Cell Communication and Signaling最新文献

{"title":"Campylobacter jejuni regulates cell cycle progression to potentiate host cell invasion.","authors":"Prabhat K Talukdar, Megan C Dines, Eric A Shelden, Brandon A Toy, Amruta Suresh Kale, Ryan R Driskell, Lisa M Gloss, Michael E Konkel","doi":"10.1186/s12964-025-02348-z","DOIUrl":"10.1186/s12964-025-02348-z","url":null,"abstract":"<p><strong>Background: </strong>Campylobacter jejuni is associated with enteritis in humans and domestic animals. Acute C. jejuni-mediated enteritis requires bacterial invasion of intestinal cells with an ensuing host inflammatory response. Known is that C. jejuni invasion of human epithelial cells is dependent on host cell-focal adhesion components, which link the extracellular matrix to the actin cytoskeleton of a cell. Based on the observation that C. jejuni cell invasion engages many of the same components involved in regulating the cell cycle, we hypothesized that C. jejuni regulates the host cell cycle.</p><p><strong>Methods: </strong>Flow cytometry was used to detect the cell cycle phases (G₁, S, G₂ and M). Single-cell RNA-sequencing (scRNA-seq) and reverse transcriptase quantitative PCR (RT-qPCR) were used to determine the differential gene expressions of uninfected and C. jejuni-infected cells. Infection assays and confocal microscopy were employed to determine the rate of bacterial invasion and intracellular localization of C. jejuni-infected cells. Quantification of Interleukin-8 (IL-8) was determined by the ELISAs.</p><p><strong>Results: </strong>INT 407 cells infected with C. jejuni showed a slower rate of cell cycle progression and a greater percentage of cells in the G₁ cell cycle phase. scRNA-seq and RT-qPCR analysis of C. jejuni-infected cells corroborated the result, revealing host genes responsive to C. jejuni infection, including genes associated with cell cycle regulation, focal adhesions, inflammatory cytokines, and oxidative stress. Cell cycle synchronization coupled with the gentamicin-protection revealed that C. jejuni preferentially invades cells in the G₁ phase. Moreover, an increase was observed in the number of bacteria colocalized with paxillin, a critical component of focal adhesion complexes, during the G₁ phase. The infection of INT 407 cells in the G₁ phase also increased the secretion of the proinflammatory cytokine IL-8 from cells.</p><p><strong>Conclusions: </strong>Based on the data, we propose that acute C. jejuni-mediated enteritis (campylobacteriosis) alters the cell cycle phase of enterocytes, cytokine production, and immune cell recruitment, disrupting the intestinal permeability barrier.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"343"},"PeriodicalIF":8.2,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12269301/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144651293","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondria from huntington´s disease striatal astrocytes are hypermetabolic and compromise neuronal branching.","authors":"Laura López-Molina, Alba Pereda-Velarde, Nadia di Franco, Imme Aerts, Elisa Sebastià, Laura Valls-Roca, Mariona Guitart-Mampel, Gloria Garrabou, Silvia Gines","doi":"10.1186/s12964-025-02341-6","DOIUrl":"10.1186/s12964-025-02341-6","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Deficits in mitochondrial bioenergetics and dynamics are strongly implicated in the selective vulnerability of striatal neurons in Huntington´s disease. Beyond these neuron-intrinsic factor, increasing evidence suggest that non-neuronal mechanisms, particularly astrocytic dysfunction involving disrupted homeostasis and metabolic support also contribute to disease progression. These findings underscore the critical role of metabolic crosstalk between neurons and astrocytes in maintaining striatal integrity. However, it remains unclear whether this impaired communication affects the transfer of mitochondria from astrocytes to striatal neurons, a potential metabolic support mechanism that may be compromised in Huntington´s Disease.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;Primary striatal astrocytes were obtained from wild-type and R6/1 mice to investigate mitochondrial dynamics. Expression levels of key mitochondrial fusion and fission proteins were quantified by Western blotting and RT-PCR. Mitochondria morphology, oxidative stress and membrane potential were assessed using confocal microscopy following staining with mitochondria-specific dyes. Mitochondrial respiration was measured using the Oxygraph-2k respirometer system (Oroboros Instruments). Transmitophagy was evaluated by confocal imaging after labeling astrocytic mitochondria with Mitotracker dyes. To assess the functional impact of mitochondrial transfer on neurons, Sholl analysis, neuronal death and oxidative stress levels were quantified using specific fluorogenic probes.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Striatal astrocytes from HD mice exhibited a significant increase in mitochondrial fission, and mitochondrial oxidative stress, mirroring alterations previously reported in striatal neurons. Analysis of mitochondrial oxygen consumption rate (OCR) revealed elevated respiration activity and enhanced ATP-linked respiration, indicative of a hypermetabolic state. Concurrently, increased lactate production suggested a shift toward dysregulated astrocytic energy metabolism. These mitochondrial alterations were functionally detrimental: astrocytic mitochondria derived from HD mice when taken up by striatal neurons via transmitophagy, led to reduced neuronal branching and disrupted oxidative homeostasis.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusions: &lt;/strong&gt;Our findings demonstrate that striatal astrocytes from HD mice exhibit a hypermetabolic phenotype, characterized by increased mitochondrial respiration, disrupted mitochondrial dynamics, and elevated mitochondrial oxidative stress. Importantly, we identify a novel mechanism of astrocyte-neuron interaction involving the transfer of dysfunctional mitochondria from astrocytes to neurons. The uptake of these compromised mitochondria by striatal neurons results in reduced neuronal branching and increased reactive oxygen species (ROS) production. Collectively, these results highlight the pathological relevance of impaired astrocyte-to-neuron mi","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"341"},"PeriodicalIF":8.2,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12265250/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144651301","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ERα-dependent crosstalk between macrophages and cancer cells potentiates vasculogenic mimicry and M2 macrophage polarization in bladder cancer.","authors":"Qing Liu, Jinpeng Wang, Shan Gao, Zhuolun Li, Wei Zhang, Weiyang Liu, Bingmei Liu, Guanglu Dong, Bosen You","doi":"10.1186/s12964-025-02297-7","DOIUrl":"10.1186/s12964-025-02297-7","url":null,"abstract":"","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"339"},"PeriodicalIF":8.2,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12261844/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144644199","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: TRIM24 regulates chromatin remodeling and calcium dynamics in cardiomyocytes.","authors":"Marco Neu, Anushka Deshpande, Ankush Borlepawar, Elke Hammer, Ahmed Alameldeen, Phillipp Vöcking, Timon Seeger, Michael Hausmann, Norbert Frey, Ashraf Yusuf Rangrez","doi":"10.1186/s12964-025-02352-3","DOIUrl":"10.1186/s12964-025-02352-3","url":null,"abstract":"","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"338"},"PeriodicalIF":8.2,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12261686/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144644198","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Degradation of voltage-gated calcium channels: mechanisms and applications in neurological and cardiovascular diseases.","authors":"Lihong Liu, Yanruo Zhou, Ping Liao, Tuck Wah Soong, Zhenyu Hu","doi":"10.1186/s12964-025-02347-0","DOIUrl":"10.1186/s12964-025-02347-0","url":null,"abstract":"<p><p>The degradation of voltage-gated calcium channels (VGCC), which are key determinants of neuronal excitability and muscle contraction, is crucial for regulating calcium homeostasis and can be targeted for analgesic drug discovery. Molecularly, both the ubiquitin-proteasomal system and lysosomal pathways play critical roles in VGCC turnover with the involvement of ubiquitin-conjugating E2 enzyme UBE2L3, multiple ubiquitin-ligating E3 ligases including Rfp2, Mdm2, Nedd4-1 and WWP1, and deubiquitinase USP5. Physiologically, a blocking peptide and small molecules interfering with the Ca_V3.2-USP5 protein interaction has been developed to treat neuroinflammation and neuropathic pain in mouse models. Moreover, two genetically encoded calcium channel blockers by using catalytic HECT domain of the E3 ubiquitin ligase Nedd4-2 and nanobodies to β subunit and Nedd4-2 have been shown to have exceptional potency to remove high voltage-gated calcium channels from the plasma membrane. These two blockers showed strong efficacy in reducing hyperalgesia response to nerve injury. Therefore, a deeper understanding of VGCC degradation offers new therapeutic strategies for diseases associated with calcium channel dysfunction, including neuroinflammation, Parkinson's disease, neuropathic pain and cardiovascular diseases.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"337"},"PeriodicalIF":8.2,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12261568/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144638690","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of calcium oxalate crystals on neutrophil cellular proteome and functions: implications for nephrolithiasis.","authors":"Chanettee Lertprapai, Paleerath Peerapen, Visith Thongboonkerd","doi":"10.1186/s12964-025-02345-2","DOIUrl":"10.1186/s12964-025-02345-2","url":null,"abstract":"<p><strong>Background: </strong>The majority of stone formers (87.5-95.9%) exhibit mild to moderate interstitial inflammation surrounding the stone. Neutrophils and neutrophil-derived genes/proteins have been found in renal papillae, stone matrix and urine of calcium oxalate monohydrate (COM) stone formers. However, neutrophil-crystal interactions, especially responses of neutrophils to COM crystals, remained unknown.</p><p><strong>Methods: </strong>This study addressed the effects of COM crystals on neutrophil cellular proteome and functions, including phagocytosis, activation/degranulation, neutrophil extracellular traps (NETs) formation and reactive oxygen species (ROS) production.</p><p><strong>Results: </strong>Label-free quantitative (LFQ) proteomics using nanoLC-ESI-Qq-TOF MS/MS with highly stringent criteria revealed that COM caused altered levels of 22 neutrophil proteins involved mainly in immune responses. Investigating neutrophil innate immune functions using flow cytometry, immunofluorescence/fluorescence imaging, ELISA and dichlorodihydrofluorescein diacetate (DCFH-DA) assay revealed that COM enhanced neutrophil phagocytic activity, NETs formation, activation/degranulation and ROS production. Moreover, secretome (a set of secretory products) from COM-treated neutrophils induced the recruitment of macrophages to phagocytose the COM-treated neutrophils.</p><p><strong>Conclusions: </strong>These findings illustrate the expression and functional responses of neutrophils to COM crystals and implicate the important roles that neutrophils play in nephrolithiasis.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"336"},"PeriodicalIF":8.2,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12255060/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144621216","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transcriptional regulation and signaling of type IV interferon in Carassius gibelio.","authors":"Caijiao Dai, Yuting Zhu, Shiyu Qian, Yihui Fan, Zekun Weng, Lijuan Li, Jianghua Wang, Junfa Yuan","doi":"10.1186/s12964-025-02342-5","DOIUrl":"10.1186/s12964-025-02342-5","url":null,"abstract":"<p><p>It was recently shown that vertebrates, ranging from fish to primitive mammals, possess type IV IFN (IFNυ). However, their precise function and elaborate signaling remains unknown. In this study, CaIFNυ was identified from Carassius gibelio and its transcriptional regulation and signaling was further investigated. Firstly, CaIFNυ displays significant differences in the distribution, magnitude, and kinetics of its antiviral properties compared with CaIFNa1, a typical type I IFN from C. gibelio. Secondly, IRF1/3/7 differentially activated CaIFNυ through homo- or heteroprotein complexes in a dose-dependent fashion and NF-κB (p65) was the most effective stimulator. Thirdly, CaIFNυ initiates the antiviral ISGs through the JAK-STAT as well as MAPK and PI3K signaling pathways by binding to the extra-cellular region of CaCRFB4 and CaCRFB12. Taken together, these findings reveal that CaIFNυ belonges to an antiviral cytokine lineage which is distinct from CaIFNa1.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"335"},"PeriodicalIF":8.2,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12255096/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144621217","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neutrophil membrane-coated circular RNA nanoparticles for targeted immunotherapy in HER2-positive breast cancer brain metastasis.","authors":"Yunpeng Liu, Wei He, Xiaoju Li, Xiyan Lu, Chihua Wu, Yuan Gao, Dong Fan, Chao Dong, Huadong Zhao","doi":"10.1186/s12964-025-02321-w","DOIUrl":"10.1186/s12964-025-02321-w","url":null,"abstract":"<p><p>Breast cancer is the most prevalent malignancy worldwide, with approximately 50% of HER2-positive advanced breast cancer patients eventually developing brain metastases, significantly reducing survival. Current HER2-targeted therapies, such as trastuzumab, exhibit limited efficacy in patients with brain metastases due to poor blood-brain barrier penetration and drug resistance. This study aimed to develop a novel strategy for treating HER2-positive breast cancer brain metastases to improve overall survival. We engineered nanoparticles encapsulating circular RNA encoding the chemokine CXCL9 and an anti-PD-1 scFv, designed to target HER2-positive brain metastases. Our results demonstrate that these nanoparticles significantly enhance anti-tumor activity both in vitro and in vivo without exhibiting significant systemic toxicity. This approach improves the local tumor immune microenvironment while inducing lower systemic toxicity. In conclusion, we have established a platform of membrane-encapsulated circular RNA nanoparticles capable of targeting brain tumor lesions, showing potential for application in various brain disorders, including metastatic brain tumors. This novel approach offers a promising strategy for addressing the urgent need for effective treatments for HER2-positive breast cancer brain metastases.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"333"},"PeriodicalIF":8.2,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12247365/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144610394","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The solute carrier family 11 transporters: a bridge between iron homeostasis and tumor biology.","authors":"Ruchira Banerjee, Bintee Bintee, Mukesh Kumar Manickasamy, Shristy Jha, Mohammed S Alqahtani, Mohamed Abbas, Arul Goel, Gautam Sethi, Zhaowu Ma, Ajaikumar B Kunnumakkara","doi":"10.1186/s12964-025-02293-x","DOIUrl":"10.1186/s12964-025-02293-x","url":null,"abstract":"<p><p>Iron is an essential trace element in the human body, and its imbalance is closely linked to the initiation and progression of various malignancies. The solute carrier family 11 (SLC11) transporters, comprising SLC11A1 and SLC11A2, play pivotal roles in iron metabolism and cellular homeostasis, processes intricately linked to oncogenesis. SLC11A1, primarily expressed in macrophages, modulates immune responses and reshapes the tumor microenvironment, while SLC11A2, a ubiquitous iron transporter, regulates dietary iron absorption and ferroptosis, an iron-dependent form of programmed cell death. Dysregulation of these transporters is associated with tumor initiation, progression, metastasis, and therapy resistance. In this review, we provide an overview of the physiological functions of SLC11 transporters in iron metabolism and their pathological roles in cancer biology. Emerging evidence highlights their involvement in key oncogenic pathways, including p53, JAK/STAT, Wnt and HIF signaling. Pharmacological and genetic interventions targeting SLC11 transporters have shown the potential to disrupt tumor progression and enhance treatment efficacy. By exploring the intricate roles of SLC11A1 and SLC11A2 in cancer progression, this review offers insights into their potential as biomarkers and therapeutic targets, paving the way for innovative cancer treatment strategies.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"332"},"PeriodicalIF":8.2,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12247208/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144610395","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IgSF11-RAP1 signaling promotes cell migration and invasion of cutaneous melanoma.","authors":"Yasuyuki Kobayashi, Kotaro Sugimoto, Minaka Ishibashi, Makoto Kobayashi, Shohei Igari, Shigeki Kitamura, Toshiyuki Yamamoto, Yuko Hashimoto, Hideki Chiba","doi":"10.1186/s12964-025-02245-5","DOIUrl":"10.1186/s12964-025-02245-5","url":null,"abstract":"<p><strong>Background: </strong>Aberrant cell adhesion signaling is known to either accelerate or inhibit cancer progression, but the underlying molecular basis has yet to be established. The immunoglobulin superfamily 11 (IgSF11) functions as a cell adhesion protein and is overexpressed in several types of cancer, including high-grade glioma. However, it remains unknown whether and how IgSF11 stimulates malignant phenotypes.</p><p><strong>Methods: </strong>Using The Cancer Genome Atlas (TCGA), we first examined the expression of IgSF11 gene in various types of cancer tissues. Next, we developed an anti-hIgSF11 monoclonal antibody (mAb) and evaluated the clinicopathological significance of high IgSF11 expression in 187 cutaneous melanoma patients via immunohistochemistry using this selective mAb. We also generated human melanoma cell lines A375 and 888mel expressing IgSF11, as well as 888mel:IgSF11^KO and 888mel:IgSF11^KO:IgSF11 cells, and compared their phenotypes with those of control cells both in vitro and in vivo. Immunoprecipitation-mass spectrometry was applied to identify an IgSF11-interacting protein, followed by validation of its association with IgSF11 and of the specific IgSF11 region responsible for the complex formation and promoting melanoma cell migration.</p><p><strong>Results: </strong>IgSF11 mRNA was highly expressed in glioblastoma tissues and skin cutaneous melanoma tissues, but not in other malignant tumors. High IgSF11 expression was observed in 57 out of the 187 melanoma cases (30.5%) and was significantly correlated with Clark's level and high budding, both of which are parameters of melanoma invasion. Using a series of established cell lines, we demonstrated that IgSF11 promotes melanoma cell migration and invasion, as well as the enrichment of a gene set associated with epithelial-mesenchymal transition (EMT). Importantly, we identified that IgSF11 forms a complex with RAS-associated protein 1 (RAP1). Furthermore, the L372-R378 region of IgSF11 was required for recruiting RAP1 and driving melanoma cell migration.</p><p><strong>Conclusions: </strong>We found that IgSF11-RAP1 signaling facilitates the migration and invasion of melanoma cells. The identification of IgSF11-RAP1 machinery highlights a novel link between cell adhesion and signaling molecules in promoting the malignant phenotypes of melanoma and may serve as a promising therapeutic target for this malignancy.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"330"},"PeriodicalIF":8.2,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12243136/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144602306","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}