NCOA1 antibody - middle region (ARP33991_P050)
- Known as:
- NCOA1 (anti-) - middle region (ARP33991_P050)
- Catalog number:
- arp33991_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- NCOA1 antibody - middle region (ARP33991_P050)
Related genes to: NCOA1 antibody - middle region (ARP33991_P050)
- Gene:
- NCOA1 NIH gene
- Name:
- nuclear receptor coactivator 1
- Previous symbol:
- -
- Synonyms:
- SRC1, F-SRC-1, NCoA-1, KAT13A, RIP160, bHLHe74
- Chromosome:
- 2p23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-17
- Date modifiied:
- 2016-10-05
Related products to: NCOA1 antibody - middle region (ARP33991_P050)
Related articles to: NCOA1 antibody - middle region (ARP33991_P050)
- Hormone receptor signaling is often interpreted through receptor abundance as a proxy for hormone responsiveness, yet the determinants of single-cell variability in hormone response remain unclear. Using murine mammary organoids, we mapped estrogen (E2) and progesterone (P4) responses at single-cell resolution. Despite controlled 3D culture conditions, basal cell-derived organoids exhibit striking variability in hormone-induced transcriptional responses, with ERα cells varying in the fraction of responsive genes engaged. This variability is not explained by receptor abundance alone. Instead, response magnitude correlates with expression of transcriptional co-regulators including , , and , suggesting that co-regulator balance contributes to variation in endocrine response magnitude. Organoids exhibit a mixed basal-luminal enhancer landscape and growth factor-dependent remodeling of ERα and PR protein abundance. MCF7 cells show delayed activation kinetics and reach a lower response plateau. Together, these findings reveal that hormone response magnitude varies independently of receptor abundance in mammary organoids and follows distinct activation dynamics in human ERα cancer cells. - Source: PubMed
Publication date: 2026/03/23
Yasar PelinDay Christopher RBennett Brian DHoffman Jackson AKammel Laura GArcher Trevor KRodriguez Joseph - Angiogenesis is essential for glioma progression, yet the epigenetic mechanisms driving this process remain incompletely defined. In this study, we investigated the role of the histone acetyltransferase EP300 in regulating VEGFA expression and promoting endothelial activation. Using glioma cell lines with EP300 overexpression or knockdown, we found that EP300 markedly enhanced endothelial proliferation, invasion, and tube formation, while its silencing produced opposite effects. Mechanistic analyses revealed that EP300 increased H3K27 acetylation at the VEGFA promoter, thereby activating VEGFA transcription. Pharmacologic blockade of EP300 activity or VEGFA neutralization abolished these pro-angiogenic effects. Through integrative analysis of TCGA data and protein complex databases, NCOA1 was identified as a key EP300-associated cofactor. Co-immunoprecipitation and nuclear-cytoplasmic assays confirmed that EP300 forms a nuclear transcriptional co-activator complex with NCOA1, which stabilizes its nuclear localization and synergistically enhances VEGFA expression. Together, these findings identify EP300 as a central epigenetic regulator of glioma angiogenesis and highlight the EP300/NCOA1-VEGFA axis as a potential therapeutic target. - Source: PubMed
Publication date: 2026/03/30
Yang ShidiYao XiaoyanLin XiuwenYang DengfengYing Xiang - The profound molecular heterogeneity of SLE remains a fundamental barrier to therapeutic progress. - Source: PubMed
Publication date: 2026/02/13
Shipa Muhammad RaBeesley ClaireMcClusky DanielGuichard VincentChung Sharon ACooney Laura AGilroy DerekEhrenstein Michael R - The purpose of this study is to explore the potential mechanism of Si-Wu-Tang (SWT) against esophageal squamous cell carcinoma (ESCC). Initially, 18 active molecules and 96 related targets of SWT obtained from publicly accessible databases. Through Genecards database queries and gene differential expression analysis combined with weighted gene correlation network analysis (WGCNA) on the GSE20347 dataset of ESCC, 3649 disease targets were identified. A subsequent analysis of Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment was performed on 51 disease-drug intersection genes using the R language. Additionally, we identified 3 target hub genes (CDK1, NCOA1, and CHRM3) utilizing machine learning tools. Single-gene GSEA results suggested that hub genes may influence several signaling pathways and biological processes. Immune infiltration analysis demonstrated that SWT might impact the tumor immune microenvironment in ESCC by acting on hub targets. Molecular docking demonstrated the presence of affinity between target hub proteins and active compounds. This study revealed that SWT might exert its therapeutic effects on ESCC through multi-targets and multi-mechanisms. - Source: PubMed
Li XinboZhang ChenchenLi JingYuan JianfengXing TiantianYang HeyuanShi Huijuan - : Obesity-associated hyperleptinemia has been linked to breast cancer (BC) progression via mechanisms that remain incompletely understood. This study explores the role of leptin and its receptor (LEPR) in facilitating BC cell proliferation, migration, epithelial-mesenchymal transition (EMT), and STAT3 signaling pathway activation. : We analyzed gene expression and survival data from TCGA BRCA dataset. MCF-7 and MDA-MB-231 BC cells were exposed to leptin at 10 ng/mL (lean-associated levels) and 100 ng/mL (elevated levels linked to obesity). MTT assays, colony formation tests, wound-healing and tumor spheroid dissemination experiments evaluated cell proliferation and migration. Immunofluorescence and Western blot analysis assessed changes in EMT markers and cytoskeletal alterations, while Western blotting and qPCR assessed STAT3 and expression and activation levels. : Elevated expression was linked with unfavorable prognosis in BC patients. Higher doses of leptin (100 ng/mL) significantly enhanced cellular proliferation rates and migratory capabilities, in both cell lines, and promoted EMT characteristics marked by downregulated E-cadherin and cytoskeleton structural changes. Whereas heightened JAK2/STAT3 signaling correlated with elevated leptin dosages, STAT3 inhibition using AG490 reversed leptin-induced migration while reinstating E-cadherin levels to baseline. Furthermore, leptin upregulated , an essential STAT3 coactivator, facilitating increased expression of and target genes. Clinical positive relationships were seen between / expressions and levels and between and various gene signatures related to STAT3/P-STAT3 within BC specimens. : Obesity-associated hyperleptinemia enhances aggressiveness in BC through a mechanism involving LEPR-mediated activation pathways encompassing NCOA1/STAT3, which drive proliferation, migration, and EMT. This assigns a potential therapeutic utility for obesity-related advancements found within BC pathology. - Source: PubMed
Publication date: 2026/01/08
Ayed KhouloudGorrab AmalBouguerra HichemAkrout RymZekri SamiAlmawi Wassim YBoughriba RahmaChoukri KhalilBacha DhouhaPagano AlessandraLouet Jean-FrançoisKovacic HervéTannour-Louet MouniaGati Asma