Browse our anti-BRD2 (BRD2) Antibodies

Human Bromodomain Containing 2 (BRD2) interaction partners

1. Results provide evidence that BRD2 is a positive regulator of epithelial-to-mesenchymal transition in breast cancer cells.

2. the bromodomain protein BRD2 is recruited to DNA double-strand breaks.

3. findings suggest that resistance to I-BET151 in U937R cells is related to constitutive activation of the NF-kappaB signaling pathway via increased expression of both BRD2 and BRD4. Targeting the NF-kappaB signaling pathway may be an effective therapeutic strategy to enhance or restore the sensitivity to I-BET151 in U937 cells.

4. The results of the present study show evidence that BRD2 promoter methylation variation is a cause of juvenile myoclonic epilepsy in Caucasians

5. acetylated peptide selectivity between human BET Brd2 bromodomains BD-I and BD-II in glioblastoma

6. In pluripotent cells, Brd2-Brd4 occupy Nodal gene regulatory elements (NREs), but only Brd4 is required for pluripotency gene expression. Brd4 downregulation facilitates pluripotent exit and drives enhanced Brd2 NRE occupancy, thereby unveiling a specific function for Brd2 in differentiative Nodal-Smad2 signalling

7. BRDs are overexpressed in castration-resistant prostate cancer and that ATAD2 and BRD2 have prognostic value.

8. The bromodomain and extraterminal domain (BET) family consists of BRDT, BRD2, BRD3, and BRD4, each containing 2 bromodomains located N-terminal to extraterminal domain, which is located near C-terminus. Data suggest that 10 distinct acylations participate in binding of BET family proteins to histone 4 (oligopeptide fragments used here); C-terminal bromodomains do not cooperatively bind multiple acylation sites.

9. The identification of RNF43 mutations in a distinct subset of intraductal papillary neoplasm of the bile ducts revealed a new molecular role in the pathogenesis of this disease

10. LRP1B, BRD2 and CACNA1D are new candidate genes in fetal metabolic programming of newborns exposed to maternal hyperglycemia.

11. This study implicates BET Brds as important regulators of IkappaB kinase/NF-kappaB-mediated synovial inflammation of RA and identifies BET proteins as novel therapeutic targets in inflammatory arthritis.

12. An unexpected role for the bromodomain and extraterminal domain (BET) proteins BRD2 and BRD4 in maintaining oncogenic IKK activity in activated B-cell-like diffuse large B-cell lymphoma.

13. BET proteins, particularly Brd2 and Brd4, may play a key role in the regulation of Nrf2-dependent antioxidant gene transcription and are hence an important target for augmenting antioxidant responses in oxidative stress-mediated diseases.

14. The C-terminal domain of Brd2 is important for chromatin interaction and regulation of transcription and alternative splicing.

15. A structural basis for BRD2/4-mediated host chromatin interaction and oligomer assembly of Kaposi sarcoma-associated herpesvirus and murine gammaherpesvirus LANA proteins.

16. The SNP alleles in BRD2, Cx-36, and ME2 and microdeletions in 15q13.3, 15q11.2, and 16p13.11 also contribute risk to juvenile myoclonic epilepsy'

17. BRD2, BRD3, and BRD4 interact with gammaretroviral INs and serve as cofactors for murine leukemia virus integration.

18. our results identify BRD2 as a new Tat-independent suppressor of HIV transcription in latently infected cells and underscore the therapeutic potential of BET inhibitors in the reversal of HIV latency.

19. Brd2 and Brd4 proteins mediatE the responses of LFs after growth factor stimulation and drivE the induction of lung fibrosis in mice in response to bleomycin challenge.

20. Our study did not confirm the presence of the genetic variants previously found to link the BRD2 gene to the idiopathic form of photosensitive epilepsy.

Mouse (Murine) Bromodomain Containing 2 (BRD2) interaction partners

1. these results provided evidence for a novel role of Brd2 in chronic inflammation and insulin resistance.

2. BRD2 acts to augment the boundary function of CTCF both by limiting the spread or range of enhancer activity and by physically preventing the formation of cross-boundary contacts genome-wide.

3. Brd2 and Brd4 genetic transcription required for Th17 cell development and adaptive immunity.

4. This study reveals an antagonistic relationship between H2A.Z.1ub and BRD2 to regulate the transcriptional balance at bivalent genes to enable proper execution of developmental programs.

5. BRD2 is involved in the modulation of neuroinflammatory responses through PAI-1 and via the regulation of epigenetic reader BET protein

6. DNA demethylation of the Brd2 promoter region induced Brd2 expression during differentiation of 3T3-L1 cells into adipocytes.

7. Brd2 inhibits adipogenesis via the ERK1/2 signaling pathway in 3T3-L1 adipocytes.

8. A structural basis for BRD2/4-mediated host chromatin interaction and oligomer assembly of Kaposi sarcoma-associated herpesvirus and murine gammaherpesvirus LANA proteins.

9. We conclude that Brd2 plays a critical, independent role in regulation of mitogenic response genes

10. Data show that infection of macrophages with Listeria monocytogenes caused binding of the BET proteins Brd2, Brd3, and, most prominently, Brd4 to the Nos2 promoter.

11. Identification of motif B of Brd2 as a dimerization domain involved in association to mitotic chromosomes and proper recognition of acetylated chromatin.

12. These findings suggest that Brd2 is required for cell cycle exit and neuronal differentiation of neuroepithelial cells through the E2F1 pathway during mouse CNS development.

13. Studies showed that although Brd2 mRNA is expressed in both the hippocampus and cerebellum, Brd2 protein only can be detected in the cerebellar Purkinje cells and not in hippocampal cells.

14. Compared to the Brd2+/+ littermates, Brd2+/- males have a decreased clonic, and females a decreased tonic-clonic, seizure threshold.

15. Knockdown of Brd2 with shRNA promotes adipogenic differentiation of 3T3-L1 preadipocytes in vitro.

16. may be involved in the transcriptional activities of genes involved in proliferation of the mammary epithelia during pregnancy

17. The distinct patterns of Brd2 localization within the adult ovary supports a role for Brd2 in mitotic and possibly meiotic cell cycle regulation

18. Brd2-deficient embryos could not be rescued by wild-type extraembryonic tissues

19. In developing a mouse model deficient in Brd2, we find that Brd2 is required for the completion of embryogenesis and proper neural tube closure during development.

Zebrafish Bromodomain Containing 2 (BRD2) interaction partners

1. these results suggest an evolutionarily conserved role for Brd2 in the proper formation and/or patterning of segmented tissues, including the vertebrate CNS, where it acts as a bi-modal regulator of apoptosis, and is necessary, directly or indirectly, for proper expression of genes that pattern the MHB and/or regulate differentiation in the anterior hindbrain.

2. brd2a on chromosome 19 exhibits both maternal and zygotic contributions to early development and patterning, analogous to the brd2 ortholog in Drosophila.