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Effect of ER stress on MUC1 kidney disease patient derived cells and and treatment by BRD4780

ABSTRACT: Effect of ER stress on MUC1 kidney disease patient derived cells and and treatment by BRD4780

PROVIDER: PRJNA533240 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8921500_1.fastq.gz	Fastqsanger.gz
	SRR8921500_2.fastq.gz	Fastqsanger.gz
	SRR8921501_1.fastq.gz	Fastqsanger.gz
	SRR8921501_2.fastq.gz	Fastqsanger.gz
	SRR8921502_1.fastq.gz	Fastqsanger.gz

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Transcriptomic of MKD (MUC1 kidney disease) patient compares to normal derived kidney epithelial cells

Project description:bulk RNAseq of MUC1 kidney disease patient derived kidney epithelial cells compare to normal kidney cells. The goal of this study was to elucidate the biological mechanism underlying MUC1 kidney disease using MUC1 expressing cells derived from either a patient or a healthy individual kidney

2019-04-18 | GSE129943 | GEO

Effect of ER stress on MUC1 kidney disease patient derived cells and and treatment by BRD4780

Project description:immortalized patient derived kidney epithelial cell were compared to cells exposed to ER stress (thapsigargin) in the absence or present of BRD4780 treatment

2019-04-18 | GSE129942 | GEO

Transcriptomic of MKD (MUC1 kidney disease) patient compares to normal derived kidney epithelial cells

Project description:Transcriptomic of MKD (MUC1 kidney disease) patient compares to normal derived kidney epithelial cells

| PRJNA533239 | ENA

RNA sequencing in kidneys of MUC1 Kidney Disease mouse model with and without treatment

Project description:MUC1 kidney disease mouse model generated by knock-in of the human mutated MUC1-fs gene. The mice were treated for 7 days, daily with either vehicle control or BRD4780, a compound showed to be beneficial to disease cells in-vitro. The kidneys were then removed and the bulk RNA was sequenced. The goal of this study was to undersand the effect of the compound on the diseased kidneys and to gain insights to its mechanism of action.

2019-04-18 | GSE129941 | GEO

MUC1(insC) affects vesicular transport in renal epithelial cells

Project description:Autosomal dominant tubulointerstitial kidney disease associated to the MUC1 gene (ADTKD-MUC1; formerly MCKD1) belongs to a heterogenous group of rare hereditary kidney diseases that is prototypically caused by frameshift mutations in the MUC1 repeat domain. The mutant MUC1(insC) lacks the transmembrane domaine, exhibits aberant cellular topology and hence might gain a function during the pathological process. To get insight into potential pathomechanisms we performed differential proteomics of extracellular vesicles shed by renal epithelia into the urine of patients. The study was based on three ADTKD patients and individual controls applying iTRAQ/LC-MS/MS. A total of 727 proteins were identified across all biological and technical replicates. A proportion of 47 proteins (6.5%) were fold-changed species. GO Term Enrichment analysis revealed proteins with significantly changed expression in ADTKD-associated extracellular vesicles as vesicular transport-associated proteins. Among these VTA1 is involved in the multivesicular body (MVB) pathway similar to the charged multivesicular body protein CHMP2B. VTA1 is also claimed to play roles as a cofactor of the AAA ATPases VPS4A and B in the disassembly of ESCRT III. Protein interaction databases list VPS4B, CHMP2A and IST1 as VTA1 binding partners.

2018-02-23 | PXD008389 | Pride

ER stress inhibits liver fatty acid oxidation while unmitigated stress leads to anorexia-induced lipolysis and both liver and kidney steatosis

Project description:The unfolded protein response (UPR), induced by endoplasmic reticulum (ER) stress, regulates the expression of factors that restore protein folding homeostasis. However, in the liver and kidney, ER stress also leads to lipid accumulation, accompanied at least in the liver by transcriptional suppression of metabolic genes. The mechanisms of this accumulation are unclear, including which pathways contribute to the phenotype in each organ. We combined gene expression profiling, biochemical assays, and untargeted lipidomics to understand the basis of stress-dependent lipid accumulation, taking advantage of enhanced hepatic and renal steatosis in mice lacking the ER stress sensor ATF6α. We found that impaired fatty acid oxidation contributed to the early development of steatosis in the liver, but not the kidney; while anorexia-induced lipolysis promoted late triglyceride and free fatty acid accumulation in both organs. These findings provide evidence for both direct and indirect regulation of peripheral metabolism by ER stress.

2017-06-23 | MTBLS472 | MetaboLights

RNA sequencing in kidneys of MUC1 Kidney Disease mouse model with and without treatment

Project description:RNA sequencing in kidneys of MUC1 Kidney Disease mouse model with and without treatment

| PRJNA533238 | ENA

Sequencing the anti-MUC1 hybridoma antibody 139H2

Project description:Mucin 1 (MUC1) is a transmembrane mucin expressed at the apical surface of epithelial cells at different mucosal surfaces including breast and intestine. The MUC1 extracellular domain contains a variable number of tandem repeats (VNTR) of 20 amino acids, which are heavily O-linked glycosylated. Monoclonal antibodies against the MUC1 VNTR can be powerful tools because of their multiplicity of binding and possible applications in the diagnosis and treatment of MUC1-expressing cancers. One such antibody is the hybridoma mouse monoclonal 139H2 which is also widely used as a research tool to study non-cancer MUC1. Here we report direct mass spectrometry-based sequencing of hybridoma-derived 139H2 IgG, which enabled reverse engineering of a recombinant 139H2.

2024-03-18 | PXD043489 | Pride

Small GTP-binding protein GDP dissociation stimulator influences cisplatin-induced acute kidney injury via PERK-dependent ER stress

Project description:Cisplatin is a common anticancer drug, but its frequent nephrotoxicity limits its clinical use. Small GTP-binding protein GDP dissociation stimulator (smgGDS), a small GTPase chaperone protein, was considerably downregulated during cisplatin-induced acute kidney injury (CDDP-AKI), especially in renal tubular epithelial cells. SmgGDS-knockdown mice was established and found that smgGDS knockdown promoted CDDP-AKI, as demonstrated by an increase in serum creatine, blood urea nitrogen levels and the appearance of tubular patterns. RNA sequencing suggested that protein kinase RNA-like ER kinase (PERK), which bridges mitochondria-associated ER membranes, was involved in smgGDS knockdown following CDDP-AKI, and then identified that smgGDS knockdown increased phosphorylated-PERK in vivo and in vitro. Furthermore, we confirmed that smgGDS deficiency aggravated apoptosis and ER stress in vivo and in vitro. And the ER stress inhibitor 4-Phenylbutyric acid and the inhibition of PERK phosphorylation mitigated smgGDS deficiency-induced ER stress related apoptosis following cisplatin treatment, while the eIF2α phosphorylation inhibitor could not reverse the smgGDS deficiency accelerated cell death. Furthermore, the over-expression of smgGDS could reverse the ER stress and apoptosis caused by CDDP. Overall, smgGDS regulated PERK-dependent ER stress and apoptosis, thereby influencing renal damage. This study identified a target for diagnosing and treating cisplatin-induced acute kidney injury.

2024-09-13 | GSE275317 | GEO

Expression of genes in the spleen of WT and MUC1.Tg mice immunized with dendritic cells loaded with MUC1 peptide

Project description:Goal of study: To determine differentially expressed genes with potential roles in tolerance and immunity in MUC1-immunized WT and MUC1.Tg mice WT (C57Bl/6) and MUC1.Tg mice were immunized (i.v.) with dendritic cells loaded with sythetic, human MUC1 peptide. At 24h and 72h splenic RNA from vaccination groups (n=3) was pooled and microarray performed.

2013-01-16 | E-GEOD-43503 | biostudies-arrayexpress

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