|
Ataxia Telangiectasia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
We observed that overexpression of MCPyV sT antigen induced the phosphorylation of histone H2AX as well as the activation of ataxia telangiectasia mutant (ATM), an upstream kinase important for H2AX phosphorylation.
|
31401636 |
2019 |
|
Ataxia Telangiectasia
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
Activation of Ataxia Telangiectasia Mediated protein kinase (ATM) by its phosphorylation on serine 1981 and phosphorylation of histone H2AX on serine 139 (γH2AX) are the key events reporting DNA damage, primarily formation of DNA double strand breaks.
|
28477120 |
2017 |
|
Ataxia Telangiectasia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Using western blotting it was shown that GA inhibited the protein expressions of MDC1, O(6)-methylguanine-DNA methyltransferase (MGMT), p-H2A.X, p53, DNA-dependent serine/threonine protein kinase (DNA-PK) and 14-3-3 proteins sigma (14-3-3σ) but increased p-p53, phosphate-ataxia-telangiectasia (p-H2A.X) and ataxia telangiectasia mutated and Rad3-related (p-ATR), phosphate-ataxia telangiectasia mutated (p-ATM) and breast cancer susceptibility protein 1 (BRCA1) in a 24-h treatment.
|
25862863 |
2015 |
|
Ataxia Telangiectasia
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
Furthermore, this growth arrest by piperine treatment was associated with DNA damage as indicated by phosphorylation of H2AX at Ser139, activation of ataxia telangiectasia and rad3-related protein (ATR) and checkpoint kinase 1 (Chk1).
|
24804719 |
2014 |
|
Ataxia Telangiectasia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Compared with controls, nuclear DNA damage response was higher (P ≤ 0.001) in diabetic subjects with increased accumulation of phospho-ataxia-telangiectasia (ATM), γ-H2AX, along with active recruitment of repair proteins (Mre11, Rad50, and Nbs1).
|
22061042 |
2011 |
|
Ataxia Telangiectasia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Therefore, we sought a possible modifier effect of H2AX gene on various clinical features in a group of patients with AT and healthy controls.
|
21199394 |
2011 |
|
Ataxia Telangiectasia
|
0.100 |
Biomarker
|
disease |
BEFREE |
This paper describes a new approach to the identification of A-T heterozygotes based on a two-tier analysis of histone H2AX phosphorylation.
|
19167771 |
2009 |
|
Ataxia Telangiectasia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Consistent with the increased cytotoxicity, cotreatment with VPA was shown to upregulate the cisplatin-mediated DNA damage revealed by phosphorylation of ataxia telangiectasia mutation and histone H2AX.
|
18429963 |
2008 |
|
Ataxia Telangiectasia
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
We have investigated the effect of hyperoxia on DNA damage signaling and show that hyperoxia is a unique stress that activates the ataxia telangiectasia mutant (ATM)- and Rad3-related protein kinase (ATR)-dependent p53 phosphorylations (Ser6, -15, -37, and -392), phosphorylation of histone H2AX (Ser139), and phosphorylation of checkpoint kinase 1 (Chk1).
|
18344416 |
2008 |
|
Ataxia Telangiectasia
|
0.100 |
Biomarker
|
disease |
BEFREE |
We established normal ranges of histone H2AX phosphorylation after 2 Gy IR by testing T-cell lines, lymphoblastoid cell lines (LCLs) and/or peripheral blood mononuclear cells (PBMCs) or both from 20 genetically proven A-T and 46 control donors.
|
18431795 |
2008 |
|
Ataxia Telangiectasia
|
0.100 |
GeneticVariation
|
disease |
LHGDN |
ATM activation accompanies histone H2AX phosphorylation in A549 cells upon exposure to tobacco smoke.
|
17594478 |
2007 |
|
Ataxia Telangiectasia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
We examined noncancerous human fibroblast strains from individuals with ataxia telangiectasia (ataxia telangiectasia mutated [ATM] deficient) or Li-Fraumeni syndrome (p53 deficient) using the neutral comet, H2AX phosphorylation, and clonogenic survival assays.
|
17126209 |
2006 |
|
Ataxia Telangiectasia
|
0.100 |
Biomarker
|
disease |
BEFREE |
The number of gamma-H2AX foci increased in proportion to the dose in both AT and normal cells after high-dose-rate irradiation.
|
16494515 |
2006 |
|
Ataxia Telangiectasia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Transfection of AT cells with ATM cDNA fully restored the association of RPA foci with gamma-H2AX illustrating the requirement of ATM gene product for this process.
|
15474997 |
2004 |
|
Ataxia Telangiectasia
|
0.100 |
Biomarker
|
disease |
BEFREE |
We also discuss how this model of H2AX function could account for some aspects of the genomic instability and cancer prone human phenotypes associated with Ataxia Telangiectasia (AT), Nijmegen Breakage Syndrome (NBS), Ataxia Telangiectasia Like Disorder (ATLD), and Bloom's Syndrome (BS).
|
14712078 |
2004 |