Membrane and Integrative Nuclear Fibroblastic Growth Factor Receptor (FGFR) Regulation of FGF-23

Han, Xiaobin; Xiao, Zhousheng; Quarles, L. Darryl

doi:10.1074/jbc.m114.609230

Cited by 47 publications

(33 citation statements)

References 65 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Low-molecular-weight FGF2 stimulates FGF23 promoter activity through PLCγ/NFAT and MAPK signaling, whereas high-molecular-weight FGF2 promotes FGF23 promoter activity through cAMP-dependent binding of FGFR1 and CREB to a conserved cAMP response element in the FGF23 promoter (Han et al 2015). Consistently, conditional deletion of Fgfr1 in osteocytes of Hyp mice, a mouse model of XLH, reduced the excessive FGF23 levels produced by osteocytes and partially rescued the bone phenotype in these mice .…”

Section: Fgf/fgfr Signaling In Osteoblastogenesismentioning

confidence: 75%

Fibroblast growth factor signaling in skeletal development and disease

2015

View full text Add to dashboard Cite

Fibroblast growth factor (FGF) signaling pathways are essential regulators of vertebrate skeletal development. FGF signaling regulates development of the limb bud and formation of the mesenchymal condensation and has key roles in regulating chondrogenesis, osteogenesis, and bone and mineral homeostasis. This review updates our review on FGFs in skeletal development published in Genes & Development in 2002, examines progress made on understanding the functions of the FGF signaling pathway during critical stages of skeletogenesis, and explores the mechanisms by which mutations in FGF signaling molecules cause skeletal malformations in humans. Links between FGF signaling pathways and other interacting pathways that are critical for skeletal development and could be exploited to treat genetic diseases and repair bone are also explored.

show abstract

Section: Fgf/fgfr Signaling In Osteoblastogenesismentioning

confidence: 75%

Fibroblast growth factor signaling in skeletal development and disease

2015

View full text Add to dashboard Cite

show abstract

“…Together, these findings suggest that hyperphosphatemia may represent a side effect of FGFR TK inhibitors rather than of extracellular inhibitors of the FGF/FGFR system. Given that both FGF23 expression and activity are under the control of a complex mechanism of regulation that includes canonical, non-canonical and intracrine FGF/FGFR pathways [158], further studies are required to elucidate this point.…”

Section: Discussionmentioning

confidence: 99%

Blocking the FGF/FGFR system as a ⿿two-compartment⿿ antiangiogenic/antitumor approach in cancer therapy

Giacomini

Chiodelli

Matarazzo

et al. 2016

Pharmacological Research

View full text Add to dashboard Cite

a b s t r a c tFibroblast growth factors (FGFs) are a family of pleiotropic factors produced by stromal and parenchymal tumor cells. Even though FGFs have been firstly characterized as angiogenic factors, they exert autocrine and paracrine functions not only on endothelial cells but also on tumor cells and other stromal components. Thus, the FGF/FGF receptor (FGFR) pathway may represent a key player in tumor growth by regulating the complex cross-talk between stromal and tumor compartments.The ligand dependent or independent activation of the FGF/FGFR system by gene upregulation, oncogenic mutation or amplification occurs in a variety of human tumors and is implicated in various key steps of tumor growth and progression. In addition, FGF/FGFR activation has been described as a mechanism of tumor escape in response to antiangiogenic/anti-VEGF therapies.Experimental and clinical evidences provide a compelling biologic rationale for the development of anti-FGF/FGFR targeting agents in cancer therapy. However, the development of drugs specifically targeting the FGF/FGFR pathway proved to be difficult, also due to the high redundancy and pleiotropic effects of FGF and FGFR family members. On the other hand, the possibility to develop "two-compartment" targeting agents endowed with both antiangiogenic and antitumor activities remains promising.Here we will review the preclinical and clinical approaches and potential therapeutics currently available to block the FGF/FGFR system in human cancer.

show abstract

“…One of the bone development controlling genes is FGF‐23 (Han et al, 2015a). In mouse ESCs only trace levels of FGF23 mRNA are detected and are further diminished in NCs (Terranova et al, 2015).…”

Section: Nfgfr1 Regulation Of Endodermal and Mesodermal Genesmentioning

confidence: 99%

Evidence‐Based Theory for Integrated Genome Regulation of Ontogeny—An Unprecedented Role of Nuclear FGFR1 Signaling

Stachowiak

2016

Journal Cellular Physiology

View full text Add to dashboard Cite

Genetic experiments have positioned the fgfr1 gene at the top of the gene hierarchy that governs gastrulation, as well as the subsequent development of the major body axes, nervous system, muscles, and bones, by affecting downstream genes that control the cell cycle, pluripotency, and differentiation, as well as microRNAs. Studies show that this regulation is executed by a single protein, the nuclear isoform of FGFR1 (nFGFR1), which integrates signals from development‐initiating factors, such as retinoic acid (RA), and operates at the interface of genomic and epigenomic information. nFGFR1 cooperates with a multitude of transcriptional factors (TFs), and targets thousands of genes encoding for mRNAs, as well as miRNAs in top ontogenic networks. nFGFR1 binds to the promoters of ancient proto‐oncogenes and tumor suppressor genes, in addition to binding to metazoan morphogens that delineate body axes, and construct the nervous system, as well as mesodermal and endodermal tissues. The discovery of pan‐ontogenic gene programming by integrative nuclear FGFR1 signaling (INFS) impacts our understanding of ontogeny, as well as developmental pathologies, and holds new promise for reconstructive medicine, and cancer therapy. J. Cell. Physiol. 231: 1199–1218, 2016. © 2016 The Authors. Journal of Cellular Physiology published by Wiley Periodicals, Inc.

show abstract

Membrane and Integrative Nuclear Fibroblastic Growth Factor Receptor (FGFR) Regulation of FGF-23

Cited by 47 publications

References 65 publications

Fibroblast growth factor signaling in skeletal development and disease

Fibroblast growth factor signaling in skeletal development and disease

Blocking the FGF/FGFR system as a ⿿two-compartment⿿ antiangiogenic/antitumor approach in cancer therapy

Evidence‐Based Theory for Integrated Genome Regulation of Ontogeny—An Unprecedented Role of Nuclear FGFR1 Signaling

Contact Info

Product

Resources

About