Ask about this productRelated genes to: TRIM56 antibody
- Gene:
- TRIM56 NIH gene
- Name:
- tripartite motif containing 56
- Previous symbol:
- -
- Synonyms:
- RNF109
- Chromosome:
- 7q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-01-03
- Date modifiied:
- 2016-10-05
Related products to: TRIM56 antibody
Related articles to: TRIM56 antibody
- EXOC5/SEC10, the central subunit of the exocyst complex, is crucial for the trafficking of secretory vesicles to the plasma membrane. However, its role in innate immunity and viral replication remains unclear. Here we demonstrate that EXOC5 acts as a negative regulator of DNA virus-triggered CGAS-STING1 signaling via targeting STING1. Mechanistically, EXOC5 facilitates the autophagic degradation of STING1 via K63-linked polyubiquitination at Lys224 and Lys338 by the E3 ligase TRIM56, which serves as a recognition signal for the cargo receptor SQSTM1/p62 (sequestosome 1). Furthermore, EXOC5 inhibits antiviral innate immunity and promotes viral replication via EXOC5-TRIM56-STING1-SQSTM1 signal transduction. More importantly, myeloid-specific deletion of in mice improves survival and reduces viral load. In general, these findings revealed a negative feedback loop of type I interferon signaling through the EXOC5-TRIM56-STING1-SQSTM1 axis, which has the potential to serve as a new target for the development of antiviral therapeutics that regulate the host immune response. BafA1: bafilomycin A1; BMDMs: bone marrow-derived macrophages; cGAMP: cyclic GMP-AMP; CGAS: cyclic GMP-AMP synthase; EXOC5/SEC10: exocyst complex component 5; HAdV-4: human adenovirus type 4; HSV-1: herpes simplex virus type 1; HT-DNA: herring testis deoxyribonucleic acid; IFN: interferon; IRF3: interferon regulatory factor 3; ISD: interferon stimulatory DNA; PMs: peritoneal macrophages; siRNA: small interfering RNA; SQSTM1/p62: sequestosome 1; TBK1: TANK binding kinase 1; VACV70: 70-mers of dsDNA representing the genome of vaccinia virus. - Source: PubMed
Publication date: 2026/04/17
Ma WenqingXu YananYu JieSun FachaoYu XiaoHe LutengLi YingyingHe Daniel ChangWang HongmeiHe Hongbin - Circular RNAs (circRNAs) are increasingly recognized as pivotal regulators of cancer development, yet their functional roles in pancreatic ductal adenocarcinoma (PDAC) remain largely elusive. Here, we identify circPLEKHM1 as a significantly upregulated circRNA in PDAC tumors, with elevated expression strongly correlated with poor patient prognosis. Functional in vitro and in vivo analyses establish an oncogenic role for circPLEKHM1, demonstrating that its overexpression promotes tumor growth and metastasis, while its knockdown exerts suppressive effects. Mechanistically, circPLEKHM1 directly interacts with the RNA-binding protein FXR1, thereby preventing TRIM56-mediated proteasomal degradation of FXR1 and enhancing global protein synthesis. Notably, serum levels of circPLEKHM1 are significantly elevated in PDAC patients compared to healthy controls and individuals with other pancreatic conditions. Importantly, combining circPLEKHM1 with CA19-9 substantially improves diagnostic accuracy of PDAC detection. Collectively, these findings delineate circPLEKHM1 as a critical driver of PDAC progression and highlight its promise as robust liquid biopsy biomarker for PDAC diagnosis and prognosis assessment. - Source: PubMed
Publication date: 2026/03/06
Yang YangLi ZhangGao LanyangMing YueZhang TingtingYe ZixiaLiu WenrongXiong QunliXu XiaomingXu FuyanGuo JiaweiLi JiaoYang XiaojuanPeng YongZhu Qing - Bufei Formula (BFF), a traditional Chinese medicine, has been widely utilized in the clinical treatment of chronic obstructive pulmonary disease (COPD), though its underlying mechanisms remain unclear and warrant further investigation. - Source: PubMed
Publication date: 2026/01/22
Xin NanZhang QinCheng MengmengZhang ZeyuWei YanxinLi JianshengZhao DiZhao Peng - Lung cancer is one of the most common cancers worldwide and the leading cause of cancer-related deaths. Non-small cell lung cancer (NSCLC) accounts for 85% of lung cancer cases and has a 5-year survival rate of ~19%. Since more than half of NSCLC patients present with metastatic disease at the time of diagnosis, early diagnosis is crucial for providing patients with the most effective treatment strategy. This study integrated transcriptome data between cancer and adjacent tissues from GEO and TCGA databases through bioinformatics analysis, and screened zinc finger CCCH-type containing 15 (ZC3H15) as a key differentially expressed gene in NSCLC. ZC3H15 expression levels were found to be significantly higher in NSCLC tissue than normal tissue and correlated with tumor size, TNM stage, lymph node metastasis and poor prognosis of patients. Overexpression of ZC3H15 promoted the proliferation, migration and invasion of NSCLC cells through activation of the AKT-mTOR signaling pathway. To elucidate the underlying molecular mechanism, we determined that ZC3H15 could bind to PTEN through its DFRP structural domain and recruited the E3 ligase TRIM56 to promote PTEN ubiquitination. In addition, overexpression of ZC3H15 increased the resistance of NSCLC cells to cisplatin. Therefore, ZC3H15 promotes the malignant phenotype of NSCLC through recruitment of TRIM56 to ubiquitinate PTEN, decreasing its expression and driving increased AKT-mTOR signaling pathway and cisplatin resistance. These findings provide a scientific basis for the development of targeted therapies against ZC3H15, which may lead to new therapeutic strategies for NSCLC patients. - Source: PubMed
Publication date: 2026/01/09
Wu PeihongYao PeifengZhao MingfangCheng Ming - (1) Background: Hepatitis B virus (HBV) belongs to the Hepadnaviridae family of viruses that interact with hepatocytes. HBV infection is a major global health problem. Most adults clear the infection quickly after being infected with HBV, while a few people develop chronic HBV infection. It is well-known that the early innate immune response of host cells plays an important role in the fight against virus infection. However, the interactions between HBV and the intrinsic innate immune system of hepatocytes are still not fully understood. The aim of this study was to confirm the interaction between HBV and hepatocytes, and to identify the interferon-stimulated genes (ISGs) regulated by HBx and their expression in association with HBV-associated HCC (HBV-HCC), so that we can refine our understanding of the interaction between HBV and ISGs and its potential influence on HBV-HCC. (2) Methods: We analyzed data concerning the stimulation of IFN-dependent genes in primary human hepatocytes (PHHs) transfected with pathogen DNA mimetics or infected with HBV in the GSE69590 database. Bioinformatic methods, such as GSEA, GO, and KEGG, were used to analyze the differentially expressed innate immunity genes and their related pathways to identify candidate intrinsic innate immune factors. qPCR on HepG2 and Huh7 cells, which highly express HBx, was used to detect relevant intrinsic innate immune factors. qPCR, RNAi, and Elisa methods were used to identify intrinsic innate immune factors in HBV-integrated HepG2.2.15 cells, and bioinformatics analysis was conducted on the HBV-infected tissues and cells in the GEO database. (3) Results: Inhibition of the JAK-STAT pathway enhanced HBV replication in HepG2 cells transfected with HBV plasmid and HepG2-NTCP cells infected with HBV. GSEA analysis of the GSE69590 data revealed significant changes in intrinsic innate immune pathways during HBV infection with PHH for 40 h. A total of 84 differentially expressed, candidate innate immunity genes were identified in GSE69590. Validation showed that and were down-regulated when HBx was expressed. Consistently, and were up-regulated following inhibition of HBx by transfection of HBx siRNA into HepG2.2.15 cells, and HBV pgRNA was up-regulated following down-regulated expression of and in HEK293 cells. Receiver operating characteristics (ROC) and overall survival (OS) analysis of 204 HBV-HCC patients showed that expression of was closely associated with HBV-HCC, and high expression of was associated with longer survival. (4) Conclusions: Innate immunity genes and are regulated by HBx, and higher expression of is closely related to longer survival of HBV-HCC patients. - Source: PubMed
Publication date: 2025/12/10
Zeng ChuiMegahed Fayed Attia KoutbGuo YiqiongSun DongmeiWang YaruLiu QinBi YanweiLi JinghangZhou QiXie QingdongSun PingnanZhou Xiaoling