Dephosphorylation is the mechanism of fibroblast growth factor inhibition of guanylyl cyclase-B.

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  • Additional Information
    • Source:
      Publisher: Elsevier Science Ltd Country of Publication: England NLM ID: 8904683 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1873-3913 (Electronic) Linking ISSN: 08986568 NLM ISO Abbreviation: Cell Signal Subsets: MEDLINE
    • Publication Information:
      Publication: Oxford : Elsevier Science Ltd
      Original Publication: Oxford ; New York : Pergamon Press, 1988-
    • Subject Terms:
      Dwarfism/*genetics ; Natriuretic Peptide, C-Type/*genetics ; Receptor, Fibroblast Growth Factor, Type 3/*genetics ; Receptors, Atrial Natriuretic Factor/*genetics; Animals ; Chondrocytes/metabolism ; Cyclic GMP/genetics ; Disease Models, Animal ; Dwarfism/metabolism ; Dwarfism/pathology ; Glutamic Acid/metabolism ; Humans ; Phosphorylation ; Rats ; Receptor, Fibroblast Growth Factor, Type 3/metabolism ; Receptors, Atrial Natriuretic Factor/metabolism ; Signal Transduction
    • Abstract:
      Activating mutations in fibroblast growth factor receptor 3 (FGFR3) and inactivating mutations of guanylyl cyclase-B (GC-B, also called NPRB or NPR2) cause dwarfism. FGF exposure inhibits GC-B activity in a chondrocyte cell line, but the mechanism of the inactivation is not known. Here, we report that FGF exposure causes dephosphorylation of GC-B in rat chondrosarcoma cells, which correlates with a rapid, potent and reversible inhibition of C-type natriuretic peptide-dependent activation of GC-B. Cells expressing a phosphomimetic mutant of GC-B that cannot be inactivated by dephosphorylation because it contains glutamate substitutions for all known phosphorylation sites showed no decrease in GC-B activity in response to FGF. We conclude that FGF rapidly inactivates GC-B by a reversible dephosphorylation mechanism, which may contribute to the signaling network by which activated FGFR3 causes dwarfism.
      (Copyright © 2017 Elsevier Inc. All rights reserved.)
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    • Grant Information:
      R01 CA174861 United States CA NCI NIH HHS; R01 GM098309 United States GM NIGMS NIH HHS; R37 HD014939 United States HD NICHD NIH HHS; T32 DK007203 United States DK NIDDK NIH HHS
    • Contributed Indexing:
      Keywords: Achondroplasia; C-type natriuretic peptide; Cyclic GMP; Dwarfism; Fibroblast growth factor; Guanylyl cyclase; NPR2
    • Accession Number:
      127869-51-6 (Natriuretic Peptide, C-Type)
      3KX376GY7L (Glutamic Acid)
      EC 2.7.10.1 (Receptor, Fibroblast Growth Factor, Type 3)
      EC 4.6.1.2 (Receptors, Atrial Natriuretic Factor)
      EC 4.6.1.2 (atrial natriuretic factor receptor B)
      H2D2X058MU (Cyclic GMP)
    • Publication Date:
      Date Created: 20171002 Date Completed: 20180613 Latest Revision: 20210429
    • Publication Date:
      20240829
    • Accession Number:
      PMC5651182
    • Accession Number:
      10.1016/j.cellsig.2017.09.021
    • Accession Number:
      28964968