Journal
GENES & DEVELOPMENT
Volume 30, Issue 7, Pages 751-771Publisher
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gad.277137.115
Keywords
fibroblast growth factor; Fgfr; receptor tyrosine kinase; Erk1/2; signaling
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Funding
- National Institutes of Health (NIH)/National Institute of Dental and Craniofacial Research (NIDCR) grant [RO1 DE022778]
- New York State Stem Cell Science (NYSTEM) grant [IIRP N11G-131]
- NIH/NIDCR fellowship [F31 DE023686]
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The fibroblast growth factor (Fgf) family of ligands and receptor tyrosine kinases is required throughout embryonic and postnatal development and also regulates multiple homeostatic functions in the adult. Aberrant Fgf signaling causes many congenital disorders and underlies multiple forms of cancer. Understanding the mechanisms that govern Fgf signaling is therefore important to appreciate many aspects of Fgf biology and disease. Here we review the mechanisms of Fgf signaling by focusing on genetic strategies that enable in vivo analysis. These studies support an important role for Erk1/2 as a mediator of Fgf signaling in many biological processes but have also provided strong evidence for additional signaling pathways in transmitting Fgf signaling in vivo.
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