Ask about this productRelated genes to: UBE2E2 antibody
- Gene:
- UBE2E2 NIH gene
- Name:
- ubiquitin conjugating enzyme E2 E2
- Previous symbol:
- -
- Synonyms:
- UbcH8, FLJ25157
- Chromosome:
- 3p24.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-12-15
- Date modifiied:
- 2016-10-05
Related products to: UBE2E2 antibody
Related articles to: UBE2E2 antibody
- While the catalytic role of ubiquitin-conjugating (UBE2/E2) enzymes within the ubiquitin-proteasome system is well established, their substrate-specifying functions in cancer, particularly at the tumor-immune interface, remain comparatively underexplored. In this review, we provide an integrative re-evaluation of the UBE2 family organized around three concepts that, we argue, distinguish recent UBE2 research from earlier descriptive accounts: (i) tumor-context-dependent functional duality, in which the same UBE2 enzyme exerts opposing effects across tissue types and substrate landscapes; (ii) convergence of mechanistically distinct UBE2 members on a small set of shared signaling and immunometabolic nodes; and (iii) the emerging role of UBE2 enzymes at the tumor-immune interface, directly linking UBE2 biology to contemporary immunotherapy paradigms. Building on this framework, we synthesize recent evidence showing how dysregulated UBE2 members shape major cancer hallmarks, including uncontrolled proliferation, oncogenic signaling, metabolic reprogramming, immune evasion, and therapeutic resistance, while emphasizing that most reported phenotypes are derived from a limited set of tumor lineages and should not be uncritically extrapolated to all malignancies. Across tumor settings, multiple UBE2 members converge on PI3K/AKT, MAPK/ERK, NF-κB, HIF-1α, antigen-presentation pathways, checkpoint-ligand regulation, and macrophage polarization. We further discuss the potential of UBE2-based signatures as candidate prognostic and immune-stratification biomarkers. While these associations are biologically compelling, most derive from retrospective cohorts and require prospective, multi-center validation before clinical consideration. We also evaluate current pharmacological strategies targeting UBE2-driven vulnerabilities, including small-molecule inhibitors, natural compounds, and combination approaches with chemotherapy and immune checkpoint blockade. Collectively, this synthesis positions UBE2 enzymes as context-resolved regulators of tumor progression and the immune microenvironment, with growing potential for biomarker-guided therapeutic exploitation in precision cancer immunopharmacology, subject to rigorous prospective validation. - Source: PubMed
Publication date: 2026/06/10
Zhao HaiYang JiaxinYang Fan - Pork is a major source of animal protein for humans, and as living standards have improved, consumer demand has shifted from quantity to quality. Amino acid and fatty acid compositions determine the nutritional value and flavor of pork. However, the genetic mechanisms underlying variation in these parameters have not been fully elucidated. In this study, we quantified 17 amino acids and 42 fatty acids in the muscle from three crossbred pig populations, namely Yorkshire × Tibetan (YT), Yorkshire × Neijiang (YN), and Duroc × Tibetan (DT). YT and YN pigs exhibited higher amino acid concentrations, while DT pigs showed elevated fatty acid levels. Subsequently, whole-genome resequencing of 73 pigs identified 24,125,658 high-quality SNPs, among which 146 were significantly associated with fatty acid traits, leading to the identification of 19 candidate genes linked to palmitic acid (i.e., , and ), oleic acid (i.e., , and ), and total fatty acids (i.e., ). Functional annotation revealed that these candidate genes participate primarily in pathways related to lipid metabolism, glucose homeostasis, and energy balance. The identified SNPs and candidate genes provide valuable insights into the genetic architecture of the fatty acid composition in pork and may serve as molecular targets for improving meat quality through breeding. - Source: PubMed
Publication date: 2026/01/29
Tang JieLiang YanAn RuiLuo GanTao XuanLiu PengliangGu Yiren - Ubiquitin modifications regulate fundamental cellular activities by modulating protein stability and function. The ubiquitin ligase COP1, which is present across species from plants to humans, plays a crucial role in the ubiquitination of developmental transcription factors. While COP1 can function independently, it can also be incorporated into CULLIN4-RING ubiquitin ligase (CRL4) complexes through the DET1 adaptor protein. Despite its biological significance, the structural and functional mechanisms of COP1 and DET1-containing complexes remains poorly understood. Here we present the cryo-electron microscopy structures of human COP1 in complex with DDB1-DDA1-DET1 and Ube2e2, revealing an inactive stacked assembly state. Co-expression with COP1 substrates including c-Jun or ETS2 disrupts this configuration, inducing a conformational rearrangement into a distinct dimeric state that allows substrate access. Structural modelling identifies the spatial organization of COP1 WD40 domains where substrate recruits. DET1 serves as a structural scaffold, bridging COP1 and Ube2e2 to initiate potential ubiquitin addition on substrates, while DDB1 recruits the CULLIN4-RBX1 complex to facilitate Ube2d3-mediated ubiquitin chain elongation. These results reveal the dynamic interplay between the structural states of the CRL4 E3 ligase complex and its substrate specific activation mechanism, offering mechanistic insights into ubiquitination regulation and a basis for future studies on E3 ligase dynamics. - Source: PubMed
Publication date: 2026/01/15
Wang ShanTeng FeiStjepanovic GoranRao FengSu Ming-Yuan - Type 2 diabetes (T2D) is a heterogeneous metabolic disorder. Recent cluster-based classifications offer insights into distinct pathophysiological subtypes. The objective of the study is to investigate the association of genetic variants in T2D-related genes with defined T2D clusters. We analyzed 678 single nucleotide polymorphisms (SNPs) from ten genes (CDKAL1, CDKN2A, CDKN2B, HHEX, KCNQ1, MTNR1B, PAX4, SLC30A8, TCF7L2, and UBE2E2) in 471 T2D patients classified into four clusters: Severe Insulin-Deficient Diabetes (SIDD), Mild Obesity-related Diabetes (MOD), Mild Age-related Diabetes (MARD), and Metabolic Syndrome-related Diabetes (MSD). Genotyping was performed using the Axiom PDMRAv2 array. Following Hardy-Weinberg Equilibrium filtering, 376 SNPs were analysed. The association between T2D clusters and SNPs was assessed by multinomial logistic regression. Nineteen SNPs showed significant differences in genotypic frequencies among clusters (p < 0.05). Eight SNPs (rs61875103 in TCF7L2; rs12576156, rs2283220, rs2074197, and rs163165 KCNQ1; rs4710943, rs9368248, and rs6456379 in CDKAL1) significantly associated with cluster assignment. Cluster-specific effects were most notable in SIDD and MOD subgroups. Our findings support genetic heterogeneity of TCF7L2, KCNQ1, and CDKAL1 in T2D clusters and underscore the potential for genetically informed precision therapy strategies. - Source: PubMed
Publication date: 2025/12/20
Plengvidhya NattachetTeerawattanapong NipapornNarkdontr TassaneeInnang SaranyaSonglilitchuwong SuavalukSuthon SarochaTangjittipokin Watip - Retinal degeneration comprises a diverse group of progressive disorders leading to visual impairment and ultimately blindness. These include inherited retinal dystrophies (IRDs), diabetic retinopathy (DR), age-related macular degeneration (AMD), and glaucoma, affecting millions worldwide. The underlying pathology involves dysfunction and death of photoreceptor cells and the retinal pigment epithelium (RPE), driven by various stress-induced cell death mechanisms. Although multiple pathways have been reported, the relative contribution of each remains incompletely understood, highlighting the need for further investigation. Therefore, we studied how different stress types that induce retinal degeneration alter the global gene expression profile in vivo (C57BL/6 mice), aiming to identify predominant cell death mechanisms as well as key genes and networks. Retinal toxicity was induced using established models of oxidative stress, hypoxia, endoplasmic reticulum (ER) stress, and chronic inflammation. Transcriptomic profiling revealed both unique and convergent gene expression changes associated with each stressor. In total, 170, 328, 146, and 151 genes were significantly altered under oxidative stress, inflammation, ER stress, and hypoxia, respectively (Log2 fold change >2 or <-2; p < 0.05). Genes such as Arhgap26, Ccdc9, Ube2e2, and Fndc3b were commonly dysregulated across ER stress, inflammation, and oxidative stress, whereas Nfix, Elp6, Naca, and Plcd3 were selectively altered in oxidative stress, inflammation, ER stress, and hypoxia, respectively. Analysis of cell death-related gene subsets revealed that pyroptosis was commonly activated across different stress types. Additionally, autophagy-mediated cell death, ferroptosis, and extrinsic apoptosis were preferentially associated with oxidative stress, chronic inflammation, and hypoxia, respectively. Both ER and oxidative stress models showed strong activation of autophagy-associated cell death. Together, these findings delineate distinct molecular signatures and predominant cell death mechanisms triggered by specific stressors, providing important insights that could aid in developing targeted therapies to prevent or slow retinal degeneration. - Source: PubMed
Publication date: 2025/12/01
Sarkar SubhradeepKannan RamarajPanigrahi TrailokyanathVeeramani KarthickrajaMb ThirumaleshShanker Bhattacharya ShomGhosh Arkasubhra