UBE2F antibody - N-terminal region (ARP52515_P050)
- Known as:
- UBE2F (anti-) - N-terminal region (ARP52515_P050)
- Catalog number:
- arp52515_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- UBE2F antibody - N-terminal region (ARP52515_P050)
Related genes to: UBE2F antibody - N-terminal region (ARP52515_P050)
- Gene:
- UBE2F NIH gene
- Name:
- ubiquitin conjugating enzyme E2 F (putative)
- Previous symbol:
- -
- Synonyms:
- NCE2
- Chromosome:
- 2q37.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-03-02
- Date modifiied:
- 2016-07-29
Related products to: UBE2F antibody - N-terminal region (ARP52515_P050)
Related articles to: UBE2F antibody - N-terminal region (ARP52515_P050)
- Natural killer (NK) cells are promising effectors for cancer immunotherapy, but their efficacy is limited by immunosuppressive tumor microenvironments. To uncover strategies for enhancing NK cell function, we establish a CRISPR loss-of-function screening platform for primary human NK cells by combining BaEVRless-pseudotyped lentiviral transduction of sgRNA libraries with Cas9 protein electroporation. This platform enables genome-scale interrogation of gene function in non-transformed NK cells. Kinome-focused and genome-wide screens identify key regulators of NK cell proliferation, cytotoxicity, and resistance to prostaglandin E (PGE)-mediated suppression. STK17B deletion enhances NK cell expansion, while loss of CCDC53 boosts degranulation and cytotoxicity. We also uncover the CRL5 complex-including RNF7, UBE2F, and CISH-as critical inhibitors of IL-2 signaling and effector function under PGE stress. These findings establish a scalable platform for CRISPR-based functional genomics in primary NK cells and reveal engineering targets to enhance NK cell persistence and efficacy in tumor microenvironments. - Source: PubMed
Publication date: 2026/04/15
Nguyen Quoc VietLan Yi-JunChang Jason Cheng-YuShih Hsin-AnFaustine JeniferChen Cheng-ChiehHo Shu-YuCheng Ching-WenChao Tsu-LanLin Steven - Pseudorabies virus (PRV) is an important swine herpesvirus that causes fatal encephalitis in newborn piglets and severe reproductive failure in pregnant sows, resulting in enormous economic losses in the pig industry worldwide. It has broad cell tropisms with the capability to infect a wide range of animals, including humans, thus posing a potential threat to human health. Neddylation is an important protein posttranslational modification that is catalyzed by an E1-E2-E3 enzyme cascade to covalently conjugate the ubiquitin-like molecule neural precursor cell expressed developmentally downregulated 8 (NEDD8) to substrate proteins. It has been demonstrated to play a key role in regulating numerous important biological processes, including cell proliferation, gene expression, signal transduction, and viral infection. However, the specific function of the neddylation pathway during PRV infection remains largely unknown. In the work described here, we identified a critically important role for neddylation in PRV replication by utilizing short hairpin RNA (shRNA)-mediated depletion of NEDD8 or the NEDD8-activating enzyme E1 subunit 1 (NAE1). Through systematic investigation of E2-E3 neddylation partners, we further demonstrated that silencing of the ubiquitin conjugating enzyme E2 F (UBE2F)-RING-box protein 2 (RBX2) axis significantly decreased PRV replication. Furthermore, knockdown of the neddylation substrate Cullin5 (CUL5) or pharmacological inhibition of CUL5 neddylation significantly attenuated PRV replication. Cumulatively, these findings demonstrate that the UBE2F-RBX2-mediated neddylation of CUL5 facilitates PRV replication. This study provides a new theoretical basis for in-depth understanding of PRV-host interaction and reveals neddylation as a novel target for antiviral strategies against PRV. - Source: PubMed
Publication date: 2025/12/30
Zheng ZhiyuanZhao FeiZhao SenhongBai YaningShi LunwenZhu BinbinHuang XiaoboZheng YiZhao QinWen YipingWu RuiDu SenyanCao SanjieYan QiguiXu ZhiwenTibbetts Scott AWang Yiping - Cullin-RING ligases (CRLs) and the anaphase-promoting complex/cyclosome (APC/C) are two major multi-subunit ubiquitin ligases essential for protein homeostasis. The underlying mechanism and biological consequence of their crosstalk remain elusive. Here, tandem affinity purification followed by LC-MS/MS is employed, and identified APC11-the RING subunit of APC/C-as a bona fide binding partner of CUL5, the scaffold of CRL5. On one hand, APC11 interacts with CUL5 and inhibits its neddylation. Consequently, APC11 knockdown enhances CUL5 neddylation by promoting its interaction with the neddylation E2 UBE2F. This leads to the degradation of SOCS3, a substrate receptor of CRL5, and the subsequent accumulation of its substrate, integrin β1, ultimately promoting cancer metastasis. On the other hand, CUL5-APC11 binding stabilizes APC11 by facilitating its atypical K27/K29/K33-linked polyubiquitylation at Lys83, a process catalyzed by ITCH E3 ligase. CUL5 loss delays mitotic exit, induces aneuploidy, and sensitizes cancer cells to the microtubule-targeting drug paclitaxel by destabilizing APC11. Collectively, the study revealed a new crosstalk between CUL5 and APC11 of two major E3 ligases, and targeting this crosstalk can provide a new strategy for blocking metastasis and triggering chemosensitization. - Source: PubMed
Publication date: 2025/10/29
Cui DanruiQu RuiruiLi TianqiWang LinchenChen XiaoyuShao ShengpengLiang XueXu JunSun YiXiong XiufangZhao Yongchao - Psoriasis is a chronic immune-mediated skin disease driven by the interleukin-23/interleukin-17 cytokine axis, yet its immunopathogenesis remains incompletely understood. Housekeeping genes, traditionally considered stably expressed across tissues and cell types, have not been systematically investigated for their role in psoriasis. Here, we aimed to identify psoriasis-associated housekeeping genes and explore their molecular mechanisms and clinical implications. - Source: PubMed
Publication date: 2025/09/01
Tang HaoWang JiachengZhang ShuhaoFeng GuanglongCheng XiangshuMeng XinChen RuiWang JiaqiJiang YongshuaiZhang RuijieLv Wenhua - Succinate dehydrogenase (SDH)-deficient paraganglioma and pheochromocytoma (PPGL) are rare neuroendocrine tumors for which no effective targeted therapies currently exist. To uncover new potential therapeutic targets, we performed an unbiased CRISPR-Cas9 genetic screen in immortalized mouse chromaffin cells (imCCs) with and without loss. Our screen identified genes that differentially affect cell proliferation in -deficient versus normal imCCs. Notably, several subunits of the transcriptional Mediator complex emerged as potential tumor suppressors, as their loss selectively promoted growth of -deficient cells. , we found that the neddylation pathway-required for ubiquitin-mediated selective protein degradation-plays a critical role in controlling cell growth and survival in -deficient imCCs. Specifically, loss of the neddylation regulator led to increased proliferation, while loss of suppressed growth of -deficient imCCs. Consequently, global neddylation inhibitor MLN4924 (Pevonedistat) and UBE2F-CRL5 axis inhibitor HA-9104 were shown to downregulate neddylation, suppressing UBE2F activity and selectively inhibiting growth of -deficient imCCs. This unexpected result highlights the neddylation pathway as a promising druggable vulnerability in this cell culture model of SDH-deficient PPGL. - Source: PubMed
Publication date: 2025/08/28
Al Khazal Fatimah JEmch Michael Jde Araujo Correia Cristina MFavier JudithHawse John RMaher L James