Ask about this productRelated genes to: RNF31 antibody
- Gene:
- RNF31 NIH gene
- Name:
- ring finger protein 31
- Previous symbol:
- -
- Synonyms:
- ZIBRA, FLJ10111, FLJ23501, HOIP, Paul
- Chromosome:
- 14q12
- Locus Type:
- gene with protein product
- Date approved:
- 2003-09-29
- Date modifiied:
- 2019-04-23
Related products to: RNF31 antibody
Related articles to: RNF31 antibody
- The early detection and diagnosis of head and neck squamous cell carcinoma (HNSCC) pose significant challenges. - Source: PubMed
Publication date: 2026/04/24
Xia YichaoLou HuiquanShao ShengjieLiu XiangLi Yongsheng - Defensins, small cationic peptides with strong antimicrobial activity, are key effectors of innate immunity. α-defensins, human neutrophil peptides, are produced primarily by neutrophils and serve as an essential component of the airway defense system against invading pathogens. However, accumulating evidence indicates that α-defensins released from human neutrophils are markedly elevated in various lung diseases, where excessive α-defensins exert cytotoxic effects on epithelial and immune cells. - Source: PubMed
Publication date: 2026/01/20
Lee JungnamMohammad NaweedMun SeyoungHan KyudongFlagg-Dowie TammyMagallon MariaBrantly Mark LSerban Karina A - Transverse tubules (T-tubules) are invaginations of the muscle plasma membrane that facilitate rapid transmission of action potentials, ensuring synchronized muscle contraction. Despite their essential role in muscle physiology, the mechanisms underlying T-tubule formation remain elusive. Here, we identify LUBEL/RNF31, a ubiquitin E3 ligase responsible for linear (M1-linked) ubiquitination, as a key regulator of T-tubule biogenesis in . Loss of LUBEL leads to Amphiphysin (Amph)-positive membrane sheets instead of tubular networks. The ubiquitin ligase activity of LUBEL and direct interaction with Amph, a BAR domain protein involved in membrane tubulation, are crucial for proper T-tubule morphology. LUBEL and M1-linked ubiquitin chains assemble into puncta on membranes through multivalent interactions, facilitating Amph-mediated tubulation. Notably, the Amph-LUBEL/RNF31 interaction is evolutionarily conserved across species, underscoring a fundamental role for linear ubiquitination in membrane remodeling. Our findings uncover an unexpected function of linear ubiquitination in membrane deformation driven by BAR proteins. - Source: PubMed
Publication date: 2026/01/07
Kawaguchi KoheiHama YutaroYoshikawa HarunoriNishino KoheiMorimoto KazukiNakamura TsuyoshiKoizumi MichikoSakamaki YurikoAbe KotaKakuta SoichiroIchimura KoichiroIkeda FumiyoKosako HidetakaFujita Naonobu - The CARD11-BCL10-MALT1 (CBM) complex drives NF-κB signaling and MALT1 protease activation after T cell receptor (TCR) stimulation, forming a central signaling hub in adaptive immunity. Both linear ubiquitin chain assembly complex (LUBAC), consisting of HOIP, HOIL-1 and SHARPIN, and TRAF6 interact with the CBM complex. Still, the coordinated activity of these E3 ligases in controlling CBM activity remains elusive. Here we demonstrate that LUBAC, unlike TRAF6, is largely dispensable for TCR-induced NF-κB activation in human CD4 T cells. However, HOIP contributes to NF-κB target gene expression and, with TRAF6, modulates MALT1 substrate recognition, influencing T cell responses. Further, LUBAC-mediated conjugation of Met1-linked ubiquitin chains to BCL10 strictly depends on TRAF6, but putative Met1-ubiquitin acceptor lysines in BCL10 serve essential structural roles that limit accessibility within BCL10-MALT1 filaments. Thus, LUBAC acts downstream of TRAF6 to modulate MALT1 substrate recognition and to catalyze BCL10 ubiquitination, which is incompatible with BCL10-MALT1 filament formation. - Source: PubMed
Publication date: 2025/11/10
Graß CarinaOber FranziskaSixt ConstanzeMoud Bahareh NematiAntoshkina IrinaEberstadt FrederickPuhach AlisaAvar GöksuKeßler AntoniaO'Neill Thomas JSeeholzer ThomasKranich JanBrocker ThomasLammens KatjaMenden Michael PZielinski Christina EKrappmann Daniel - Hepatocellular carcinoma (HCC) is a leading cause of cancer-related mortality worldwide, and identifying novel biomarkers for diagnosis and prognosis is critical for improving patient outcomes. In this study, we identified 44 differentially expressed necroptosis-related genes (DE-NERGs) in HCC using the GSE121248 dataset. Functional analyses, including GO and KEGG pathway analyses, revealed that these genes were associated with key pathways such as NF-κB signaling, apoptosis, and cancer-related pathways. Through machine learning algorithms (SVM-RFE and LASSO), we selected 13 diagnostic genes (FAS, MAPK8, TNFRSF1B, SQSTM1, DNMT1, ID1, HSPA4, BCL2, FLT3, MPG, GATA3, ATRX, and RNF31), which were further validated as potential biomarkers for differentiating HCC from normal samples. Notably, HSPA4 was identified as a novel prognostic biomarker, with high expressions correlating with shorter overall survival and disease-specific survival in HCC patients. Pan-cancer analysis demonstrated dysregulation of HSPA4 across multiple cancer types, further supporting its role in cancer progression. Results from both in vitro and in vivo tests showed that HSPA4 knockdown considerably reduced migration, invasion, and proliferation of HCC cells, while changing the Wnt/β-catenin/EMT signaling pathway. Furthermore, it was shown that ATF4 was a critical transcription factor that increased HSPA4 expression. Knockdown of ATF4 reduced HSPA4 levels and suppressed HCC progression. These findings suggest that HSPA4, regulated by ATF4, may serve as a promising therapeutic target and prognostic biomarker for HCC. - Source: PubMed
Publication date: 2025/11/05
Li RuixiWang KunnanHou NaijingTian YuGong BiyanTang Min