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PMID |
Sentence |
1 |
9398851
|
Atm is required for proper assembly of Rad51 onto the chromosomal axial elements during meiosis.
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2 |
20208057
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ATM, mutated in ataxia telangiectasia, is critical for the genotoxic stress response, and its deficiency is associated with accelerated atherosclerosis and insulin resistance in humans and mice.
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3 |
20357360
|
In obese women, CD11c(+) ATM density was greater in subcutaneous than omental adipose tissue and correlated with markers of insulin resistance.
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4 |
20357360
|
Tissue culture medium conditioned by CD11c(+) ATMs, but not CD11c(-) ATMs or other stromovascular cells, impaired insulin-stimulated glucose uptake by human adipocytes.
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5 |
20736911
|
This phosphorylation of H2AX is mediated by the phosphatidyl-inosito 3-kinase (PI3K) family of proteins, ataxia telangiectasia mutated (ATM), DNA-protein kinase catalytic subunit and ATM and RAD3-related (ATR).
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6 |
20956556
|
ATM phosphorylates the p53 tumor suppressor on a site (Ser15) that regulates transcription activity.
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7 |
20956556
|
This analysis demonstrates that p53 phosphorylation on an ATM site is an important mechanism in the physiological regulation of glucose homeostasis.
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8 |
21315178
|
Particular attention is given to the role of ATM in insulin signaling and Akt activation.
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9 |
15187252
|
The checkpoint kinase Chk2 is activated in response to DNA damage through pathways requiring protein kinases ATM and/or ATR.
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10 |
18534819
|
The role of ATM in activation of Akt was further confirmed in mouse embryonic fibroblast (MEF) A29 (ATM+/+) and A38 (ATM-/-) cells.
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11 |
20676049
|
In different cellular models where ATM expression was disrupted, we demonstrated that the absence of ATM leads to an increased expression of both subunits of the transcription factor Hypoxia Inducible Factor 1 (HIF-1).
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12 |
20676049
|
Interestingly, we demonstrated that ATM disruption positively regulates both expression and function of the basal glucose transporter GLUT-1 as well as the proangiogenic factor, VEGF.
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13 |
20676049
|
In addition, our results suggest that the absence of ATM increases HIF-1 proteins biosynthesis, and this effect is dependant on the oxidative stress existing in ATM deficient cells.
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