NCOA3 antibody - middle region (ARP32487_P050)
- Known as:
- NCOA3 (anti-) - middle region (ARP32487_P050)
- Catalog number:
- arp32487_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- NCOA3 antibody - middle region (ARP32487_P050)
Related genes to: NCOA3 antibody - middle region (ARP32487_P050)
- Gene:
- NCOA3 NIH gene
- Name:
- nuclear receptor coactivator 3
- Previous symbol:
- -
- Synonyms:
- RAC3, AIB1, ACTR, p/CIP, TRAM-1, CAGH16, TNRC16, KAT13B, bHLHe42, SRC-3, SRC3
- Chromosome:
- 20q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-17
- Date modifiied:
- 2016-10-05
Related products to: NCOA3 antibody - middle region (ARP32487_P050)
Related articles to: NCOA3 antibody - middle region (ARP32487_P050)
- Metabolic dysfunction-associated steatotic liver disease (MASLD) and steatohepatitis (MASH) are leading causes of cirrhosis and hepatocellular carcinoma. Defects in autophagy contribute to the development of MASLD, however, the role of the Unc-51-like autophagy-activating kinase 1 (ULK1) in the pathophysiology of MASLD remains unclear. Herein, we show that ULK1, a serine/threonine kinase and core autophagy protein, is significantly repressed in human MASH livers, and that hepatocyte-specific loss of ULK1, unexpectedly, promotes hepatic steatosis and progression to liver fibrosis, without affecting basal autophagy flux. Phospho-proteomics identified the transcriptional coactivator NCOA3 as a downstream phospho-target of ULK1. Mechanistically, ULK1 phosphorylates NCOA3 to repress its transcriptional activity and restrain the CREB/CBP-mediated de novo lipogenic program. Accordingly, a phosphorylation-deficient NCOA3 mutant drives CREB/CBP-mediated lipogenesis, whereas genetic or pharmacological NCOA3 inhibition prevents steatosis, hepatic inflammation, and profibrotic signaling. Hence, ULK1-mediated NCOA3 phosphorylation is a fundamental and druggable checkpoint against the entire MASLD spectrum. - Source: PubMed
Publication date: 2026/04/02
Koo Young DoCastillo Romilia TatianaSukumaran Nair AshaGarneau MichaelGochee ChadCampbell Zachary VVakil Tashya ShreyasHa JuaMarti AlexSoto JamieDas DebajyotiMartinez-Lopez NuriaSharma ShipraDelgado YenniferPhung CallieAshley Immy AKapelczak Edmund DJacobo RashelWeatherford Eric TDai Dao-FuBenhammou Jihane NMarshall Andrea GHinton AntentorYang LingPereira Renata OTeSlaa TaraBouhaddou MehdiSingh RajatAbel E Dale - In dairy sheep, mammary morphology-related phenotypes are crucial functional traits due to their connection to machine milking aptitude, udder health, particularly mastitis, and animal welfare. This study aimed to dissect the genetic architecture underlying 5 mammary morphology traits (Udder depth, Udder attachment, Teat placement, Teat size, and Udder shape) in Churra dairy sheep by using data generated with the Illumina OvineSNP50 BeadChip. The analyzed population, part of the Churra Dairy Selection Nucleus (ANCHE), comprised 1,680 ewes distributed across 16 half-sib families. Genome scans using linkage analysis and a GWAS detected 5 genome-wide significant QTL regions. Comparison with previously reported sheep QTL revealed no direct overlap; however, several of the identified regions coincided with QTL reported in cattle for mammary morphology and mastitis resistance traits, suggesting the possibility of conserved genetic mechanisms underlying these traits across ruminant species and further supporting the relevance and validity of the genomic regions detected in this study. Interestingly, the genome-wide significant QTL region detected on OAR13 for Teat placement showed overlapping with chromosome-wide effects on Udder shape, suggesting for this region a potential pleiotropy effect or the presence of closely linked variants affecting multiple udder traits. To further explore the genome-wide significant regions identified in this study, all genes within each region were annotated. Among the 84 annotated genes, 3 of them, NCOA3, ASS1, and TMEFF2, directly overlapped with a previously defined reference gene list for udder traits and were therefore considered direct functional candidate genes. These genes were associated with epithelial branching, extracellular matrix regulation, cytoskeletal dynamics, and signaling pathways. For the remaining annotated genes in the target regions, a prioritization analysis was performed to identify additional potential candidate genes that may be relevant to the traits under study. The results reported here offer a valuable insight into the genetic basis of udder morphology traits in dairy sheep and are a first step into the identification of genetic markers that could improve the efficiency of future genomic selection programs in dairy sheep. - Source: PubMed
Publication date: 2026/03/02
Vrcan MSuárez-Vega AMarina HDzidic AArranz J JGutiérrez-Gil B - Steroid receptor coactivator 3 (SRC-3) is highly expressed in regulatory T cells (Tregs) and is important for their immunosuppressive activity. Recently, we demonstrated that disrupting SRC-3 expression in Tregs eliminates triple-negative breast cancer (TNBC) and prostate cancer in syngeneic animal models by generating an anti-tumor immune microenvironment without inducing immune-related adverse events (irAEs). Further analysis of these mice revealed that SRC-3 knockout (KO) Tregs infiltrated breast tumors and facilitated the infiltration of CD8, CD4, and natural killer (NK) immune cells into the tumor microenvironment (TME). Given the anti-tumor effects of SRC-3KO Tregs in two different solid cancers, we sought to extend our studies to additional cancer types. Here, we showed that SRC-3KO Tregs exerted a potent antitumor immunity-like effect, capable of eradicating glioblastoma, melanoma, and lung cancer in their respective syngeneic mouse models by generating an anti-tumor immune environment. These results support the translational development of SRC-3-targeted Treg modulation as a safe and effective immunotherapy platform for treatment-refractory cancers. - Source: PubMed
Publication date: 2026/03/02
Sung NuriKim EunsuGilad YosefPark YuriDean Adam MXia YanXu JianmingDacso Clifford CLonard David MHan Sang Jun - Diabetes-related cognitive dysfunction (DCD) represents a significant complication of diabetes mellitus, yet its underlying molecular mechanisms remain incompletely elucidated. In this study, we aimed to investigate the potential role of nuclear receptor coactivator 3 (NCOA3) in DCD pathogenesis using both conditional knockout (cKO) and lentivirus-mediated overexpression mouse models. Diabetes was induced through combined high-fat diet feeding and low-dose streptozotocin (STZ) administration. Comprehensive behavioral assessments, including novel object recognition test (NORT), Y-maze, and contextual fear conditioning (CFC), were performed alongside molecular analyses of NCOA3/AGO2 expression and downstream targets. Our results suggested a significant downregulation of NCOA3 expression in cortical and hippocampal tissues of diabetic mice. Genetic ablation of NCOA3 in forebrain excitatory neurons markedly appeared to exacerbate hippocampus-dependent cognitive deficits, while targeted hippocampal NCOA3 overexpression effectively ameliorated these impairments. At the mechanistic level, NCOA3 deficiency was associated with reduced protein levels of AGO2, along with downregulation of the synaptic markers synaptophysin (SYP) and postsynaptic density protein 95 (PSD-95). In vitro studies using primary neuronal cultures indicated that high glucose treatment similarly reduced the expression of both NCOA3 and AGO2, while pharmacological inhibition or genetic knockdown of NCOA3 was found to significantly upregulate miR-138-5p levels. These findings collectively suggested a potential regulatory axis wherein NCOA3 is associated with synaptic plasticity via AGO2/miR-138-5p signaling, providing insights into DCD pathogenesis. - Source: PubMed
Publication date: 2026/01/20
Su YanfangZhang LijingCui HengzhenZhang ChunMeng Xianfang - The molecular pathogenesis of uterine adenosarcoma (uAS; synonym: Müllerian adenosarcoma) is confounded by its pathologic heterogeneity, with DICER1 mutations and TP53 pathway alterations reported in most tumors with high-grade morphology, stromal overgrowth and/ or rhabdomyoblastic differentiation. However, a small subset of tumors harbor gene fusions, but their molecular spectrum and clinicopathological correlations have not been defined. We identified 12 uAS-like neoplasms in our files carrying ESR1 gene fusions and reviewed 4 previously reported cases (total: 16). Patient's age range was 34 - 76 years (median, 54). The tumors originated in the uterus body (5), unspecified uterus segment (5), cervix (1) and isthmus (1). Follow-up was available for 6 patients (median 44 months, range 9 months-20 years). One patient developed lung metastasis 52 months later and one had an abdominopelvic recurrence > 20 years later. Four patients were disease-free at 9-55 months. All tumors harbored in-frame ESR1 fusions (10 with ESR1::NCOA3, 1 ESR1:NCOA2 and 1 ESR1::MAMLD1). Nine tumors were low-grade and 3 high-grade. All lacked heterologous elements. Stromal overgrowth was recorded in three (all high-grade) and sex cord-like elements in 4 tumors. Phyllodiform architecture, admixed Mullerian glands, and periglandular stromal condensation distinguished the 4 tumors with sex cord-like elements from conventional uterine tumors resembling ovarian sex cord tumor (UTROSCT). This study expands the overlapping morphologic and molecular spectrum of uterine neoplasms resembling uAS showing recurrent fusions (mostly ESR1::NCOA3/2), associated with mostly low-grade histology, lack of heterologous elements and paucity of stromal overgrowth. The nosological relationship of these uAS-like tumors to UTROSCT (driven similarly by ESR1::NCOA3/2 fusions) and to fusion-negative high-grade uAS remains to be verified in future studies utilizing epigenetics and other tools. - Source: PubMed
Publication date: 2026/01/20
Agaimy AbbasChiang SarahMichal MichaelDermawan Josephine KClarke Blaise AEmons JuliusStoehr RobertBeckmann Matthias WHartmann ArndtHodgson AnjelicaMatias-Guiu XavierAntonescu Cristina RDickson Brendan C