Cellular signalling最新文献

Retraction notice to "Exploring the role of biologics in depression" [Cellular Signalling 98 (2022) 110409]. 关于“探索生物制剂在抑郁症中的作用”的撤回通知[细胞信号98(2022)110409]。

IF 4.4 2区生物学

Cellular signalling Pub Date : 2025-05-28 DOI: 10.1016/j.cellsig.2025.111902

Tarapati Rani, Tapan Behl, Neelam Sharma, Hafiz A Makeen, Mohammed Albratty, Hassan A Alhazmi, Abdulkarim M Meraya, Saurabh Bhatia, Simona Gabriela Bungau

引用次数: 0

The AKT-USP15 axis modulates autophagy in MPP⁺-induced Parkinson's disease model of SN4741 cells. AKT-USP15轴调节MPP+诱导的SN4741帕金森病模型细胞自噬。

IF 4.4 2区生物学

Cellular signalling Pub Date : 2025-05-27 DOI: 10.1016/j.cellsig.2025.111879

Xian Wu, Yue Wen, Tianyao Bai, Nanfei Yang, Yuyu Yuan, Lingling Xu, Yujie Ma, Peng Su, Wenjing Luo, Wenjun Li

{"title":"The AKT-USP15 axis modulates autophagy in MPP<sup>+</sup>-induced Parkinson's disease model of SN4741 cells.","authors":"Xian Wu, Yue Wen, Tianyao Bai, Nanfei Yang, Yuyu Yuan, Lingling Xu, Yujie Ma, Peng Su, Wenjing Luo, Wenjun Li","doi":"10.1016/j.cellsig.2025.111879","DOIUrl":"https://doi.org/10.1016/j.cellsig.2025.111879","url":null,"abstract":"<p><p>In Parkinson's disease (PD), maintaining the balance between protein synthesis and degradation is critical for cellular homeostasis. Ubiquitination, which marks proteins for degradation, and its reverse process deubiquitination, are essential regulators for protein turnover. Recent research implicate that deubiquitinating enzymes involve in PD pathogenesis. Specially, Ubiquitin Specific Protease 15 (USP15) has been shown to antagonize Parkin, an E3 ubiquitin ligase that facilitates mitophagy - the selective clearance of damaged mitochondria.. However, the regulatory mechanisms governing the activity of USP15 in PD remain unclear. Our study revealed a novel regulatory mechanism: USP15 served as a phosphorylation substrate for protein kinase B (AKT). AKT-mediated phosphorylation triggered translocation of USP15 from the nucleus to the cytoplasm, subsequently restoring autophagy levels. These data identified that AKT mediated phosphorylation of USP15 regulated autophagy in MPP<sup>+</sup>-induced PD models. Collectivelly, our research elucidates the complex interplay among AKT, USP15, and autophagy in PD. These mechanistic insights advance our understanding of potential therapeutic targets to enhance autophagic flux and ameliorate cellular dysfunction in Parkinson's disease.</p>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":" ","pages":"111879"},"PeriodicalIF":4.4,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144181023","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Curcumin alleviates lipopolysaccharide-induced alveolar epithelial Glycocalyx damage by modulating the Rac1/NF-κB/HPSE pathway 姜黄素通过调节Rac1/NF-κB/HPSE通路减轻脂多糖诱导的肺泡上皮糖萼损伤

IF 4.4 2区生物学

Cellular signalling Pub Date : 2025-05-27 DOI: 10.1016/j.cellsig.2025.111909

Wenxia Xu , Dinqin Ou , Yufei Zhao , Yuan Liu , Peng Yan , Shuang Li , Qimao Sun , Xiong Zhang , Hong Liu , Jie Huang , Yu Fang

{"title":"Curcumin alleviates lipopolysaccharide-induced alveolar epithelial Glycocalyx damage by modulating the Rac1/NF-κB/HPSE pathway","authors":"Wenxia Xu , Dinqin Ou , Yufei Zhao , Yuan Liu , Peng Yan , Shuang Li , Qimao Sun , Xiong Zhang , Hong Liu , Jie Huang , Yu Fang","doi":"10.1016/j.cellsig.2025.111909","DOIUrl":"10.1016/j.cellsig.2025.111909","url":null,"abstract":"<div><div>The glycocalyx, a cell surface component implicated in various diseases, has recently been recognized for its role in acute lung injury (ALI). Also known as the alveolar epithelial polysaccharide coat, it is vital for maintaining lung barrier integrity, fluid homeostasis, and defense against pathogens. This study investigated the protective effects and mechanisms of curcumin, a natural polyphenol, against lipopolysaccharide (LPS) -induced alveolar epithelial glycocalyx damage. Key findings include: in vitro pretreatment with 20 μM curcumin for 2 h before a 24-h exposure to 10 μg/mL LPS markedly reduced heparan sulfate (HS) degradation by regulating heparanase (HPSE) expression. Mechanistic studies demonstrated that curcumin suppressed LPS-induced Ras-related C3 botulinum toxin substrate 1 (Rac1) expression and downstream nuclear factor kappa B (NF-κB) pathway activation, while upregulation of Rac1 protein abolished its protective effects. Furthermore, in vivo, administration of 200 mg/kg curcumin significantly reduced lung inflammation induced by 5 mg/kg LPS in mice. This treatment enhanced alveolar-capillary barrier function, evidenced by reduced levels of interleukin-6 (IL-6), IL-8, tumor necrosis factor-alpha (TNF-α), and HPSE. Curcumin also reduced damage to HS and syndecan-1 (SDC-1), a crucial component of the glycocalyx. This study is the first to indicate that curcumin protects against LPS-induced lung injury by reducing damage to the alveolar epithelial glycocalyx by inhibiting the Rac1/NF-κB/HPSE pathway.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"134 ","pages":"Article 111909"},"PeriodicalIF":4.4,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144170052","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Effects of higenamine on M1/M2 polarization and osteoclast differentiation in rheumatoid arthritis via the THBS-1/TGF-β signaling pathway 高铁胺通过THBS-1/TGF-β信号通路对类风湿关节炎M1/M2极化和破骨细胞分化的影响

IF 4.4 2区生物学

Cellular signalling Pub Date : 2025-05-27 DOI: 10.1016/j.cellsig.2025.111905

De-ta Chen , Zi-jian Wan , Xiao-ping Sheng, Wu Rao, Xin-hua Zhan, Jing-liang Gu, Xian-zhen Wei, Tian-you Fan

{"title":"Effects of higenamine on M1/M2 polarization and osteoclast differentiation in rheumatoid arthritis via the THBS-1/TGF-β signaling pathway","authors":"De-ta Chen , Zi-jian Wan , Xiao-ping Sheng, Wu Rao, Xin-hua Zhan, Jing-liang Gu, Xian-zhen Wei, Tian-you Fan","doi":"10.1016/j.cellsig.2025.111905","DOIUrl":"10.1016/j.cellsig.2025.111905","url":null,"abstract":"<div><div>This study investigated the therapeutic efficacy of Higenamine (HG), an extract from Monkshood, in the context of rheumatoid arthritis (RA). As an autoimmune disorder, RA is characterized by significant bone destruction primarily driven by inflammatory processes. Analysis demonstrated marked infiltration of macrophages within RA immune cells. HG inhibited iNOS, TNF-α, and IL-1β expression in M1 macrophages while enhancing IL-10, Arg-1, and MCP-1 levels in M2 macrophages. Flow cytometry confirmed HG's capacity to promote the M1 to M2 macrophage transition. Transcriptomic analysis established connections between HG, RA, osteoclast differentiation, and the THBS-1/TGF-β signaling pathway, indicating its potential to mitigate bone destruction. In vitro studies showed that HG diminished osteoclast differentiation and downregulated V-ATPase, Ctsk, TRAP, THBS-1, and TGF-β expression. In vivo, HG alleviated arthritis symptoms in collagen-induced arthritis (CIA) mice, reduced M1 macrophage accumulation, modulated THBS-1/TGF-β signaling, and lessened joint damage. Micro-CT imaging and staining corroborated the reduction in osteoclast numbers and improvement in bone homeostasis. In summary, HG presents a promising therapeutic avenue for RA and associated bone destruction through modulation of the THBS-1/TGF-β signaling pathway.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"134 ","pages":"Article 111905"},"PeriodicalIF":4.4,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144170053","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

LINC02593 impedes cell senescence via COP1-mediated p53 degradation in cervical cancer 在宫颈癌中，LINC02593通过cop1介导的p53降解阻碍细胞衰老

IF 4.4 2区生物学

Cellular signalling Pub Date : 2025-05-27 DOI: 10.1016/j.cellsig.2025.111907

Qian Jing , Qin Chen , Guosong Wang , Tong Wu , Lingli Wang , Qunli Xiong , Xiaojuan Yang , Lei Qiu , Junhong Han

{"title":"LINC02593 impedes cell senescence via COP1-mediated p53 degradation in cervical cancer","authors":"Qian Jing , Qin Chen , Guosong Wang , Tong Wu , Lingli Wang , Qunli Xiong , Xiaojuan Yang , Lei Qiu , Junhong Han","doi":"10.1016/j.cellsig.2025.111907","DOIUrl":"10.1016/j.cellsig.2025.111907","url":null,"abstract":"<div><div>Evasion of cellular senescence is one of the hallmarks of cervical carcinoma (CC) to maintain malignant development. Even though the regulators driving CC cell senescence are widely recognized, the underlying upstream mechanisms are still not fully understood. Long non-coding RNAs (lncRNAs) are emerging as important regulators in cell senescence. Here, we conducted a lncRNA profiling and identified LINC02593 as a significantly downregulated lncRNA in induced senescent cervical squamous cell carcinoma (CSCC) cells. LINC02593 is upregulated in CSCC tissues. Depletion of LINC02593 resulted in a marked cellular senescence phenotype and tumor growth inhibition in vitro and in vivo, whereas LINC02593 overexpression suppressed doxorubicin-induced cell senescence. LINC02593 was shown to impede cell senescence by inhibiting p21 expression, and this regulation was mainly dependent on p53 protein degradation. Mechanistically, LINC02593 served as a scaffold, bridging the coiled-coil domain of COP1 and the C-terminal domain of p53, enhancing the affinity between p53 and its E3 ubiquitin ligase COP1. The “scaffold” function facilitated p53 degradation by COP1 as well as the downstream p21 repression, eventually evading cell senescence. Overall, we characterized a previously unknown mechanism by which LINC02593 manipulated senescence to promote CC progression.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"134 ","pages":"Article 111907"},"PeriodicalIF":4.4,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144170051","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Panx3 mediates ferroptosis via the AKT/mTOR signaling pathway in oral squamous cell carcinoma Panx3在口腔鳞状细胞癌中通过AKT/mTOR信号通路介导铁下垂

IF 4.4 2区生物学

Cellular signalling Pub Date : 2025-05-27 DOI: 10.1016/j.cellsig.2025.111908

Xuan Li , Yan Zhao , Yang Liu , Chang-Song Zhang , Zhao-Yuan Xu , Shi-Rui Wang , Tong-Mei Zhang , Yan Zhang , Su-Xia Liang , Ying-Bin Yan

{"title":"Panx3 mediates ferroptosis via the AKT/mTOR signaling pathway in oral squamous cell carcinoma","authors":"Xuan Li , Yan Zhao , Yang Liu , Chang-Song Zhang , Zhao-Yuan Xu , Shi-Rui Wang , Tong-Mei Zhang , Yan Zhang , Su-Xia Liang , Ying-Bin Yan","doi":"10.1016/j.cellsig.2025.111908","DOIUrl":"10.1016/j.cellsig.2025.111908","url":null,"abstract":"<div><div>Pannexin 3 (Panx3) has been the subject of numerous studies across different cell types, predominantly concentrating on bone remodeling, wound repair, and dermal inflammation. However, the link between Panx3 and cancer remains minimally explored. Here, we showed for the first time that the expression of Panx3 was lower in oral squamous cell carcinoma (OSCC) tissues than in normal oral mucosa tissues, and was associated with the differentiation of OSCC. We found that overexpression of Panx3 significantly promotes ferroptosis while inhibiting proliferation, migration, and invasion in SCC15 and CAL27 cells. Furthermore, in Panx3-overexpressing OSCC cells, the expression levels of P-AKT, P-mTOR, GPX4, and SLC7A11 were significantly decreased, whereas ACSL4 expression was markedly upregulated. Subsequently, the enhanced ferroptosis was significantly rescued upon the addition of the AKT activator SC79 to Panx3-overexpressing SCC15 and CAL27 cells. The tumor-suppressive role of Panx3 through ferroptosis induction was further confirmed by xenograft assays, which demonstrated significantly inhibited tumor growth. In conclusion, the results suggested that Panx3 overexpression reduced the survival of OSCC cells and inhibited the progression of OSCC by promoting ferroptosis via the inhibition of AKT/mTOR signaling pathway.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"134 ","pages":"Article 111908"},"PeriodicalIF":4.4,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144170436","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

HBV upregulates TNNT1 expression through PI3K/AKT/mTOR-c-Myc axis, which in turn induces EMT and liver fibrosis in mice. HBV通过PI3K/AKT/mTOR-c-Myc轴上调TNNT1表达，进而诱导小鼠EMT和肝纤维化。

IF 4.4 2区生物学

Cellular signalling Pub Date : 2025-05-27 DOI: 10.1016/j.cellsig.2025.111899

Haoran Qu, Yan Xie, Shan Hu, Sujuan Sun, Yufeng Yuan, Yuchen Xia, Min Liu, Xiao-Lian Zhang

{"title":"HBV upregulates TNNT1 expression through PI3K/AKT/mTOR-c-Myc axis, which in turn induces EMT and liver fibrosis in mice.","authors":"Haoran Qu, Yan Xie, Shan Hu, Sujuan Sun, Yufeng Yuan, Yuchen Xia, Min Liu, Xiao-Lian Zhang","doi":"10.1016/j.cellsig.2025.111899","DOIUrl":"https://doi.org/10.1016/j.cellsig.2025.111899","url":null,"abstract":"<p><p>Hepatitis B virus (HBV) infection is a major etiological factor in the development of hepatocellular carcinoma (HCC). Despite extensive research efforts, the precise molecular mechanisms and critical host factors driving HBV-induced epithelial-mesenchymal transition (EMT), liver fibrosis and hepatocarcinogenesis remain to be explored. Emerging evidence has identified aberrant expression of Troponin T1 (TNNT1) in malignancies, implicating its potential role in HCC progression. However, the specific role and mechanism of TNNT1 in HBV-associated HCC remain elusive. In this study, we demonstrate that TNNT1 expression is markedly upregulated in HBV-positive HCC tissues, HBV infection/replication cell models and AAV-HBV1.3-infected mouse models. Mechanistically, HBV activates the transcription factor c-Myc via the PI3K/AKT/mTOR signaling pathway. HBV promotes HCC cell proliferation and EMT markers (Cyclin D1, Vimentin increased, E-cadherin decreased) and liver fibrosis marker α-smooth muscle actin (α-SMA) expression in a TNNT1-dependent manner. HBV infection-induced EMT and liver fibrosis can be abolished by hepatic-specific TNNT1 knockout or knockdown in mice. These findings provide novel insights into the role of TNNT1 in HBV-driven EMT and liver fibrosis, and establish a foundation for further exploration of TNNT1 as a potential therapeutic target in HBV-associated HCC progress.</p>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":" ","pages":"111899"},"PeriodicalIF":4.4,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144181330","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

IL-6/KIAA1429 promotes ferroptosis resistance in endometrial cancer through m6A modification of DDIT3 IL-6/KIAA1429通过m6A修饰DDIT3促进子宫内膜癌铁下垂抵抗

IF 4.4 2区生物学

Cellular signalling Pub Date : 2025-05-26 DOI: 10.1016/j.cellsig.2025.111906

Xiaoyu Shen , Wan Shu , Jun Zhang , Ting Zhou , Kejun Dong , Jiarui Zhang , Yuwei Yao , Haojia Li , Shuangshuang Cheng , Tangansu Zhang , Guanxiao Chen , Shuyang Yu , Qi Zhang , Hongbo Wang , Yan Liu

{"title":"IL-6/KIAA1429 promotes ferroptosis resistance in endometrial cancer through m6A modification of DDIT3","authors":"Xiaoyu Shen , Wan Shu , Jun Zhang , Ting Zhou , Kejun Dong , Jiarui Zhang , Yuwei Yao , Haojia Li , Shuangshuang Cheng , Tangansu Zhang , Guanxiao Chen , Shuyang Yu , Qi Zhang , Hongbo Wang , Yan Liu","doi":"10.1016/j.cellsig.2025.111906","DOIUrl":"10.1016/j.cellsig.2025.111906","url":null,"abstract":"<div><div>Endometrial cancer (EC) exhibits significant resistance to ferroptosis. Interleukin (IL)-6 is a pleiotropic cytokine that is a regulator of the expression of various oncogenes and tumour suppressor genes. Notably, N6-methyladenosine (m6A) modification has been demonstrated to play a significant role in tumour occurrence and development. However, IL-6 regulatory role in ferroptosis during carcinogenesis and whether it affects m6A modification in EC remain unclear. The present study aimed to investigate the effect of IL-6 on m6A modification in EC. The degree of ferroptosis of EC in vitro and in vivo was evaluated using a cell proliferation assay, western blotting, total reactive oxygen species (ROS) detection, a lipid peroxidation assay, and a subcutaneous xenograft tumour model. The regulation of downstream molecules by KIAA1429 was confirmed using dot blot, RNA and methylated RNA immunoprecipitation (RIP), a RNA stability assay, and fluorescence in situ hybridisation (FISH). IL-6 upregulated overall m6A levels in EC cells, with the KIAA1429 expression upregulation being the most significant. Functionally, IL-6 inhibited EC cell ferroptosis and promoted proliferation. The downregulation of KIAA1429 triggered ferroptosis, subsequently suppressing the proliferation of EC cells in vitro and tumour growth in vivo. Mechanistically, IL-6 activated KIAA1429 expression through the JAK1/STAT3 pathway. KIAA1429 regulated DDIT3 expression and promoted its degradation through m6A modification. IL-6 is crucial in EC cell ferroptosis resistance. Overall, the IL-6/KIAA1429/DDIT3 axis is a novel pathway that promotes EC progression and provides novel directions for targeted EC therapy.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"134 ","pages":"Article 111906"},"PeriodicalIF":4.4,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144170435","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Aerobic exercise alleviates chronic allergic airway inflammation by regulating the circMETTL9/EIF4A3/IGFBP3 axis 有氧运动通过调节circmetl9 /EIF4A3/IGFBP3轴减轻慢性变应性气道炎症

IF 4.4 2区生物学

Cellular signalling Pub Date : 2025-05-26 DOI: 10.1016/j.cellsig.2025.111889

Haixia Wang , Yuanmin Jia , Bin Ma , Ting Gao , Hui Wei , Danyang Li , Junlian Gu , Ou Chen , Shouwei Yue

{"title":"Aerobic exercise alleviates chronic allergic airway inflammation by regulating the circMETTL9/EIF4A3/IGFBP3 axis","authors":"Haixia Wang , Yuanmin Jia , Bin Ma , Ting Gao , Hui Wei , Danyang Li , Junlian Gu , Ou Chen , Shouwei Yue","doi":"10.1016/j.cellsig.2025.111889","DOIUrl":"10.1016/j.cellsig.2025.111889","url":null,"abstract":"<div><div>Aerobic exercise has been recommended as a non-pharmacological treatment for asthma. Previous studies have shown that circMETTL9 regulates cellular inflammation, apoptosis, and oxidative stress levels. However, whether aerobic exercise can modulate the expression of circMETTL9 to alleviate chronic allergic airway inflammation remains unclear. In this study, we established a mouse model of chronic allergic lung inflammation with aerobic exercise intervention to assess its effects. Our results demonstrate that aerobic exercise exerts anti-inflammatory, anti-proliferative, anti-apoptotic, and anti-oxidative stress effects by regulating the circMETTL9/EIF4A3/IGFBP3 axis. Mechanistically, we found that circMETTL9 binding to EIF4A3 does not affect EIF4A3 expression. However, EIF4A3 positively regulates both the protein and mRNA levels of IGFBP3. Specifically, circMETTL9 binds to EIF4A3 to inhibit IGFBP3 transcription and translation. This study identifies a novel potential target and research direction for treating chronic allergic lung inflammation.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"134 ","pages":"Article 111889"},"PeriodicalIF":4.4,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144170050","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A brief overview of the E3 ubiquitin ligase: TRIM7 E3泛素连接酶TRIM7简介

IF 4.4 2区生物学

Cellular signalling Pub Date : 2025-05-24 DOI: 10.1016/j.cellsig.2025.111886

Jun-Jie Fan , Can Hu , Min Hu , Wen-Sheng Dong , Kang Li , Yun-Jia Ye , Xin Zhang

{"title":"A brief overview of the E3 ubiquitin ligase: TRIM7","authors":"Jun-Jie Fan , Can Hu , Min Hu , Wen-Sheng Dong , Kang Li , Yun-Jia Ye , Xin Zhang","doi":"10.1016/j.cellsig.2025.111886","DOIUrl":"10.1016/j.cellsig.2025.111886","url":null,"abstract":"<div><div>TRIM7, a member of the E3 ubiquitin ligase family, has garnered significant attentions in different research fields since its discovery. This enzyme plays indispensable roles in various pathophysiological processes through ubiquitination-mediated degradation of diverse protein substrates. This review systematically summarizes the current knowledge on the protein structure and biological functions of TRIM7. Structurally, TRIM7 features a conserved RBCC motif (RING, B-box, and coiled-coil domains) coupled with a variable C-terminal region that dictates the substrate specificity. In infectious contexts, TRIM7 is required for the pathogen-specific regulation, and exerts paradoxical effects by either promoting host defense or facilitating viral pathogenesis depending on pathogen type. Within oncology, TRIM7 manifests tumor-suppressive properties through regulating metastasis, apoptosis, and tumor immunology. In addition, it might serve as a reliable biomarker for monitoring the progression of idiopathic pulmonary fibrosis and also inhibits the progression of atherosclerosis. In summary, TRIM7 plays critical roles in different pathophysiological processes, and it might be a predictive and therapeutic target in certain human diseases.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"134 ","pages":"Article 111886"},"PeriodicalIF":4.4,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149540","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0