BRD3 antibody - middle region (ARP34431_P050)
- Known as:
- BRD3 (anti-) - middle region (ARP34431_P050)
- Catalog number:
- arp34431_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- BRD3 antibody - middle region (ARP34431_P050)
Related genes to: BRD3 antibody - middle region (ARP34431_P050)
- Gene:
- BRD3 NIH gene
- Name:
- bromodomain containing 3
- Previous symbol:
- -
- Synonyms:
- RING3L, ORFX, KIAA0043
- Chromosome:
- 9q34.2
- Locus Type:
- gene with protein product
- Date approved:
- 2000-07-25
- Date modifiied:
- 2016-10-05
Related products to: BRD3 antibody - middle region (ARP34431_P050)
Related articles to: BRD3 antibody - middle region (ARP34431_P050)
- Respiratory disease in goats is frequently assessed using non-species-specific clinical scoring schemes, yet evidence on their agreement with thoracic ultrasonography (TUS) is limited. This study compared standardized clinical respiratory scores with TUS lung consolidation in adult goats and developed a goat-adapted triage score (Caprine Respiratory Triage Score, CRTS). - Source: PubMed
Publication date: 2026/08/21
Borriello GiulianoFerrini SaraZantonelli AliceCagnotti GiuliaReinero LisaSannazzaro MartinaZoppi SimonaD'Angelo AntonioBellino Claudio - Proteolysis-targeting chimeras (PROTACs) are heterobifunctional molecules that induce selective degradation of target proteins by hijacking the ubiquitin-proteasome system (UPS). Despite their transformative potential in eliminating disease-associated proteins, comprehensively identifying off-target degradation events remains technically challenging. Here, we employed an integrated proteomic and ubiquitinomic strategy to systematically profile the degradation landscape of the PROTAC molecule dBET1 in Jurkat T cells. By capturing the upstream ubiquitination events─which serve as earlier and more sensitive indicators than total protein abundance─our approach enabled the identification of previously overlooked off-target candidates. While dBET1 efficiently degraded its canonical BET family targets, our data also revealed the mitochondrial outer membrane protein VDAC1 as a putative off-target, evidenced by its depletion and increased multisite ubiquitination. Notably, our analysis framework enabled site-specific resolution of degradation events within BRD3, revealing preferential ubiquitination at functionally essential bromodomains, suggesting that degron-enriched regions may underlie domain-selective degradation. Additionally, dBET1 treatment was associated with mitochondrial depolarization and calcium homeostasis disruption, defects that we hypothesize may be functionally linked to the observed VDAC1 depletion. Together, this study demonstrates that integrating ubiquitomics provides a superior sensitivity layer for PROTAC safety assessment, capable of uncovering mechanism-based liabilities that escape conventional global proteomic screening. - Source: PubMed
Wen HongtaoLiu HuiLiu JinfangYang BendongDai JiaxingChang LeiLi YanchangZhang YaoYu LiyanXu Ping - Acute myeloid leukaemia (AML) is a therapeutically challenging malignancy driven by the self-renewal, quiescence, and therapy resistance of leukaemic stem cells (LSCs). CDK8, a kinase component of the Mediator complex, regulates oncogenic transcription, and the selective CDK8/CDK19 inhibitor RVU120 (Romaciclib) targets AML cells with CD34/pSTAT5-high LSC-like characteristics; however, the epigenetic and transcriptional consequences of CDK8 blockade and actionable combinatorial strategies remain incompletely defined. Using the TEX cell line, an LSC-enriched surrogate model, we performed time-resolved RNA-seq, whole-proteome and phosphoproteomics mass spectrometry (MS), and CUT&Tag chromatin profiling following treatment with RVU120 and CCT251921. CDK8 protein-protein interactions were mapped by co-immunoprecipitation MS across five AML models, and synergy with Pelabresib (BET inhibitor) or CB6644 (RUVBL1/2 inhibitor) was assessed by high-content screening in three cell lines and three patient-derived xenograft (PDX) models. Both inhibitors suppressed STAT5 phosphorylation, induced loss of the CD34/CD38 LSC-enriched phenotype, and drove erythromegakaryocytic differentiation. Transcriptomic and proteomic responses were concordant, and CDK8 inhibition triggered widespread enhancer activation with redistribution of RNAP2, BRD3, and NFRKB. CDK8 combined with Pelabresib acted synergistically in MOLM-16 cells and two of three PDX models. These findings identify CDK8 as a transcriptional node of LSC-associated programs and provide a mechanistic rationale for combined CDK8-BET inhibition in molecularly defined AML subsets, which will require validation in functional LSC assays and primary specimens. - Source: PubMed
Publication date: 2026/08/04
Statkiewicz MalgorzataRumienczyk IzabelaPakulska UrszulaObacz MartaKulecka MariaCendrowski JarosławCubulska-Lubak MagdalenaKaniuga EwelinaSandowska-Markiewicz ZuzannaSlusarczyk-Kacprzyk WiolettaGoryca KrzysztofRubel TymonBakun MagdalenaSwiderska BiankaKruczkowska-Tarantowicz KamilaRzepecki PiotrKorsak JolantaKyc-Wachowiak KrystynaPolak AnnaJuszczynski PrzemyslawMazan MilenaRzymski TomaszOstrowski JerzyMikula Michal - Paternal influences on offspring development extend beyond Mendelian inheritance, but how sire genetics shape fetal transcription and -regulatory landscapes across tissues is unclear. Using a reciprocal backcross in pigs (F×German Landrace vs. F×Piétrain) and a haplotype-agnostic RNA-seq pipeline, we profiled six fetal tissues to test sire-breed effects. We identified paternal breed-driven transcriptional divergence, with 1,176 genes differentially expressed. Transcriptional divergence was most pronounced in metabolic tissues, revealing a tissue-specific trade-off: F × GL conceptuses prioritized metabolic and energy pathways, whereas F × Pi conceptuses upregulated developmental and cell cycle processes. Allele-specific expression analysis revealed extensive, tissue-dependent -regulatory divergence, and differential ASE highlighted candidate mediators, including and (kidney), (brain), and (liver). These results indicate that paternal genetics programs fetal tissues via -regulatory variation, informing strategies to improve livestock traits. Notably, many loci overlapped known QTLs, suggesting that regulatory variants connect sire background to performance-related phenotypes and fetal programming. - Source: PubMed
Publication date: 2026/07/13
Iqbal Muhammad ArsalanMurani EduardHadlich FriederReyer HenryOster MichaelTrakooljul NaresWimmers KlausPonsuksili Siriluck - Bromodomain-containing protein 4 (BRD4) is an important therapeutic target for anticancer, antiviral, and anti-inflammatory responses. Although its role in transcription, chromatin dynamics, and epigenetic programs is well recognized, recent studies have expanded the functions of BRD4 and its related bromodomain and extra-terminal (BET) family members (BRD2, BRD3, and BRDT) to other molecular and biological processes. How a universal epigenetic regulator is tailored for context-specific gene/pathway regulation is mechanistically intriguing. In this review, we highlight the importance of protein isoforms and posttranslational modifications, particularly phosphorylation, in generating the protein diversity necessary for selective factor recruitment and context-dependent regulation. Three BRD4 protein isoforms have been identified, including the universally expressed BRD4-L and BRD4-S(a) (simplified as BRD4-S), representing the long and short isoform a, and cell-/stress-specific short isoform b, BRD4-S(b). A phospho-switch mechanism controlling the open/closed state of the bromodomain and BRD4 interaction with partner proteins will also be discussed. Mechanistic understanding of BET protein action has led not only to the development of diverse bromodomain-binding compounds currently used in clinical trials but also to the discovery of a new class of small-molecule inhibitors targeting an intrinsically disordered region (IDR) of phospho-BRD4 to alter specific protein-protein interaction (PPI) networks without globally perturbing transcription programs and chromatin landscapes, thus significantly reducing off-target effects and providing new directions for therapeutic drug development. - Source: PubMed
Publication date: 2026/07/23
Wu Shwu-YuanChiang Cheng-Ming