Journal of Cell Communication and Signaling最新文献

{"title":"Dual impacts of mesenchymal stem cell-derived exosomes on cancer cells: unravelling complex interactions.","authors":"Babak Jahangiri, Mohammad Khalaj-Kondori, Elahe Asadollahi, Ali Kian Saei, Majid Sadeghizadeh","doi":"10.1007/s12079-023-00794-3","DOIUrl":"10.1007/s12079-023-00794-3","url":null,"abstract":"<p><p>Mesenchymal stem cells (MSCs) are multipotent, self-renewing stromal cells found in a variety of adult tissues. MSCs possess a remarkable ability to migrate towards tumor sites, known as homing. This homing process is mediated by various factors, including chemokines, growth factors, and extracellular matrix components present in the tumor microenvironment. MSCs release extracellular vesicles known as exosomes (MSC-Exos), which have been suggested to serve a key role in mediating a wide variety of MSC activities. Through cell-cell communication, MSC-Exos have been shown to alter recipient cell phenotype or function and play as a novel cell-free alternative for MSC-based cell therapy. However, MSC recruitment to tumors allows for their interaction with cancer cells and subsequent regulation of tumor behavior. MSC-Exos act as tumor niche modulators via transferring exosomal contents, such as specific proteins or genetic materials, to the nearby cancer cells, leading to either promotion or suppression of tumorigenesis, angiogenesis, and metastasis, depending on the specific microenvironmental cues and recipient cell characteristics. Consequently, there is still a debate about the precise relationship between tumor cells and MSC-Exos, and it is unclear how MSC-Exos impacts tumor cells. Although the dysregulation of miRNAs is caused by the progression of cancer, they also play a direct role in either promoting or inhibiting tumor growth as they act as either oncogenes or tumor suppressors. The utilization of MSC-Exos may prove to be an effective method for restoring miRNA as a means of treating cancer. This review aimed to present the existing understanding of the impact that MSC-Exos could have on cancer. To begin with, we presented a brief explanation of exosomes, MSCs, and MSC-Exos. Following this, we delved into the impact of MSC-Exos on cancer growth, EMT, metastasis, angiogenesis, resistance to chemotherapy and radiotherapy, and modulation of the immune system. Opposing effects of mesenchymal stem cells-derived exosomes on cancer cells.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":" ","pages":"1229-1247"},"PeriodicalIF":4.1,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10713965/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136397572","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Potential of extracellular vesicles for early prediction of severity and potential risk stratification in critical inflammatory diseases.","authors":"Yuchuan Deng, Yu Zou, Xiaoshuang Song, Ailing Jiang, Mao Wang, Qin Qin, Yiran Song, Chao Yue, Dujiang Yang, Bo Yu, Huimin Lu, Yu Zheng","doi":"10.1007/s12079-023-00763-w","DOIUrl":"10.1007/s12079-023-00763-w","url":null,"abstract":"<p><p>Some acute inflammatory diseases are often exacerbated during or after hospitalization, leading to some severe manifestations like systemic inflammatory response syndrome, multiple organ failure, and high mortality. Early clinical predictors of disease severity are urgently needed to optimize patient management for better prognosis. The existing clinical scoring system and laboratory tests cannot circumvent the problems of low sensitivity and limited specificity. Extracellular vesicles (EVs) are heterogeneous nanosecretory vesicles containing various biomolecules related to immune regulation, inflammation activation, and inflammation-related complications. This review provides an overview of EVs as inflammatory mediators, inflammatory signaling pathway regulators, promoters of inflammatory exacerbation, and markers of severity and prognosis. Currently, although relevant biomarkers are clinically available or are in the preclinical research stage, searching for new markers and detection methods is still warranted, as the problems of low sensitivity/specificity, cumbersome laboratory operation and high cost still plague clinicians. In-depth study of EVs might open a door in the search for novel predictors.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":" ","pages":"1283-1292"},"PeriodicalIF":4.1,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10189682/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9491316","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Farewell Springer… Hello Wiley : The tale of an academic scientific periodical -\"20 years later\" the Journal of Cell Communication and Signaling.","authors":"Bernard Perbal","doi":"10.1007/s12079-023-00796-1","DOIUrl":"10.1007/s12079-023-00796-1","url":null,"abstract":"<p><p>Academic publishing is the support for dissemination of research findings that constitute the grounds upon which new orientations and improvements are based on sharing breaking ideas, critical analyses of data, and argumentations that sustain the development of collaborative research projects. The wide diffusion of new scientific findings is pivotal to the progress of medical sciences, a salient feature of human societal fullness and intellectual welfare. In a practical way, the value of academic publishing can be ascertained by its capacity to reach a wide number of readers from different fields that may provide the soil for interactive projects. The challenges are numerous (Zul in Challenges in Academic Publishing; Navigating the Obstacles, 2023). An examination of the means developed to survey the individual performances of scientists, based on their publications, has led me to comment in this editorial on pitfalls that muddle the way to upstanding evaluations mainly based on irrelevant metrics.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":" ","pages":"1123-1129"},"PeriodicalIF":3.6,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10713886/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138498501","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metformin combined with rapamycin ameliorates podocyte injury in idiopathic membranous nephropathy through the AMPK/mTOR signaling pathway.","authors":"Meichen Ma, Yue Pan, Yue Zhang, Mei Yang, Ying Xi, Baoxu Lin, Wudi Hao, Jianhua Liu, Lina Wu, Yong Liu, Xiaosong Qin","doi":"10.2139/ssrn.4257549","DOIUrl":"https://doi.org/10.2139/ssrn.4257549","url":null,"abstract":"Autophagy activation protects against podocyte injury in idiopathic membranous nephropathy (IMN). The AMPK/mTOR signaling pathway is a vital autophagy regulatory pathway. Metformin promotes autophagy, whereas rapamycin is an autophagy agonist. However, the therapeutic mechanisms of metformin and rapamycin in IMN remain unclear. Thus, we examined the mechanisms of action of metformin and rapamycin in IMN by regulating the AMPK/mTOR autophagy signaling pathway. Female Sprague-Dawley (SD) rats were treated with cationic bovine serum albumin (C-BSA) to establish an IMN model and were randomly divided into IMN model, metformin, rapamycin, and metformin + rapamycin groups. A control group was also established. Metformin and rapamycin were used as treatments. Renal histological changes, urinary protein excretion, the protein expression levels of key AMPK/mTOR signaling pathway proteins, renal tissue cell apoptosis, and autophagy-associated proteins (Beclin 1 and LC3) were examined. In addition, a C5b-9 sublysis model using the MPC-5 mouse podocyte cell line was established to verify the effect of metformin combined with rapamycin on podocytes. Metformin combined with rapamycin improved urinary protein excretion in IMN rats. Metformin combined with rapamycin attenuated the inflammatory response, renal fibrosis, and podocyte foot process fusion. In addition, it improved autophagy in podocytes as demonstrated by the enhanced expression of Beclin-1, p-AMPK/AMPK, LC3-II/I, and autophagosomes in podocytes and decreased p-mTOR/mTOR expression. In conclusion, metformin combined with rapamycin decreased proteinuria, improved renal fibrosis and podocyte autophagy via AMPK/mTOR pathway in IMN rats. The metformin and rapamycin decreased proteinuria and inproved renal fibrosis in IMN model rats.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"1 1","pages":""},"PeriodicalIF":4.1,"publicationDate":"2023-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47747792","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Emerging roles of the long non-coding RNA NEAT1 in gynecologic cancers","authors":"Maryam Farzaneh,&nbsp;Mahrokh Abouali Gale Dari,&nbsp;Amir Anbiyaiee,&nbsp;Sajad Najafi,&nbsp;Dian Dayer,&nbsp;Abdolah Mousavi Salehi,&nbsp;Mona Keivan,&nbsp;Mehri Ghafourian,&nbsp;Shahab Uddin,&nbsp;Shirin Azizidoost","doi":"10.1007/s12079-023-00746-x","DOIUrl":"10.1007/s12079-023-00746-x","url":null,"abstract":"<div>\u0000 \u0000 <p>Gynecologic cancers are a worldwide problem among women. Recently, molecular targeted therapy opened up an avenue for cancer diagnosis and treatment. Long non-coding RNAs (lncRNAs) are RNA molecules (&gt; 200 nt) that are not translated into protein, and interact with DNA, RNA, and proteins. LncRNAs were found to play pivotal roles in cancer tumorigenesis and progression. Nuclear paraspeckle assembly transcript 1 (NEAT1) is a lncRNA that mediates cell proliferation, migration, and EMT in gynecologic cancers by targeting several miRNAs/mRNA axes. Therefore, NEAT1 may function as a potent biomarker for the prediction and treatment of breast, ovarian, cervical, and endometrial cancers. In this narrative review, we summarized various NEAT1-related signaling pathways that are critical in gynecologic cancers.</p>\u0000 </div>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"17 3","pages":"531-547"},"PeriodicalIF":4.1,"publicationDate":"2023-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10409959/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9972980","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction Note: Long non-coding RNA TP73-AS1 promotes TFAP2B-mediated proliferation, metastasis and invasion in retinoblastoma via decoying of miRNA-874-3p","authors":"Lina Wang,&nbsp;Chaokui Wang,&nbsp;Tong Wu,&nbsp;Fengyuan Sun","doi":"10.1007/s12079-023-00774-7","DOIUrl":"10.1007/s12079-023-00774-7","url":null,"abstract":"<p><b>Retraction Note: Journal of Cell Communication and Signaling (2020) 14:193–205</b></p><p>https://doi.org/10.1007/s12079-020-00550-x</p><p>The Editor-in-Chief has retracted this article. After publication, concerns were raised regarding high similarity between Fig. 5g (HXO-RB44 pcDNA-TP73-AS1 + NC mimic) in this article and Fig. 4g (HCT116 group 2) in Wang et al. (<span>2019</span>). The authors have been unable to provide raw data to address these concerns. The Editor-in-Chief therefore no longer has confidence in the presented data.</p><p>Fengyuan Sun does not agree to this retraction. Lina Wang, Chaokui Wang and Tong Wu have not responded to any correspondence from the editor or publisher about this retraction.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"17 3","pages":"1121"},"PeriodicalIF":4.1,"publicationDate":"2023-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10409937/pdf/12079_2023_Article_774.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10024270","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CCNs and other extracellular matrix proteins: an introduction to the special issue","authors":"Ralf Weiskirchen","doi":"10.1007/s12079-023-00770-x","DOIUrl":"10.1007/s12079-023-00770-x","url":null,"abstract":"&lt;p&gt;The extracellular matrix (ECM) is a specialized, highly organized and dynamic three-dimensional network composed of a complex mixture of proteins and other molecules forming the physical scaffolding of a cell and determining the tissue architecture of organs (Rais et al., &lt;span&gt;2023&lt;/span&gt;). It is of fundamental importance in cell growth, cell migration, and cellular communication. It is further a reservoir for growth factors and an anchor for cell-matrix, cell adhesion, and signaling receptors (Kyriakopoulou et al. &lt;span&gt;2023&lt;/span&gt;). Altered composition or dysregulated ECM remodeling can result in a wide range of diseases that include tissue stiffening, connective tissue disorders, muscular dystrophy, fibrosis, and cancer. Therefore, there is hope that increasing knowledge on the mechanisms that regulate ECM composition will lead to improved diagnostics and novel strategies for repair and regeneration of affected tissues (Keane et al. &lt;span&gt;2018&lt;/span&gt;). In particular, the six centralized coordinating network (CCN1-CCN6) factors represent general hubs that operate through diverse signaling pathways, thereby impacting a wide array of biological properties in tissue homeostasis and malignancy (Yeger and Perbal &lt;span&gt;2021&lt;/span&gt;).&lt;/p&gt;&lt;p&gt;This Special Issue of &lt;i&gt;Journal of Cell Communication and Signaling&lt;/i&gt; (JCCS) entitled “&lt;i&gt;CCNs and other extracellular matrix proteins&lt;/i&gt;” contains a comprehensive editorial, 7 reviews, and 4 original research articles reporting novel concepts and major advances in our understanding of basic and clinical aspects on CCN biology. The collection of these articles demonstrates the eminent progress made in the CCN field during the last years and supports the hope that this knowledge will help establishing novel therapies for various pathologies associated with imbalance or de-regulation of CCN proteins and pathways modulated by this multifaceted protein family.&lt;/p&gt;&lt;p&gt;The first contribution in this Special Issue is a profound Editorial by Perbal et al. (&lt;span&gt;2023&lt;/span&gt;) in which exciting basic principles, concepts, new views and considerations on the CCN family of protein are discussed. The article highlights important theoretical and conceptual considerations on how CCN family members can coordinate different signaling pathways. Strikingly, individual CCN members are functional “bipartite-acting” mediators, with members acting negatively and/or positively on cell proliferation and differentiation. As such, it is critical that expression of CCN members is under strict time- and tissue-specific regulation. The article further provides an extensive reference work for the CCN interactome. Importantly, the four structural modules of CCNs (i.e., insulin-like growth factor binding domain, von Willebrand factor-C domain, thrombospondin type 1 repeat domain, and carboxy-terminal cysteine knot domain) can interact with a high number of distinct ligands. Thus, it is estimated that different combinations of possible bindin","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"17 2","pages":"229-232"},"PeriodicalIF":4.1,"publicationDate":"2023-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10326176/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10153352","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CCN1 is predominantly elevated in human skin dermis by solar-simulated ultraviolet irradiation and accumulated in dermal extracellular matrix","authors":"Zhaoping Qin,&nbsp;Tianyuan He,&nbsp;Chunfang Guo,&nbsp;Jun Young Kim,&nbsp;Taihao Quan","doi":"10.1007/s12079-023-00767-6","DOIUrl":"10.1007/s12079-023-00767-6","url":null,"abstract":"<div>\u0000 \u0000 <p>Skin primarily comprises a collagen-rich extracellular matrix (ECM) that provides structural and functional support to the skin. Aging causes progressive loss and fragmentation of dermal collagen fibrils, leading to thin and weakened skin (Dermal aging). We previously reported that CCN1 is elevated in naturally aged human skin, photoaged human skin, and acute UV-irradiated human skin dermal fibroblasts in vivo. Elevated CCN1 alters the expression of numerous secreted proteins that have deleterious effects on the dermal microenvironment, impairing the structural integrity and function of the skin. Here we show that CCN1 is predominantly elevated in the human skin dermis by UV irradiation and accumulated in the dermal extracellular matrix. Laser capture microdissection indicated that CCN1 is predominantly induced in the dermis, not in the epidermis, by acute UV irradiation in human skin in vivo. Interestingly, while UV-induced CCN1 in the dermal fibroblasts and in the medium is transient, secreted CCN1 accumulates in the ECM. We explored the functionality of the matrix-bound CCN1 by culturing dermal fibroblasts on an acellular matrix plate that was enriched with a high concentration of CCN1. We observed that matrix-bound CCN1 activates integrin outside-in signaling resulting in the activation of FAK and its downstream target paxillin and ERK, as well as elevated MMP-1 and inhibition of collagen, in human dermal fibroblasts. These data suggest that accumulation of CCN1 in the dermal ECM is expected to progressively promote the aging of the dermis and thereby negatively impact the function of the dermis.</p>\u0000 </div>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"17 2","pages":"287-296"},"PeriodicalIF":4.1,"publicationDate":"2023-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10326203/pdf/12079_2023_Article_767.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9797738","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recent progress on the role of cellular communication network factors (CCN) 3, 4 and 6 in regulating adiposity, liver fibrosis and pancreatic islets","authors":"Viktoria Xega,&nbsp;Tara Alami,&nbsp;Jun-Li Liu","doi":"10.1007/s12079-023-00765-8","DOIUrl":"10.1007/s12079-023-00765-8","url":null,"abstract":"<div>\u0000 \u0000 <p>CCN/WISP (cellular communication network factors, or Wnt-inducted secreted proteins) family of proteins consists of six extracellular matrix (ECM)-associated proteins that regulate development, cell adhesion and proliferation, ECM remodeling, inflammation, and tumorigenesis. In the last two decades, metabolic regulation by these matricellular proteins has been studied extensively, several excellent reviews have covered the roles of CCN1, -2 and − 5. In this brief review, we will focus on those lesser-known members and more recent discoveries, together with other recent articles presenting a more complete picture of the current state of knowledge. We have found that CCN2, -4, and − 5 promote pancreatic islet function, while CCN3 plays a unique and negative role. CCN3 and − 4 are pro-adiposity leading to insulin resistance, but CCN5 and − 6 are anti-adiposity. While CCN2 and − 4 promote tissue fibrosis and inflammation, all other four members are clearly anti-fibrotic. As for cellular signaling, they are known to interact with integrins, other cell membrane proteins and ECM thereby regulate Akt/protein kinase B, myocardin-related transcription factor (MRTF), and focal adhesion kinase. Yet, a cohesive mechanism of action to comprehensively explain those major functions is still lacking.</p>\u0000 </div>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"17 2","pages":"297-306"},"PeriodicalIF":4.1,"publicationDate":"2023-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10326175/pdf/12079_2023_Article_765.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9795081","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Structural insights into regulation of CCN protein activities and functions","authors":"Vivi Talstad Monsen,&nbsp;Håvard Attramadal","doi":"10.1007/s12079-023-00768-5","DOIUrl":"10.1007/s12079-023-00768-5","url":null,"abstract":"<div>\u0000 \u0000 <p>CCN proteins play important functions during development, in repair mechanisms following tissue injury, as well as in pathophysiologic mechanisms of metastasis of cancer. CCNs are secreted proteins that have a multimodular structure and are categorized as matricellular proteins. Although the prevailing view is that CCN proteins regulate biologic processes by interacting with a wide array of other proteins in the microenvironment of the extracellular matrix, the molecular mechanisms of action of CCN proteins are still poorly understood. Not dissuading the current view, however, the recent appreciation that these proteins are signaling proteins in their own right and may even be considered preproproteins controlled by endopeptidases to release a C-terminal bioactive peptide has opened new avenues of research. Also, the recent resolution of the crystal structure of two of the domains of CCN3 have provided new knowledge with implications for the entire CCN family. These resolved structures in combination with structural predictions based upon the AlphaFold artificial intelligence tool provide means to shed new light on CCN functions in context of the notable literature in the field. CCN proteins have emerged as important therapeutic targets in several disease conditions, and clinical trials are currently ongoing. Thus, a review that critically discusses structure - function relationship of CCN proteins, in particular as it relates to interactions with other proteins in the extracellular milieu and on the cell surface, as well as to cell signaling activities of these proteins, is very timely.</p>\u0000 </div>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"17 2","pages":"371-390"},"PeriodicalIF":4.1,"publicationDate":"2023-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10326224/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9797732","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}