UEV1A (UBE2V1) Active Human Recombinant Protein
- Known as:
- UEV1A (UBE2V1) Active Human Recombinant Protein
- Catalog number:
- 80325
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- BPS Bioscience
- Gene target:
- UEV1A (UBE2V1) Active Human Recombinant Protein
Related genes to: UEV1A (UBE2V1) Active Human Recombinant Protein
- Gene:
- UBE2V1 NIH gene
- Name:
- ubiquitin conjugating enzyme E2 V1
- Previous symbol:
- UBE2V
- Synonyms:
- UEV-1, CROC-1, UEV1A, CROC1
- Chromosome:
- 20q13.13
- Locus Type:
- gene with protein product
- Date approved:
- 1998-03-20
- Date modifiied:
- 2016-10-05
Related products to: UEV1A (UBE2V1) Active Human Recombinant Protein
Related articles to: UEV1A (UBE2V1) Active Human Recombinant Protein
- Aberrant histone lactylation is emerging as a pivotal player in tumorigenesis. However, its role in epithelial ovarian cancer (EOC) has not been fully elucidated to date. - Source: PubMed
Publication date: 2026/06/29
Jiang YahuiLyu TianjiaoZhou TianyuZhu ChongyingFeng Weiwei - 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 - Circular RNA (circRNA), which encompasses a large range of endogenous RNA, can control the expression of genes in cancer. However, the function of circRNA in tumor stem cells remains largely unknown. In this study, we obtained circRNA and mRNA microarray data from bladder cancer stem cells (BCSCs) and non-bladder cancer stem cells (NBCSCs) derived from 3 patients. We performed functional validation of putative mechanisms using established low expression of cZFR bladder cancer cell lines. We found that the circRNA cZFR is overexpressed in BCSCs. Downregulation of cZFR inhibited cell sphere formation, invasion, migration, and BC cell proliferation. By analyzing the co-expression network of expressed circRNAs and dysregulated mRNAs, we determined that UBE2V1 is a target gene regulated by cZFR. Mechanistically, cZFR shares miRNA response elements with UBE2V1. cZFR binds to miR-511 and prevents miR-511 from decreasing the level of UBE2V1, which was upregulated in BCSCs and correlated with poor prognosis. Finally, we found that the expression of cZFR in the urine exosomes of patients was increased compared to normal. Our results suggest that cZFR may have regulatory functions in BC. cZFR is expected to be a biomarker for prognostic evaluation and a therapeutic target in BC. - Source: PubMed
Publication date: 2026/05/29
Zheng HaoxiangTian YeCai ZihanHuang GuixiaoXu SiqiLiu XiaocenLi ChongTao Tao - Oncogenic is known to induce DNA replication stress, leading to cellular senescence or death. In contrast, we found that it can also trigger polyploid ovarian nurse cells to die by inducing aberrant division stress. To explore intrinsic protective mechanisms against this specific form of cellular stress, here, we conducted a genome-wide genetic screen and identified the E2 enzyme Uev1A as a key protector. Reducing its expression levels exacerbates the nurse cell death induced by oncogenic , while overexpressing it or its human homologs, UBE2V1 and UBE2V2, mitigates this effect. Although Uev1A is primarily known for its non-proteolytic functions, our studies demonstrate that it collaborates with the E3 APC/C complex to mediate the proteasomal degradation of Cyclin A, a key cyclin that drives cell division. Furthermore, Uev1A and UBE2V1/2 also counteract oncogenic -driven tumorigenesis in diploid cells, suppressing the overgrowth of germline tumors in and human colorectal tumor xenografts in nude mice, respectively. Remarkably, elevated expression levels of UBE2V1/2 correlate with improved survival rates in human colorectal cancer patients harboring oncogenic mutations, indicating that their upregulation could represent a promising therapeutic strategy. - Source: PubMed
Publication date: 2026/03/25
Zhang QiWang YunfengFu XueliWang ZiguangZhang YangYan LizhongWang YuejiaYang MuhanSong DongzeZhang RuixingZhang HongruWu ShianZhao Shaowei - Hepatocellular carcinoma (HCC) is characterized by a profoundly hypoxic microenvironment, which drives tumor aggressiveness and poor clinical outcomes. However, the precise regulatory mechanisms through which hypoxia promotes HCC progression remain incompletely understood. Here, we identified ubiquitin conjugating enzyme E2 variant 1 () as a novel hypoxia-responsive gene that is transcriptionally activated by hypoxia-inducible factor-1α (HIF-1α) through direct binding to a hypoxia-response element located between -208 and -201 bp in the promoter. Overexpression of UBE2V1 was frequently detected in HCC tissues and correlated strongly with advanced tumor stage and unfavorable patient prognosis. Moreover, UBE2V1 facilitated the proliferation and migration of HCC cells. Further investigation revealed that up-regulated UBE2V1 competes with HIF-1α for binding to the β-domain of von Hippel-Lindau (VHL) protein and, in complex with UBE2S, catalyzes K11/K48-linked ubiquitination at VHL K196, leading to its proteasomal degradation. This disruption of VHL function attenuates HIF-1α ubiquitination and degradation, resulting in sustained HIF-1α stabilization, increased nuclear accumulation, and enhanced transcriptional activity. Consistent with these findings, genetic knockdown of or pharmacological inhibition of HIF-1α markedly suppresses HCC tumorigenesis and metastasis in vivo. Altogether, our study unveils a previously unrecognized HIF-1α-UBE2V1 positive feedback loop that is self-reinforcing and critically sustains the hypoxic microenvironment to drive HCC progression, highlighting UBE2V1 as both a promising prognostic biomarker and a compelling therapeutic target for HCC. - Source: PubMed
Publication date: 2025/12/23
Yuan ZiboHu SipinZhu QingweiFang YuliangLiu XinLi ShuangshuangHu XiaogeTu KangshengXu QiuranHuang DongshengCui Di