UBE2T

Last update 08 May 2025

Basic Info

Synonyms

Cell proliferation-inducing gene 50 protein, E2 ubiquitin-conjugating enzyme T, FANCT

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Introduction

Accepts ubiquitin from the E1 complex and catalyzes its covalent attachment to other proteins. Catalyzes monoubiquitination. Involved in mitomycin-C (MMC)-induced DNA repair. Acts as a specific E2 ubiquitin-conjugating enzyme for the Fanconi anemia complex by associating with E3 ubiquitin-protein ligase FANCL and catalyzing monoubiquitination of FANCD2, a key step in the DNA damage pathway (PubMed:16916645, PubMed:17938197, PubMed:19111657, PubMed:19589784, PubMed:28437106). Also mediates monoubiquitination of FANCL and FANCI (PubMed:16916645, PubMed:17938197, PubMed:19111657, PubMed:19589784). May contribute to ubiquitination and degradation of BRCA1 (PubMed:19887602). In vitro able to promote polyubiquitination using all 7 ubiquitin Lys residues, but may prefer 'Lys-11'-, 'Lys-27'-, 'Lys-48'- and 'Lys-63'-linked polyubiquitination (PubMed:20061386).

100 Clinical Results associated with UBE2T

100 Translational Medicine associated with UBE2T

0 Patents (Medical) associated with UBE2T

177

Literatures (Medical) associated with UBE2T

19 Apr 2025·Cureus

Analysis of Ubiquitin-Conjugating Enzyme E2T (UBE2T) Protein Levels in the Bone Marrow Biopsy Specimens of Patients With Multiple Myeloma

Article

Author: Wang, Fei ; Xia, Rong ; Yu, Na

Introduction Several studies have reported that the ubiquitin-conjugating enzyme E2 T (UBE2T) is overexpressed in multiple myeloma (MM). This has been assessed via bioinformatic analysis, which represents mRNA expression. However, biological experimental evidence is lacking. Moreover, the protein levels of UBE2T in tissue obtained via bone marrow biopsy are not clear. To identify newer potential therapeutic targets for MM, this study aimed to assess the expression of the UBE2T protein by immunohistochemical (IHC) staining of bone marrow biopsy specimens and also collected clinical data for a correlation analysis. Methods Bone marrow biopsy specimens were obtained from the pathology department between December 2022 and December 2024. The expression of UBE2T protein in them was evaluated by IHC staining. Clinical data of the patients were also collected. These included gender, age, Revised International Staging System (R-ISS) staging category, overall survival and progression-free survival time, and concentrations of hemoglobin (Hb), creatinine (Cr), calcium (Ca), serum beta-2-microglobulin (β2-MG), serum albumin (ALB), and serum lactate dehydrogenase (LDH). Furthermore, we investigated the expression of UBE2T in patients with MM belonging to different R-ISS staging categories and its relationship with Hb, Cr, Ca, ALB, β2-MG, and LDH concentrations. Finally, a survival analysis was performed. Results Bone marrow biopsy specimens were obtained from 77 patients with MM and 16 patients with non-hematological conditions (control group). The UBE2T protein was weakly expressed in the control group (IHC results were negative or weakly positive), while it was significantly greater in specimens obtained from patients with MM (P< 0.001 vs. control). The patients with MM were further divided into three groups according to their clinical Revised International Staging System (R-ISS) staging. Compared to patients in R-ISS stage I, the UBE2T protein expression was significantly increased in those in stage II (P<0.05) and III (P<0.0001), whereas patients in stage III showed significantly higher levels than patients in stage II (P<0.01). Additionally, the level of UBE2T protein expression was positively correlated with the serum concentrations of β2-MG (P < 0.001, R²=0.211) and LDH (P < 0.001, R²=0.192). Further, the one-year progression-free survival rate was significantly higher in the low-expression (87.18%, 34/39) vs. the high-expression group (71.05%, 27/38; P<0.05). Conclusions The UBE2T protein is highly expressed in bone marrow biopsy specimens from patients with MM and positively correlates with R-ISS staging categories and serum concentrations of β2-MG and LDH. The comparative one-year progression-free survival rate was also significantly higher in the low-expression vs. the high-expression group. Although larger scale and longer follow-up studies are needed, UBE2T may become a potential indicator for MM detected via bone marrow biopsy and a novel target for its therapy.

06 Mar 2025·Current Cancer Drug Targets

Biological Functions and Therapeutic Potential of UBE2T in Human Cancer

Article

Author: Yu, Zeyuan ; Wang, Tao ; Wang, Keshen ; He, Qichen ; Ma, Yong ; Zhou, Huinian ; Jiang, Xiangyan ; Jiao, Zuoyi

The ubiquitin-proteasome system is a fundamental regulatory mechanism that governs protein stability and intracellular signaling in eukaryotic cells. This system relies on a coordinated cascade of enzymatic activities involving activating enzymes, conjugating enzymes, and ligases to assemble distinct ubiquitin signals. These signals are subsequently edited, removed, or interpreted by deubiquitinases and ubiquitin-binding proteins. While E3 ligases have traditionally been recognized as the primary determinants of substrate specificity in the ubiquitination process, recent studies have revealed that the dysregulation of E2 enzymes can also lead to significant pathological outcomes, including chromatin instability, immune dysregulation, metabolic dysfunction, and an elevated risk of cancer. Consequently, E2 enzymes have emerged as promising therapeutic targets for the treatment of various dis-eases. This review provides a comprehensive examination of the roles and mechanisms of the ubiquitin-conjugating enzyme E2T (UBE2T) in cancer initiation, progression, and therapy resistance, highlighting its potential as a compelling target for cancer therapeutics.

01 Feb 2025·Journal for ImmunoTherapy of Cancer

UBE2T/CDC42/CD276 signaling axis mediates brain metastasis of triple-negative breast cancer via lysosomal autophagy

Article

Author: Liang, Tao ; Jiang, Xiaobing ; Wang, Min Jie ; Qiao, Xin Wei ; Cheng, Qi Hong ; Li, Lin ; Xie, Ming Xing ; Chen, Yan ; Li, Jun Jun ; Chen, Qian Zhi ; Fu, Rong ; Yao, Jin ; Shi, Liang Liang

BackgroundAdvanced triple-negative breast cancer (TNBC) is prone to brain metastasis (BrM). The precise molecular mechanism responsible for this phenomenon has not yet been completely established, so it is vital to comprehend the molecular mechanism behind it.MethodsThe protein chip analysis was conducted to identify any abnormal UBE2T protein expression in TNBC, especially BrM. Here, we used public databases and bioinformatics analysis as well as clinical samples from different cohorts to investigate the interrelationship between UBE2T/CDC42/CD276. This predicted relationship was then repeatedly validated using different in vivo and in vitro experimental methods. Additionally, multiple experimental approaches were implemented, encompassing western blotting, Co-IP, GST pull-down, flow cytometry, mass spectrometry, immunofluorescence, immunohistochemistry, and qRT-PCR to reveal the molecular mechanism of UBE2T-mediated immune escape and BrM.ResultsOur results indicate that expressed at elevated levels in breast cancer, UBE2T is negatively linked to patient prognosis, especially in BrM of TNBC. Data from clinical samples from our different cohorts and TCGA indicate a significant correlation between UBE2T and immunosuppression. Mechanistically, UBE2T directly interacts with CDC42, promoting its K48-linked polyubiquitination and proteasomal degradation, thereby inhibiting CDC42 from degrading CD276 via the autophagy-lysosomal pathway, indirectly upregulating CD276 and thereby impairing the CD8+T cells function, ultimately mediating tumor immune escape and BrM. Finally, animal experimental results also showed that inhibition of UBE2T elevated the TNBC sensitivity to immune checkpoint CD276 blockade and inhibited BrM of TNBC.ConclusionsIn conclusion, our results indicate a new mechanism whereby UBE2T-mediated ubiquitination positively controls the UBE2T/CDC42/CD276 axis to upregulate tumor cell expression of CD276 and thereby impair CD8+T cells function, ultimately leading to tumor cell immune escape and BrM.

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