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
- 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 - Radioresistance is one of the primary causes of prostate cancer treatment failure and post-radiotherapy progression. However, there is currently a lack of effective targets to increase radiotherapy sensitivity and inhibit malignant progression. We identified AKR1C3 as a potential key target associated with radioresistance and malignant progression through integrated bioinformatic analysis of RNA sequencing (RNA-seq) data from prostate cancer clinical samples in The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. The promotion of radioresistance by AKR1C3 in both AR-positive and AR-negative prostate cancer cells was further validated through in vivo and in vitro experiments. Mechanistic studies revealed that AKR1C3 can bind to PKM2 and accelerate its degradation, thereby inhibiting glycolytic flux and enhancing oxidative phosphorylation (OXPHOS). Increased OXPHOS boosts ROS production, which further promotes NRF2 nuclear translocation, activating the transcription of DNA repair protein UBE2T. This enhanced DNA damage repair ability enables prostate cancer cells with high AKR1C3 expression to exhibit greater resistance to radiotherapy. In summary, this study reveals the molecular mechanism by which AKR1C3 is involved in metabolic reprogramming to promote radioresistance in prostate cancer through PKM2/UBE2T. These findings indicate that targeting AKR1C3 has potential for overcoming radioresistance, providing novel insight into the clinical treatment of prostate cancer. - Source: PubMed
Publication date: 2026/03/30
Zhang JinyuLi JiongzhengYan YufeiWang BinghuanWang RuojiaCui XiaoliZhan YangLiang ZuowenLi Jing - Triple-negative breast cancer (TNBC), particularly the androgen receptor-low (AR-low) subtype, is one of the most aggressive and hard-to-treat forms of BC, characterized by a high index of proliferation, chromosomal instability (CIN), and high prevalence of TP53 mutations. These features fuel therapy resistance, metastases, and poor clinical outcomes. An integrated framework describing the dysregulated molecular networks that support the pathobiology of AR-low TNBC is lacking. Multiple published studies in breast cancer have previously proposed mechanistic links between TP53 loss, AR-low states, and heightened FOXM1-driven G2/M transcriptional programs, potentially via deregulation of E2F activity, chromatin-associated co-regulators (e.g., ATAD2), and disruption of repressive networks involving p53-p21-DREAM and SPDEF. Additional reports suggest that FOXM1-associated circuitry may be reinforced by chromatin regulators such as WDR5 and by mitotic/spindle factors such as ASPM, including through feedback interactions and condensate-associated transcriptional organization. We previously showed that FOXM1, a master regulator transcription factor, is upregulated and is a biomarker of poor prognosis in AR-low TNBC. In this study, we filtered a set of "TNBC core genes" known to promote transcriptional chaos downstream of FoxM1. We identified a set of 15 cell cycle regulators-including mitotic kinesin motors (KIF14, KIF11, KIF4A, KIF2C, and KIF20A), centromeric proteins (CENPA, CENPO, CENPL, CENPF, and OIP5), and regulators of proteolysis (UBE2C, UBE2S, UBE2T, PSMD14, and TUBA1B). These 15 genes, which were ranked highly among genes overexpressed in TNBC featured prominently in gene signatures of chromosomal instability and were also overexpressed among AR-low TNBCs and TP53-mutant breast tumors. We show that expression of each of these 15 genes correlates positively with proliferation markers (Ki67, PCNA, and MCM2) in TNBC, and that the overexpression of this gene set is associated with shorter relapse-free survival and distinct immune/stromal infiltration patterns. In light of prior work, our findings point to a FOXM1-associated 15-gene signature enriched in AR-low TNBC and associated with the high-proliferation and high-CIN phenotypes of this clinically challenging tumor type. This 15-gene set represents an actionable vulnerability with therapeutic potential for AR-low TNBC and provides a framework for rethinking how to manage highly proliferative, genomically unstable BCs. - Source: PubMed
Publication date: 2026/02/14
Rida PadmashreeAndreae RaphaelBikhazi NoahJackson BeneciaWang IvanJinna Nikita - Although glycolysis is a metabolic hallmark of pancreatic ductal adenocarcinoma (PDAC), it remains unclear whether the excessive lactate produced regulates CAF lactylation to promote extracellular matrix (ECM) deposition. The multi-omics and spontaneous model findings indicate that lactate accumulation in the tumor microenvironment (TME) promotes histone H3 lysine 18 lactylation (H3K18la) and activation of cancer-associated fibroblasts (CAFs), leading to both ECM densification and impaired immunotherapy efficacy in PDAC. Mechanistically, ubiquitin-conjugating enzyme E2T (UBE2T) acts as an initiating factor that promotes p53 positive feedback degradation through modulation of ribosome biogenesis, thereby enhancing lactate metabolic crosstalk via glycolytic reprogramming. Genetic ablation or pharmacological inhibition of UBE2T using the selective inhibitor pentagalloylglucose (PGG) disrupts lactate metabolic crosstalk, suppresses stromal deposition, and promotes intratumoral CD8 T cells infiltration. Furthermore, the combination of PGG and anti-PD-1 therapy exhibits synergistic effects and survival benefits in spontaneous PDAC mice and immune-reconstituted patient-derived xenografts. Collectively, these findings reveal that UBE2T drives p53 positive feedback degradation to enhance glycolysis of PDAC, leading to excessive lactate production, which promotes H3K18la in CAFs and subsequent ECM deposition. Targeting UBE2T represents a potential strategy to improve the efficacy of immunotherapy in PDAC. - Source: PubMed
Publication date: 2026/02/15
Ma YongLiu WenboLi MingdouWang TaoZhao BinWang KeshenHe QichenSun HaonanQing HuiguoGuan XiaoyingShi WenguiQin LongDong YumanZhou HuinianYu ZeyuanJiang XiangyanJiao Zuoyi - Psoriasis is a chronic, inflammatory autoimmune skin disease, characterized by epidermal hyperplasia and abnormal immune system activation. It is influenced by both genetic and environmental factors. - Source: PubMed
Publication date: 2026/02/11
Chen JuntaoPeng LiYang TengfeiChen ShuiqinTang YingLi DongfangYuan Xiaoqing