HCSGD entry for H2AFX
1. General information
| Official gene symbol | H2AFX |
|---|---|
| Entrez ID | 3014 |
| Gene full name | H2A histone family, member X |
| Other gene symbols | H2A.X H2A/X H2AX |
| Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network
3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
|---|---|---|---|
| GO:0000077 | DNA damage checkpoint | IDA | biological_process |
| GO:0000724 | Double-strand break repair via homologous recombination | TAS | biological_process |
| GO:0000781 | Chromosome, telomeric region | IDA | cellular_component |
| GO:0000786 | Nucleosome | IEA | cellular_component |
| GO:0000790 | Nuclear chromatin | IEA | cellular_component |
| GO:0000794 | Condensed nuclear chromosome | IEA | cellular_component |
| GO:0001673 | Male germ cell nucleus | IEA | cellular_component |
| GO:0001741 | XY body | IEA | cellular_component |
| GO:0003677 | DNA binding | NAS | molecular_function |
| GO:0003684 | Damaged DNA binding | IEA | molecular_function |
| GO:0005515 | Protein binding | IPI | molecular_function |
| GO:0005634 | Nucleus | IDA | cellular_component |
| GO:0005654 | Nucleoplasm | TAS | cellular_component |
| GO:0005657 | Replication fork | IEA | cellular_component |
| GO:0006281 | DNA repair | TAS | biological_process |
| GO:0006302 | Double-strand break repair | NAS TAS | biological_process |
| GO:0006334 | Nucleosome assembly | NAS | biological_process |
| GO:0006974 | Cellular response to DNA damage stimulus | IDA | biological_process |
| GO:0007126 | Meiosis | IEA | biological_process |
| GO:0007283 | Spermatogenesis | IEA | biological_process |
| GO:0010212 | Response to ionizing radiation | NAS | biological_process |
| GO:0019899 | Enzyme binding | IPI | molecular_function |
| GO:0035861 | Site of double-strand break | IDA | cellular_component |
| GO:0042393 | Histone binding | IPI | molecular_function |
| GO:0045739 | Positive regulation of DNA repair | NAS | biological_process |
| GO:0046982 | Protein heterodimerization activity | IEA | molecular_function |
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4. Expression levels in datasets
- Meta-analysis result
| p-value up | p-value down | FDR up | FDR down |
|---|---|---|---|
| 0.9934508985 | 0.0068370085 | 0.9999902473 | 0.1653088342 |
- Individual experiment result
( "-" represent NA in the specific microarray platform )
( "-" represent NA in the specific microarray platform )
| Data source | Up or down | Log fold change |
|---|---|---|
| GSE11954 | Down | -0.2083175693 |
| GSE13712_SHEAR | Up | 0.0045811887 |
| GSE13712_STATIC | Down | -0.1286833597 |
| GSE19018 | Down | -0.1606432483 |
| GSE19899_A1 | Down | -0.4063905657 |
| GSE19899_A2 | Down | -0.4328740164 |
| PubMed_21979375_A1 | Up | 0.2757657180 |
| PubMed_21979375_A2 | Down | -0.7320772839 |
| GSE35957 | Down | -0.3426800608 |
| GSE36640 | Down | -1.7592676094 |
| GSE54402 | Down | -0.2035185427 |
| GSE9593 | Down | -0.2646094629 |
| GSE43922 | Down | -0.1299045296 |
| GSE24585 | Down | -0.2044475770 |
| GSE37065 | Down | -0.3041883460 |
| GSE28863_A1 | Down | -0.4039402597 |
| GSE28863_A2 | Up | 0.0192120239 |
| GSE28863_A3 | Down | -0.3760406441 |
| GSE28863_A4 | Up | 0.1177315788 |
| GSE48662 | Down | -1.0353234737 |
5. Regulation relationships with compounds/drugs/microRNAs
- Compounds
Not regulated by compounds
- Drugs
Not regulated by drugs
- MicroRNAs
- mirTarBase
- mirTarBase
MiRNA_name | mirBase ID | miRTarBase ID | Experiment | Support type | References (Pubmed ID) |
|---|---|---|---|---|---|
| hsa-miR-138-5p | MIMAT0000430 | MIRT006493 | Luciferase reporter assay//Western blot | Functional MTI | 21693595 |
| hsa-miR-328-3p | MIMAT0000752 | MIRT019531 | Reporter assay;Western blot;qRT-PCR | Functional MTI | 19377482 |
| hsa-miR-24-3p | MIMAT0000080 | MIRT030383 | Reporter assay;Western blot;qRT-PCR | Functional MTI | 19377482 |
| hsa-miR-24-3p | MIMAT0000080 | MIRT030383 | qRT-PCR;Microarray | Functional MTI (Weak) | 19748357 |
| hsa-miR-484 | MIMAT0002174 | MIRT042120 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-miR-320a | MIMAT0000510 | MIRT044465 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-miR-16-5p | MIMAT0000069 | MIRT051262 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-let-7d-5p | MIMAT0000065 | MIRT051722 | CLASH | Functional MTI (Weak) | 23622248 |
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- mirRecord
No target information from mirRecord
- mirRecord
6. Text-mining results about the gene
Gene occurances in abstracts of cellular senescence-associated articles: 25 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
|---|---|
| 27286367 | The DNA breaks and DNA repair were examined by alkaline comet assay and by immunofluorescence staining of the phosphorylated histone variant H2AX (gammaH2AX), respectively |
| 26934368 | Exposure to radiation promoted a parallel induction of autophagy and senescence that was strongly correlated with the extent of persistent H2AX phosphorylation in both cell lines, however, inhibition of autophagy failed to suppress senescence, indicating that the two responses were dissociable |
| 26718258 | Previously, we showed that the sesquiterpene lactone, dehydroleucodine (DhL), promotes the accumulation of DNA damage markers, such as H2AX and 53BP1, in human tumor cells |
| 26596544 | One of the earliest cellular responses to DNA double strand breaks (DSBs) is the phosphorylation of the core histone protein H2AX (termed gammaH2AX) |
| 25712102 | Multiple facets of histone variant H2AX: a DNA double-strand-break marker with several biological functions |
| 25712102 | In the last decade, many papers highlighted that the histone variant H2AX and its phosphorylation on Ser 139 (gammaH2AX) cannot be simply considered a specific DNA double-strand-break (DSB) marker with a role restricted to the DNA damage response, but rather as a 'protagonist' in different scenarios |
| 25712102 | This review will present and discuss an up-to-date view regarding the 'non-canonical' H2AX roles, focusing in particular on possible functional and structural parts in contexts different from the canonical DNA DSB response |
| 25712102 | The authors will emphasize that, just as H2AX phosphorylation signals chromatin alteration and serves the canonical function of recruiting DSB repair factors, so the modification of H2AX in contexts other than the DNA damage response may contribute towards creating a specific chromatin structure frame allowing 'non-canonical' functions to be carried out in different cell types |
| 25293814 | To develop a more efficient, inclusive and sensitive methodology, we examined the phosphorylation of histone H2AX and the p53 levels in normal human periosteal cells exposed to x-rays or other oxidative stressors |
| 25293814 | The cell cycle, electric nuclear volume and CD44 expression were evaluated using flow cytometry, and the phosphorylated H2AX (gamma-H2AX), p53, p21 and proliferating cell nuclear antigen (PCNA) levels were evaluated by Western blot analyses |
| 25293814 | In parallel, each oxidative stress rapidly phosphorylated H2AX and stabilized p53, and intense stress sustained these high levels for at least 8 days |
| 24552809 | Interestingly, Ppm1d(-/-) MEFs showed increased H2AX phosphorylation levels without increased levels of reactive oxygen species (ROS) or DNA base damage compared with wild-type (Wt) MEFs, suggesting a decreased threshold for DDR activation or sustained DDR activation during recovery |
| 24552809 | Notably, the increased H2AX phosphorylation levels observed in Ppm1d(-/-) MEFs were primarily associated with S-phase cells and predominantly dependent on the activation of ATM |
| 23941874 | Consistent with this shift in favor of excessive reactive oxygen species, DFs also displayed a significant increase in senescence-associated beta-galactosidase activity and phospho-gamma-histone H2AX (pH2AX) level |
| 23811199 | The phosphorylation of p53 and histone H2Ax and the induction of the two proapoptotic genes Bax and Noxa were evident in SOD1-deficient MEFs and more enhanced under normoxic culture than under hypoxic culture |
| 23272087 | This mechanism appears to preserve androgen induced autophosphorylation of ATM and phosphorylation of H2AX, lesion processing and repair pathway yet restrain ATM/CHK1/CHK2 and p53 signaling pathway |
| 23050037 | Foci of phosphorylated histone H2AX and ATM are the surrogate markers of DNA double strand breaks |
| 23050037 | Large phosphorylated H2AX foci (>1 |
| 23050037 | Importantly, large foci of phosphorylated H2AX were always colocalized with phosphorylated ATM foci |
| 21149450 | The TopBP1-ablated mouse cells exhibit phosphorylation of H2AX and Chk2, indicating that the cells contain DNA breaks |
| 21118958 | Importantly, depletion of the DNA-SCARS-stabilizing component histone H2AX did not deplete 53BP1 from DNA-SCARS but diminished the presence of MDC1 and activated CHK2 |
| 21118958 | Furthermore, depletion of H2AX reduced both the p53-dependent senescence growth arrest and p53-independent cytokine secretion |
| 21081476 | We examined phosphorylation of H2AX, a marker for DNA double-strand breaks over the life of a human fibroblast cell line |
| 20889973 | Embryos lacking ATMIN (atmin(Delta/Delta)) died in utero and showed increased numbers of cells positive for phosphorylated histone H2aX, indicative of increased DNA damage |
| 20372780 | Phosphorylation of histone H2AX (gammaH2AX) is a sensitive marker of DNA damage, particularly induction of DNA double-strand breaks |
| 20372780 | Using multiparameter cytometry we explored the effects of doxorubicin (DOX), cisplatin (CDDP) and 5-fluorouracil (5-FU) on four types of endometrioid adenocarcinoma cell lines (HEC-1A, HEC-1B, Ishikawa, KLE) correlating the drug-induced increases in phosphorylated H2AX (gammaH2AX) with cell cycle phase, induction of apoptosis and induction of cell senescence, the latter detected by analysis of beta-galactosidase |
| 20372780 | Treatment with CDDP and 5-FU led to phosphorylation of H2AX preferentially in S-phase cells, consistent with the induction of replication stress |
| 20107320 | We further show that CAPNS1 depletion is coupled to reduced levels of H2AX phosphorylation, not only in Ras(v12) induced BJ-ET fibroblasts, but also in a number of cellular systems upon genotoxic stress |
| 18723444 | We show that human atherosclerotic plaque VSMCs exhibit increased levels of double-stranded DNA breaks and basal activation of DNA repair pathways involving ataxia telangiectasia-mutated (ATM) and the histone H2AX in vivo and in vitro |
| 18497977 | WI-38 and A549 cells were exposed to 200 microM H2O2 in the absence or presence of HA and induction of histone H2AX phosphorylation and activation of ATM, the reporters of DNA damage, was assessed by multiparameter cytometry |
| 18497977 | Also explored was effect of HA on constitutive H2AX phosphorylation that reflects DNA damage caused by endogenous oxidants generated during aerobic metabolism |
| 18497977 | 1% (w/v) in culture medium totally prevented the H2O2-induced H2AX phosphorylation in both cell types whereas effect of 60,000 average MW (low MW) HA was somewhat less pronounced |
| 18497977 | Constitutive H2AX phosphorylation in WI-38 cells growing in the presence of 0 |
| 18005250 | To understand quantitative and qualitative changes in the DNA damage response during human aging, DNA damage-induced foci of phosphorylated histone H2AX (gamma-H2AX), which occurs specifically at sites of DNA double-strand breaks (DSBs) and eroded telomeres, were examined in human young and senescing fibroblasts, and in lymphocytes of peripheral blood |
| 18001825 | We have shown that RNF8 facilitates the accumulation of checkpoint mediator proteins BRCA1 and 53BP1 to the damaged chromatin, on one hand through the phospho-dependent FHA domain-mediated binding of RNF8 to MDC1, on the other hand via its role in ubiquitylating H2AX and possibly other substrates at damage sites |
| 17879239 | The level of ATM activation and H2AX phosphorylation, detected immunocytochemically, has been monitored in WI-38, A549, and TK6 cells treated with H2O2 as well as growing under conditions known or suspected to affect the level of endogenous oxidants |
| 17879239 | Thirty- to 60-min exposure of cells to 100 or 200 microM H2O2 led to an increase in the level of H2AX phosphorylation and ATM activation, particularly pronounced (nearly fivefold) in S-phase cells |
| 17227291 | Constitutive histone H2AX phosphorylation and ATM activation are strongly amplified during mitogenic stimulation of lymphocytes |
| 16820894 | Constitutive histone H2AX phosphorylation on Ser-139 in cells untreated by genotoxic agents is cell-cycle phase specific and attenuated by scavenging reactive oxygen species |
| 16820894 | DNA damage, particularly when it involves formation of double-strand breaks (DSBs), triggers phosphorylation of histone H2AX on Ser-139 |
| 16820894 | Phosphorylated H2AX has been named gammaH2AX, and induction of gammaH2AX in cells exposed to genotoxic agents is considered a sensitive and specific reporter of DNA damage |
| 16820894 | However, in untreated normal cells as well in the cells of various tumor lines cells, a fraction of histone H2AX molecules remain phosphorylated |
| 16820894 | In the present study, we observed that the extent of this constitutive H2AX phosphorylation varies depending on the cell type (line) and on cell cycle phase and, in most cell types, S and G(2)/M phase cells exhibit greater levels of H2AX phosphorylation than do cells in the G(1) phase |
| 16820894 | Furthermore, constitutive H2AX phosphorylation in human pulmonary carcinoma A549, lymphoblastoid TK6, and in normal bronchial epithelial cells was reduced following cell exposure to N-acetyl-L-cysteine, a scavenger of reactive oxygen intermediates; the reduction was most pronounced for G(2)M cells |
| 16820894 | Growth of A549 cells in the presence of buthionine sulfoximine, an inhibitor of glutathione synthetase, amplified the level of constitutive H2AX phosphorylation in A549 cells |
| 16820894 | The observed constitutive H2AX phosphorylation may be a reflection of the ongoing DNA damage mediated by reactive oxygen species (ROS) generated by metabolic activity during progression through the cell cycle, leading to formation of DSBs during the S phase |
| 16820894 | Because cumulative DNA damage in proliferating cells mediated by ROS is considered the key mechanism for cell ageing, the present approach to estimate the degree of attenuation of constitutive H2AX phosphorylation by antioxidants may provide a convenient tool to assess the DNA-protective and possible anti-ageing properties of other agents |
| 16436511 | We find an ATR-dependent phosphorylation of the histone H2AX (gamma-H2AX) |
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