ReviewF1000Research2018
A threshold model for receptor tyrosine kinase signaling specificity and cell fate determination.
Review in F1000Research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
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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
48 citing papers in PubMed, 64 citations in OpenAlex.
- Growth factor applications and clinical translation: advances and challenges.Annals of medicine · 2026Review
- Article
- Mechanisms and Manifestations of Ligand Bias in Signaling: Focus on Receptor Tyrosine Kinases.Chemical reviews · 2026Review
- KRAS signaling networks, mutational heterogeneity, and emerging therapeutic strategies for cancer treatment.Biomarker research · 2026Review
- Engineered fibroblast growth factor 1 variants uncouple glucose-lowering effects from mitogenic activity with therapeutic potential for type 2 diabetes.Molecular biomedicine · 2026Article
- The role of fibroblast growth factors in cell and cancer metabolism.FEBS letters · 2026Review
- Colonic epithelial-derived FGF1 drives intestinal stem cell commitment toward goblet cells to suppress inflammatory bowel disease.Nature communications · 2025Article
- Visualizing the Cellular and Subcellular Distribution of Fms-like Tyrosine Kinase 3 (Flt3) and Other Neuronal Proteins Using Alkaline Phosphatase (AP) Immunolabeling.International journal of molecular sciences · 2025Article
- Hepatocyte-Derived FGF1 Alleviates Isoniazid and Rifampicin-Induced Liver Injury by Regulating HNF4α-Mediated Bile Acids Synthesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- A viral insulin-like peptide inhibits IGF-1 receptor phosphorylation and regulates IGF1R gene expression.Molecular metabolism · 2024Article
- Article
- Quantification of ligand and mutation-induced bias in EGFR phosphorylation in direct response to ligand binding.Nature communications · 2023Article
- Quantitative assessment of ligand bias from bias plots: The bias coefficient "kappa".Biochimica et biophysica acta. General subjects · 2023Article
- Molecular and cellular factors determining the functional pleiotropy of cytokines.The FEBS journal · 2023Review
- Receptor clustering by a precise set of extracellular galectins initiates FGFR signaling.Cellular and molecular life sciences : CMLS · 2023Article
- Platelets, Protean Cells with All-Around Functions and Multifaceted Pharmacological Applications.International journal of molecular sciences · 2023Review
- Editorial: Special 2021 Frontiers in Endocrinology collection for the 100Frontiers in endocrinology · 2023Article
- Functional selectivity of Receptor Tyrosine Kinases regulates distinct cellular outputs.Frontiers in cell and developmental biology · 2023Review
- New developments in the biology of fibroblast growth factors.WIREs mechanisms of disease · 2022Review
- Activation of neurotrophin signalling with light‑inducible receptor tyrosine kinases.Molecular medicine reports · 2022Article
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
Upon ligand engagement, the single-pass transmembrane receptor tyrosine kinases (RTKs) dimerize to transmit qualitatively and quantitatively different intracellular signals that alter the transcriptional landscape and thereby determine the cellular response. The molecular mechanisms underlying these fundamental events are not well understood. Considering recent insights into the structural biology of fibroblast growth factor signaling, we propose a threshold model for RTK signaling specificity in which quantitative differences in the strength/longevity of ligand-induced receptor dimers on the cell surface lead to quantitative differences in the phosphorylation of activation loop (A-loop) tyrosines as well as qualitative differences in the phosphorylation of tyrosines mediating substrate recruitment. In this model, quantitative differences on A-loop tyrosine phosphorylation result in gradations in kinase activation, leading to the generation of intracellular signals of varying amplitude/duration. In contrast, qualitative differences in the pattern of tyrosine phosphorylation on the receptor result in the recruitment/activation of distinct substrates/intracellular pathways. Commensurate with both the dynamics of the intracellular signal and the types of intracellular pathways activated, unique transcriptional signatures are established. Our model provides a framework for engineering clinically useful ligands that can tune receptor dimerization stability so as to bias the cellular transcriptome to achieve a desired cellular output.
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What OpenQuestion 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 OpenQuestion graph.