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1 ompanied by a change in the abundance of the ATM protein.
2 d by western blot for abnormal expression of ATM protein.
3  acid changes or premature truncation of the ATM protein.
4                        All four cases lacked ATM protein.
5 ing to generate mice that do not express the Atm protein.
6 era raised against the approximately 350 kDa ATM protein.
7 of p53 or the ataxia telangiectasia mutated (ATM) protein.
8 ated with the ataxia telangiectasia mutated (ATM) protein.
9                                          The ATM protein, a member of the phosphatidylinositol 3-kina
10 uggested that ataxia-telangiectasia mutated (ATM) protein, a protein kinase, is a direct target of mi
11  is the human Ataxia Telangiectasia Mutated (ATM) protein, a wortmannin-sensitive protein kinase that
12                                          The ATM protein acts as a sensor of radiation-induced cellul
13 in A-T cells; AMOs restored up to 20% of the ATM protein and corrected the A-T cellular phenotype.
14 ex of approximately 500 kDa containing the X-ATM protein and other, as yet unidentified component(s).
15 ecombinant X-ATM are highly specific for the ATM protein and recognize a single polypeptide of 370-kD
16               Ataxia telangiectasia mutated (ATM) protein and AT- and Rad9-related protein kinases, b
17 ctors such as ataxia telangiectasia mutated (ATM) protein and combined deficiencies in classical non-
18 Inhibition of ataxia telangiectasia mutated (ATM) protein and DNA-PK could not suppress the induction
19 reatment-induced apoptosis by activating the ATM protein, and that the presence of the XPC protein is
20                                          The ATM protein appears to be a regulator of ABL activity in
21  pattern and the nuclear localization of the ATM protein are consistent with the proposed function of
22 nd immunoblot analysis, we show that Atr and Atm proteins are approximately 300 and 350 kD relative m
23 ntly reduced episome levels, suggesting that ATM proteins are playing an important role in HPV episom
24                                  Kinase-dead ATM protein (Atm-KD), but not loss of ATM (Atm-null), pr
25              We have observed purified human ATM protein, ATM-DNA and ATM-DNA-avidin bound complexes
26 ases of B-CLL were studied for expression of ATM protein by Western blot analysis and RIA.
27 by using X-ray crystal structures of a Vps34-ATM protein chimera where the Vps34 ATP-binding site was
28 nase' subclass of kinases which includes the ATM protein defective in ataxia telangiectasia patients.
29 de a progressive neurodegeneration caused by ATM protein deficiency.
30                               The level of X-ATM protein did not change throughout the meiotic divisi
31 now show that ATM kinase inhibition, but not ATM protein disruption, also inhibits DNA synthesis.
32 reported that ATM kinase inhibition, but not ATM protein disruption, blocks sister chromatid exchange
33         Furthermore, we demonstrate that the Atm protein exists as two discrete molecular species, an
34 es with LOH at the ATM gene were studied for ATM protein expression by Western blot analysis.
35                      In addition, we analyse ATM protein expression in a variety of A-T patients.
36                                         When ATM protein expression was suppressed by short hairpin R
37 y, monoubiquitination of Fanconi protein D2, ATM protein expression, and non-homologous DNA end joini
38 rve any change in the level or mobility of X-ATM protein following gamma-irradiation of embryos.
39 o the translation of full-length, functional ATM protein for at least 84 h in the three cell lines ex
40  (A-T) is a syndrome associated with loss of ATM protein function.
41                Pharmacological inhibition of ATM proteins had no effect on episome levels, but ATM kn
42                     We find that in neurons, ATM protein has a substantial cytoplasmic distribution.
43                                          The ATM protein has been implicated in pathways controlling
44                                    Since the ATM protein has been implicated in telomere metabolism o
45                                          The ATM protein has roles in DNA repair and in the regulatio
46 y at 11q22-23 and, more recently, absence of ATM protein, have been associated with poor prognosis in
47 ng compounds consistently induced functional ATM protein in ATM-deficient cells containing disease-ca
48 important function of catalytically inactive ATM protein in DNA repair.
49  findings are consistent with a role for the ATM protein in ensuring the fidelity of DNA repair and c
50 of human A-T and found evidence for residual ATM protein in seven of them.
51 cent study suggests the presence of residual ATM protein in the brain of one such model.
52  telangiectasia based on their effect on the ATM protein, including five that caused a protein trunca
53 ion experiment further demonstrated that the ATM protein interacted with the TFIIH basal transcriptio
54                       Abnormal expression of ATM protein is a frequent finding in B-CLL.
55                                          The ATM protein is a member of the PI 3-kinase-like superfam
56                                          The ATM protein is a single, high-molecular weight protein p
57                                A fraction of ATM protein is localized in mitochondria, and it is rapi
58                                              ATM protein is normally present at high levels primarily
59 as been previously proposed and that loss of ATM protein is not sufficient to induce cerebellar degen
60               In addition, we found that the ATM protein is predominantly cytoplasmic in Purkinje cel
61                                          The ATM protein is therefore critical both for cellular resp
62 show that the ataxia-telangiectasia mutated (ATM) protein is activated and forms telomeric foci in re
63           The ataxia-telangiectasia mutated (ATM) protein is an apical kinase that orchestrates the m
64 astogens, the ataxia telangiectasia mutated (ATM) protein is rapidly activated, which in turn initiat
65           The ataxia telangiectasia mutated (ATM) protein is the principal activator of the p53 prote
66 emonstrate that DNA-PKcs, unlike the related ATM protein, is not essential for the activation of p53
67               In response to DNA damage, the ATM protein kinase activates signal transduction pathway
68                                          The Atm protein kinase and Mre11-Rad50-nibrin (MRN) complex
69  patients are deficient in activation of the Atm protein kinase and phosphorylation of downstream Atm
70 l function in facilitating activation of the ATM protein kinase at sites of DNA double-strand breaks
71                        Here we show that the ATM protein kinase directly phosphorylates T68 within th
72 cell cycle checkpoint protein related to the ATM protein kinase family.
73 tasia, a disorder caused by mutations in the Atm protein kinase gene.
74  double-strand break (DSB) activates ATR and ATM protein kinase homologs Mec1 and Tel1, which then ac
75  a consensus site for phosphorylation by the ATM protein kinase in cells; and TAO and p38 activation
76                                          The ATM protein kinase is a critical intermediate in a numbe
77                                              ATM protein kinase is activated by DNA damage and respon
78                                          The ATM protein kinase is activated by intermolecular autoph
79                                          The Atm protein kinase is central to the DNA double-strand b
80                                          The ATM protein kinase is essential for cells to repair and
81                                          The ATM protein kinase is mutated in ataxia telangiectasia,
82                    The gene that encodes the ATM protein kinase is mutated in ataxia-telangiectasia (
83                                          The ATM protein kinase regulates the cell's response to DNA
84                                          The ATM protein kinase regulates the DNA damage response by
85                                          The ATM protein kinase regulates the response of the cell to
86                  Acute ex vivo inhibition of ATM protein kinase significantly decreased mitochondrial
87                                          The ATM protein kinase, mutations of which are associated wi
88                                          The ATM protein kinase, the product of the gene mutated in A
89 e chief mobilizer of the DSB response is the ATM protein kinase.
90 nzymes, end tethering, and activation of the ATM protein kinase.
91 tasia (A-T) results from inactivation of the ATM protein kinase.
92 licit a rapid signaling response through the ATM protein kinase.
93 , in response to IR also is dependent on the ATM protein kinase.
94 trated by the ataxia-telangiectasia mutated (ATM) protein kinase and involves interruption of Hdm2-me
95           The ataxia-telangiectasia mutated (ATM) protein kinase blocks cell cycle progression in res
96           The ataxia telangiectasia mutated (ATM) protein kinase is a critical component of a DNA-dam
97           The ataxia-telangiectasia mutated (ATM) protein kinase is a master regulator of the DNA dam
98           The ataxia-telangiectasia mutated (ATM) protein kinase is activated by DNA double-strand br
99           The ataxia-telangiectasia-mutated (ATM) protein kinase is rapidly and specifically activate
100           The Ataxia Telangiectasia-Mutated (ATM) protein kinase is recruited to sites of double-stra
101           The ataxia-telangiectasia mutated (ATM) protein kinase is widely known for its function as
102            The Ataxia Telangietasia mutated (ATM) protein kinase promotes DNA repair and activates ch
103            The ataxia telangiectasia mutant (ATM) protein kinase regulates the cell's response to DNA
104           The ataxia telangiectasia mutated (ATM) protein kinase regulates the cellular response to d
105               Ataxia-telangiectasia mutated (ATM) protein kinase regulates the DNA damage response (D
106 gest that the ataxia-telangiectasia-mutated (ATM) protein kinase signal-transduction pathway is prima
107 diated by the ATAXIA TELANGIECTASIA MUTATED (ATM) protein kinase, representing candidate factors that
108 m, led by the ataxia telangiectasia mutated (ATM) protein kinase, represses MITF transcriptional acti
109  on activation of the ataxia-telangiectasia (ATM) protein kinase, which phosphorylates cell-cycle eff
110 ctivating the ataxia-telangiectasia mutated (ATM) protein kinase.
111 ogated by caffeine and requires ATR, but not ATM, protein kinase.
112                                  The ATR and ATM protein kinases are known to be involved in a wide v
113  PRMT1 and PRMT5 as modulators that regulate ATM protein level.
114                                              ATM protein levels and localization remain constant thro
115                                              ATM protein levels remained constant throughout the cell
116                       We revealed that total ATM protein levels were high in some human melanoma line
117 e reduced in ataxia telangiectasia cells and ATM protein levels were low in primary murine fibroblast
118                                     Cellular Atm protein levels were lower in AS-IGF1R-transfected ce
119 metic drug neocarzinostatin had no effect on ATM protein levels, in contrast to a noted rise in p53 l
120 RCA-associated cancers (without DDR-GAs), or ATM protein loss as determined by immunohistochemistry.
121 d by DNA damage, indicating that the Nbs and Atm proteins may participate in common pathways.
122 ypothesized that the absence of a functional ATM protein might involve perturbations to the ubiquitin
123 , in contrast to the nuclear localization of ATM protein observed in cultured cells.
124               Ataxia telangiectasia mutated (ATM) protein plays a central role in DNA damage response
125           The ataxia telangiectasia mutated (ATM) protein plays a central role in early stages of DNA
126  homolog of the human ataxia telangiectasia (ATM) protein, prevents these translocations, whereas the
127 e the acetyltransferase Tip60 must acetylate ATM proteins prior to their full activation by autophosp
128 lines lacking ataxia telangiectasia mutated (ATM) protein produced wild-type levels of infectious vir
129 ns, as demonstrated by direct measurement of ATM protein, restored ATM kinase activity, and colony su
130  A-T patients with 5-20% of normal levels of ATM protein show slower neurological progression, A-T ma
131               Expression of kinase-dead (KD) ATM protein solely accelerates lymphomagenesis beyond AT
132 to R3047X in human ATM) severely compromises ATM protein stability and causes T cell developmental de
133 vation of ATM without consistently affecting ATM protein stability and recruitment.
134 t a physiological role of the FATC domain in ATM protein stability and show that the presence of mini
135 anslated and produces a catalytically active ATM protein that responds to DNA damage by phosphorylati
136                                          The ATM protein that the gene encodes is involved in DNA dou
137                    The central region of the ATM protein therefore contains multiple sequences which
138      In brain, although Bal/Bal mice have no ATM protein, they have nearly normal amounts of Atm mRNA
139 62ins137) that express a low level of normal ATM protein to evaluate the impact of residual Nbs1 func
140 tein was required for the association of the ATM protein to genomic DNA.
141 ino acids 1-150 of ATM were required for the ATM protein to regulate cellular radiosensitivity.
142  XPC protein is essential for recruiting the ATM protein to the DNA template.
143 -T patients and mouse models that express no ATM protein undergo normal embryonic development but exh
144                       Steady-state levels of ATM protein varied from undetectable in most AT cell lin
145                                 The restored ATM protein was close to normal levels in cells with hom
146                                           No ATM protein was detected by western blotting in any AT c
147 ne ATM mutation, and a variable reduction in ATM protein was detected in all 4 patients examined.
148                               In adult mice, ATM protein was detected in all tissues examined and was
149  that the aminoglycoside-induced full-length ATM protein was functional and corrected, to various ext
150                            Expression of the ATM protein was impaired in eight (40%) of the 20 tumour
151                                    Truncated ATM protein was not detected in lymphoblasts from ataxia
152                                   Functional ATM protein was required for HuCds1 modification after i
153                  A significant amount of the ATM protein was still detected 21 days after a single 5
154  help clarify the physiological roles of the ATM protein, we disrupted the ATM gene in mice through h
155  Here, we show that the expression levels of Atm protein were gradually increased during liver regene
156 the status of ataxia-telangiectasia mutated (ATM) protein, which activates p53 in response to DNA dam
157                            Pre-incubation of ATM protein with active DNA-PKcs also significantly redu
158 stration of a nuclear association of Atr and Atm proteins with meiotic chromosomes and suggests a dir
159 expression of Ataxia Telangiectasia Mutated (ATM) protein within melanocytes in anagen hair follicle
160                                      Xenopus ATM protein (X-ATM) is 85% identical to human ATM within

 
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