{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wang Q"],"funding":["NEI NIH HHS","National Eye Institute"],"pagination":["RP103615"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12055001"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13"],"pubmed_abstract":["Fibroblast growth factor (FGF) signaling elicits multiple downstream pathways, most notably the Ras/MAPK cascade facilitated by the adaptor protein Grb2. However, the mechanism by which Grb2 is recruited to the FGF signaling complex remains unresolved. Here, we showed that genetic ablation of FGF signaling prevented murine lens induction by disrupting transcriptional regulation and actin cytoskeletal arrangements, which could be reproduced by deleting the juxtamembrane region of the FGF receptor and rescued by Kras activation. Conversely, mutations affecting the Frs2-binding site on the FGF receptor or the deletion of Frs2 and Shp2 primarily impact later stages of lens vesicle development involving lens fiber cell differentiation. Our study further revealed that the loss of Grb2 abolished "],"journal":["eLife"],"pubmed_title":["Shc1 cooperates with Frs2 and Shp2 to recruit Grb2 in FGF-induced lens development."],"pmcid":["PMC12055001"],"funding_grant_id":["R01EY025933","P30 EY019007","R01 EY018868","R01 EY017061","R01 EY025933","EY018868","K99EY032171","R01EY017061","K99 EY032171"],"pubmed_authors":["Li H","Wang Q","Garg A","Park ES","Zhang X","Peregrin J","Chow A","Mao Y","Wu Y"],"additional_accession":[]},"is_claimable":false,"name":"Shc1 cooperates with Frs2 and Shp2 to recruit Grb2 in FGF-induced lens development.","description":"Fibroblast growth factor (FGF) signaling elicits multiple downstream pathways, most notably the Ras/MAPK cascade facilitated by the adaptor protein Grb2. However, the mechanism by which Grb2 is recruited to the FGF signaling complex remains unresolved. Here, we showed that genetic ablation of FGF signaling prevented murine lens induction by disrupting transcriptional regulation and actin cytoskeletal arrangements, which could be reproduced by deleting the juxtamembrane region of the FGF receptor and rescued by Kras activation. Conversely, mutations affecting the Frs2-binding site on the FGF receptor or the deletion of Frs2 and Shp2 primarily impact later stages of lens vesicle development involving lens fiber cell differentiation. Our study further revealed that the loss of Grb2 abolished ","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 May","modification":"2026-05-29T15:19:42.341Z","creation":"2026-04-08T05:16:27.413Z"},"accession":"S-EPMC12055001","cross_references":{"pubmed":["40327534"],"doi":["10.7554/eLife.103615"]}}