BRD8 antibody Polyclonal Antibodies Primary antibodies
- Known as:
- BRD8 (anti-) Polyclonal Antibodies Primary antibodies
- Catalog number:
- orb100138
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- BRD8 antibody Polyclonal Antibodies Primary antibodies
Related genes to: BRD8 antibody Polyclonal Antibodies Primary antibodies
- Gene:
- BRD8 NIH gene
- Name:
- bromodomain containing 8
- Previous symbol:
- -
- Synonyms:
- SMAP, p120
- Chromosome:
- 5q31.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-02-07
- Date modifiied:
- 2016-10-05
Related products to: BRD8 antibody Polyclonal Antibodies Primary antibodies
Related articles to: BRD8 antibody Polyclonal Antibodies Primary antibodies
- Patients with hormone receptor-positive/HER2-positive (HR+/HER2+) breast cancer represent a historically underrecognized subgroup demonstrating poor response to combined endocrine and HER2-targeted therapies. Here, using single-cell transcriptomic and epigenomic sequencing of ER+/HER2+ models, we identified BRD8, an acetyl-lysine reader in the EP400 histone acetyltransferase complex, as a critical mediator of ER/HER2 signaling crosstalk. BRD8 expression rapidly increased following anti-HER2 treatment, while its depletion disrupted ER-HER2 interaction and enhanced drug sensitivity. Single-nucleus ATAC-sequencing revealed that chromatin regions opening after anti-HER2 treatment were enriched for ER, FOX, and ETS transcription factor motifs, coinciding with BRD8-dependent gene activation through EP400-mediated H2AZac deposition. BRD8 regulated ER-dependent and independent growth pathways, and depletion of BRD8 abolished neratinib-induced ER activation and restored drug sensitivity in resistant cells. A 3-gene BRD8 signature successfully predicted anti-HER2 therapy response in two human clinical trials. Together, these findings establish BRD8 as both a predictive biomarker for anti-HER2 response and a therapeutic target to overcome resistance in HR+/HER2+ breast cancer. - Source: PubMed
Publication date: 2026/03/26
Gao AngKhatri Parth HMa GuiLiu PengFernandez-Martinez AranzazuDonahue KristineWang YidanKim Eui-JunHu MingshanLiu FabaoZhou JingjingChan Ngai TingYang XingjianWelch Schwartz ReneOng Irene MBurkard Mark EWisinski Kari BPerou Charles MDinh Huy QXu Wei - Genetic effects due to long term exposure to low doses of ionizing radiation (LDIR) in humans are not well understood. Human population living in high level natural radiation areas (HLNRAs) of Kerala coast in India are continuously exposed to chronic LDIR emanating from monazite containing beach sand for many generations. The background radiation level in this area varies from < 1.0 to 45mGy/year. The people residing in HLNRAs sometimes receives background radiation dose which is approximately 10-40 times higher than the people living in adjacent normal level natural radiation areas (NLNRAs). This population provides a unique opportunity to identify, if present, a mutational signature due to chronic low-dose radiation exposure in humans. We have employed whole exome sequencing approach to determine germline mutational changes in the lymphocytes of healthy individuals from HLNRAs (mean background dose: 31.8 ± 5.4 mGy/year, mean age: 43.0 ± 5.9 years) and compared them with healthy individuals from NLNRAs (mean background dose: 0.9 ± 0.2 mGy/year, mean age: 43.0 ± 11.3 years). - Source: PubMed
Publication date: 2026/02/27
Jain VinaySaini DivyalakshmiSabarinathan RadhakrishnanDas Birajalaxmi - Merkel cell carcinomas (MCCs) are rare, highly aggressive skin cancers with poor outcome due to early lymphatic tumor spread and frequent recurrences. MCCs mostly occur in the head and neck and are mainly caused by an infection with the Merkel cell polyomavirus (MCPyV). Increasing evidence suggests that Piwil-2 and small non-coding PIWI-interacting RNAs (piRNAs) play an important role in solid malignancies and we thought that this might also be the case for MCCs. Therefore, Piwil-2 expression was first evaluated in 27 MCC specimens and correlated with oncological outcome. We found an association with high Piwil-2 expression and advanced tumor stage, MCPyV positivity and poor outcome. Next, we utilized siRNAs for Piwil-2 knock-down in MCC cells. Downregulation of Piwil-2 caused a significant change of 202 different piRNAs and 419 proteins. Interestingly, proteins related to viral driven MCC pathways (TRRAP, BRD8, PRIM2, ORC4) were significantly downregulated. Moreover, there was a moderate cell cycle arrest of cells in the G0/G1-phase, as well as a significant upregulation of SOX-2, a key regulator of Merkel cells. Altogether, Piwil-2 poses a poor prognosticator in MCCs, which is linked to MCC oncogenesis and SOX-2. Further research is needed to better understand underlying mechanisms and to prove their clinical relevance. - Source: PubMed
Publication date: 2025/11/10
Janik StefanPammer JohannesSimader ElisabethKotowski UlanaGrasl StefanHouben RolandCopic DraganMildner MichaelMitulovic GoranBilban MartinDerdak SophiaUnterwurzacher MarkusKratochwill KlausErovic Boban M - Colorectal cancer (CRC) ranks as one of the most malignant solid tumors worldwide. Bromodomain containing 8 (BRD8) functions as an oncogene in various cancers. This study aimed to investigate the roles of BRD8 in CRC. mRNA expression was detected using reverse transcription-quantitative PCR (RT-qPCR). Protein expression was detected using Western blot. The expression of macrophage markers was detected using immunohistochemistry and immunofluorescence. Cell viability was detected using Cell Counting Kit-8 (CCK-8) assay. Macrophage function was detected using flow cytometry. Cell migration and invasion was detected using transwell assays. We found that high levels of BRD8 mediated the predominance of M2-like tumor-associated macrophages (TAM2) and predicted poor prognosis of CRC patients. However, BRD8 knockdown suppressed TAM2 polarization as well as the migration and invasion of CRC cells. Mechanically, BRD8-mediated the upregulation of transforming growth factor β1 (TGF-β1), overexpression of which promoted TAM2 polarization and aggressiveness of CRC cells. Taken together, BRD8 deficiency suppressed TAM2 polarization, inhibiting the progression of CRC. Therefore, BRD8 may be a therapeutic target for CRC. - Source: PubMed
Publication date: 2025/07/28
Xu LiangMo YejiaYu BingqiFan Sunfu - We report an unusual uterine polypoid mesenchymal tumor in a 52-year-old resembling the soft tissue neoplasm ossifying fibromyxoid tumor (OFMT). The neoplasm was morphologically low-grade with hypocellular areas containing bland spindle cells in a fibromyxoid stroma, cellular areas resembling typical low-grade endometrial stromal sarcoma (LGESS), and abundant mature bone. The cellular areas were ER and CD10 positive and cyclin D1 negative, and the hypocellular areas were ER and CD10 negative, with approximately 50% of the nuclei being cyclin D1 positive. The tumor harbored a BRD8::PHF1 fusion. This fusion has been reported rarely in uterine mesenchymal neoplasms, which have been designated as LGESS or high-grade endometrial stromal sarcoma. In reporting this case, we review previously reported uterine mesenchymal neoplasms with a BRD8::PHF1 fusion. Since OFMT commonly contains PHF1 fusions, we discuss the most appropriate terminology for the neoplasm we report and suggest that it is best classified as an LGESS with OFMT-like morphology. - Source: PubMed
Publication date: 2025/07/16
O'Neill NiallSampson JamesMcCluggage W Glenn