UBE2B 293T Cell Transient Overexpression Lysate(Denatured)
- Known as:
- UBE2B 293T Cell Transient Overexpression Lysate(Denatured)
- Catalog number:
- H00007320-T03
- Product Quantity:
- 100 uL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- UBE2B 293T Cell Transient Overexpression Lysate(Denatured)
Related genes to: UBE2B 293T Cell Transient Overexpression Lysate(Denatured)
- Gene:
- UBE2B NIH gene
- Name:
- ubiquitin conjugating enzyme E2 B
- Previous symbol:
- -
- Synonyms:
- UBC2, HHR6B, RAD6B
- Chromosome:
- 5q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 1992-12-02
- Date modifiied:
- 2016-03-14
Related products to: UBE2B 293T Cell Transient Overexpression Lysate(Denatured)
Related articles to: UBE2B 293T Cell Transient Overexpression Lysate(Denatured)
- The initial COVID-19 outbreak precipitated unprecedented health crises, with research impeded by containment protocols and the high mortality rate. While SARS-CoV-2 perturbs immune ubiquitin dynamics, the causal interplay between them remains uncharacterized. - Source: PubMed
Publication date: 2026/06/10
Wang YueyueCai SiruiSun YuboZhang JunqiDing JiaqiWang JingZhang XiyangChang YuanhangFang ZhenchiYue AnqiYang KunJiang Dongbo - Protein ubiquitination regulates diverse cellular processes, and its dysregulation contributes to human disease, including cancer. E2 ubiquitin-conjugating enzymes share a conserved UBC fold in which surface loops fine-tune catalysis and partner interactions, yet the roles of individual loops remain incompletely defined. Here, we identify loop 3-a component of the "backside" β2-β3 hairpin-as a conserved structural and allosteric element in Rad6-family E2s. Structural and bioinformatic analyses of yeast Rad6 and its human homologs (UBE2A/UBE2B) reveal that loop 3 forms an overlapping triple β-turns, with variable first turn and a highly conserved second/third turn that links catalytic regulation to E3 ligase engagement. Systematic mutagenesis of the yeast Rad6 backside β-turn (residues 42-51) shows that this element is required in vivo for Bre1-dependent histone H2B Lys123 monoubiquitination, Rad18-dependent PCNA monoubiquitination, and Ubr1/Ubr2-dependent polyubiquitination and degradation of Sml1 and N-end rule substrates, and related biological processes. Charge-reversal mutations at backside β-turn Glu49 and Asp50 disrupt E3 binding, whereas cancer-relevant substitutions in kink-inducing prolines (Pro43/Pro47) impair mono- and polyubiquitination without abolishing E3 interactions. Certain backside β-turn mutations, including cancer-relevant variants, compromise steady-state levels following DNA damage, revealing them as conditional null or loss-of-function alleles. Nuclear magnetic resonance spectroscopy demonstrates that Pro43/Pro47 mutations induce long-range structural perturbations from backside β-turn into the front-face catalytic pocket, correlating with reduced in vitro ubiquitination activity. Deletion or alanine replacement of the β-turn destabilizes yeast Rad6 and human UBE2A/UBE2B. Together, these findings establish the loop 3/backside β-turn as a critical structural element of Rad6-family enzymes. - Source: PubMed
Shukla Prakash KLeng Andrew MChen Hui-HsuanGanguly RajarshiNewell NicholasChandrasekharan Mahesh B - Ubiquitin (Ub)-conjugating enzymes (E2 enzyme) are essential mediators of Ub-dependent signaling cascades, governing diverse cellular processes such as proteolysis and transcriptional regulation. Despite increasing evidence linking E2 enzymes to tumorigenesis, their precise roles in gastric cancer remain incompletely defined. In this study, we identified UBE2B as a key oncogenic E2 enzyme significantly upregulated in gastric cancer tissues through integrative bioinformatics analysis and clinical validation. High UBE2B expression was associated with poor patient prognosis and aggressive clinicopathologic features. Functional assays demonstrated that UBE2B promotes gastric cancer cell proliferation both in vitro and in vivo. Mechanistically, UBE2B interacts with the E3 ligase baculoviral IAP repeat-containing 2 (BIRC2) to catalyze K63-linked ubiquitination of TNF receptor-associated factor 1 (TRAF1), thereby amplifying NF-κB signaling. Furthermore, chromatin immunoprecipitation and luciferase reporter assays revealed that the NF-κB subunit P65 directly binds to the UBE2B promoter, enhancing its transcription and forming a feedforward regulatory loop. This UBE2B-BIRC2-TRAF1 axis, coupled with the UBE2B-TRAF1-P65 feedback circuitry, establishes a self-sustaining mechanism that drives NF-κB hyperactivation and tumor cell proliferation. Collectively, our findings highlight UBE2B as a critical modulator of gastric cancer progression and a potential target for therapeutic intervention. - Source: PubMed
He JianchengHuang XinkunXing DanjieChen ShunChen YuXue WanjiangHu Yilin - More and more evidence indicates that type 2 diabetes mellitus (T2DM) can cause muscle lesions and lead to the occurrence of sarcopenia. The changes in the gastrocnemius muscle of T2DM rats were investigated by using tandem mass tag (TMT) proteomics technology, with the aim of discovering biomarkers of muscle lesions induced by T2DM and clarifying their potential biological relationships. - Source: PubMed
Publication date: 2026/01/05
Wang TianruiZhang LiangJiang YuZhao XiaHou KehaoZhang YingzeYu NingXu Kuishuai - Understanding the genetic basis of male reproduction in mammals remains challenging. Commercial pig populations offer a unique model for studying fertility, as semen traits are routinely recorded using high-throughput systems. - Source: PubMed
Publication date: 2025/12/15
Sá PedroGòdia MartaGodinho Rodrigo MSevillano Claudia AHarlizius BarbaraMadsen OleBovenhuis Henk