Ask about this productRelated genes to: UBE2T antibody
- Gene:
- UBE2T NIH gene
- Name:
- ubiquitin conjugating enzyme E2 T
- Previous symbol:
- -
- Synonyms:
- HSPC150, FANCT
- Chromosome:
- 1q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-03-21
- Date modifiied:
- 2019-04-23
Related products to: UBE2T antibody
Related articles to: UBE2T antibody
- Fanconi anemia complement group I (FANCI), a core component of the Fanconi anemia pathway, has emerged as a potential oncogenic factor across multiple cancer types. Located on chromosome 15q26.1, FANCI encodes a protein named FANCI that forms a stable heterodimer with FANCD2, playing a central role in the DNA damage response and repair. Beyond its involvement in DNA repair, FANCI participates in ribosome biogenesis, meiosis, and mRNA export, underscoring its essential role in maintaining genomic stability. Although FANCI deficiency has traditionally been associated with Fanconi anemia, recent studies have demonstrated that FANCI is overexpressed in various malignancies, where it promotes tumor progression and correlates with poor prognosis. The expression and activity of FANCI are tightly regulated at multiple levels, including transcriptional and post-transcriptional regulation by transcription factors and non-coding RNAs, as well as post-translational modifications such as phosphorylation mediated by PP2A and ATR, monoubiquitination catalyzed by the FANCL-UBE2T complex, and deubiquitination by USP1-UAF1. This review summarizes the functional mechanisms of FANCI across diverse physiological and pathological processes, highlighting its role as a crucial molecular bridge linking genomic stability maintenance to cancer development, and emphasizing its potential as a promising therapeutic target in cancer. - Source: PubMed
Publication date: 2026/06/29
Zhang XiaoyueZhang YangChen MengyingWei JinmeiLi YanlingDai TaoHe JunyuHan ChenZhou Yanhong - Endocrine therapy (ET) selection in estrogen receptor-positive breast cancer (ER + BC) is guided by menopausal status and tolerability rather than tumor biology, despite substantial heterogeneity in recurrence. We hypothesized that baseline gene expression differentially associates with recurrence depending on initial ET class. In a retrospective cohort of 74 ER+/HER2- patients treated with adjuvant ET, we profiled baseline tumor RNA and fitted adjusted Cox models for gene and ET interactions on time-to-recurrence and time-to-switch. Among selective estrogen receptor modulators-initiated patients, higher expression of , , , , and was associated with markedly increased recurrence, while no comparable association was observed among aromatase inhibitors-initiated patients. Forty-one percent of patients switched ET at least once, predominantly due to intolerance (joint pain, unspecified side effects); switching was not consistently associated with tumor biology. These hypothesis-generating findings identify candidate gene and ET interactions and motivate validation in larger, independent cohorts. - Source: PubMed
Publication date: 2026/06/30
Jones VeronicaWang YongzheQuinones ChristineAljaber DanaNelson EvaNath AritroKang IreneRugo HopeYee LisaSeewaldt VictoriaMortimer Joanne - Mural granulosa cells (MGCs) secrete C-type natriuretic peptide (CNP) to maintain oocyte meiotic arrest, yet the upstream regulatory networks remain unclear. This study aimed to investigate how the ubiquitin-conjugating enzyme E2T (UBE2T) in MGCs modulates CNP signaling to influence oocyte quality and to apply these findings to optimize in vitro maturation (IVM) efficiency. Expression analysis showed that UBE2T was highly expressed in the ovine ovary and preferentially enriched in MGCs (P < 0.05). Functional validation demonstrated that UBE2T in MGCs elevated intra-oocyte cAMP and cGMP levels, preventing spontaneous meiotic resumption (P < 0.05). Concurrently, UBE2T facilitated cytoplasmic maturation, characterized by enhanced mitochondrial membrane potential, uniform cortical granule distribution, and increased secretion of CNP and estradiol (E) (P < 0.05). Integrated multi-omics and experimental assays revealed that UBE2T upregulated mTOR protein expression, thereby increasing CNP level to maintain meiotic arrest. Furthermore, an optimized two-step IVM protocol featuring a 4h pre-maturation co-culture with MGCs significantly improved oocyte quality, evidenced by increased mitochondrial DNA copy number compared with conventional IVM (P < 0.05). Oocytes matured under this optimized protocol exhibited enhanced subsequent embryonic developmental competence, yielding blastocysts with significantly higher total cell numbers and upregulated expression of key pluripotency and maternal effect genes (P < 0.05). This study identifies the MGC-specific UBE2T-mTOR-CNP signaling axis as a critical driver of meiotic arrest, offering an evidence-based strategy to improve ovine oocyte IVM efficiency and embryonic development. - Source: PubMed
Publication date: 2026/07/06
Yu YangXia WeiTao ChenyuFang XiaohuanQi YatianZhang WentaoQin TianmiaoYang JingyiDu DongyanLiu ZhihuiZhang WeiyaLi Junjie - Chronic obstructive pulmonary disease (COPD) is the primary cause of deaths related to respiratory diseases. Epigenetic modifications are crucial in the development of mammals, and any disruption to epigenetic regulation may result in disease. - Source: PubMed
Publication date: 2026/06/07
Xie JianpengHuang LinhuiChen XinWang Xilong - Endometrial cancer (EC) is a prevalent malignancy in women. UBE2T, a member of the E2 ubiquitin-conjugating enzyme family, has emerged as a potential regulator of cancer progression. In this study, we conducted WGCNA and machine learning analysis using the GEO dataset to identify UBE2T as a key target. Various experimental techniques, including qPCR, WB, IHC, CCK8, EdU, LDH release assays, MeRIP-qPCR and CHX experiments were employed to investigate the expression and function of UBE2T in EC. Additionally, we investigated the mechanism by which UBE2T is regulated through m6A modification. UBE2T is highly expressed in EC and exhibits low m6A modification levels. Knockdown of UBE2T significantly inhibits EC cell proliferation. Both FTO knockdown and METTL3 overexpression increase m6A modification of UBE2T and reduce its expression, respectively. Cycloleucine (CYC) treatment also promoted EC cell proliferation, and overexpression of FTO increased UBE2T expression and enhanced EC cell proliferation. Rescue experiments demonstrated that CYC treatment can reverse the increased m6A modification and restored UBE2T expression following FTO knockdown. Additionally, CYC treatment also rescues the proliferation inhibition caused by UBE2T knockdown in EC cells. Furthermore, UBE2T accelerates P53 protein degradation in EC cell lines. UBE2T is regulated by m6A modification and plays a crucial role in the progression of endometrial cancer by modulating key cellular processes. Targeting its expression or activity may offer a promising therapeutic strategy for intervention. - Source: PubMed
Publication date: 2026/05/20
Zhang WenyiLi YanfangWang ZhenhuiKang ChuyunZhao PanpanRen DanZhang JingyanLu Xiaoqin