Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Chemical dissection of vtamin D activity

ABSTRACT: Chemical dissection of vtamin D activity

PROVIDER: PRJNA556890 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Chemical dissection of vtamin D activity

Project description:Vitamin D3 metabolites are capable of controlling gene expression in mammalian cells through two independent pathways: vitamin D receptor (VDR) and sterol regulatory element-binding protein (SREBP) pathways. In the present study, we dissect the complex biological activity of vitamin D by designing synthetic vitamin D3 analogs specific for VDR or SREBP pathway, i.e., a VDR activator that lacks SREBP inhibitory activity, or an SREBP inhibitor devoid of VDR activity.

2019-07-27 | GSE134965 | GEO

Single cell dissection of Chemical Reprogramming from Fibroblasts into functional Chondrocytes

Project description:Single cell dissection of Chemical Reprogramming from Fibroblasts into functional Chondrocytes

| PRJNA485015 | ENA

High-Resolution Dissection of Chemical Reprogramming from Fibroblasts into Functional Articular Chondrocytes

Project description:High-Resolution Dissection of Chemical Reprogramming from Fibroblasts into Functional Articular Chondrocytes

| PRJNA484940 | ENA

Selective chemical tracking of Dnmt1 catalytic activity in live cells

Project description:Selective chemical tracking of Dnmt1 catalytic activity in live cells

| PRJNA756279 | ENA

High-resolution genome-wide dissection of transcriptional regulatory activity and function in human cells

Project description:Genome-wide profiling of epigenomic marks allows rapid prediction of transcriptional regulatory regions, including promoters and enhancers. However, experimental validation of predicted regions’ effect on gene expression, and high-resolution dissection of driver sequence elements within them, have remained infeasible on a high throughput scale. Here, we describe HiDRA (High-Definition Reporter Assay), a high-throughput episomal assay for the high-resolution dissection of promoter and enhancer activity genome-wide. We applied HiDRA on millions of DNA fragments preferentially extracted from open chromatin. We applied HiDRA to the GM12878 lymphoblastoid cell line, generating a 6.83 million fragment library preferentially extracted from open chromatin, and revealed tens of thousands of genomic regions that significantly drive reporter gene transcription. These regions are enriched for H3K9ac, H3K27ac, other active histone marks, known regulatory motifs, and regions bound by immune regulators. We developed a new algorithm, SHARPR2, to deconvolve fragment-level activity measurements from regulatory regions tiled by dozens to hundreds of offset fragments to enable high-resolution maps of activity patterns, pinpointing individual driver regulatory motifs and predicting driver genetic variants underlying immune diseases. Our results indicate that HiDRA provides a general and scalable high-throughput and high-resolution strategy for experimental dissection of regulatory regions and nucleotides in the context of human biology and disease.

2017-09-26 | GSE104001 | GEO

Miz1 Limits Tumor-promoting Function of Hepatocyte NF-κB independently of Its Transcriptional Activity in Chemical Hepatocarcinogenesis

Project description:NF-κB has a crucial tumor-suppression role in chemical hepatocarcinogenesis (HCC) by preventing hepatocyte apoptosis-induced compensatory proliferation. However, NF-κB is typically activated in chemical HCC animal models and in ~40% HCC patients, in which its role in tumor progression is largely not known. Here we report that transcription factor Miz1 limits tumor-promoting function of NF-κB independently of its transcriptional activity in chemical HCC. In a murine model, hepatocyte-specific deletion of Miz1 exacerbates HCC progression. Miz1 loss results in a unique sub-group of hepatocytes with upregulated NF-κB activity and pro-inflammatory cytokine production, skewing infiltrating macrophages toward M1-like pro-inflammatory phenotype. Mechanistically, Miz1 sequestrates and prevents IKK-phosphorylation of Metadherin (MTDH), thereby inhibiting NF-κB nuclear translocation and transcription activity. In HCC patient specimens, Miz1 expression is inversely correlated with phosphorylation of RelA and MTDH, and poor prognosis. Thus, Miz1 preventing hepatocytes from promoting infiltrating macrophage M1-like phenotype and inflammation in chemical HCC progression.

2021-07-13 | GSE142868 | GEO

Transcriptional changes associated with chemical induction of adenylyl cyclase activity in Mtb

Project description:Transcriptional changes associated with chemical induction of adenylyl cyclase activity in Mtb

| PRJNA788789 | ENA

Functional dissection of QTL-region affecting fat-deposition

Project description:Functional dissection of QTL-region affecting fat-deposition

2018-10-15 | E-MTAB-1434 | biostudies-arrayexpress

High-resolution genome-wide dissection of transcriptional regulatory activity and function in human cells

Project description:High-resolution genome-wide dissection of transcriptional regulatory activity and function in human cells

| PRJNA407924 | ENA

chemical production metagenome

Project description:chemical production metagenome Metagenome