Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

10 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ChIP seq for H4K5ac, JunD , and MED1 in Parental and Paclitaxel resistant L3.6pl cell line

ABSTRACT: Identification of occupancy for H4K5ac, MED1, and JunD in chemo resistance

INSTRUMENT(S): NextSeq 2000

ORGANISM(S): Homo sapiens

SUBMITTER: Feda Hamdan

PROVIDER: E-MTAB-12707 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

H3K4me3 HiChIP for Paclitaxel resistant L3.6pl pancreatic cancer cells (Non targeting vs siJunD)

Project description:Identification of JunD dependent interaction in paclitaxel resistance

2023-03-21 | E-MTAB-12708 | biostudies-arrayexpress

leChRO-seq in L3.6pl (Parental and Paclitaxel-resistant)

Project description:Evaluate the nascent RNA-seq production in L3.6pl

2023-03-24 | E-MTAB-11744 | biostudies-arrayexpress

Genome-wide profiling of MED1 and RUNX1 binding in MED1 wild-type and knockout human pre-B ALL cell line 697 (ChIP-seq)

Project description:CRISPR/Cas9 system was used to generate mediator complex subunit 1 (MED1) knockout human pre-B ALL cell line 697. ChIP-seq was performed to identify genomic regions responsible for recruitment of MED1 and RUNX1.

2020-05-13 | E-MTAB-8177 | biostudies-arrayexpress

Med1 overexpression induces cell proliferation

2013-07-18 | GSE48950 | GEO

Med1 overexpression induces cell proliferation

Project description:Med1 overexpression leads to induction of a wide spectrum of genes. Adenovirally-driven overexpression of Med1 in mouse liver stimulates hepatocyte DNA synthesis with enhanced expression of DNA replication, cell cycle control and liver specific genes as observed at day 3 and day 5 post injection. Med1 gene is amplified in a number of cancers so in this study we tested the hypothesis that Med1 by itself has the capacity to induce cell proliferation. Analysis of the Med1- induced gene expression showed a robust induction of a wide spectrum of genes involved in hepatocellular proliferation. Med1 floxed mice (Med1fl/fl) were injected with Ad-His-Med1 (adenovirus expressing Med1 gene) via tail vein and killed 3 or 5 days after injection. Ad-LacZ (adenovirus expression beta-galactosidase gene) injected mouse liver served as control. Total RNA were isolated from the liver and subjected to the microarray.

2013-07-18 | E-GEOD-48950 | biostudies-arrayexpress

H3K4me3 HiChIP for L3.6pl cells (parental and paclitaxel-resistant)

Project description:Identification of TSS-centric interaction

2023-04-21 | E-MTAB-11732 | biostudies-arrayexpress

RNA seq for PacR cells (Non-targeting vs siJunD)

Project description:This experiment investigates the effects of JunD depletion in Paclitaxel resistant L3.6pl pancreatic cancer cells

2023-03-21 | E-MTAB-12705 | biostudies-arrayexpress

CDK7 inhibition suppresses Castration-Resistant Prostate Cancer through MED1 inactivation

Project description:We performed RNA-seq and ChIP-seq in three prostate cell lines (VCaP, LNCaP and DU145) to ascertain the role of the mediator complex MED1 in AR signaling. Upon androgen stimulation, MED1 undergoes phosphorylation by CDK7 and physically engages with AR at super-enhancer sites, which is essential for AR-mediated transcription. The CDK7 specific inhibitor THZ1 blunts AR-dependent neoplastic growth by preventing the co-recruitment of AR/MED1 in a genome-wide fashion, and reverts the enzalutamide resistance characterized by hyper-phosphorylated MED1. The effect of THZ1 phenocopies that for MED1 and CDK7 knockdown.

2019-08-20 | GSE125245 | GEO

MED1 is a lipogenesis co-activator required for postnatal adipose expansion

Project description:MED1 often serves as a surrogate of the general transcription coactivator complex Mediator for identifying active enhancers. MED1 is required for phenotypic conversion of fibroblasts to adipocytes in vitro but its role in adipose development and expansion in vivo has not been reported. Here we show that MED1 is not generally required for transcription during adipogenesis in culture and that MED1 is dispensable for adipose development in mice. Instead, MED1 is required for postnatal adipose expansion and the induction of fatty acid and triglyceride synthesis genes after pups switch diet from high-fat maternal milk to carbohydrate-based chow. During adipogenesis, MED1 is dispensable for induction of lineage-determining transcription factors (TFs) PPARγ and C/EBPα but is required for lipid accumulation in the late phase of differentiation. Mechanistically, MED1 controls the induction of lipogenesis genes by facilitating lipogenic TF ChREBP- and SREBP1a-dependent recruitment of Mediator to active enhancers. Together, our ﬁndings identify a cell- and gene-specific regulatory role of MED1 as a lipogenesis coactivator required for postnatal adipose expansion.

2021-03-17 | GSE160605 | GEO

Phosphorylated MED1 Links Transcription Recycling and Cancer Growth

Project description:Mammalian RNA polymerase II (Pol II) initiation, elongation, termination and reinitiation are well studied, but how Pol II dynamically recycles after the transcription cycle remains unclear. By establishing in vitro and in vivo transcription recycling systems, we find that human Mediator 1 (MED1), when phosphorylated at the mammal-specific threonine 1032 by cyclin-dependent kinase 9, dynamically travels with Pol II throughout the transcribed genes to drive Pol II recycling. Mechanistically, MED1 phosphorylation leads to an increase of recycled Pol II via the molecular bridge of MED31, enhancing mRNA output during the transcription recycling process. Importantly, MED1 phosphorylation increases during prostate cancer progression to the lethal phase, and pharmacological inhibition of CDK9 decreases prostate tumor growth through decreasing MED1 phosphorylation and Pol II recycling. Our findings reveal essential mechanisms underlying Pol II recycling and suggest a neglected, yet fundamental Pol II transcription process for therapeutic intervention.

2022-04-20 | GSE127894 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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