TCF12 Mouse Monoclonal Antibody
- Known as:
- TCF12 Mouse Monoclonal Antibody
- Catalog number:
- ENZ-006938-M01
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- TCF12 Mouse Monoclonal Antibody
Related genes to: TCF12 Mouse Monoclonal Antibody
- Gene:
- TCF12 NIH gene
- Name:
- transcription factor 12
- Previous symbol:
- -
- Synonyms:
- HEB, HTF4, HsT17266, bHLHb20, p64
- Chromosome:
- 15q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1994-06-17
- Date modifiied:
- 2018-02-20
Related products to: TCF12 Mouse Monoclonal Antibody
Related articles to: TCF12 Mouse Monoclonal Antibody
- Transcription factor 12 (TCF12) is a basic helix-loop-helix transcription factor implicated in tissue differentiation and pathogenesis in many types of cancer. Its role in breast and ovarian cancer remains poorly understood. TCF12 protein expression was assessed by immunohistochemistry in 1,514 primary breast tumours and 423 ovarian tumours. TCF12 mRNA expression was analysed in the Molecular Taxonomy of Breast Cancer International Consortium cohort (n=1,980). Associations between protein expression with clinicopathological variables and patient survival were evaluated. In breast cancer, TCF12 was predominantly expressed in the nucleus with low nuclear expression observed in 32% of cases. Both TCF12 protein and mRNA expression were significantly associated with adverse clinicopathological features, including larger tumour size, higher Nottingham Prognostic Index category, and oestrogen receptor-negative tumours. Low nuclear TCF12 expression was associated with adverse breast cancer-specific survival, particularly in oestrogen receptor-positive tumours; it remained an independent adverse prognostic factor in the multivariate analysis. Similar findings were observed when assessing TCF12 mRNA. No association was observed between TCF12 expression and survival of ovarian cancer patients. Low TCF12 expression identified a biologically aggressive subset of breast cancers with poor prognosis. These findings highlight the potential of TCF12 as a prognostic biomarker in breast cancer. No association between TCF12 expression and survival was observed in ovarian cancer patients, suggesting tumour-specific roles. - Source: PubMed
Publication date: 2026/08/04
Polchai NuanphanNdeke DenysAlshammari KhalidGreener Megan RMarak Tangkam RHenman MaisieDeen SuhaGreen Andrew REllis Ian ORakha Emad AMartin Stewart GStorr Sarah J - The genetic dissection of complex traits in livestock continues to pose a significant challenge in the field of animal genetics and breeding. Although traditional genome-wide association studies (GWAS) are capable of localizing genetic variants associated with specific traits, they are insufficient to elucidate the underlying physiological mechanisms. An integrated analysis of multi-trait GWAS and multi-transcriptomic data systematically identifies key tissues and cell types influencing complex traits in beef cattle and elucidates their genetic regulatory basis. - Source: PubMed
Publication date: 2026/07/28
Zhang BoyuQiu ShiyuanDu ZhenweiXiao HaoSu YingxiaoTang AnyiBao BinwuZhu BoChen YanGao XueXu LingyangWang ZezhaoZhang LupeiGao HuijiangLi JunyaZheng Caihong - Therapeutic resistance to trastuzumab remains a critical limitation in the management of HER2-positive (HER2+) breast cancer. Emerging evidence implicates epigenetic regulators, including microRNAs and histone demethylases, in modulating HER2 signaling and drug responsiveness. This study aimed to investigate the mechanistic role of miR-770-5p and its interplay with KDM5B in the context of trastuzumab resistance. An integrative approach combining in silico analyses with in vitro functional assays was employed in trastuzumab-sensitive and -resistant HER2 + breast cancer cell lines. Molecular, subcellular, and phenotypic effects of miR-770-5p modulation were assessed using qRT-PCR, Western blotting, immunofluorescence, RNA-FISH, luciferase reporter assays, and live-cell imaging. KDM5B was significantly overexpressed in HER2 + tumors and inversely correlated with HER2 expression. miR-770-5p directly targeted KDM5B and was associated with coordinated regulation of HER2 signaling at both transcription-associated and post-transcriptional levels. Overexpression of miR-770-5p was associated with reduced expression of KDM5B, TCF12, and GRB7, supporting the involvement of a KDM5B-TCF12-GRB7 regulatory network in HER2 modulation. Functionally, miR-770-5p reversed EMT-associated phenotypic features and enhanced trastuzumab sensitivity. Clinically, reduced KDM5B expression was associated with improved distant metastasis-free survival in ER+/HER2-high breast cancer patients. Collectively, miR-770-5p functions as a nuclear-associated regulatory microRNA that modulates HER2 signaling through epigenetic regulation of KDM5B and associated downstream networks. These findings suggest a previously unrecognized regulatory mechanism contributing to trastuzumab response and provide potential therapeutic avenues for HER2-positive breast cancer. - Source: PubMed
Publication date: 2026/07/20
Noyan SenemGurdal HakanCan AlpGur Dedeoglu Bala - Autism spectrum disorder (ASD) is a genetically complex neurodevelopmental condition with a high heritability. However, genomic studies of ASD have been underrepresented in East Asian populations, and the molecular yield in ASD cohorts remains modest. Here, we present a whole-genome sequencing analysis of 3109 samples across 1033 Chinese ASD families. By examining a wide spectrum of genetic variation, we identified rare ASD-associated variants in 19.2% of affected individuals, providing a population-specific view of the genetic architecture of ASD. We identify significant enrichment of de novo variants in probands, nominate or strengthen candidate risk genes (e.g., NCL, SPPL3, ADGRB1, SLC9A3, KIF1B) through mutational burden, evolutionary constraint, recurrent missense site, and functional assays, and implicate convergent pathways including protein palmitoylation. By integrating over 40,000 ASD cases across unpublished and published global cohorts, we identify 245 ASD risk genes, including 45 with limited prior evidence and 32 with no prior association. Single-cell transcriptomic profiling of the developing human cortex reveals that ASD risk genes exhibit widespread yet heterogeneous expression across all major cell types, with peak expression in excitatory neurons, particularly intratelencephalic neurons, and enriched expression in microglia (e.g., C1QC, CARD11, SNX13, MEF2C, FOXP2, TCF12, MED13L), suggesting convergent involvement of both synaptic and neuroimmune mechanisms. Together, our findings expand the ASD genetic landscape and suggest convergent pathogenic axes involving transcriptional regulation, synaptic signaling and plasticity, and neuroimmune interactions. This work supports the development of inclusive diagnostic strategies and provides a foundation for mechanistic and intervention exploration in ASD. - Source: PubMed
Publication date: 2026/07/16
Tan SenweiLyu YongqingSun XiaoyueGuo RuolanZhang XiaoleiSong ZhuoChen KewenLi ChenzhangZheng YiJiang CanhuiQin CaiBai TingTang GuizhiLi JuanLong ZhigaoPan QianTan JieqiongZhao NingxiaHao YanZhang YuShen YidongOu JianjunCui YonghuaHao ChanjuanJia XiangbinXia LuLi JinchenHu ZhengmaoLi WeiGuo HuiXia Kun - Childhood Nephrotic Syndrome (NS) is a common kidney disease. This study investigates the role of LncRNA GATA3-AS1 and miR-2116-5p in childhood NS and their impact on podocyte function. - Source: PubMed
Publication date: 2026/07/16
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