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Omics score: 0

E-GEOD-43498

ABSTRACT: Differentially expressed genes in H2AX knockdown cells undergoing apoptosis

OTHER RELATED OMICS DATASETS IN: PRJNA186599

PROVIDER: E-GEOD-43498 | ExpressionAtlas | 2025-01-24

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-GEOD-43498-analysis-methods.tsv	Tabular
	E-GEOD-43498-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-43498-configuration.xml	Xml
	E-GEOD-43498-percentile-ranks.tsv	Tabular
	E-GEOD-43498.condensed-sdrf.tsv	Tabular

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

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

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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

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 ＜0.05 were identified as differentially expressed genes between C and P1 cells both with apoptosis induction.

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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.

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