Ask about this productRelated genes to: BRD1 antibody
- Gene:
- BRD1 NIH gene
- Name:
- bromodomain containing 1
- Previous symbol:
- -
- Synonyms:
- BRL, BRPF2
- Chromosome:
- 22q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1999-10-29
- Date modifiied:
- 2015-08-26
Related products to: BRD1 antibody
Related articles to: BRD1 antibody
- BRCA1/BARD1 is a chromatin-associated E3 ubiquitin ligase that ubiquitylates histone H2A to coordinate DNA damage repair, transcriptional repression, and genome stability. In , the orthologous BRC-1/BRD-1 complex performs analogous functions but exhibits structural variation, most notably through an additional 11-residue loop in BRD-1 that is absent from human BARD1. Prior experiments indicate this worm-specific insertion promotes nucleosome engagement and may alter the preferred lysine target for ubiquitylation. Here, we provide a cross-species comparison by integrating computational and experimental investigation to clarify how a discrete structural variation can tune BRCA1-family ligase behavior and, consequently, chromatin regulation. ubiquitylation assays and mass spectrometry reveal BRC-1/BRD-1 ubiquitylate the C-terminal tail of histone H2A with less specificity than the human homologs. All-atom molecular dynamics simulations of both the BRC-1/BRD-1-LET-70-Ubiquitin assembly and the human BRCA1/BARD1-UbcH5c-Ubiquitin complex in the presence of the nucleosome core particle uncover that the BRD-1 loop makes transient contacts with nucleosomal DNA and histone tails, thereby modulating the positioning and conformational flexibility of the bound E2 (ubiquitin-conjugating enzyme). Together, our results suggest that the BRD-1 loop alters the E3-E2 geometry, thereby altering ubiquitylation-site specificity. - Source: PubMed
Publication date: 2026/07/01
Heidari SaharLightle CaitlinHerrington LaurenShah TejasHossain FarihaMorcos FaruckWeintraub Susan TStewart Mikaela DTorabifard Hedieh - Antiretroviral therapy suppresses HIV replication but fails to eliminate the virus due to the persistence of a transcriptionally silent reservoir, which remains the primary barrier to a cure. HIV latency is maintained through chromatin-mediated repression, making epigenetic regulators attractive therapeutic targets. To identify new modulators of latency, we screened a focused library of 84 chromatin-targeting small molecules. This screen identified BAY-299, a bromodomain inhibitor selective for TAF1 and BRD1, as a latency-modulating compound. BAY-299 reactivated HIV expression and enhanced the efficacy of established latency-reversing agents, including vorinostat, prostratin, and iBET-151, in cell line models. CRISPR/Cas9-mediated knockout experiments demonstrated that TAF1, but not BRD1, is essential for maintaining HIV latency and that TAF1 depletion selectively increases HIV transcription with minimal effects on host gene expression. Dual knockout of TAF1 and Tat revealed that reactivation of HIV in the absence of TAF1 is partially Tat-dependent. Cleavage Under Targets and Release Using Nuclease analysis further showed that TAF1 depletion increased histone acetylation at the viral promoter and across the HIV gene body, suggesting a chromatin-based mechanism. These findings identify TAF1 as a novel regulator of HIV latency and demonstrate the utility of targeted chemical screening to uncover therapeutic vulnerabilities within the latent reservoir. - Source: PubMed
Publication date: 2026/06/15
Burgos Samuel DWard Airlie MAshokkumar ManickamEnders Kimberly PJames Lindsey IMargolis David MBrowne Edward P - Phelan-McDermid syndrome (PMS) is caused in the majority of cases by the loss or mutation of one allele of the SHANK3 gene, located in human chr 22q13.33. PMS displays large interindividual differences in clinical severity and longitudinal trajectory. Other genes located in this chromosomal region are known to contribute to the clinical phenotype (CELSR1, TCF20) in patients with larger deletions. The aim of this study is to identify clinically-relevant phenotypic features significantly influenced by the size of chromosome 22q terminal deletion and to identify new potential candidate genes likely to be involved in these phenotypic effects. - Source: PubMed
Publication date: 2026/05/26
Sandoni LauraChehbani FethiaAsta LisaCamia MichelaRicciardello AriannaTomaiuolo PasqualeCucinotta FrancescaTurriziani LauraBoncoddo MariaBellomo FabianaBaccarin MarcoPicinelli ChiaraCastronovo PaolaSacco RobertoLintas CarlaPiras Ignazio StefanoPelagatti FrancescoBanchelli FedericoCostantini Riccardo CuoghiD'Amico RobertoPersico Antonio M - BRD1 is an epigenetic regulator implicated in neurodevelopmental and psychiatric disorders, yet its role in human neuronal differentiation, maturation, and function remains poorly understood. Here we show that haploinsufficiency disrupts early neuronal programming, resulting in accelerated maturation and altered neurodevelopmental trajectories in human induced glutamatergic neurons. Transcriptomic profiling reveals an early shift toward neuronal identity, characterized by downregulation of pluripotency markers and persistent upregulation of genes involved in synapse assembly and organization, including . Despite this, neurons form significantly smaller synapses and display increased neuronal activity. Our findings highlight BRD1 as a key regulator of neurodevelopmental timing and synaptic maturation, and network activity reinforcing growing evidence that disruptions in chromatin-mediated control of differentiation and synaptic organization contribute to neurodevelopmental disorders. - Source: PubMed
Publication date: 2026/02/16
Qvist PerDonskov JulieDeans P JPediotidis-Maniatis DimitriosHøgfeldt JacobBorglum AndersDenham MarkBrennand Kristen - Phenotypic diversity arises from the process of development and is shaped by genomic variation in plants. However, the genetic basis of growth dynamics remains poorly understood in maize. - Source: PubMed
Publication date: 2026/01/29
Wu ChengxiuGeng ZedongLi WeikunYe JunliHao XiaoyuanXu JietingJin MinliangWu XiaoyuDu YuanhaoChen YunyuMa ChengGao YuChen YuyueXie TianjinGui SongtaoChen YuanyuanLuo JingyunLiu YupengYang WenyuYan JianbingYang WannengXiao Yingjie