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
- 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 - Based on PCR with complementary primer pairs and Pfu DNA polymerase, QuickChange site-directed mutagenesis has been widely employed, but its efficiency varies from mutation to mutation. An alternative strategy relies on partially overlapping primer pairs with 3'-overhangs, and this strategy has led to the recent development of P3a and P3b site-directed mutagenesis, in which the use of SuperFi II and Q5 polymerases raises the mutagenesis efficiency to ~100%. It is unclear whether these two DNA polymerases also improve the QuickChange method. Herein, we have evaluated this possibility by engineering 46 mutations on seven expression plasmids, two of which possess extremely GC-rich sequences. As Pfu DNA polymerase is a slow enzyme, its replacement with SuperFi II and Q5 polymerases reduced PCR length. Moreover, the average efficiency for each of the seven plasmids ranged from 48% to 69%, thereby outperforming the original QuickChange method. However, this efficiency is still lower than that from the P3a and P3b methods, supporting the superiority of primer pairs with 3'-overhangs. Analysis of the incorrect plasmids from the improved QuickChange method revealed frequent insertions at primer sites. The insertions were derived from primers and varied from mutation to mutation, with certain sites much more prone to such insertions. In comparison, these insertions occurred at a much lower frequency with the P3a and P3b methods, suggesting that primer pairs with 3'-overhangs enhance mutagenesis efficiency by reducing the likelihood to introduce insertions at primer sites. Thus, this study improves the QuickChange mutagenesis method, supports the superiority of the P3a and P3b methods, and uncovers a novel molecular mechanism by which the efficiency of PCR-based mutagenesis with completely overlapping primer pairs is negatively affected. - Source: PubMed
Publication date: 2026/01/13
Varela-Castillo PaulinaRazavi ArezousadatMousavi NegarRobinson NicoleYang Xiang-Jiao - Polycystic ovary syndrome (PCOS) is a common endocrine-metabolic disorder in which skeletal muscle insulin resistance contributes substantially to cardiometabolic risk. Pioglitazone improves insulin sensitivity in women with PCOS, yet the underlying transcriptional changes and their potential as treatment-response biomarkers remain incompletely defined. We aimed to reanalyse skeletal muscle gene expression from pioglitazone-treated PCOS patients using modern machine learning and network approaches to identify candidate biomarkers and regulatory hubs that may support precision therapy. - Source: PubMed
Publication date: 2025/12/29
Al Athamneh AhmadFarfoura Mahmoud EKhaleel AnasConnie Tee - Cytochrome P450 enzymes (CYPs) are central to metabolism and stress adaptation. In Caenorhabditis elegans, the CYP-13 family performs diverse and conserved functions beyond xenobiotic detoxification. cyp-13 links lifespan regulation to the APP ortholog apl-1 and the heterochronic factor lin-14, integrating with DAF-16/FOXO, HSF-1, and DAF-12 pathways. In apoptosis, cyp-13 contributes to the degradosome complex with CPS-6/EndoG and WAH-1, facilitating DNA degradation. Several isoforms are inducible by aflatoxin B1 and PCB1254, underscoring roles in toxicant metabolism. Notably, cyp-13A12 regulates behavioral responses to reoxygenation via the EGL-9-HIF-1-PUFA-eicosanoid pathway, paralleling mammalian ischemia-reperfusion responses. Epigenetic regulation adds another layer, as BRCA1/BARD1 homologs brc-1 and brd-1 repress distinct subsets of cyp-13A genes through H2A ubiquitylation. Collectively, CYP-13 emerges as a multifunctional hub linking developmental, apoptotic, metabolic, stress, and chromatin-level processes, with clear parallels to human CYPs, highlighting its translational relevance to aging, cancer, and toxicology. - Source: PubMed
Publication date: 2026/01/14
Lim Sharoen Yu Ming