ArticleMolecular and cellular biology2009
Structural and functional basis of a role for CRKL in a fibroblast growth factor 8-induced feed-forward loop.
Article in Molecular and cellular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 36 citations in OpenAlex.
- The Caenorhabditis elegans protein SOC-3 permits an alternative mode of signal transduction by the EGL-15 FGF receptor.Developmental biology · 2024Article
- FGF1 ameliorates obesity-associated hepatic steatosis by reversing IGFBP2 hypermethylation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- Fibroblast growth factor signalling influences homologous recombination-mediated DNA damage repair to promote drug resistance in ovarian cancer.British journal of cancer · 2022Article
- Modeling development of genitourinary birth defects to understand disruption due to changes in gene dosage.American journal of clinical and experimental urology · 2022Review
- Fibroblast Growth Factor Receptors (FGFRs) and Noncanonical Partners in Cancer Signaling.Cells · 2021Review
- Fibroblast growth factor signalling in osteoarthritis and cartilage repair.Nature reviews. Rheumatology · 2020Review
- Targeting FGFR overcomes EMT-mediated resistance in EGFR mutant non-small cell lung cancer.Oncogene · 2019Article
- Paracrine Fibroblast Growth Factor 1 Functions as Potent Therapeutic Agent for Intrahepatic Cholestasis by Downregulating Synthesis of Bile Acid.Frontiers in pharmacology · 2019Article
- Targeting of FGF-Signaling Re-Sensitizes Gastrointestinal Stromal Tumors (GIST) to Imatinib In Vitro and In Vivo.Molecules (Basel, Switzerland) · 2018Article
- Article
- Uncoupling the Mitogenic and Metabolic Functions of FGF1 by Tuning FGF1-FGF Receptor Dimer Stability.Cell reports · 2017Article
- Murine model indicates 22q11.2 signaling adaptorProceedings of the National Academy of Sciences of the United States of America · 2017Article
- Fibroblast growth factors, old kids on the new block.Seminars in cell & developmental biology · 2016Review
- Genetic insights into the mechanisms of Fgf signaling.Genes & development · 2016Review
- Molecular mechanisms of fibroblast growth factor signaling in physiology and pathology.Cold Spring Harbor perspectives in biology · 2013Review
- The neural crest in cardiac congenital anomalies.Differentiation; research in biological diversity · 2012Review
- Domain organization differences explain Bcr-Abl's preference for CrkL over CrkII.Nature chemical biology · 2012Article
- Plasticity in interactions of fibroblast growth factor 1 (FGF1) N terminus with FGF receptors underlies promiscuity of FGF1.The Journal of biological chemistry · 2012Article
- The structural biology of the FGF19 subfamily.Advances in experimental medicine and biology · 2012Review
- A specific need for CRKL in p210BCR-ABL-induced transformation of mouse hematopoietic progenitors.Cancer research · 2010Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
The adapter protein CRKL is required for the normal development of multiple tissues that rely on fibroblast growth factor 8 (FGF8). The precise role of CRKL in receptor signaling has been unclear, however. To address this issue, we first modeled the three-dimensional structure of CRKL by molecular dynamics. By taking advantage of structural simulations, we performed in silico analysis of the interactions of the autophosphorylation sites of FGR receptor 1 (FGFR1) with the SH2 domain of CRKL or a highly related protein, CRK. As predicted by simulations, we confirm the specific physical interaction of phosphorylated Y463 (pY463) in FGFR1 with the CRKL SH2 domain at an affinity approximately 30-fold stronger than that of CRK. We also provide evidence that interactions outside of the core YXXP motif have a significant impact on physical association, which is consistent with predictions from molecular-dynamics simulations. Furthermore, we identify CRKL as an essential component of an FGF8-induced feed-forward loop permissive for efficient activation of the mitogen-activated protein kinase Erk1/2, as well as FGF8-induced anchorage-independent cell growth, using Crkl-deficient cells or a pY463 synthetic peptide. Although many cells generally require cell-matrix adhesion, our results demonstrate that CRKL permits cells to bypass the strict need for adhesion in response to FGF8 through direct interaction with receptor.
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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 Socratic graph.