ReviewFrontiers in genetics2019
Structural Biology of the FGF7 Subfamily.
Review in Frontiers in genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
47 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.
- Phenotypic spectrum ofPeerJ · 2022Pooled it
- Fibroblast growth factors in ischemic stroke: Therapeutic potential and clinical challenges.Acta pharmacologica Sinica · 2026Review
- Fibroblast Growth Factor 7 Limits Fibroblast-Driven Matrix Remodeling in Abdominal Aortic Aneurysm.Cardiovascular drugs and therapy · 2026Article
- A Conformal Wearable Ultrasound Bioelectronics for Mechanotherapy Reprogramming of Fibroblast Plasticity via Wnt-FGF10 Axis to Overcome Fibrotic Healing in Urethral Regeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- Fibroblast Growth Factor-7 and Hair Biology: Bridging Basic Science and Therapeutic Applications.Current issues in molecular biology · 2026Review
- FGF7 promotes load-bearing tendon regeneration and suppresses fibrosis.Nature communications · 2025Article
- Unveiling Key Genes Modulating Retinal Cell Survival and Autophagy in Glaucoma.Molecular biotechnology · 2025Article
- N-terminal helix formation and dimer-monomer transition of FGF10 in specific recognition of FGFR2b.The FEBS journal · 2025Article
- High-Fat Diet Differentially Regulates Fibroblast Growth Factor Expression in Metabolic Tissues of Young and Aged Male Mice.Journal of the Endocrine Society · 2025Article
- Pathology and Therapeutic Significance of Fibroblast Growth Factors.Targets (Basel) · 2025Article
- The Regulatory Role of CircAGGF1 in Myogenic Differentiation and Skeletal Muscle Development.Animals : an open access journal from MDPI · 2025Article
- Fibroblast Growth Factors: Roles and Emerging Therapeutic Applications.Current drug targets · 2025Review
- Signaling of Mitogenic and Metabolic Activities by Fibroblast Growth Factors.Journal of cellular signaling · 2025Article
- Decoding FGF/FGFR Signaling: Insights into Biological Functions and Disease Relevance.Biomolecules · 2024Review
- LowerBiology · 2024Article
- Article
- Screening of CAD-related secretory genes associated with type II diabetes based on comprehensive bioinformatics analysis and machine learning.BMC cardiovascular disorders · 2024Article
- The use of ectopic volar fibroblasts to modify skin identity.Science (New York, N.Y.) · 2024Article
- The Intricacies of Renal Phosphate Reabsorption-An Overview.International journal of molecular sciences · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Mammalian fibroblast growth factor (FGF) signaling is intricately regulated via selective binding interactions between 18 FGF ligands and four FGF receptors (FGFR1-4), three of which (FGFR1-3) are expressed as either epithelial ("b") or mesenchymal ("c") splice isoforms. The FGF7 subfamily, consisting of FGF3, FGF7, FGF10, and FGF22, is unique among FGFs in that its members are secreted exclusively by the mesenchyme, and specifically activate the "b" isoforms of FGFR1 (FGFR1b) and FGFR2 (FGFR2b) present in the overlying epithelium. This unidirectional mesenchyme-to-epithelium signaling contributes to the development of essentially all organs, glands, and limbs. Structural analysis has shown that members of the FGF7 subfamily achieve their restricted specificity for FGFR1b/FGFR2b by engaging in specific contacts with two alternatively spliced loop regions in the immunoglobulin-like domain 3 (D3) of these receptors. Weak basal receptor-binding affinity further constrains the FGF7 subfamily's specificity for FGFR1b/2b. In this review, we elaborate on the structural determinants of FGF7 subfamily receptor-binding specificity, and discuss how affinity differences among the four members for the heparin sulfate (HS) co-receptor contribute to their disparate biological activities.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.