Ask about this productRelated genes to: RNF139 Blocking Peptide
- Gene:
- RNF139 NIH gene
- Name:
- ring finger protein 139
- Previous symbol:
- -
- Synonyms:
- TRC8, RCA1, HRCA1
- Chromosome:
- 8q24.13
- Locus Type:
- gene with protein product
- Date approved:
- 2003-05-21
- Date modifiied:
- 2018-05-04
Related products to: RNF139 Blocking Peptide
Related articles to: RNF139 Blocking Peptide
- Human cytomegalovirus (HCMV) has evolved diverse strategies for immune evasion. In this study, we identified HCMV-pUS2 as an indirect antagonist of the cGAS-STING pathway by promoting the degradation of lectin mannose-binding 2-like protein (LMAN2L), an unrecognized host factor involved in STING pathway. First, we discovered that HCMV, but not other DNA viruses such as HSV-1 and VACV, induces proteasomal degradation of LMAN2L during the immediate-early stage of infection. We then demonstrated that HCMV-pUS2 mediates LMAN2L degradation by recruiting the host E3 ubiquitin ligase RNF139 and E2 ubiquitin-conjugating enzyme UBE2G2, directing LMAN2L to the endoplasmic reticulum (ER)-associated protein degradation (ERAD) pathway. LMAN2L knockout diminishes HCMV-induced expression of type I interferons and interferon-stimulated genes. Furthermore, LMAN2L co-localizes and interacts with STING. Though it does not affect STING dimerization or TBK1 recruitment, it is essential for STING translocation from the ER to the Golgi. Our findings uncover LMAN2L as a novel host regulator of the STING pathway and identify pUS2-mediated ERAD as a previously unrecognized viral immune evasion strategy. - Source: PubMed
Publication date: 2026/05/18
Zhou Yue-PengYao Yong-XuanWu Jin-PengPan Yu-TingZeng Wen-BoSun Jin-YanZhao YueCheng HanLuo Min-HuaYang Bo - Growing evidence indicates that nanoplastics (NPs), particularly polystyrene nanoparticles (PS-NPs), cross the blood-brain barrier and reach the hippocampus, where they induce neurotoxicity through oxidative stress, neuroinflammation, and synaptic damage. In the present study, we demonstrate that PS-NPs downregulate RNF139 in microglia, impairing the degradation of SCAP. Elevated SCAP levels trigger SREBP activation, disordered lipid metabolism, and enhanced lipid synthesis. Subsequently, mitochondrial dynamics are dysregulated, characterized by elevated mitochondrial reactive oxygen species, a drop in membrane potential, and diminished ATP synthesis. Under these pathological conditions, microglia become abnormally activated and secrete inflammatory factors such as TNF-α, IL-1β, and IL-6. This neuroinflammatory cascade induces neuronal damage and apoptosis, resulting in spatial cognitive impairment. Thus, our findings reveal a link between PS-NPs exposure, changes in microglial lipid metabolism, and nerve damage. They also identify targets for treating NP-induced neurological disorders. - Source: PubMed
Publication date: 2026/02/19
Du QingBu NingZhou XuanWang HailanJiang ZhenhaoXia HaiboCheng ChengSun JingLiu Qizhan - Bladder cancer (BCa) is a prevalent malignancy with high recurrence and metastasis rates. Nuclear receptor subfamily 4 group A member 3 (NR4A3), a member of the orphan nuclear receptor superfamily, is implicated in various cancers, but its functional role and mechanisms in BCa have not been well understood. This study aimed to explore the functional significance and diagnostic value of NR4A3 in BCa, with a focus on its regulation of endoplasmic reticulum (ER) stress and anoikis sensitivity via ATF6 and RNF139. - Source: PubMed
Publication date: 2025/11/21
Cui HaiyangFan Xuejiao - Protein-lipid crosstalk is fundamental to homeostasis in the endoplasmic reticulum (ER). The ER-associated degradation (ERAD) pathway, a branch of the ubiquitin-proteasome system, maintains ER membrane properties by degrading lipid metabolic enzymes. However, the ERAD components that sense membrane properties and their mechanisms remain poorly defined. Using reconstituted systems with purified ERAD factors, we show that membrane composition modulates the ubiquitination cascade at multiple levels. The membrane-anchored E2 UBE2J2 acts as a sensor for lipid packing: in loosely packed membranes, UBE2J2 becomes inactive due to membrane association that impedes ubiquitin loading, while tighter packing promotes its active conformation and interaction with E1. UBE2J2 activity directs ubiquitin transfer by the E3 ligases RNF145, MARCHF6, and RNF139, targeting both themselves and the substrate squalene monooxygenase. Additionally, RNF145 senses cholesterol, altering its oligomerization and activity. These findings reveal that ERAD integrates multiple lipid signals, with UBE2J2 relaying and extending the effect of lipid signals through its cooperation with multiple E3 ligases. - Source: PubMed
Publication date: 2025/10/09
Vrentzou AikateriniLeidner FlorianSchmidt Claudia CGrubmüller HelmutStein Alexander - The study aimed to identify key genes related to lipid metabolism in chronic sinusitis and understand their biological implications, considering the growing interest in the association between chronic sinusitis - a complex inflammatory condition - and lipid metabolism due to lipids' role in inflammation and immunity. - Source: PubMed
Publication date: 2025/07/30
Xiong PanhuiLiu LeiPi JingtingWang JiLu TaoKe XiaJiang YuShen YangYang Yucheng