Fibroblast Growth Factor 14 Proteins (FGF14)

Human Fibroblast Growth Factor 14 (FGF14) interaction partners

1. The data implicate FGF14 as an organizer of channel localization in the axon initial segment and provide insight into the coordination of KCNQ (show KCNQ1 Proteins) and voltage-gated sodium channel conductances in the regulation of membrane potential.

2. Either the FGF14(V160A) or the FGF14(K74A/I76A) mutation was sufficient to abolish the FGF14-dependent regulation of peak transient Na(+) currents and the voltage-dependent activation and steady-state inactivation of Nav1.6 (show SCN8A Proteins); but only V160A with a concomitant alanine mutation at Tyr (show TYR Proteins)-158 could impede FGF14-dependent modulation of the channel fast inactivation.

3. study reports on a two-generation French Canadian family affected with autosomal dominant episodic ataxia caused by a frameshift mutation leading to a premature stop codon in FGF14

4. identified the PI3K/Akt pathway, the cell-cycle regulator Wee1 kinase, and protein kinase C (PKC) as prospective regulatory nodes of neuronal excitability through modulation of the FGF14:Nav1.6 complex.

5. family demonstrates phenotypic variability of FGF14 deletions (SCA 27), fever sensitivity of ataxia and the added value of SNP-array analysis in making a diagnosis

6. inhibition of GSK3 reduces the assembly of the FGF14.Nav channel complex, modifies FGF14-dependent regulation of Na(+) currents, and induces dissociation and subcellular redistribution of the native FGF14.Nav channel complex in hippocampal neurons.

7. THe present study demonstrates that Spinocerebellar ataxia type 27 (SCA27) caused by FGF14 mutation is rare in Chinese SCA patients.

8. A mutation in the fibroblast growth factor 14 gene is associated with autosomal dominant cerebral ataxia

9. A G->A variant was found in a single spinocerebellar ataxia patient in the 3' untranslated region, 31 bp to the STOP codon; it did not affect the polyadenylation site. FGF14 mutations are not a major cause of SCA in Caucasians.

10. Frameshift mutation and polymorphisms in the fibroblast growth factor 14 gene is associated with ataxias

Mouse (Murine) Fibroblast Growth Factor 14 (FGF14) interaction partners

1. These new insights into the biology of FGF14 in neurogenesis shed light into the signaling pathways associated with disrupted functions in complex brain diseases.

2. These results indicate that Fgf14(-/-) mice recapitulate salient molecular, cellular, functional and behavioral features associated with human cognitive impairment, and FGF14 loss of function might be associated with the biology of complex brain disorders such as schizophrenia.

3. TWEAK (show TNFSF12 Proteins)/Fn14 (show TNFRSF12A Proteins) pathway instrumental in the pathogenesis of spontaneous lupus nephritis

4. FGF14 is localized in a decreasing proximal to distal gradient along the axon initial segment of Purkinje neurons.

5. FGF14 regulates presynaptic Ca2 (show CA2 Proteins)+ channels and synaptic transmission in cultured rat neurons.

6. inhibition of GSK3 reduces the assembly of the FGF14.Nav channel complex, modifies FGF14-dependent regulation of Na(+) currents, and induces dissociation and subcellular redistribution of the native FGF14.Nav channel complex in hippocampal neurons.

7. Fgf14-deficient mice developed ataxia and a paroxysmal hyperkinetic movement disorder. FGF14 may mediate neuronal signaling, axonal trafficking and synaptosomal function.

8. FGF14 in regulating synaptic plasticity via presynaptic mechanisms by affecting the mobilization, trafficking, or docking of synaptic vesicles to presynaptic active zones.

9. these results suggest a role for FGF14 in certain spatial learning functions and synaptic plasticity

10. Sodium channels in Fhf1 (show FGF12 Proteins)-/-Fhf4-/- granule neurons inactivate at more negative membrane potential, inactivate more rapidly, and are slower to recover from the inactivated state.