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1 d by western blot for abnormal expression of ATM protein.
2 acid changes or premature truncation of the ATM protein.
3 All four cases lacked ATM protein.
4 ing to generate mice that do not express the Atm protein.
5 era raised against the approximately 350 kDa ATM protein.
6 ompanied by a change in the abundance of the ATM protein.
7 of p53 or the ataxia telangiectasia mutated (ATM) protein.
8 ated with the ataxia telangiectasia mutated (ATM) protein.
10 is the human Ataxia Telangiectasia Mutated (ATM) protein, a wortmannin-sensitive protein kinase that
12 in A-T cells; AMOs restored up to 20% of the ATM protein and corrected the A-T cellular phenotype.
13 ex of approximately 500 kDa containing the X-ATM protein and other, as yet unidentified component(s).
14 ecombinant X-ATM are highly specific for the ATM protein and recognize a single polypeptide of 370-kD
16 ctors such as ataxia telangiectasia mutated (ATM) protein and combined deficiencies in classical non-
17 Inhibition of ataxia telangiectasia mutated (ATM) protein and DNA-PK could not suppress the induction
18 reatment-induced apoptosis by activating the ATM protein, and that the presence of the XPC protein is
20 pattern and the nuclear localization of the ATM protein are consistent with the proposed function of
21 nd immunoblot analysis, we show that Atr and Atm proteins are approximately 300 and 350 kD relative m
22 ntly reduced episome levels, suggesting that ATM proteins are playing an important role in HPV episom
26 nase' subclass of kinases which includes the ATM protein defective in ataxia telangiectasia patients.
29 now show that ATM kinase inhibition, but not ATM protein disruption, also inhibits DNA synthesis.
30 reported that ATM kinase inhibition, but not ATM protein disruption, blocks sister chromatid exchange
35 y, monoubiquitination of Fanconi protein D2, ATM protein expression, and non-homologous DNA end joini
37 o the translation of full-length, functional ATM protein for at least 84 h in the three cell lines ex
44 y at 11q22-23 and, more recently, absence of ATM protein, have been associated with poor prognosis in
45 ng compounds consistently induced functional ATM protein in ATM-deficient cells containing disease-ca
47 findings are consistent with a role for the ATM protein in ensuring the fidelity of DNA repair and c
50 telangiectasia based on their effect on the ATM protein, including five that caused a protein trunca
51 ion experiment further demonstrated that the ATM protein interacted with the TFIIH basal transcriptio
57 as been previously proposed and that loss of ATM protein is not sufficient to induce cerebellar degen
60 show that the ataxia-telangiectasia mutated (ATM) protein is activated and forms telomeric foci in re
62 astogens, the ataxia telangiectasia mutated (ATM) protein is rapidly activated, which in turn initiat
64 emonstrate that DNA-PKcs, unlike the related ATM protein, is not essential for the activation of p53
67 patients are deficient in activation of the Atm protein kinase and phosphorylation of downstream Atm
68 l function in facilitating activation of the ATM protein kinase at sites of DNA double-strand breaks
72 double-strand break (DSB) activates ATR and ATM protein kinase homologs Mec1 and Tel1, which then ac
73 a consensus site for phosphorylation by the ATM protein kinase in cells; and TAO and p38 activation
91 trated by the ataxia-telangiectasia mutated (ATM) protein kinase and involves interruption of Hdm2-me
102 gest that the ataxia-telangiectasia-mutated (ATM) protein kinase signal-transduction pathway is prima
103 on activation of the ataxia-telangiectasia (ATM) protein kinase, which phosphorylates cell-cycle eff
109 e reduced in ataxia telangiectasia cells and ATM protein levels were low in primary murine fibroblast
111 metic drug neocarzinostatin had no effect on ATM protein levels, in contrast to a noted rise in p53 l
113 ypothesized that the absence of a functional ATM protein might involve perturbations to the ubiquitin
116 homolog of the human ataxia telangiectasia (ATM) protein, prevents these translocations, whereas the
117 e the acetyltransferase Tip60 must acetylate ATM proteins prior to their full activation by autophosp
118 lines lacking ataxia telangiectasia mutated (ATM) protein produced wild-type levels of infectious vir
119 ns, as demonstrated by direct measurement of ATM protein, restored ATM kinase activity, and colony su
120 A-T patients with 5-20% of normal levels of ATM protein show slower neurological progression, A-T ma
121 anslated and produces a catalytically active ATM protein that responds to DNA damage by phosphorylati
124 In brain, although Bal/Bal mice have no ATM protein, they have nearly normal amounts of Atm mRNA
125 62ins137) that express a low level of normal ATM protein to evaluate the impact of residual Nbs1 func
129 -T patients and mouse models that express no ATM protein undergo normal embryonic development but exh
133 ne ATM mutation, and a variable reduction in ATM protein was detected in all 4 patients examined.
135 that the aminoglycoside-induced full-length ATM protein was functional and corrected, to various ext
140 help clarify the physiological roles of the ATM protein, we disrupted the ATM gene in mice through h
141 Here, we show that the expression levels of Atm protein were gradually increased during liver regene
142 the status of ataxia-telangiectasia mutated (ATM) protein, which activates p53 in response to DNA dam
144 stration of a nuclear association of Atr and Atm proteins with meiotic chromosomes and suggests a dir
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