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ataxia telangiectasia/tyrosine
Linkki tallennetaan leikepöydälle
Sivu 1 alkaen 79 tuloksia
Ataxia telangiectasia mutant protein activates c-Abl tyrosine kinase in response to ionizing radiation.
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Ataxia telangiectasia (AT) is a rare human autosomal recessive disorder with pleiotropic phenotypes, including neuronal degeneration, immune dysfunction, premature ageing and increased cancer risk. The gene mutated in AT, ATM, encodes a putative lipid or protein kinase. Most of the human AT patient
c-Abl tyrosine kinase is not essential for ataxia telangiectasia mutated functions in chromosomal maintenance.
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c-Abl is activated by DNA damage in an ataxia telangiectasia mutated (ATM)-dependent manner and plays important roles in growth arrest and apoptosis induced by DNA damage. c-Abl also interacts physically and functionally with Rad51, a key molecule in homologous recombinational (HR) DNA repair. To
Receptor tyrosine kinase EphA5 is a functional molecular target in human lung cancer.
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Lung cancer is often refractory to radiotherapy, but molecular mechanisms of tumor resistance remain poorly defined. Here we show that the receptor tyrosine kinase EphA5 is specifically overexpressed in lung cancer and is involved in regulating cellular responses to genotoxic insult. In the absence
Defective radiation signal transduction in ataxia-telangiectasia cells.
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OBJECTIVE
The product of the gene ATM mutated in the human genetic disorder ataxia-telangiectasia (A-T) is predominantly present in the nucleus Compatible with a role in DNA-damage recognition and cell-cycle control. However, ATM is also present outside the nucleus in cytoplasmic and membrane
Defect in Radiation Signal Transduction in Ataxia-telangiectasia.
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Exposure of mammalian cells to ionizing radiation causes a delay in progression through the cycle at several checkpoints. Cells from patients with ataxia-telangiectasia (A-T) ignore these checkpoint controls postirradiation. The tumour suppressor gene product p53 plays a key role at the G1/S
Defect in radiation signal transduction in ataxia-telangiectasia.
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Exposure of mammalian cells to ionizing radiation causes a delay in progression through the cycle at several checkpoints. Cells from patients with ataxia-telangiectasia (A-T) ignore these checkpoint controls postirradiation. The tumour suppressor gene product p53 plays a key role at the G1/S
Defect in radiation signal transduction in ataxia-telangiectasia.
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Exposure of mammalian cells to ionizing radiation causes a delay in progression through the cycle at several checkpoints. Cells from patients with ataxia-telangiectasia (A-T) ignore these checkpoint controls postirradiation. The tumour suppressor gene product p53 plays a key role at the G1/S
Human topoisomerase II function, tyrosine phosphorylation and cell cycle checkpoints.
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Three DNA damage-responsive cell cycle checkpoints can be shown to operate in diploid human fibroblasts. One checkpoint arrests growth in G1, another inhibits replicon initiation in S phase cells, and the third delays progression from G2 into mitosis. Progression from G2 into M is controlled in part
Expression of the ATDC (ataxia telangiectasia group D-complementing) gene in A431 human squamous carcinoma cells.
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The ATDC gene was originally identified by its ability to complement the radiosensitivity defect of an ataxia telangiectasia (AT) fibroblast cell line. Because hypersensitivity to ionizing radiation is an important feature of the AT phenotype, we reasoned that ATDC may function generally in the
Impaired ionizing radiation-induced activation of a nuclear signal essential for phosphorylation of c-Jun by dually phosphorylated c-Jun amino-terminal kinases in ataxia telangiectasia fibroblasts.
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The c-Jun amino-terminal kinases (JNKs) participate in intracellular signaling in response to cytokines and cellular stresses. JNKs are activated by phosphorylation on two critical residues, the threonine 183 and tyrosine 185, within the TPY motif. The activated JNKs, in turn, phosphorylate the
Activation of p53 by oxidative stress involves platelet-derived growth factor-beta receptor-mediated ataxia telangiectasia mutated (ATM) kinase activation.
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Phosphorylation of the p53 tumor suppressor protein is a critical event in the up-regulation and activation of p53 during cellular stress. In this study, we characterized the signaling pathway linking oxidative stress to p53 through the platelet-derived growth factor beta (PDGF beta) receptor and
Ataxia telangiectasia mutated impacts insulin-like growth factor 1 signalling in skeletal muscle.
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Reports that ataxia telangiectasia mutated (ATM) is required for full activation of Akt raise the hypothesis that ATM plays a role in insulin-like growth factor 1 (IGF-1) signalling through the Akt/mammalian target of rapamycin (mTOR) pathway. Differentiated C2C12 cells harbouring either
Lyn tyrosine kinase promotes silencing of ATM-dependent checkpoint signaling during recovery from DNA double-strand breaks.
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DNA damage activates the DNA damage checkpoint and the DNA repair machinery. After initial activation of DNA damage responses, cells recover to their original states through completion of DNA repair and termination of checkpoint signaling. Currently, little is known about the process by which cells
Inhibition of c-Abl tyrosine kinase activity by filamentous actin.
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The catalytic activity of c-Abl tyrosine kinase is reduced in fibroblasts that are detached from the extracellular matrix. We report here that a deletion of the extreme C terminus of c-Abl (DeltaF-actin c-Abl) can partially restore kinase activity to c-Abl from detached cells. Because the extreme C
Progressive sensorimotor impairment is not associated with reduced dopamine and high energy phosphate donors in a model of ataxia-telangiectasia.
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Ataxia-telangiectasia (A-T) is a genetic disease, associated with progressive motor impairment and a lack of functional ATM protein. It has been reported that immunoreactive tyrosine hydroxylase and dopamine transporter are reduced in an Atm-/- mouse model of A-T. These observations led to a
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