Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Adaptation to chronic ER stress enforces pancreatic beta-cell plasticity

ABSTRACT: Adaptation to chronic ER stress enforces pancreatic beta-cell plasticity

PROVIDER: PRJNA731067 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR14585400.fastq.gz	Fastqsanger.gz
	SRR14585401.fastq.gz	Fastqsanger.gz
	SRR14585402.fastq.gz	Fastqsanger.gz
	SRR14585403.fastq.gz	Fastqsanger.gz
	SRR14585404.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 18

Similar Datasets

Adaptation to chronic ER stress enforces pancreatic β-cell plasticity.

Project description: Not available

| S-EPMC9360004 | biostudies-literature

Adaptation to chronic ER stress enforces pancreatic beta-cell plasticity

Project description:The next-generation-sequencing (NGS) of ribosome footprintings and poly(A) enriched RNA-seq have been proformed to examine transcriptional and translational changes in an mouse insulinoma cell MIN6 under acute and chronic endoplasmic reticular stresses.

2021-05-20 | GSE174679 | GEO

Posttranscriptional reprogramming controls MASLD progression through chronic ER stress adaptation (RNAseq)

Project description:Metabolic dysfunction-associated steatohepatitis (MASH) and its progression to hepatocellular carcinoma remain major clinical challenges. Chronic endoplasmic reticulum (ER) stress, induced by sustained high-fat diet (HFD) intake, promotes hepatic inflammation, lipid accumulation, and hepatocellular dysfunction during MASH pathogenesis. While transcriptional responses are well-characterized, the post-transcriptional mechanisms underlying hepatocyte adaptation to chronic ER stress remain poorly understood. Using an integrative approach combining transcriptomics, ribosome profiling, cytoplasmic polyadenylation analysis, and cis-regulatory mapping, we define the post-transcriptional landscape induced by chronic HFD exposure. To delineate the specific role of chronic ER stress, we use a hepatocyte-specific knockout of a key regulator of translational control under prolonged ER stress. We show that ~70% of HFD-induced gene expression changes are modulated at the translational level. A distinct subset of mRNAs - enriched in suboptimal codons and bearing short poly(A) tails under normal diet - becomes selectively activated upon HFD-induced poly(A) tail elongation. These transcripts, associated with cell cycle, immune response, fibrosis, and tissue remodeling, correlate with MASH severity in both murine models and human samples. Their regulation is mediated by cis-elements in the 3'UTR that coordinate polyadenylation and deadenylation. Loss of this adaptive response exacerbates liver damage and tumor burden in HFD-fed mice.

2026-03-05 | E-MTAB-16295 | biostudies-arrayexpress

Posttranscriptional reprogramming controls MASLD progression through chronic ER stress adaptation (Riboseq)

Project description:Metabolic dysfunction-associated steatohepatitis (MASH) and its progression to hepatocellular carcinoma remain major clinical challenges. Chronic endoplasmic reticulum (ER) stress, induced by sustained high-fat diet (HFD) intake, promotes hepatic inflammation, lipid accumulation, and hepatocellular dysfunction during MASH pathogenesis. While transcriptional responses are well-characterized, the post-transcriptional mechanisms underlying hepatocyte adaptation to chronic ER stress remain poorly understood. Using an integrative approach combining transcriptomics, ribosome profiling, cytoplasmic polyadenylation analysis, and cis-regulatory mapping, we define the post-transcriptional landscape induced by chronic HFD exposure. To delineate the specific role of chronic ER stress, we use a hepatocyte-specific knockout of a key regulator of translational control under prolonged ER stress. We show that ~70% of HFD-induced gene expression changes are modulated at the translational level. A distinct subset of mRNAs - enriched in suboptimal codons and bearing short poly(A) tails under normal diet - becomes selectively activated upon HFD-induced poly(A) tail elongation. These transcripts, associated with cell cycle, immune response, fibrosis, and tissue remodeling, correlate with MASH severity in both murine models and human samples. Their regulation is mediated by cis-elements in the 3' UTR that coordinate polyadenylation and deadenylation. Loss of this adaptive response exacerbates liver damage and tumor burden in HFD-fed mice.

2026-03-05 | E-MTAB-16293 | biostudies-arrayexpress

Posttranscriptional reprogramming controls MASLD progression through chronic ER stress adaptation (RNAseq 2)

Project description:Metabolic dysfunction-associated steatohepatitis (MASH) and its progression to hepatocellular carcinoma remain major clinical challenges. Chronic endoplasmic reticulum (ER) stress, induced by sustained high-fat diet (HFD) intake, promotes hepatic inflammation, lipid accumulation, and hepatocellular dysfunction during MASH pathogenesis. While transcriptional responses are well-characterized, the post-transcriptional mechanisms underlying hepatocyte adaptation to chronic ER stress remain poorly understood. Using an integrative approach combining transcriptomics, ribosome profiling, cytoplasmic polyadenylation analysis, and cis-regulatory mapping, we define the post-transcriptional landscape induced by chronic HFD exposure. To delineate the specific role of chronic ER stress, we use a hepatocyte-specific knockout of a key regulator of translational control under prolonged ER stress. We show that ~70% of HFD-induced gene expression changes are modulated at the translational level. A distinct subset of mRNAs - enriched in suboptimal codons and bearing short poly(A) tails under normal diet - becomes selectively activated upon HFD-induced poly(A) tail elongation. These transcripts, associated with cell cycle, immune response, fibrosis, and tissue remodeling, correlate with MASH severity in both murine models and human samples. Their regulation is mediated by cis-elements in the 3' UTR that coordinate polyadenylation and deadenylation. Loss of this adaptive response exacerbates liver damage and tumor burden in HFD-fed mice.

2026-03-05 | E-MTAB-16294 | biostudies-arrayexpress

Posttranscriptional reprogramming controls MASLD progression through chronic ER stress adaptation (RIP Seq)

Project description:Metabolic dysfunction-associated steatohepatitis (MASH) and its progression to hepatocellular carcinoma remain major clinical challenges. Chronic endoplasmic reticulum (ER) stress, induced by sustained high-fat diet (HFD) intake, promotes hepatic inflammation, lipid accumulation, and hepatocellular dysfunction during MASH pathogenesis. While transcriptional responses are well-characterized, the post-transcriptional mechanisms underlying hepatocyte adaptation to chronic ER stress remain poorly understood. Using an integrative approach combining transcriptomics, ribosome profiling, cytoplasmic polyadenylation analysis, and cis-regulatory mapping, we define the post-transcriptional landscape induced by chronic HFD exposure. To delineate the specific role of chronic ER stress, we use a hepatocyte-specific knockout of a key regulator of translational control under prolonged ER stress. We show that ~70% of HFD-induced gene expression changes are modulated at the translational level. A distinct subset of mRNAs - enriched in suboptimal codons and bearing short poly(A) tails under normal diet - becomes selectively activated upon HFD-induced poly(A) tail elongation. These transcripts, associated with cell cycle, immune response, fibrosis, and tissue remodeling, correlate with MASH severity in both murine models and human samples. Their regulation is mediated by cis-elements in the 3' UTR that coordinate polyadenylation and deadenylation. Loss of this adaptive response exacerbates liver damage and tumor burden in HFD-fed mice.

2026-03-05 | E-MTAB-16346 | biostudies-arrayexpress

Posttranscriptional reprogramming controls MASLD progression through chronic ER stress adaptation (Riboseq)

Project description:Posttranscriptional reprogramming controls MASLD progression through chronic ER stress adaptation (Riboseq)

| PRJEB104354 | ENA

Posttranscriptional reprogramming controls MASLD progression through chronic ER stress adaptation (RNAseq)

Project description:Posttranscriptional reprogramming controls MASLD progression through chronic ER stress adaptation (RNAseq)

| PRJEB104356 | ENA

Posttranscriptional reprogramming controls MASLD progression through chronic ER stress adaptation (RIP Seq)

Project description:Posttranscriptional reprogramming controls MASLD progression through chronic ER stress adaptation (RIP Seq)

| PRJEB104696 | ENA

Posttranscriptional reprogramming controls MASLD progression through chronic ER stress adaptation (RNAseq 2)

Project description:Posttranscriptional reprogramming controls MASLD progression through chronic ER stress adaptation (RNAseq 2)