Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Dynamic Ca2+-dependent transcription links metabolic stress to impaired β-cell identity

ABSTRACT: Dynamic Ca2+-dependent transcription links metabolic stress to impaired β-cell identity

PROVIDER: PRJEB83006 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	ERR14008724_1.fastq.gz	Fastqsanger.gz
	ERR14008724_2.fastq.gz	Fastqsanger.gz
	ERR14008725_1.fastq.gz	Fastqsanger.gz
	ERR14008725_2.fastq.gz	Fastqsanger.gz
	ERR14008726_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 96

Similar Datasets

Impaired store-operated Ca2+ entry in mouse epidermis

Project description:Impaired store-operated Ca2+ entry in mouse epidermis

| PRJNA1311974 | ENA

Dynamic Transformations of Genome-wide Epigenetic Marking and Transcriptional Control Establish T Cell Identity

Project description:This SuperSeries is composed of the following subset Series: GSE31233: Dynamic transformations of epigenetic marking and genome-wide transcriptional regulation that establish T cell identity [ChIP-Seq] GSE31234: Dynamic transformations of epigenetic marking and genome-wide transcriptional regulation that establish T cell identity [RNA-Seq] Refer to individual Series

2012-04-13 | E-GEOD-31235 | biostudies-arrayexpress

Staphylococcus lentus Ca2

Project description:Staphylococcus lentus Ca2 genome sequence

| PRJEB278 | ENA

Global transcriptomic changes following elevated carbon dioxide (5%) in the wild-type (WT) and mutant (M2; RNAi-knockdown line of carbonic anhydrase (CA2)) Nannochloropsis oceanica IMET1: Illumina sequencing

Project description:In Nannochloropsis oceanica IMET1, transcript knockdown of a cytosolic carbonic anhydrase (CA2; g2018) specifically inhibited by HC resulted in ~45%, ~30% and ~40% elevation of photosynthetic oxygen evolution rate, growth rate and biomass accumulation rate under high CO2 (5% ), respectively. This CA2-knockdown mutant is demonated as M2. To probe mechanistic links underlying the mutant (M2; RNAi-knockdown line of carbonic anhydrase (CA2)) phenotypes, temporal transcriptomic profiles are compared between RNAi-knockdown line of carbonic anhydrase (CA2) and WT, at 12 h and 24h under high CO2 (5%).

2020-10-28 | GSE115445 | GEO

Impaired CHD6 function links misregulation of autophagy and DNA damage response to premature ageing

Project description:Impaired CHD6 function links misregulation of autophagy and DNA damage response to premature ageing

| PRJNA675606 | ENA

Oxaliplatin Pharmacokinetics With and Without Ca2+/MG2+ Infusion in Colorectal Cancer Patients

Project description:The investigators hypothesize that Ca2+/MG2+ infusions will not have a significant effect on oxaliplatin pharmacokinetics.

| 2091675 | ecrin-mdr-crc

Suppression of NCALD protects against spinal muscular atrophy by restoring impaired endocytosis

Project description:Spinal muscular atrophy (SMA) is a common genetic motor neuron (MN) disease caused by low levels of the ubiquitously expressed housekeeping survival motor neuron (SMN) protein, whereas concomitant overexpression of plastin 3 (PLS3) protects from SMA. Here we identify neurocalcin delta (NCALD), a neuronal calcium sensor, as a second fully protective SMA modifier, which counteracts SMA pathology when downregulated. We show reduced Ca2+ influx and impaired endocytosis in SMA, which are crucial processes in synaptic vesicle recycling and neurotransmission. Remarkably, both reduced NCALD or increased PLS3 restore endocytosis in cell culture and MN function across species in zebrafish, worm and mouse SMA models, whereas Ca2+ influx remains disturbed. Furthermore, NCALD physically binds clathrin in a Ca2+-dependent manner. We propose that NCALD acts as a Ca2+-regulated inhibitor of endocytosis, and that endocytosis is critically affected in SMA. This finding opens new therapeutic avenues for SMA. Multifactorial design comparing affected patients and unaffected disease carriers against severly affected control group to identify disease modifying transcripts

2015-01-01 | E-GEOD-58316 | biostudies-arrayexpress

SMARCA4/2 loss inhibits chemotherapy-induced apoptosis by restricting IP3R3-mediated Ca2+ flux to mitochondria

Project description:Inactivating mutations in SMARCA4 and concurrent epigenetic silencing of SMARCA2 characterize subsets of ovarian and lung cancers. Concomitant loss of these key subunits of SWI/SNF chromatin remodeling complexes in both cancers is associated with chemotherapy resistance and poor prognosis. Here, we discover that SMARCA4/2 loss inhibits chemotherapy-induced apoptosis through disrupting intracellular organelle calcium ion (Ca2+) release in these cancers. By restricting chromatin accessibility to ITPR3, encoding Ca2+ channel IP3R3, SMARCA4/2 deficiency causes reduced IP3R3 expression leading to impaired Ca2+ transfer from the endoplasmic reticulum to mitochondria required for apoptosis induction. Reactivation of SMARCA2 by a histone deacetylase inhibitor rescues IP3R3 expression and enhances cisplatin response in SMARCA4/2-deficient cancer cells both in vitro and in vivo. Our findings elucidate the contribution of SMARCA4/2 to Ca2+-dependent apoptosis induction, which may be exploited to enhance chemotherapy response in SMARCA4/2-deficient cancers.

| EGAS00001005448 | EGA

Impaired store-operated Ca2+ entry in mouse epidermis

Project description:The purpose of this study was to investigate the role of SOCE in the skin epidermis in vivo, using female mice with epithelial tissue-specific Stim1 and Stim2 knockout (Stim1/2 cKO) and control mice (Stim1/2fl/fl).　This study found that SOCE dysfunction led to hyperkeratosis and impaired epidermal barrier function via Klk activation without affecting skin cell proliferation in vivo.

2025-10-15 | GSE306726 | GEO

Store operated Ca2+ entry (SOCE) controls ameloblast cell function and enamel development

Project description:Abstarct:Mutations in the endoplasmic reticulum (ER) Ca2+ sensor stromal interaction molecule 1 (STIM1) result is a number of disease states including abnormal enamel formation. However, these defects in enamel have remained unclear given a lack of animal models available. We generated Stim1/2K14Cre mice to ablate the activity of STIM1 and its homologue STIM2 in enamel cells. These mice showed impaired Ca2+ entry in enamel cells and although enamel formed, it was severely hypomineralized and mechanically weak. RNA-sequencing of enamel cells provided a global overview of loss of Ca2+ sensor activity. ER stress markers associated with unfolded protein response (UPR) were increased. Cell morphology was altered showing loss of the typical ruffled-border and mislocalized mitochondria. We also identified decreased glutathione system and potentially associated with this, increased ROS and abnormal mitochondria. The Ca2+ extrusion system and enamel gene expression were also altered. These data might represent the first in vivo study linking Stim1/2 ablation with increased UPR function, decreased glutathione metabolism, increased ROS and abnormal mitochondria. Loss of ER Ca2+ sensors Stim1/2 in enamel cells has substantial detrimental effects at the cell and mineral phase level.

2017-01-17 | GSE93655 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data