Ab'/> Dephosphorylation is the mechanism of fibroblast growth factor inhibition of guanylyl cyclase-B
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Dephosphorylation is the mechanism of fibroblast growth factor inhibition of guanylyl cyclase-B

机译：去磷酸化是围式环胞嘧啶-B的成纤维细胞生长因子抑制的机制

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AbstractActivating 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.Highlights?Guanylyl cyclase-B is expressed in rat chondrosarcoma cells.?FGF2 induces a rapid, potent, and reversible inhibition of GC-B.?
机译：<！[cdata [ 抽象 激活成纤维细胞生长因子受体3（FGFR3）中的激活突变和瓜武环酶-B的灭活突变（GC-B ，也称为NPRB或NPR2）导致侏儒症。 FGF暴露抑制软骨细胞系中的GC-B活性，但灭活的机制是不知道的。在这里，我们认为FGF暴露导致大鼠软骨肉瘤细胞中GC-B的脱磷酸化，其与GC-B的C型Natriesurect肽依赖性活化的快速，有效且可逆抑制相关。表达GC-B的磷酸化突变体的细胞不能通过去磷酸化灭活，因为它含有谷氨酸取代，用于所有已知的磷酸化位点，响应于FGF而没有降低GC-B活性。我们得出结论，FGF通过可逆的去磷酸化机制迅速灭活GC-B，这可能导致激活的FGFR3导致侏儒症的信令网络。 突出显示 ？ uAnylyl cyclase-b在大鼠软骨肉瘤细胞中表达。 < CE：list-item id =“li0010”> ？ FGF2诱导GC的快速，有效和可逆抑制GC -B。 ？

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