Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Differentially expressed genes in H2AX knockdown cells undergoing apoptosis

ABSTRACT: H2AX has been characterized as a novel tumor suppressor protein. Difficiency of H2AX will result in apoptotic inhibition of cancer cells. However, how H2AX epigenetically regulates apoptosis of cancer cells is still unclear. To reveal the genes expression regulated by H2AX and involved in apoptosis, the microarray profiling analysis was employed to identify differentially expressed genes in H2AX knockdown lung cancer cells and control ones after apoptotic induction. H2AX was knockdown by miRNA interfering system in human lung cancer originated cell A549 and the stable cell line named P1, while the control stable cell line named C. Genes with greater than 1.2-fold change and P-value ＜0.05 were identified as differentially expressed genes between C and P1 cells both with apoptosis induction.

ORGANISM(S): Homo sapiens

PROVIDER: GSE43498 | GEO | 2013/01/16

SECONDARY ACCESSION(S): PRJNA186599

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Differentially expressed genes in H2AX knockdown cells undergoing apoptosis

Project description:H2AX has been characterized as a novel tumor suppressor protein. Difficiency of H2AX will result in apoptotic inhibition of cancer cells. However, how H2AX epigenetically regulates apoptosis of cancer cells is still unclear. To reveal the genes expression regulated by H2AX and involved in apoptosis, the microarray profiling analysis was employed to identify differentially expressed genes in H2AX knockdown lung cancer cells and control ones after apoptotic induction. H2AX was knockdown by miRNA interfering system in human lung cancer originated cell A549 and the stable cell line named P1, while the control stable cell line named C. Genes with greater than 1.2-fold change and P-value ï¼0.05 were identified as differentially expressed genes between C and P1 cells both with apoptosis induction. The two groups including control (C) and H2AX knockdown lung cancer cells (P1) were harvested 48 h after VP-16 treatment. Three independent experiments were performed for each group.

2013-01-16 | E-GEOD-43498 | biostudies-arrayexpress

Differentially expressed miRNAs in H2AX knockdown cells undergoing apoptosis

Project description:H2AX has been characterized as a novel tumor suppressor protein. Difficiency of H2AX will result in apoptotic inhibition of cancer cells. However, how H2AX epigenetically regulates apoptosis of cancer cells is still unclear To reveal the miRNA expression regulated by H2AX and involved in apoptosis, the microarray profiling analysis was employed to identify differentially expressed miRNAs in H2AX knockdown lung cancer cells and control ones after apoptotic induction. H2AX was knockdown by miRNA interfering system in human lung cancer originated cell A549 and the stable cell line named P1, while the control stable cell line named C. Genes with greater than 1.5-fold change and P-value ?0.05 were identified as differentially expressed genes between C and P1 cells both with apoptosis induction. The two groups including control (C) and H2AX knockdown lung cancer cells (P1) were harvested 48 h after VP-16 treatment. Three independent experiments were performed for each group.

2015-04-25 | E-GEOD-68233 | biostudies-arrayexpress

Differentially expressed miRNAs in H2AX knockdown cells undergoing apoptosis

Project description:H2AX has been characterized as a novel tumor suppressor protein. Difficiency of H2AX will result in apoptotic inhibition of cancer cells. However, how H2AX epigenetically regulates apoptosis of cancer cells is still unclear To reveal the miRNA expression regulated by H2AX and involved in apoptosis, the microarray profiling analysis was employed to identify differentially expressed miRNAs in H2AX knockdown lung cancer cells and control ones after apoptotic induction. H2AX was knockdown by miRNA interfering system in human lung cancer originated cell A549 and the stable cell line named P1, while the control stable cell line named C. Genes with greater than 1.5-fold change and P-value ＜0.05 were identified as differentially expressed genes between C and P1 cells both with apoptosis induction.

2015-04-25 | GSE68233 | GEO

Whole-genome landscape of histone H2AX and γ-H2AX

Project description:Phosphorylation of the histone variant H2AX forms γ-H2AX that marks DNA double-strand break (DSB). Here we generated the sequencing-based maps of H2AX and γ-H2AX positioning in resting and proliferating cells before and after ionizing irradiation. Genome-wide locations of possible endogenous and exogenous DSBs were identified based on γ-H2AX distribution in dividing cancer cells without irradiation and that in resting cells upon irradiation, respectively. γ-H2AX-enriched regions of endogenous origin in replicating cells included telomeres and active transcription start sites, apparently reflecting replication- and transcription-mediated stress during rapid cell division. Surprisingly, H2AX itself, prior to phosphorylation, was specifically located at these endogenous hotspots. This phenomenon was only observed in dividing cancer cells but not in resting cells. Endogenous H2AX was concentrated on the transcription start site of actively transcribed genes but was irrelevant to pausing of RNA polymerase II (pol II), which precisely coincided with γ-H2AX of endogenous origin. γ-H2AX enrichment upon irradiation also coincided with actively transcribed regions, but unlike endogenous γ-H2AX, it extended into the gene body and was not specifically concentrated on the pausing site of pol II. Subtelomeres were not responsive to external DNA damage. Our findings provide insight into DNA repair programs of cancer and may have implications for cancer therapy.

2012-04-04 | GSE25577 | GEO

Whole-genome landscape of histone H2AX and M-NM-3-H2AX

Project description:Phosphorylation of the histone variant H2AX forms M-NM-3-H2AX that marks DNA double-strand break (DSB). Here we generated the sequencing-based maps of H2AX and M-NM-3-H2AX positioning in resting and proliferating cells before and after ionizing irradiation. Genome-wide locations of possible endogenous and exogenous DSBs were identified based on M-NM-3-H2AX distribution in dividing cancer cells without irradiation and that in resting cells upon irradiation, respectively. M-NM-3-H2AX-enriched regions of endogenous origin in replicating cells included telomeres and active transcription start sites, apparently reflecting replication- and transcription-mediated stress during rapid cell division. Surprisingly, H2AX itself, prior to phosphorylation, was specifically located at these endogenous hotspots. This phenomenon was only observed in dividing cancer cells but not in resting cells. Endogenous H2AX was concentrated on the transcription start site of actively transcribed genes but was irrelevant to pausing of RNA polymerase II (pol II), which precisely coincided with M-NM-3-H2AX of endogenous origin. M-NM-3-H2AX enrichment upon irradiation also coincided with actively transcribed regions, but unlike endogenous M-NM-3-H2AX, it extended into the gene body and was not specifically concentrated on the pausing site of pol II. Subtelomeres were not responsive to external DNA damage. Our findings provide insight into DNA repair programs of cancer and may have implications for cancer therapy. Profiles of H2AX and gamma-H2AX in normal resting and cancer T cells with and without ionizing irradiation.

2012-04-03 | E-GEOD-25577 | biostudies-arrayexpress

Whole-genome landscape of histone H2AX and γ-H2AX along with related factors in activated cells

Project description:Phosphorylation of the histone variant H2AX forms γ-H2AX, which serves as a marker of DNA repair response. Here we provide ChIP-seq-based maps of histone H2AX, γ-H2AX, H2AZ, INO80, SRCAP, and RNA polymerase II in activated T cells. Matched data for H2AX and γ-H2AX in resting T cells and Jurkat cancer T cells are available in GSE25577.

2014-04-01 | GSE44309 | GEO

Whole-genome landscape of histone H2AX and Î³-H2AX along with related factors in activated cells

Project description:Phosphorylation of the histone variant H2AX forms Î³-H2AX, which serves as a marker of DNA repair response. Here we provide ChIP-seq-based maps of histone H2AX, Î³-H2AX, H2AZ, INO80, SRCAP, and RNA polymerase II in activated T cells. Matched data for H2AX and Î³-H2AX in resting T cells and Jurkat cancer T cells are available in GSE25577. CD4+ T cells were stimulated in two different ways (IL-2 alone or IL-2 plus anti-CD3 and anti-CD28), and H2AX, Î³-H2AX, H2AZ, INO80, and SRCAP profiles were examined by ChIP-seq

2014-04-01 | E-GEOD-44309 | biostudies-arrayexpress

Homo sapiens

Project description:Differentially expressed genes in H2AX knockdown cells undergoing apoptosis

| PRJNA186599 | ENA

H2AX controls motor learning and response to oxidative stress

Project description:ATM drives DNA repair through rapid phosphorylation of the histone variant H2AX. Similarities between ATM and H2AX are evident in the phenotypes of their knockout mouse models, but the role of H2AX in the brain remains obscure. Here, we provide the first evidence that H2AX loss leads to neurobehavioral deficits. H2AX regulates proper response to oxidative stress through Nrf2-transcriptional targets and treatment with antioxidant ameliorates the neurobehavioral deficits.

2018-03-09 | GSE102548 | GEO