Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Intracellular free zinc mediates compressive stress-induced mechanotransduction in pancreatic cancer

ABSTRACT: Intracellular free zinc mediates compressive stress-induced mechanotransduction in pancreatic cancer

PROVIDER: PRJNA804136 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Intracellular free zinc mediates compressive stress-induced mechanotransduction in pancreatic cancer

Project description:In this study, Nihei et al. show that unknown function of the intracellular free zinc in mechanical compressive stress-induced signaling and altered gene expression in pancreatic cancer cells, provide novel perspectives on zinc as a signal transducer and therapeutic target. We explored the roles of compressive stress in pancreatic cancer progression by investigating the changes in gene expression induced by it using microarray.

2022-08-01 | GSE196275 | GEO

Intracellular zinc protects tumors from T cell-mediated cytotoxicity

Project description:Intracellular zinc protects tumors from T cell-mediated cytotoxicity

| PRJNA1021499 | ENA

Differential gene expression of static and intermittent compressive force treated human periodontal ligament cells

Project description:Mechanical force has been shown to regulate periodontal ligament cells (PDLs) behaviors. However, different force types lead to distinct PDLs’ responses. Here, the differential gene expression profiling of PDLs subjected to static and intermittent compressive forces was examined using RNA sequencing technique. Results demonstrated that the static and intermittent compressive force treated PDLs exhibited the differential regulation genes. KEGG pathway enrichment analysis revealed that focal adhesion and transforming growth factor beta signaling pathway were commonly upregulated while calcium signaling pathway was downregulated in both static and intermittent compressive force-treated PDLs. Interestingly, Wnt signaling pathway was upregulated only in the PDLs that subjected to the intermittent compressive force.

2019-07-23 | GSE112122 | GEO

Intracellular zinc protects tumors from T cell-mediated cytotoxicity [MC38 RNAseq]

Project description:Intracellular zinc protects tumors from T cell-mediated cytotoxicity [MC38 RNAseq]

| PRJNA1021506 | ENA

Intracellular zinc protects tumors from T cell-mediated cytotoxicity [E0771 RNAseq]

Project description:Intracellular zinc protects tumors from T cell-mediated cytotoxicity [E0771 RNAseq]

| PRJNA1021507 | ENA

Differential gene expression of intermittent compressive force treated mouse gingival fibrpblast derived induced pluripiotent stem cells

Project description:Mechanical force regulates various biological responses in many cell types. Here, the retinoic acid treated mouse gingival fibroblast derived induced pluripotent stem cells were treated with intermittent compressive for 24 h and gene expression profiling was evaluated using RNA sequencing technique. Results indicated that intermittent compressive stress regulated various pathways in these cells including p53 signaling and other metabolic pathways.

2021-12-31 | GSE118952 | GEO

The long non-coding RNA landscape of periodontal ligament stem cells subjected to compressive force

Project description:To explore the lncRNA landscape of periodontal ligament stem cells (PDLSCs) subjected to compressive force.

2021-07-09 | GSE116787 | GEO

Effects of dynamic compressive loading on MSC chondrogenesis

Project description:Long-term dynamic compression enhanced the mechanical properties of MSC-seeded constructs only when loading was initiated after 21 days of chondrogenic differentiation. This study examined the molecular differences of chondrogenic MSCs compared to undifferentiated MSCs (TGF-beta vs no TGF-beta) and the effects of dynamic loading on MSC chondrogenesis (loading vs free-swelling). Free-swelling MSC-seeded constructs were cultured for 21 days in chemically defined media. Chondrogenesis was induced with TGF-beta3. Undifferentiated controls were maintained in parallel. After 21 days of chondrogenic differentiation, a subset of constructs were subjected to 21 days of dynamic compressive loading. On days 21 and 42, construct mechanical properties and biochemical content were assessed. Microarray analysis was carried out on day 3, day 21 and day 42 constructs. 6 arrays.

2010-11-01 | E-GEOD-18879 | biostudies-arrayexpress

Motexafin Gadolinium and Zinc Induce Oxidative Stress Responses and Apoptosis in B-Cell Lymphoma Lines

Project description:We report the effect of motexafin gadolinium (MGd) and exogenous zinc on intracellular levels of free zinc, oxidative stress, proliferation, cell cycle, and cell death in exponential phase human B-cell lymphoma and other hematologic cell lines. We find that increased levels of oxidative stress and intracellular free zinc precede and correlate with cell cycle arrest and apoptotic response. Treatment with exogenous zinc increased oxidative stress and, conversely, oxidative stress resulted in increased intracellular free zinc levels. To better understand the molecular basis of these results, gene expression profiling analyses were conducted on Ramos cell cultures treated with MGd and/or zinc acetate. Cultures treated with MGd or zinc acetate alone elicited transcriptional responses characterized by induction of MTF-1 and HIF-1 regulated genes. Cultures co-treated with MGd and zinc acetate displayed further increases in the levels of MTF-1 and HIF-1 regulated transcripts as well as additional transcripts regulated by NRF-2. Overall, these studies suggest that co-treatment of Ramos cells with MGd and zinc acetate increase intracellular zinc levels with a concomitant rise in oxidative stress levels that activate adaptive survival responses but eventually lead to cell death. Keywords: Dose response

2006-01-01 | GSE2964 | GEO

Mycobacterial p(1)-type ATPases mediate resistance to zinc poisoning in human macrophages.

Project description:Mycobacterium tuberculosis thrives within macrophages by residing in phagosomes and preventing them from maturing and fusing with lysosomes. A parallel transcriptional survey of intracellular mycobacteria and their host macrophages revealed signatures of heavy metal poisoning. In particular, mycobacterial genes encoding heavy metal efflux P-type ATPases CtpC, CtpG, and CtpV, and host cell metallothioneins and zinc exporter ZnT1, were induced during infection. Consistent with this pattern of gene modulation, we observed a burst of free zinc inside macrophages, and intraphagosomal zinc accumulation within a few hours postinfection. Zinc exposure led to rapid CtpC induction, and ctpC deficiency caused zinc retention within the mycobacterial cytoplasm, leading to impaired intracellular growth of the bacilli. Thus, the use of P(1)-type ATPases represents a M. tuberculosis strategy to neutralize the toxic effects of zinc in macrophages. We propose that heavy metal toxicity and its counteraction might represent yet another chapter in the host-microbe arms race. [Data is also available from http://bugs.sgul.ac.uk/E-BUGS-122]

2012-01-27 | E-BUGS-122 | biostudies-arrayexpress

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