Project description:We report the application of Calling Card sequencing technology for high-throughput profiling of Brd4-bound enhancers in male and female mouse glioblastoma.

2020-08-23 | GSE156678 | GEO

Brd4-bound enhancers drive cell-intrinsic sex differences in glioblastoma.

Project description: Not available

| S-EPMC8072233 | biostudies-literature

Brd4-bound enhancers drive cell intrinsic sex differences in glioblastoma

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-08-25 | GSE156821 | GEO

Brd4-bound enhancers drive cell intrinsic sex differences in glioblastoma [ChIP-Seq]

Project description:We report the application of ChIP-seq for high-throughput profiling of histone mark H3K27ac in male and female mouse glioblastoma.

2020-08-26 | GSE156820 | GEO

Brd4-bound enhancers drive cell intrinsic sex differences in glioblastoma [RNA-Seq]

Project description:We report the application of RNA-seq for high-throughput profiling of transcriptom in male and female mouse glioblastoma.

2020-08-26 | GSE156819 | GEO

BRD4 degradation via stabilization of a native interaction with DCAF16

Project description:Targeted protein degradation is a modality based on small molecules that induce proximity between a protein of interest (POI) and an E3 ubiquitin ligase, thus prompting POI ubiquitination and degradation. To expand the reach of TPD, current research is geared to unlock novel E3s. To that end, the transcriptional co-activator protein BRD4 has emerged as a frequently used POI. Derivatization of known BRD4 ligands with structurally diverse substituents has yielded a suite of potent BRD4 degraders, thus generating the notion that BRD4 is particularly amenable to TPD. Here, we mechanistically characterize two BRD4 degraders via orthogonal CRISPR screens. Despite their structural dissimilarity, both degraders functionally converge on a unifying mechanism of action that involves the CRL4DCAF16 ligase complex. Using recombinant reconstitution, as well as biophysical and structural elucidation, we demonstrate that BRD4 has an intrinsic activity for DCAF16, which is further enhanced by both compounds. We uncover a novel mode of molecular recognition based on multivalent "gluing" of BRD4 onto DCAF16 that requires both bromodomains of BRD4. Our data thus imply a substantial conceptual overlap between PROTACs and molecular glue degraders, and highlight multivalency as a novel concept in the design of proximity-inducing drugs.

2024-01-08 | PXD040570 | Pride

Chromatin occupancy assessment an AML cell line treated with vehicle control, BETi, MDM2i, or a drug combination (BRD4-bound profiles)

Project description:BRD4 chromatin occupancy changes in human OCI-AML3 cells treated with DMSO (vehicle control), the BET inhibitor CPI-203, the MDM2 inhibitor Nutlin-3a, or a combination of both drugs, were compared. Method: Genomic DNA from the OCI-AML3 cell line treated for 24 hrs with either DMSO, CPI-203, Nutlin-3a or a combination of both drugs was extracted, BRD4-bound chromatin was immunoprecipitated, then DNA was sequenced with an Illumina NextSeq 500 sequencer. Sequence reads passing the quality control filters were aligned using Bowtie2 and then analysed with SICER.

2020-11-04 | GSE132247 | 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