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 phorylation target for the apical DDR kinase ataxia-telangiectasia mutated.

5 tion of BRCA1 on Ser (1387) was dependent on ataxia-telangiectasia mutated.

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

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

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

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

10 alter Ataxia Telangiectasia and Rad3-related/Ataxia Telangiectasia Mutated activity but increased inh

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

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

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

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

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

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

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

18 8 motif is also present in the 3'-UTR of the ataxia telangiectasia mutated and Rad3-related (ATR) mRN

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 yotic cells requires the protein kinase ATR (ataxia telangiectasia mutated and rad3-related), which i

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

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

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

27 and protein levels of claspin, an adaptor of ataxia telangiectasia-mutated and Rad3-related protein-m

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

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

30 orks activate and are stabilized by the ATR (ataxia-telangiectasia mutated and Rad3 related)-mediated

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

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

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

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

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

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

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

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

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

40 NA damage response pathways mediated by ATM (ataxia-telangiectasia, mutated) and ATR (ATM and Rad3-re

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

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

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

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

45 The MRN complex (Mre11/RAD50/NBS1) and ATM (ataxia telangiectasia, mutated) are critical for the cel

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

66 including activation of the protein kinases ataxia telangiectasia mutated (ATM) and DNA-dependent pr

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

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

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

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

71 Telomere deprotection activates both ataxia telangiectasia mutated (ATM) and telangiectasia a

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

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

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

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

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

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

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

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

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

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

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

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

84 Ataxia telangiectasia mutated (ATM) deficiency predispos

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

86 The Ataxia Telangiectasia Mutated (ATM) gene is frequently i

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

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

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

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

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

92 Ataxia telangiectasia mutated (ATM) is a protein kinase

93 Ataxia telangiectasia mutated (ATM) is activated upon DN

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

95 Ataxia telangiectasia mutated (ATM) is an important sign

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

97 Moreover, the ataxia telangiectasia mutated (ATM) kinase activates ant

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

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

100 this process due to the lack of a functional ataxia telangiectasia mutated (ATM) kinase and elicit ra

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

102 expressing TgMYST-B have increased levels of ataxia telangiectasia mutated (ATM) kinase and phosphory

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

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

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

106 resent study was to elucidate the effects of ataxia telangiectasia mutated (ATM) kinase on the regula

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

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

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

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

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

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

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

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

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

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

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

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

119 In response to clastogens, the ataxia telangiectasia mutated (ATM) protein is rapidly a

120 The ataxia telangiectasia mutated (ATM) protein kinase regul

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

122 of poly(ADP)ribosyl polymerase 1 (PARP1) and ataxia telangiectasia mutated (ATM) result in synthetic

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

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

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

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

127 The role of ataxia telangiectasia mutated (ATM), a DNA double-strand

128 Ataxia telangiectasia mutated (ATM), a target gene of mi

129 80, ARTEMIS, DNA-PKcs, DNA ligase IV (LIG4), Ataxia telangiectasia mutated (ATM), and ATM- and Rad3-r

130 h inhibitors of the serine-threonine kinases ataxia telangiectasia mutated (ATM), AT- and Rad3-relate

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

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

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

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

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

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

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

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

139 However, in ataxia telangiectasia mutated (ATM)-deficient lymphocyte

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

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

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

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

144 Here we show that hypoxia results in ataxia telangiectasia mutated (ATM)-dependent phosphoryl

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

146 The ataxia telangiectasia mutated (ATM)-interacting protein

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

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

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

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

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

152 ain sensor of double-strand breaks in cells, ataxia telangiectasia mutated (ATM).

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

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

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

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

157 Ataxia telangiectasia-mutated (ATM) and ataxia telangiec

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

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

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

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

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

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

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

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

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

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

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

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

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

171 By crossing the FX premutation mice to Ataxia Telangiectasia-Mutated (Atm) mutant mice, we show

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

173 n of DSB responses through activation of the ataxia telangiectasia-mutated (ATM) serine-threonine kin

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

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

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

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

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

179 nase-related protein kinases (PIKKs) such as ataxia telangiectasia-mutated (ATM).

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

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

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

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

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

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

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

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

191 The p53 activation depends on the ataxia-telangiectasia mutated (ATM) gene product and inc

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

193 Ataxia-telangiectasia mutated (ATM) is a cellular damage

194 Ataxia-telangiectasia mutated (ATM) is a high molecular

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

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

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

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

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

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

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

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

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

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

205 The ataxia-telangiectasia mutated (ATM) protein kinase is ac

206 Ataxia-telangiectasia mutated (ATM) protein kinase regul

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

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

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

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

211 Ataxia-telangiectasia mutated (ATM), ATM and Rad3-relate

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

213 Its role in activating Ataxia-Telangiectasia Mutated (ATM), the central checkpo

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

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

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

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

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

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

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

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

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

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

224 A (siRNA) knockdowns, we identified the ATR (ataxia-telangiectasia mutated [ATM] and Rad3 related) si

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

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

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

228 angiectasia and Rad-3 related)/CHK1 and ATM (Ataxia telangiectasia mutated)/CHK2 pathways in addition

229 Inhibition of ataxia telangiectasia mutated decreased the induction of

230 We previously reported that ataxia-telangiectasia mutated deficiency resets the prim

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

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

233 find that the absence of 53BP1 results in an ataxia telangiectasia mutated-dependent increase in DNA

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

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

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

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

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

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

240 ine 139 by DNA damage sensor kinases such as ataxia telangiectasia-mutated, forming gamma-H2AX.

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

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

243 CI 1.22-1.49) at a locus containing ATM, the ataxia telangiectasia mutated gene.

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

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

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

247 elling was significantly increased by p53 or ataxia telangiectasia mutated inhibition (ATM), indicati

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

249 Ataxia telangiectasia-mutated inhibition only retards re

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

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

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

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

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

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

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

257 Ataxia telangiectasia-mutated kinase activity can compen

258 We discovered that both ATM (ataxia telangiectasia-mutated kinase) and ATR (ATM- and

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

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

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

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

263 f DNA damage initiates signaling through the ataxia-telangiectasia mutated kinase (ATM) and the ATM-

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

265 Ataxia-telangiectasia mutated kinase and JNK mediated th

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

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

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

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

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

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

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

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

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

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

276 RAD51C recruitment depends on ataxia telangiectasia mutated, NBS1, and replication pro

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

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

279 homeostatic role in reversing the effects of ataxia telangiectasia-mutated phosphorylation of H2AX.

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

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

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

283 The ataxia telangiectasia-mutated protein (ATM) detects DSBs

284 Stimulated histone H2AX phosphorylation was ataxia telangiectasia-mutated protein-dependent.

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

286 The ATM (ataxia telangiectasia mutated) protein responds to clast

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 age signals (e.g. gamma-H2AX, phosphorylated ataxia telangiectasia mutated (Ser-1981), and phosphoryl

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

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

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

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

294 Knock down of ataxia telangiectasia mutated suppressed gammaH2AX and C

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

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