UEV1A (UBE2V1) Active Human Recombinant Protein
- Known as:
- UEV1A (UBE2V1) Active Human Recombinant Protein
- Catalog number:
- 80325
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Biotech support group
- 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
- 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 - - Source: PubMed
Publication date: 2025/11/19
Wang XuXia CuicuiZhang Xiaofei - BackgroundHepatocellular carcinoma (HCC) is a major global health burden, with limited tools for early diagnosis and prognosis. This study explores serum-derived exosomal miR-1275 as a potential non-invasive biomarker for HCC.MethodsExosomes were isolated from serum samples of 50 HCC patients and 50 matched healthy controls. miR-1275 expression was quantified by qRT-PCR and compared with traditional biomarkers (AFP, CEA, CA199, DCP, AFP-L3%). Diagnostic performance was evaluated using ROC curves. Bioinformatic analyses, including TCGA pan-cancer data, target gene prediction, and pathway enrichment, were performed to explore regulatory mechanisms.ResultsExosomal miR-1275 levels were significantly reduced in HCC patients and correlated with advanced clinical stage, tumor burden, and metastasis. miR-1275 showed strong diagnostic value (AUC = 0.869), outperforming CEA and CA199, and improved significantly when combined with other biomarkers (AUC = 0.982). UBE2V1 was identified as a key miR-1275 target involved in cancer-related pathways, including ubiquitination and mTOR signaling.ConclusionSerum exosomal miR-1275 is a promising biomarker for early diagnosis and prognosis of HCC. Its integration into multimarker panels could enhance clinical decision-making and patient management. - Source: PubMed
Publication date: 2025/11/13
Jun YangYeng ChenSainan ShenJingwen XiaoYu HeAbdul Khalil Khalilah BintiMusa Maslinda Binti - A deeper understanding of how teriparatide exerts its anabolic effects on bone tissue may open new avenues for osteoanabolic treatment. Our study aimed to identify long non-coding RNAs and messenger RNAs (mRNAs) regulated by teriparatide. Bone marrow mesenchymal stem cells (MSCs) were treated with teriparatide during osteogenic differentiation, and long RNA sequencing was performed. We identified 7 622 differentially expressed lncRNAs in both continuous and intermittent treatment groups compared to untreated MSCs. In intermittent treatment, the most upregulated lncRNAs were VCP, EMP1, OXA1L, LPP, and SCARB2, while in continuous treatment, they were XLOC_055533, SCARB2, HNRNPC, VCP, and CALM3. The most downregulated lncRNAs in intermittent treatment were KRTAP4-11, DUBR, MEG3, DIABLO, and ABI3BP, while in continuous treatment, they were XLOC_055164, SLC2A3, COPG1, and SMTN. Among mRNAs, the most upregulated in intermittent treatment were DNAJC25-GNG10, ZBTB4, SLC2A6, TMEM189-UBE2V1, and BDP1, whereas SLC2A6, ZBTB4, MX1, BDP1, and RSAD2 were the most upregulated in continuous treatment. The most downregulated mRNAs in intermittent treatment were PIP4K2B, GFI1B, ISY1-RAB43, AC010422.5, SESN2 and ISY1-RAB43, whereas ZDBF2, KLKB1, RPS10-NUDT3, and XLOC_055092 were the most downregulated mRNAs in continuous treatment. AC008622.2, MED17, and RNF213 emerged as the most critical lncRNAs for elucidating the mechanism of intermittent teriparatide therapy, while XLOC_055533, SPG7, and HOOK3 were highlighted as the most important lncRNAs in the continuous treatment. Additionally, we identified novel lncRNAs (KRTAP4-11, CEBPZOS, and CDC42SE2) that may have a role in teriparatide effects on MSCs. Identified lncRNAs and mRNAs could serve as therapeutic targets or diagnostic markers to improve osteoanabolic treatments. - Source: PubMed
Publication date: 2025/07/02
Vrščaj Lucija AnaMarc JanjaOstanek Barbara