UBE2Q1

Last update 23 Jan 2025

Basic Info

Synonyms

E2 ubiquitin-conjugating enzyme Q1, NICE-5, NICE5

+ [8]

Introduction

Catalyzes the covalent attachment of ubiquitin to other proteins (PubMed:22496338). May be involved in hormonal homeostasis in females. Involved in regulation of B4GALT1 cell surface expression, B4GALT1-mediated cell adhesion to laminin and embryoid body formation (By similarity).

100 Clinical Results associated with UBE2Q1

100 Translational Medicine associated with UBE2Q1

0 Patents (Medical) associated with UBE2Q1

Literatures (Medical) associated with UBE2Q1

01 Dec 2024·International Immunopharmacology

Bortezomib induces cell apoptosis and increases the efficacy of αPD-1 in BCR::ABL T315I mutation CML by targeting UBE2Q1

Article

Author: Gao, Anran ; Lin, Siwei ; Zhang, Qin ; Liu, Wenjie ; Li, Cenming ; Zhou, Yanyu ; Xue, Yangyang ; Yu, Xiaoxuan ; Shao, Miaomiao ; Jiang, Fengyu ; Zhang, Wan ; Liao, Shanting ; Ma, Tonghui

The BCR:ABL T315I mutation presents a significant challenge in the current management of Chronic Myeloid Leukemia (CML), highlighting the need to identify novel targets and drugs. In our study, we observed the elevated expression of UBE2Q1 in KBM5-T315I cells compared to KBM5 cells, where it interacted with DDX3, regulating its ubiquitination. Furthermore, we found that Bortezomib (BTZ) targeted UBE2Q1, reducing its protein level expression. Consequently, BTZ dose-dependently inhibited the growth vitality of KBM5-T315I cells, inducing increased ROS production, mitochondrial membrane potential collapse, cytochrome C release, and expression of apoptosis-related proteins. These events collectively induced apoptosis in KBM5-T315I cells. Moreover, BTZ enhanced the therapeutic effects of anti-PD-1 treatment. In NOD/SCID mice bearing KBM5-T315I cell line xenografts, BTZ administration (2 mg/kg, ip, every other day for 4 weeks) significantly inhibited the growth of KBM5-T315Iderived xenografts and extended survival. In conclusion, our study sheds new light on the BTZ-induced apoptosis mechanism, suggesting the potential of BTZ as a promising chemo-immunotherapy agent against BCR:ABL T315I mutation CML.

01 Oct 2024·The American Journal of the Medical Sciences

UBE2Q1 as a novel cancer biomarker for lung adenocarcinoma

Article

Author: Wang, Yuchao ; Jiang, Wei ; Li, Li ; Xu, Chunhua ; Zou, Jue

PURPOSEUbiquitin-conjugating enzymes (E2s) participate in various tumor-promoting processes. UBE2Q1 is a member of the E2 family. This research aimed to detect the expression level of UBE2Q1 in human lung adenocarcinoma and to study its malignant biological function.METHODSWestern blot, qRT-PCR and immunohistochemistry was used to measure the expression of UBE2Q1 in human lung adenocarcinoma tissues. The association between UBE2Q1 expression and clinic-pathological variables in 99 lung adenocarcinoma samples was analyzed by immunohistochemistry. In vitro experiment, establishing UBE2Q1 knockdown pattern, the markers of apoptosis, cell cycle and epithelial-mesenchymal transition (EMT) were analyzed by Western blot. CCK8, colony formation, Transwell and invasion assay analyzed the effect of UBE2Q1 knockdown on the proliferation, metastasis and invasion of lung cancer cells.RESULTSUBE2Q1 was overexpressed in lung adenocarcinoma, and the expression level of UBE2Q1 was related with TNM stage, tumor size, and lymph node metastasis. The high level of UBE2Q1 expression was also associated with poor survival and was an independent risk factor. In vitro, It was also confirmed that steady downregulation of UBE2Q1 could promote apoptosis, induce G2/M cell cycle arrest and regulate EMT. UBE2Q1 silencing dramatically reduce lung tumor cells proliferation, migration and invasion capacities.CONCLUSIONSUBE2Q1 may serve as a prognostic biomarker and a new therapeutic target of lung adenocarcinoma.

01 Nov 2023·Microbial Pathogenesis

Characterization of cellular immune response in hamsters immunized with recombinant vaccines against leptospirosis based on LipL32:LemA:LigAni chimeric protein

Article

Author: Dellagostin, Odir Antônio ; Bunde, Tiffany Thurow ; Pedra, Ana Carolina Kurz ; de Oliveira, Natasha Rodrigues ; Maia, Mara Andrade Colares ; Santos, Francisco Denis Souza ; Oliveira Bohn, Thaís Larré

In the last 20 years, various research groups have endeavored to develop recombinant vaccines against leptospirosis to overcome the limitations of commercially available bacterins. Numerous antigens and vaccine formulations have been tested thus far. However, the analysis of cellular response in these vaccine formulations is not commonly conducted, primarily due to the scarcity of supplies and kits for the hamster animal model. Our research group has already tested the Q1 antigen, a chimeric protein combining the immunogenic regions of LipL32, LemA, and LigANI, in recombinant subunit and BCG-vectored vaccines. In both strategies, 100 % of the hamsters were protected against clinical signs of leptospirosis. However, only the recombinant BCG-vectored vaccine provided protection against renal colonization. Thus, the objective of this study is to characterize the cellular immune response in hamsters immunized with different vaccine formulations based on the Q1 antigen through transcriptional analysis of cytokines. The hamsters were allocated into groups and vaccinated as follows: recombinant subunit (rQ1), recombinant BCG (rBCG:Q1), and saline and BCG Pasteur control vaccines. To assess the cellular response induced by the vaccines, we cultured and stimulated splenocytes, followed by RNA extraction from the cells and analysis of cytokines using real-time PCR. The results revealed that the recombinant subunit vaccine elicited a Th2-type response, characterized by the expression of cytokines IL-10, IL-1α, and TNF-α. This pattern closely resembles the cytokines expressed in severe cases of leptospirosis. On the other hand, the rBCG-vectored vaccine induced a Th1-type response with significant up-regulation of IFN-γ. These findings suggest the involvement of the cellular response and the IFN-γ mediated inflammatory response in the sterilizing immunity mediated by rBCG. Therefore, this study may assist future investigations in characterizing the cellular response in hamsters, aiming to elucidate the mechanisms of efficacy and establish potential correlates of protection.

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UBE2Q1

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