The ins and outs of fibroblast growth factors

Mason, Ivor

doi:10.1016/0092-8674(94)90520-7

Cited by 515 publications

(298 citation statements)

References 29 publications

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“…The ®broblast growth factors (FGFs) comprise a family of at least 18 growth factors and oncogenes that share a signi®cant degree of sequence homology and often exhibit overlapping biological activities (for reviews, see Fernig and Gallagher, 1994;Mason, 1994). Individual FGFs play important roles in various physiological and pathological processes, including embryonic development, cell growth, tissue repair, morphogenesis, in¯ammation, angiogenesis, vascular tone (Zhou et al, 1998), and tumor growth and invasion (reviewed by Mason, 1994).…”

Section: Introductionmentioning

confidence: 99%

“…Individual FGFs play important roles in various physiological and pathological processes, including embryonic development, cell growth, tissue repair, morphogenesis, in¯ammation, angiogenesis, vascular tone (Zhou et al, 1998), and tumor growth and invasion (reviewed by Mason, 1994). FGF-1 (acidic FGF) and FGF-2 (basic FGF) were identi®ed as mitogens for a variety of cell types (Gospodarowicz et al, 1978(Gospodarowicz et al, , 1986, whereas FGF-3 (int-2), FGF-4 (hst/K-FGF) and FGF-5 were ®rst identi®ed as oncogenes (reviewed by Basilico and Moscatelli, 1992;Burgess and Maciag, 1989).…”

Section: Introductionmentioning

confidence: 99%

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Human fibroblast growth factor-18 stimulates fibroblast cell proliferation and is mapped to chromosome 14p11

Wang

Qiu

1999

Oncogene

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Human fibroblast growth factor-18 stimulates fibroblast cell proliferation and is mapped to chromosome 14p11

Wang

Qiu

1999

Oncogene

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“…FGFs can also induce di erentiation of certain cell types or inhibit di erentiation (e.g. of myoblasts into myotubes) Mason, 1994). The action of FGFs is mediated by their interaction with high a nity RTKs.…”

Section: Introductionmentioning

confidence: 99%

Activation of FGF receptors by mutations in the transmembrane domain

Mangasarian

Mansukhani

et al. 1997

Oncogene

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Signaling through FGF receptors, which constitute a family of membrane-spanning tyrosine kinases, can stimulate cell proliferation, induce or inhibit cell di erentiation and plays an important role in development. Recently, mutations in FGF receptors have been shown to be associated with a number of genetically dominant human skeletal disorders. A remarkably conserved mutation (Gly 380?Arg) in the transmembrane region of FGFR-3 has been shown to be responsible for achondroplasia (ACH) but it was not clear whether such mutations result in loss of receptor function or constitutive activation. We have therefore made mutations in the transmembrane regions of murine FGFR-2 and FGFR-3 and studied their e ect on receptor activity. We show here that the ACH mutation in FGFR-3 as well as two similar mutations in FGFR-2 result in constitutive activation of these receptors. This is manifested in their ability to become autophosphorylated in the absence of ligand in L6 cells, transforming activity on NIH3T3 ®broblasts, and the ability to inhibit myogenic di erentiation in the absence of growth factor. Thus the transmembrane region of FGFR-2 and FGFR-3 plays a regulatory role in receptor function and the ACH mutation produces a dominant oversignaling receptor which is no longer regulated by FGF binding. These ®ndings also support the newly identi®ed role of FGF signaling as a negative regulator of bone growth.

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“…Growth Factors, Signaling Molecules, and Their Receptors-Soluble/ diffusible molecules involved in formation and patterning of mesoderm include growth factors from the WNT family (McMahon et al, 1992;Parr and McMahon, 1994), the fibroblast growth factor (FGF) family (Mason, 1994), and the transforming growth factor (TGFβ) superfamily (Kingsley, 1994b) and their respective receptors (Attisano et al, 1994;Givol and Yayon, 1992). Inactivation of the Wnt3a gene impairs development of dorsal, somitic mesoderm, and Ieads to a disrupted notochord, a lack of caudal somites, and a failure of tail bud formation.…”

Section: Gastrulation and Formation Of Paraxial Mesodermmentioning

confidence: 99%

Molecular basis for skeletal variation: insights from developmental genetic studies in mice

Kappen

Neubüser

Balling

et al. 2007

Birth Defects Research Pt B

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Skeletal variations are common in humans, and potentially are caused by genetic as well as environmental factors. We here review molecular principles in skeletal development to develop a knowledge base of possible alterations that could explain variations in skeletal element number, shape or size. Environmental agents that induce variations, such as teratogens, likely interact with the molecular pathways that regulate skeletal development. Birth Defects Res (Part B), 80:425–450, 2007. © 2007 Wiley‐Liss, Inc.

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The ins and outs of fibroblast growth factors

Cited by 515 publications

References 29 publications

Human fibroblast growth factor-18 stimulates fibroblast cell proliferation and is mapped to chromosome 14p11

Human fibroblast growth factor-18 stimulates fibroblast cell proliferation and is mapped to chromosome 14p11

Activation of FGF receptors by mutations in the transmembrane domain

Molecular basis for skeletal variation: insights from developmental genetic studies in mice

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