Ask about this productRelated genes to: TCL1A protein
- Gene:
- TCL1A NIH gene
- Name:
- T cell leukemia/lymphoma 1A
- Previous symbol:
- -
- Synonyms:
- TCL1
- Chromosome:
- 14q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-03
- Date modifiied:
- 2017-12-06
Related products to: TCL1A protein
Related articles to: TCL1A protein
- Aromatase Inhibitors Associated Musculoskeletal Symptoms (AIMSS) are common side effects among hormone receptor-positive breast cancer patients, significantly affecting patients' treatment adherence and quality of life. The individual genetic susceptibility mechanism underlying AIMSS was not well understood yet. This study aimed to validate the association between genetic polymorphisms and AIMSS among Chinese breast cancer patients. - Source: PubMed
Publication date: 2026/03/18
Jing FengJiang LingyunCao YulingTian MaotingQiu JiajiaTang LichenHu Yan - Pathogenic variants in NLRP7, implicated in 55% of recurrent hydatidiform mole characterized by hypomethylation at maternally methylated imprinted regions, are proposed to disrupt de novo DNA methylation in human oocytes. However, the precise mechanism remains unclear. Here, we identify TCL1A, a DNMT3A inhibitor, as an endogenous NLRP7-interacting partner. The cryo-EM structure of the NLRP7-TCL1A complex reveals its fundamental architecture. Comprehensive analysis demonstrates that the majority of recurrent hydatidiform mole-causing NLRP7 variants impair its interaction with TCL1A. Mechanistically, NLRP7 potentially safeguards oocyte methylome by sequestering TCL1A in the cytoplasm, thereby preventing its nuclear entry and subsequent suppression of DNMT3A-mediated de novo methylation. Combining in silico predictions and interaction analysis, we identify L766R as a pathogenic variant. These findings propose a cytoplasmic regulatory mechanism governing nuclear DNA methylation, explaining the hypomethylation pathogenesis in NLRP7 variant-associated recurrent hydatidiform mole. - Source: PubMed
Publication date: 2026/03/05
Gao ZhengLiu QingtingLi LeiHu TingLu XukunWu YuQin DandanWang XiaoxiaoGu ChenLi JinhongXu ChengpengZhou DanZhou FanBai YanLingKang XiangjinLiu JianqiaoDeng DongLi Lei - DNA methyltransferases DNMT3A/B mediate de novo DNA methylation, essential for embryonic development and cell fate determination. Dysregulation of DNMT3A/B causes developmental defects and tumorigenesis. TCL1A is critical for embryogenesis but promotes lymphomagenesis when deregulated. Previous studies suggested TCL1A binds DNMT3A/B and inhibits their activity, but the mechanism remained unclear. Here, we report the cryo-EM structure of the DNMT3A-TCL1A complex, which comprises a DNMT3A dimer bound by two TCL1A dimers. TCL1A interacts with the catalytic domain of DNMT3A, overlapping with the DNMT3L-binding site, and induces extended conformational rearrangements. The target recognition domain and catalytic loop shift markedly, reducing DNA accessibility, while the catalytic loop occupies the SAM-binding pocket, thereby blocking methyltransferase activity. Supported by biochemical assays and molecular dynamics simulations, we propose a dynamic inhibition mechanism in which TCL1A exploits DNMT3A conformational plasticity to suppress de novo DNA methylation. - Source: PubMed
Publication date: 2026/03/05
Liu QingtingLi JinhongWang XiaoxiaoLi YaozongWu YuHan ZhuoGuo ZixinGuo LiWang XiangYuan GangGao ZhengLi LeiDeng Dong - Cancer of unknown primary (CUP) encompasses a highly heterogeneous group of cancers with limited therapeutic options and a dismal prognosis. To date, the pathogenesis and immune profiling of CUP have not been fully characterized which could provide more therapeutic targets.Samples of thirteen breast CUPs and five known metastatic breast cancers were subjected to gene expression analysis. The identified cancer stem cell (CSC) phenotype induced by the overexpression of T-cell leukemia/lymphoma-1 A (TCL1A) was validated via cytological experiments.Compared with known metastatic breast cancers, breast CUPs presented various genetic abnormalities mainly involving pluripotency in stem cells and upregulation of immune-related signaling pathways. CUPs also had significantly greater immune cell infiltration and tumor inflammation signature scores, accompanied by a higher trend of PD-L1 expression and tumor-infiltrating lymphocytes. TCL1A, a gene associated with stem cell-like features, was more highly expressed in various types of CUP than in metastases with known primary sites. In triple-negative breast cancer cell lines, overexpression of TCL1A promoted cell proliferation, invasion, and sphere formation and inhibited apoptosis; it also markedly upregulated CSC and epithelial-mesenchymal transition marker expression. Analysis of the downstream signaling pathways affected by TCL1A revealed notable enrichment of the AKT pathway.Breast CUP is characterized by complex genomic alterations and an inflamed immune microenvironment. The significant overexpression of TCL1A and the enrichment of CSC signatures suggest that the TCL1A-AKT axis may serve as a potential therapeutic target, highlighting the CSC phenotype as a critical biological mechanism in the tumorigenesis and progression of CUP. - Source: PubMed
Publication date: 2026/02/23
Ren MinChen ChenHu ZijuanYang YuWei PingZhou Xiaoyan - Dysfunctional mitochondria increase oxidative stress and inflammation, driving atherosclerosis. Understanding gene expression and regulatory mechanisms is crucial. - Source: PubMed
Publication date: 2026/02/09
Kong De ZhaoZhang Xue ZhiZhou Yuan YuanWang QunPan Yi HuiLu YiYe HuiHong Xiong Yi