various DNA damage responses including ATM (Ataxia telangiectasia mutated) activation, homologous re

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

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

10 Ataxia telangiectasia mutated and RAD3 related (ATR) pro

11 ght to play a key role in activation of ATR (ataxia telangiectasia mutated and Rad3 related) and CHK1

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

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

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

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

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

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

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

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

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

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

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

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

24 , DNA-dependent protein kinase (DNA-PK), and ataxia telangiectasia-mutated and Rad3-related (ATR) sig

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

26 ATR (ataxia telangiectasia-mutated and Rad3-related) contains

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

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

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

30 The ataxia-telangiectasia mutated and RAD3-related (ATR) kin

31 leta becomes phosphorylated at Ser601 by the ataxia-telangiectasia mutated and Rad3-related (ATR) kin

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

33 In contrast, ataxia-telangiectasia mutated and Rad3-related kinase (A

34 n problem is specified by six pathways [ATM (ataxia telangiectasia mutated) and ATR (ataxia telangiec

35 The ATR (ATM (ataxia telangiectasia mutated) and rad3-related) checkpo

36 that p30 specifically binds to cellular ATM (ataxia telangiectasia mutated) and REGgamma (a nuclear 2

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

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

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

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

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

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

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

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

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

46 ectrometry approach and have identified Atm (ataxia-telangiectasia mutated) as a candidate Tcl1-inter

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

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

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

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

51 in HO-1-deficient cells resulted in loss of ataxia-telangiectasia mutated/ataxia telangiectasia and

52 us recombination-mediated DNA repair through ataxia-telangiectasia mutated/ataxia telangiectasia and

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

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

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

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

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

58 We demonstrated that ataxia telangiectasia mutated (ATM) and ataxia telangiec

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

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

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

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

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

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

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

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

67 other DNA damage response pathways, such as ataxia telangiectasia mutated (ATM) and BRCA1, promotes

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

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

70 Ataxia telangiectasia mutated (ATM) and DNA-dependent pr

71 eloping lymphocytes, where they activate the ataxia telangiectasia mutated (Atm) and DNA-PKcs kinases

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

73 DDR markers such as the phosphorylations of ataxia telangiectasia mutated (ATM) and histone H2A.x (H

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

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

76 promotes cancer cell death via activation of ataxia telangiectasia mutated (ATM) and the resultant up

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

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

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

80 es DNA-dependent protein kinase (DNA-PK) and ataxia telangiectasia mutated (ATM) as bulky DNA damage-

81 ilencing prevented sustained accumulation of ataxia telangiectasia mutated (ATM) at DNA damage sites

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

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

84 H3K56Ac restoration is regulated by ataxia telangiectasia mutated (ATM) checkpoint kinase.

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

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

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

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

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

90 AT patients have mutations in the ataxia telangiectasia mutated (ATM) gene.

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

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

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

94 Ataxia telangiectasia mutated (ATM) is a protein kinase

95 Ataxia telangiectasia mutated (ATM) is activated upon DN

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

97 Ataxia telangiectasia mutated (ATM) is an important sign

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

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

100 RE11-RAD50-NBS1 (MRN) complex that activates ataxia telangiectasia mutated (ATM) kinase and early che

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

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

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

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

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

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

107 Upon DNA damage, ataxia telangiectasia mutated (ATM) kinase triggers mult

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

109 or of DNA damage checkpoint 1 (MDC1) and the ataxia telangiectasia mutated (ATM) kinase, both key reg

110 lar DNA damage response to NF-kappaB via the ataxia telangiectasia mutated (ATM) kinase.

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

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

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

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

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

116 nding protein 1 foci, and increases baseline ataxia telangiectasia mutated (ATM) phosphorylation.

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

118 fects in DNA damage response factors such as ataxia telangiectasia mutated (ATM) protein and combined

119 The ataxia telangiectasia mutated (ATM) protein kinase regul

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

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

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

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

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

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

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

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

128 80, ARTEMIS, DNA-PKcs, DNA ligase IV (LIG4), Ataxia telangiectasia mutated (ATM), and ATM- and Rad3-r

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

130 ein kinase (DNA-PK) catalytic subunit, Ku80, ataxia telangiectasia mutated (ATM), BRCA2, or XRCC3 com

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

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

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

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

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

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

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

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

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

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

141 esponse to genotoxic stimuli, which involves ataxia telangiectasia mutated (ATM)-dependent histone me

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

143 The ataxia telangiectasia mutated (ATM)-interacting protein

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

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

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

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

148 raction blocks the phosphorylation of p53 by ataxia telangiectasia mutated (ATM).

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

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

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

152 erines 15 and 46) and autophosphorylation of ataxia telangiectasia mutated (ATM); depleting p53 or AT

153 Ataxia telangiectasia-mutated (ATM) and ataxia telangiec

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

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

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

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

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

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

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

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

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

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

164 e, resulting from biallelic mutations in the ataxia telangiectasia-mutated (ATM) gene.

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

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

167 DNA-PKcs and the ataxia telangiectasia-mutated (ATM) kinase are members o

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

169 B) domain-associated protein (KAP-1), by the ataxia telangiectasia-mutated (ATM) kinase.

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

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

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

173 The DNA damage response kinases ataxia telangiectasia-mutated (ATM), DNA-dependent prote

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

190 In the present study, we demonstrate that ataxia-telangiectasia mutated (ATM) directly phosphoryla

191 on toward lymphoma, as seen in patients with ataxia-telangiectasia mutated (ATM) dysfunction.

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

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

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

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

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

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

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

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

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

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

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

203 Ataxia-telangiectasia mutated (ATM) plays a central role

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

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

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

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

208 Ataxia-telangiectasia mutated (ATM) protein kinase regul

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

224 ic stress induces TG2 expression through the Ataxia-Telangiectasia, Mutated (ATM)/Nuclear Factor kapp

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

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

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

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

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

230 We demonstrate that the ataxia-telangiectasia-mutated (ATM) kinase phosphorylate

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

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

233 p38 kinases and PI3K isoforms and Torin1 to ataxia telangiectasia mutated, ATM and Rad3-related prot

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

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

236 Inhibition of ataxia telangiectasia mutated decreased the induction of

237 hat the increase in L1 retrotransposition in ataxia telangiectasia mutated-deficient cells most likel

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

253 Ataxia telangiectasia-mutated inhibition only retards re

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

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

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

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

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

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

260 Here, we show that activation of Ataxia telangiectasia-mutated kinase (ATM) by endogenous

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

262 Ataxia telangiectasia-mutated kinase activity can compen

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

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

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

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

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

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

269 a functional DNA damage sensor complex, and ataxia-telangiectasia mutated kinase.

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

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

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

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

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

275 Rather, because phosphorylated ataxia telangiectasia mutated levels were increased in p

276 omologue of mammalian nuclear protein of the ataxia telangiectasia-mutated locus that is encoded by t

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

293 Knock down of ataxia telangiectasia mutated suppressed gammaH2AX and C

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

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

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

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

298 2) is required for the recruitment of active ataxia telangiectasia mutated to DNA damage foci, thus a

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

300 Ataxia telangiectasia mutated was activated but not its