Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA sequencing of HeLa cells overexpression CHIKV structural protein TF and 6K

ABSTRACT: The analysis indicates that overexpression of tf leads to the upregulation of genes related to endoplasmic reticulum stress, and KEGG analysis also identified pathways related to endoplasmic reticulum stress in biological metabolism.

ORGANISM(S): Homo sapiens

PROVIDER: GSE299288 | GEO | 2026/05/10

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

RNA sequencing of HeLa cells overexpression CHIKV structural protein TF and 6K

Project description:RNA sequencing of HeLa cells overexpression CHIKV structural protein TF and 6K

| PRJNA1273851 | ENA

Transcriptomics DNAJC15 and DNAJC19 knockdown in HeLa cells

Project description:To better understand how OMA1 affects mitochondrial proteostasis and stress responses, we performed a proteomic survey of OMA1-deficient cells for proteolytic substrates. We demonstrate that OMA1 cleaves the mitochondrial chaperone DNAJC15 facilitating its degradation by the mitochondrial m-AAA protease. The loss of DNAJC15 alters protein import by TIM23 protein translocases in the IM and limits the accumulation of OXPHOS-related mitochondrial matrix and IM proteins. Non-imported mitochondrial preproteins accumulate at the endoplasmic reticulum (ER) and trigger an ATF6-related unfolded protein response. These results demonstrate that OMA1 allows to adapt mitochondrial protein biogenesis to stress and reveal an intricate network of cellular stress responses to proteostasis disturbances.

2025-12-19 | GSE299431 | GEO

Effect of knockout ERO1α on gene expression in mTORC1 activated mouse embryonic fibroblasts

Project description:Endoplasmic reticulum oxidoreductase 1 alpha (ERO1α) is an endoplasmic reticulum stress–related gene, which improves cell perseverance against challenges of high levels of protein misfolding during endoplasmic reticulum stress by retaining good activity of oxidative protein folding. Numerous studies have shown abnormal expression of ERo1α in various diseases, but its downstream target are not fully understood. Our work will help in the elucidation of the downstream molecular mechanism of ERO1α.

2024-04-17 | GSE246899 | GEO

Overexpression of PTHrP in beta cells reveals key effects on endoplasmic reticulum stress

Project description:Administration of parathyroid hormone-related protein (PTHrP) has been shown to increase insulin content and secretion in mice. PTHrP also increases beta-cell mass and proliferation. However, the mechanisms for these effects are unknown, and investigations have yet to examine PTHrP in the transcriptome. In this study, we transiently transfected a mouse beta-cell line (MIN6) with either full-length PTHrP or DSred vector. Insulin content and glucose-stimulated insulin secretion were measured, and RNA from the cells after incubating in 20mM glucose was collected. The results showed that PTHrP overexpression increased insulin content and the ratio of insulin secretion between low and high glucose (stimulation index). RNA-sequencing showed that PTHrP overexpression downregulated many genes associated with responses to endoplasmic reticulum (ER) stress such as Hspa40, Dnajc3 and Xbp1. Among enriched KEGG pathways, the ER stress gene pathway was the most strongly downregulated by far, and the most upregulated pathway was for biosynthesis of amino acids required for protein synthesis. These pathways suggest increased rates of protein biosynthesis. qPCR supported RNA-sequencing results for several ER stress genes (Xbp1, Bax, Bip). MIN6 cells transfected with PTHrP also had lower proinsulin-to-insulin ratio, indicting that PTHrP enhanced insulin processing in the ER. Our working hypothesis is that PTHrP augments insulin production and ER efficiency, which is consistent with observations of increased insulin content, decreased proinsulin-to-insulin ratio and reduced ER stress markers in MIN6 cells. In conclusion, our findings suggest a previously unknown role for PTHrP in beta-cell endoplasmic reticulum, which may have therapeutic implications for enhancing insulin production.

2025-04-29 | GSE295339 | GEO

CUT&RUN of 3 months old wild type and hepatocyte-specific ATF6 overexpression mice

Project description:Hepatocellular carcinoma (HCC) is the fastest growing cause of cancer-related mortality with limited therapies. While endoplasmic reticulum (ER)-stress and the unfolded protein response (UPR) are implicated in HCC, the involvement of the UPR-transducer activating transcription factor 6 alpha (ATF6α) remains unclear. We generated hepatocyte specific n-ATF6 overexpression transgenic mice via Cre-mediated recombination.

2024-12-28 | GSE285262 | GEO

RNAi knock down of VCP in human HeLa cells

Project description:Study of the effects of the VCP knockdown. VCP (p97, yeast cdc48) is a hexameric AAA ATPase involved in various cellular functions including degradation of proteins by the ubiquitin-proteasome system. We examine the consequences of the reduction of VCP levels after RNAi of VCP in HeLa cells. We find ~30 transcripts upregulated in a sequence independent manner. Those transcripts encode proteins involved in endoplasmic reticulum stress, apoptosis, and amino acid starvation.

2006-08-23 | E-MEXP-817 | biostudies-arrayexpress

ATAC-seq of 3 months old wild type and hepatocyte-specific ATF6 overexpression mice

2024-12-28 | GSE285261 | GEO

Neurocellular Endoplasmic Reticulum Stress Response in Alzheimer's Disease and Related Dementias (ADRD) Risk

Project description:Neurocellular Endoplasmic Reticulum Stress Response in Alzheimer's Disease and Related Dementias (ADRD) Risk

| PRJNA1096693 | ENA

Liver transcriptomic profile of 6 months old wild type and hepatocyte-specific ATF6 overexpression mice

2025-11-05 | GSE244213 | GEO

Liver transcriptomic profile of 3 months old wild type and hepatocyte-specific ATF6 overexpression mice

2025-11-05 | GSE244212 | GEO