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Pancreatic cancer cells require the transcription factor MYRF (Myelin Regulatory Factor) to maintain ER homeostasis (RNA-Seq).

ABSTRACT: Pancreatic cancer cells require the transcription factor MYRF (Myelin Regulatory Factor) to maintain ER homeostasis (RNA-Seq).

PROVIDER: PRJNA607769 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11123260.fastq.gz	Fastqsanger.gz
	SRR11123261.fastq.gz	Fastqsanger.gz
	SRR11123262.fastq.gz	Fastqsanger.gz
	SRR11123263.fastq.gz	Fastqsanger.gz
	SRR11123264.fastq.gz	Fastqsanger.gz

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Similar Datasets

Pancreatic cancer cells require the transcription factor MYRF (Myelin Regulatory Factor) to maintain ER homeostasis

Project description:Pancreatic cancer cells require the transcription factor MYRF (Myelin Regulatory Factor) to maintain ER homeostasis

| PRJNA607766 | ENA

Pancreatic cancer cells require the transcription factor MYRF (Myelin Regulatory Factor) to maintain ER homeostasis (RNA-Seq).

Project description:Many tumors of endodermal origin are composed of highly secretory cancer cells that must adapt endoplasmic reticulum (ER) activity to enable proper folding of secretory proteins, prevent ER stress and thus maintain their viability. In pancreatic ductal adenocarcinoma (PDAC), well-differentiated and secretory cancer cells coexist with poorly differentiated cells with quasi-mesenchymal features. We found that the differentiated PDAC cells, but not the undifferentiated ones, expressed an ER membrane-associated transcription factor (TF), Myelin Regulatory Factor (MYRF), that is released by self-cleavage and translocates to the nucleus. MYRF expression was directly controlled by HNF1B, a TF maintaining epithelial identity in PDAC, and it acted to fine-tune the expression of genes encoding highly glycosylated and cysteine-rich secretory proteins, thus preventing ER overload. MYRF-deficient PDAC cells showed anatomical and biochemical signs of ER stress, impaired proliferation and inability to form spheroids in vitro, while in vivo they generated highly secretory but poorly proliferating and hypo-cellular tumors. These data indicate a role of MYRF in the control of homeostasis and proliferation of cancer cells with high secretory activity

2020-09-18 | GSE145628 | GEO

Pancreatic cancer cells require the transcription factor MYRF (Myelin Regulatory Factor) to maintain ER homeostasis (ChIP-Seq).

2020-09-18 | GSE145627 | GEO

Pancreatic cancer cells require the transcription factor MYRF (Myelin Regulatory Factor) to maintain ER homeostasis (ChIP-Seq).

Project description:Pancreatic cancer cells require the transcription factor MYRF (Myelin Regulatory Factor) to maintain ER homeostasis (ChIP-Seq).

| PRJNA607770 | ENA

Pancreatic cancer cells require the transcription factor MYRF (Myelin Regulatory Factor) to maintain ER homeostasis

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-09-18 | GSE145629 | GEO

RNA Sequencing Analysis of Wild Type and Myrf +/− mice Retina

Project description:We have created a Myrf knockdown (Myrf +/−) mutant mouse strain and investigated the molecular phenotype of reduced MYRF expression in the retina using RNA-sequencing. As an initial finding, photoreceptor defects with impaired functions of spatial vision and retinal electrophysiology were found in Myrf +/− mice, indicating an important role of MYRF in retinal development.It was revealed through RNA-seq that the expression of phototransduction and estrogen signaling pathways reduced in Myrf +/− mice. Thus, alterations of phototransduction and estrogen signaling pathways seem to play important roles in connecting Myrf deficiency with retinal photoreceptor defects.

2020-09-12 | GSE157806 | GEO

Comparative MicroRNA Sequencing Analysis in Late L1 Larvae of C. elegans: Wild Type N2 Versus myrf-1(ju1121) Mutants

Project description:Our research revealed that the transmembrane transcription factors MYRF-1 and MYRF-2 are crucial for activating the microRNA lin-4 at the end of the first larval stage in C. elegans. To determine whether MYRF regulates other microRNA genes during this period, we conducted a microRNA sequencing analysis to compare microRNA expression in late L1 larvae of wild type and myrf-1(ju1121) mutants. The myrf-1(ju1121) mutation causes a loss of function in both MYRF-1 and MYRF-2. Our analysis identified a subset of microRNAs that were differentially expressed between the wild type and the myrf-1(ju1121) mutants.

2024-03-31 | GSE262766 | GEO

Progressive axonopathy when oligodendrocytes lack the myelin protein CMTM5

Project description:Chemokine-like factor-like MARVEL-transmembrane domain containing protein 5 (CMTM5) is a tetraspan-transmembrane protein highly enriched in oligodendrocytes and central nervous system (CNS) myelin. We analyzed the proteome of myelin biochemically purified from mouse brains upon genetic disruption of the Cmtm5-gene specifically in myelinating cells. An ion mobility-enhanced version of data-independent acquisition (DIA) workflow with alternating low and elevated energy (referred to as UDMSE) was used to compare protein abundance in Cmtm5 cKO and CTRL samples by label-free quantification. Specifically, dynamic range enhancement (DRE)-UDMSE was applied as a dedicated data acquisition mode recently introduced for routine differential myelin proteome profiling. We found that Cmtm5 cKO mice displayed a largely similar myelin proteome composition as control mice and, together with other data such as electron micrographs, concluded that CMTM5 is not essential for myelin biogenesis and composition. However, oligodendroglial Cmtm5-deficiency causes an early-onset progressive axonopathy, presumably following a Wallerian-like pathomechanism. These results indicate that CMTM5 is involved in the function of oligodendrocytes to maintain axonal integrity rather than myelin biogenesis.

2022-04-04 | PXD029443 | Pride

The role of ATP citrate lyase in myelin formation and maintenance

Project description:Schwann cell-specific knockout of ATP citrate lyase (ACLY) revealed that this pathway is important for myelin maintenance rather than formation, and ACLY is required to maintain expression of a myelin-associated gene program.

2024-05-03 | MSV000094670 | MassIVE

Identification of Myelin-gene Regulatory Factor as a Critical Transcriptional Regulator Required for CNS Myelination

Project description:The transcriptional control of CNS myelin gene expression is poorly understood. Here we identify gene model 98, which we have named Myelin-gene Regulatory Factor (MRF), as a transcriptional regulator required for CNS myelination. Within the CNS, MRF is specifically expressed by postmitotic oligodendrocytes. MRF is a nuclear protein containing an evolutionarily conserved DNA binding domain homologous to a yeast transcription factor. Knockdown of MRF in oligodendrocytes by RNA interference prevents expression of most CNS myelin genes; conversely, overexpression of MRF within cultured oligodendrocyte progenitors or the chick spinal cord promotes expression of myelin genes. In mice lacking MRF within the oligodendrocyte lineage, pre-myelinating oligodendrocytes are generated but display severe deficits in myelin gene expression and fail to myelinate. These mice display severe neurological abnormalities, and die due to seizures during the third postnatal week. These findings establish MRF as a critical transcriptional regulator essential for oligodendrocyte maturation and CNS myelination. We used microarrays to compare cultured oligodendrocytes (differentiated in vitro for 4 days) from MRF conditional knockouts and control litteramates to look at the effects of MRF deficiency on myelin gene expression. Mouse OPCs grown in vitro in the presence of PDGF serve as a baseline for gene expression prior to differentiation.

2009-05-31 | GSE15303 | GEO

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