BRD2 (bromodomain containing 2)
Also known as: BRD2 · bromodomain containing 2
In patient-derived xenograft models, PTEN loss recruited BRD2 to MES gene promoters; genetic ablation of BRD2 bromodomains reversed the MES transition and increased radiation sensitivity. VC0095
Review pending Version 0.1.0 · status: draft · last expert review: not yet reviewed
External identifiers
- HGNC symbol
- BRD2
- HGNC
- HGNC:1103
- UniProt
- P25440
Identifiers were checked against the public registry (HGNC, UniProt, MONDO via EBI OLS, NCBI GEO) and are listed only when certain.
Relations
| Subject | Relation | Object | Confidence | Evidence (role) |
|---|---|---|---|---|
| BRD2 | promotes | Mesenchymal-like state | high | VC0095 supports Evidence is from patient-derived xenograft and cell models: PTEN loss recruited BRD2 to MES gene promoters and bromodomain ablation reversed the MES transition. |
| BRD2 | validated by | Patient-derived xenograft models | high | VC0095 supports Tested in patient-derived xenografts; not shown in patients. |
| BRD2 | associated with | Radiotherapy | medium | VC0095 supports Genetic ablation of BRD2 bromodomains increased radiation sensitivity in xenografts. |
Appears in research topics
- Mesenchymal-like (MES-like) glioblastoma cell state (Cell states)
- Therapy-induced plasticity in glioblastoma (Transitions)
Appears in library items (1)
Items whose title, tags or one-line summary match this entity (derived from the data), plus the items cited as evidence for the description.
- VC0095 BRD2 bromodomain-mediated regulation of cell state plasticity modulates therapy response in glioblastoma. — Vadla R et al., Neuro-oncology, 2025
For research and education only. Not medical advice and not a recommendation of any diagnosis, treatment or product. Patients should consult their own physicians.