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10.1002/advs.202513286 http://scihub22266oqcxt.onion/10.1002/advs.202513286 41319267!?!41319267 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=41319267&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Adv+Sci+(Weinh) 2025 ; ? (?): e13286 Nephropedia Template TP {{tp|p=41319267|t=2025. Surface-Associated Proteins on Extracellular Vesicles Remodel the Tumor Microenvironment by Potentiating TGF-beta Signaling in a Contact-Dependent Manner |pdf=|usr=}}{{41319267}} gab.com Text Surface-Associated Proteins on Extracellular Vesicles Remodel the Tumor Microenvironment by Potentiating TGF-beta Signaling in a Contact-Dependent Manner JO: Adv Sci (Weinh) http://www.kidney.de/pget.php?&tw=1&pmid=41319267 #FOAvip Cancer-associated fibroblasts (CAFs) are a major stromal cell type within the tumor microenvironment (TME), where they drive extracellular matrix remodeling and influence tumor progression through the secretion of bioactive molecules. Transforming growth factor-beta (TGF-beta) is a key regulator of CAF activation, yet its impact on the composition and function of extracellular vesicles (EVs) secreted by CAFs remains largely unexplored. Here, it is shown that TGF-beta activation alters the protein cargo and function of CAF-derived EVs (TGF-beta-EVs), leading to a distinct enrichment of surface-associated proteins. One such protein is tumor necrosis factor-stimulated gene-6 protein (TSG6), which interacts with receptor CD44 and its ligand hyaluronan on EVs. The EV surface-associated proteins facilitate EV docking to cell membranes by binding to transmembrane receptors. Elevated TSG6 on CAF-derived EV surface promotes the clustering of the co-receptor CD44 and TGF-beta type I receptor (TGFBR1) on recipient cells, enhancing TGF-beta signaling. Functionally, TGF-beta-EVs further activate CAFs and contribute to CD8(+) T cell immunosuppression, thereby promoting cancer progression. Overall, the findings reveal a contact-dependent mechanism by which CAF-derived EVs influence cellular signaling in the TME, suggesting a broader paradigm in which EV surface-associated proteins regulate receptor clustering and downstream signaling, particularly in cells with low EV uptake. Twit Text FOAVip Surface-Associated Proteins on Extracellular Vesicles Remodel the Tumor Microenvironment by Potentiating TGF-beta Signaling in a Contact-Dependent Manner ????Adv Sci (Weinh) http://www.kidney.de/pget.php?&tw=1&pmid=41319267 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=41319267 #FOAvip English Wikipedia <ref>{{Cite pmid|41319267}}</ref> Surface-Associated Proteins on Extracellular Vesicles Remodel the Tumor Microenvironment by Potentiating TGF-beta Signaling in a Contact-Dependent Manner #MMPMID41319267 Li C; Enciso-Martinez A; Zhu L; Rotman SA; van Veelen PA; Koning RI; Mei H; Ten Dijke P Adv Sci (Weinh) 2025[Nov]; ? (?): e13286 PMID41319267show ga Cancer-associated fibroblasts (CAFs) are a major stromal cell type within the tumor microenvironment (TME), where they drive extracellular matrix remodeling and influence tumor progression through the secretion of bioactive molecules. Transforming growth factor-beta (TGF-beta) is a key regulator of CAF activation, yet its impact on the composition and function of extracellular vesicles (EVs) secreted by CAFs remains largely unexplored. Here, it is shown that TGF-beta activation alters the protein cargo and function of CAF-derived EVs (TGF-beta-EVs), leading to a distinct enrichment of surface-associated proteins. One such protein is tumor necrosis factor-stimulated gene-6 protein (TSG6), which interacts with receptor CD44 and its ligand hyaluronan on EVs. The EV surface-associated proteins facilitate EV docking to cell membranes by binding to transmembrane receptors. Elevated TSG6 on CAF-derived EV surface promotes the clustering of the co-receptor CD44 and TGF-beta type I receptor (TGFBR1) on recipient cells, enhancing TGF-beta signaling. Functionally, TGF-beta-EVs further activate CAFs and contribute to CD8(+) T cell immunosuppression, thereby promoting cancer progression. Overall, the findings reveal a contact-dependent mechanism by which CAF-derived EVs influence cellular signaling in the TME, suggesting a broader paradigm in which EV surface-associated proteins regulate receptor clustering and downstream signaling, particularly in cells with low EV uptake. ?Surface-Associated Proteins on Extracellular Vesicles Remodel the Tumo(epmc).pdf DeepDyve Pubget Overpricing