ArticleThe Journal of biological chemistry2013
Fibroblast growth factor receptor like-1 (FGFRL1) interacts with SHP-1 phosphatase at insulin secretory granules and induces beta-cell ERK1/2 protein activation.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
30 citing papers in PubMed, 50 citations in OpenAlex.
- FGFR1 signaling in rheumatoid arthritis: Mechanisms of bone destruction and therapeutic targeting (Review).International journal of molecular medicine · 2026Review
- FGFR Like1 drives esophageal cancer progression via EMT, PI3K/Akt, and notch signalling: insights from clinical data and next-generation sequencing analysis.FEBS open bio · 2026Article
- FGFRL1: Structure, Molecular Function, and Involvement in Human Disease.Current issues in molecular biology · 2025Review
- Review
- Aberrant Expression of FGFRL1 in Esophageal Cancer and Its Regulation by miR-107.Asian Pacific journal of cancer prevention : APJCP · 2023Article
- Laminin matrix regulates beta-cell FGFR5 expression to enhance glucose-stimulated metabolism.Scientific reports · 2022Article
- Src acts with WNT/FGFRL signaling to pattern the planarian anteroposterior axis.Development (Cambridge, England) · 2022Article
- Molecular study of the proliferation process of beta cells derived from pluripotent stem cells.Molecular biology reports · 2022Review
- Article
- Review
- The aging mouse lens transcriptome.Experimental eye research · 2021Article
- Pathophysiological Implications of Imbalances in Fibroblast Growth Factor 23 in the Development of Diabetes.Journal of clinical medicine · 2021Review
- Review
- Fibroblast Growth Factor Receptors (FGFRs) and Noncanonical Partners in Cancer Signaling.Cells · 2021Review
- Cell Type-specific Adaptive Signaling Responses to KRASClinical cancer research : an official journal of the American Association for Cancer Research · 2021Article
- FGFRL1 affects chemoresistance of small-cell lung cancer by modulating the PI3K/Akt pathway via ENO1.Journal of cellular and molecular medicine · 2020Article
- Establishment of an erythroid progenitor cell line capable of enucleation achieved with an inducible c-Myc vector.BMC biotechnology · 2019Article
- MicroRNA and Human Bone Health.JBMR plus · 2019Review
- Targeting Cellular Trafficking of Fibroblast Growth Factor Receptors as a Strategy for Selective Cancer Treatment.Journal of clinical medicine · 2018Review
- Fibroblast growth factor receptor 5 (FGFR5) is a co-receptor for FGFR1 that is up-regulated in beta-cells by cytokine-induced inflammation.The Journal of biological chemistry · 2018Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
FGFRL1 is a newly identified member of the fibroblast growth factor receptor (FGFR) family expressed in adult pancreas. Unlike canonical FGFRs that initiate signaling via tyrosine kinase domains, the short intracellular sequence of FGFRL1 consists of a putative Src homology domain-2 (SH2)-binding motif adjacent to a histidine-rich C terminus. As a consequence of nonexistent kinase domains, FGFRL1 has been postulated to act as a decoy receptor to inhibit canonical FGFR ligand-induced signaling. In pancreatic islet beta-cells, canonical FGFR1 signaling affects metabolism and insulin processing. This study determined beta-cell expression of FGFRL1 as well as consequent effects on FGFR1 signaling and biological responses. We confirmed FGFRL1 expression at the plasma membrane and within distinct intracellular granules of both primary beta-cells and βTC3 cells. Fluorescent protein-tagged FGFRL1 (RL1) induced a significant ligand-independent increase in MAPK signaling. Removal of the histidine-rich domain (RL1-ΔHis) or entire intracellular sequence (RL1-ΔC) resulted in greater retention at the plasma membrane and significantly reduced ligand-independent ERK1/2 responses. The SHP-1 phosphatase was identified as an RL1-binding substrate. Point mutation of the SH2-binding motif reduced the ability of FGFRL1 to bind SHP-1 and activate ERK1/2 but did not affect receptor localization to insulin secretory granules. Finally, overexpression of RL1 increased cellular insulin content and matrix adhesion. Overall, these data suggest that FGFRL1 does not function as a decoy receptor in beta-cells, but rather it enhances ERK1/2 signaling through association of SHP-1 with the receptor's intracellular SH2-binding motif.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.