Structural basis for fibroblast growth factor receptor activation

Mohammadi, Moosa; Olsen, Shaun K.; Ibrahimi, Omar A.

doi:10.1016/j.cytogfr.2005.01.008

Cited by 643 publications

(645 citation statements)

References 159 publications

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“…To do this, we removed the retina at E4 and added FGF7 (also called keratinocyte growth factor, KGF) to the eye. FGF7 preferentially binds to FGFR2 isoform IIIb (FGFR2-IIIb; reviewed in Itoh and Ornitz, 2004;Mohammadi et al, 2005). After 3 days of exposure to FGF7, we observed some regeneration from the CB/CMZ (not shown), although this was not as robust as regeneration stimulated by FGF2.…”

Section: Shh Up-regulates Fgf and Fgfr1 Mrnamentioning

confidence: 89%

Fibroblast growth factor–hedgehog interdependence during retina regeneration

Spence

Aycinena

Rio‐Tsonis

2007

Developmental Dynamics

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Section: Shh Up-regulates Fgf and Fgfr1 Mrnamentioning

confidence: 89%

Fibroblast growth factor–hedgehog interdependence during retina regeneration

Spence

Aycinena

Rio‐Tsonis

2007

Developmental Dynamics

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“…In general, in order for FGF to bind to and activate the FGFR system, heparin sulphate proteoglycans or heparin-like molecules are required (Amaya et al, 1991;Mohammadi et al, 2005a;Mohammadi et al, 2005b;Ornitz et al, 1992) FGF-23 is a recently identified member of the FGF family, and is significantly distinct from other FGFs in that it contains a proconvertase processing site. Whether FGF-23 also needs heparin-like molecules to activate the FGFR system is an intense area of research (Yu et al, 2005), but it is becoming increasingly clear that FGF-23 needs klotho as a cofactor to induce its receptor activities to exert biological effects.…”

Section: Fgf-23 Klotho and Receptor Interactionsmentioning

confidence: 99%

Premature aging in klotho mutant mice: Cause or consequence?

Lanske¹,

Razzaque²

2007

Ageing Research Reviews

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Suitable mammalian models for aging with wide range of age-associated pathology are desirable to study molecular mechanisms of human aging. Recent studies have identified that fibroblast growth factor 23 (Fgf-23) null mice and klotho hypomorphs could generate multiple premature aging-like features, including shortened lifespan, infertility, kyphosis, atherosclerosis, extensive soft tissue calcifications, skin atrophy, muscle wasting, T-cell dysregulation, pulmonary emphysema, osteoporosis/osteopenia, abnormal mineral ion metabolism, and impaired vitamin-D homeostasis. The strikingly similar in vivo phenotypes of two separate genetically altered mouse lines implicate that the premature aging-like features may be partly regulated through a common signaling pathway involving both Fgf-23 and klotho; such speculation is experimentally supported by the observation that Fgf-23 requires klotho as a cofactor to exert its functions. Despite about 2,000 fold higher serum levels of Fgf-23 in klotho mutants (compared to wild-type animals), these mice show physical, biochemical and morphological features similar to Fgf-23 null mice, but not as Fgf-23 transgenic mice; these observations suggest that widely encountered premature aging-like features in klotho mutant mice are due to the inability of Fgf-23 to exert its bioactivities in absence of klotho. The results of recent studies showing klotho as a cofactor in Fgf-23 signaling consequently explains that the premature aging-like features in klotho deficient mice is not a primary cause, rather a consequence of lacking Fgf-23 activity. These understandings will help us to redefine the role of klotho as an aging factor. Keywords FGF-23; Kotho; Vitamin-D; Calcification; Premature aging Phosphate homeostasisMaintaining phosphate homeostasis is of crucial biological importance, as it regulates fundamental cellular functions and skeletal mineralization; it is also an important component of nucleic acids, biologically active signaling proteins, coenzymes, and lipid bilayer of the cell membranes. Ingested phosphate is mostly absorbed in the small intestine and is either incorporated in cells in organic forms, deposited as a component of bone mineral, or eliminated by the kidney; the rate of renal reabsorption and/or excretion is determined by the specific needs of the body.Roughly 70% of the phosphate is absorbed in the duodenum and jejunum, through a sodiumdependent active transport, a process stimulated by 1,25-dihydroxyvitamin D 3 [1,25 (OH) 2 D 3 ]; besides parathyroid hormone (PTH) and low-phosphate diets can also stimulate Corresponding authors: Tel.

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“…The FGF family comprises 23 distinct, structurally-related proteins described to date that exert biologic effects in different cells and organ systems, including tumor growth and angiogenesis (82)(83)(84)(85). FGFs are heparin-binding proteins, which interact with low affinity heparan sulfate proteoglycans (HSPGs).…”

Section: Fibroblast Growth Factors and Fibroblast Growth Factor-bindimentioning

confidence: 99%

The Angiogenic Switch Molecule, Secreted FGF-Binding Protein, an Indicator of Early Stages of Pancreatic and Colorectal Adenocarcinoma

Tassi

Wellstein

2006

Seminars in Oncology

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Tumor angiogenesis has been related to the initiation as well as progression toward more aggressive behavior of human tumors. We will discuss genetic events underlying the initiation and progression of colorectal and pancreatic adenocarcinoma with a particular focus on the modulation of angiogenesis. A secreted fibroblast growth factor (FGF) binding protein (FGF-BP), which is an extracellular chaperone molecule for FGFs, has been shown to enhance FGF-mediated biochemical and biologic events and to be a crucial rate-limiting factor for tumor-dependent angiogenesis. Histochemical and in situ hybridization studies with archival samples show that FGF-BP is induced early during the initiation of colorectal and pancreatic adenocarcinoma. We will discuss the potential of this secreted protein as a serum marker to identify at-risk subjects.

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Structural basis for fibroblast growth factor receptor activation

Cited by 643 publications

References 159 publications

Fibroblast growth factor–hedgehog interdependence during retina regeneration

Fibroblast growth factor–hedgehog interdependence during retina regeneration

Premature aging in klotho mutant mice: Cause or consequence?

The Angiogenic Switch Molecule, Secreted FGF-Binding Protein, an Indicator of Early Stages of Pancreatic and Colorectal Adenocarcinoma

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