Proteins UBE2T , Human
- Known as:
- Proteins UBE2T , Human
- Catalog number:
- C187
- Product Quantity:
- 10μg
- Category:
- -
- Supplier:
- Novoprotein
- Gene target:
- Proteins UBE2T Human
Related genes to: Proteins UBE2T , Human
- 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: Proteins UBE2T , Human
Related articles to: Proteins UBE2T , Human
- 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 - Diffusion-based generative models have emerged as powerful tools for structure-based molecular design, yet their effectiveness depends critically on how prior information about protein-ligand interactions is incorporated into the generative process. In this work, we propose and systematically investigate structural hotspot conditioning as a mechanism to inject interaction-relevant chemical knowledge into pocket-conditioned diffusion models. We evaluate three complementary strategies developed for defining atom-level reference points: docking score-based atom selection, structure-based pharmacophore localization, and data-driven prediction of hydrogen-bonding sites. Using MolSnapper as a unified diffusion-based generative model, we benchmark these strategies on a standardized CrossDocked2020 test set, evaluating docking-derived affinity estimates, physicochemical quality, structural plausibility, and chemical diversity. Compared to established baselines, our explicit hotspot-based conditioning systematically alters generative behavior, enabling controllable trade-offs between affinity, chemical feasibility, and diversity. An iterative case study on the shallow allosteric pocket of Ube2T further illustrates how alternating hotspot strategies supports effective exploration and prioritization of ligand candidates for challenging targets. Overall, this work establishes structural hotspot conditioning as a flexible and tunable design variable for guiding diffusion-based molecular generation toward chemically meaningful solutions. - Source: PubMed
Publication date: 2026/05/21
Masone DiegoCaparotta Marcelo - Growing evidence has revealed that DEAD-box RNA helicase 5 (DDX5, also known as p68) and ubiquitin-conjugating enzyme E2T (UbE2T) are two emerging and highly promising cancer therapeutic targets. This article provides the first comprehensive review of the physical and functional relationship between these two cancer targets, further refining their therapeutic potentials in solid cancers. In addition, the consequences of simultaneously degrading DDX5 and UbE2T proteins by the small-molecule dual molecular glue degrader FL118 in difficult-to-treat advanced cancers are presented.Specifically, this article reviews: (1) the roles of DDX5 and UbE2T in diverse cancer DNA repair pathways; (2) the physical binding relationship and potential functional roles of DDX5 in topoisomerase regulation; (3) the involvement of DDX5 in EZH2- and NANOG-associated prostate cancer stem cell (PCSC)-driven neuroendocrine prostate cancer (NEPC), castration-resistant prostate cancer (CRPC), and metastatic CRPC (mCRPC); (4) the contributions of DDX5 and UbE2T to inflammatory and immune regulation within the tumor microenvironment (TME); (5) FL118 as a small-molecule dual molecular glue degrader selectively targeting both DDX5 and UbE2T; (6) the high efficacy of FL118 against multiple difficult-to-treat advanced and metastatic cancers, including advanced colorectal cancer (CRC), pancreatic ductal adenocarcinoma (PDAC), osteosarcoma, Ewing sarcoma, ovarian cancer, and glioma/glioblastoma; (7) the resistance of ABCG2-expressing cancer cells to common anticancer agents but not to FL118; (8) the favorable pharmacokinetic and toxicology profiles of FL118 in mice, rats, and dogs; (9) the distinct functions of DDX5 in normal tissues, cells, and organs versus cancer; and (10) FL118 as a drug platform enabling the development of novel analogs and derivatives.Based on this review, we conclude that DDX5 and UbE2T represent superior anticancer therapeutic targets, and that the high efficacy of FL118 against multiple difficult-to-treat cancers is attributable to its function as a bona fide small-molecule dual molecular glue degrader that physically targets and degrades both DDX5 and UbE2T. Strikingly, this activity is observed regardless of the expression status of ABC transporter proteins, ABCG2/BCRP, ABCB1/Pgp/MDR1, and/or ABCC1/MRP1 in cancer cells. - Source: PubMed
Publication date: 2026/05/18
Li FengzhiLing XiangChakraborty SayanTang Dean GMcLean KarenWu WenjieSule NorbertVadehra DeepakFountzilas ChristosGupta AjayTwist ClareOhm JoyceChatta GurkamalAbrams Scott I - Bone metastasis remains a major clinical challenge in advanced prostate cancer (PCa). Although β-elemene has been shown to suppress cancer stem cells and tumor progression, its mechanism in PCa is not fully understood. - Source: PubMed
Publication date: 2026/04/25
Huang RenlunChen ChiweiWang ZhichaoZhang QiuhongCao JiadongWang WeiXiang Songtao - Breast cancer brain metastasis (BCBrM) remains one of the most lethal manifestations of breast cancer. Its response to immunotherapy is severely limited by the blood-brain barrier, which restricts immune cell infiltration and antigen presentation, thereby creating an immunosuppressive microenvironment. To overcome these barriers, recent studies have focused on novel immune checkpoints, including the Lymphocyte-Activated Gene 3-Galectin 3 (LAG3-LGALS3) and T-Cell Immunoreceptor with Ig and ITIM Domains-Nectin Cell Adhesion Molecule 2 (TIGIT-NECTIN2) axes, as well as on the reprogrammed metastatic ecosystem driven by immunosuppressive cells such as Forkhead Box P3-positive (FOXP3⁺) Regulatory T (Treg) cells, Lysosomal-Associated Membrane Protein 3-positive (LAMP3⁺) tolerogenic dendritic cells (DCs), C-C Motif Chemokine Ligand 18-positive (CCL18⁺) M2-like macrophages, Regulator of G-Protein Signaling 5-positive (RGS5⁺) cancer-associated fibroblasts (CAFs), Galectin 1-positive (LGALS1⁺) and TANK-Binding Kinase 1-positive (TBK1⁺) microglia, and phosphorylated Signal Transducer and Activator of Transcription 3-positive (pSTAT3⁺) reactive astrocytes. In addition, targeted inhibition of tumor-derived N-acetyltransferase 8-like (NAT8L) and metabolites N-Acetylaspartate (NAA), suppression of the N-Methyl-D-Aspartate Receptor (NMDAR) signaling pathway in tumor cells, and interventions against γ-Aminobutyric Acid (GABA)ergic reprogramming in BCBrM cells. Moreover, targeted interventions against distinct immune escape pathways-such as the Ubiquitin-Conjugating Enzyme E2T (UBE2T)/Cell Division Cycle 42 (CDC42)/Cluster of Differentiation 276 (CD276) and C-C Motif Chemokine Ligand 2-C-C Motif Chemokine Receptor 2/C-C Motif Chemokine Receptor 4 (CCL2-CCR2/CCR4) axes-have shown promise in reshaping the immune microenvironment and enhancing the efficacy of conventional immunotherapy. Collectively, this perspective outlines evolving strategies in immune checkpoint modulation, cellular ecosystem reprogramming, and neuroimmune intervention, providing a forward-looking framework to enhance the efficacy of immunotherapy in BCBrM. - Source: PubMed
Publication date: 2026/04/02
Zou YutianWu JiadiYuan ZeHe XiaofangTang Hailin