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 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; but only V160A with a concomitant alanine mutation at Tyr-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

11. these findings implicate FGF14 as a unique modulator of Nav channel activity in the CNS.

12. a distinct SCA (spinocerebellar ataxia)phenotype (SCA27) is associated with a F145S mutation in the fibroblast growth factor 14 (FGF14) gene on chromosome 13q34.

13. FGF14 mutations in Ataxia and childhood onset postural tremor.

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/Fn14 pathway instrumental in the pathogenesis of spontaneous lupus nephritis

4. The results of this study demonstrated that iFGF14 is required for spontaneous and evoked action potential firing in adult Purkinje neurons, thereby controlling the output of these cells and the regulation of motor coordination and balance.

5. These data suggest that the FGF14b N-terminus is a potent regulator of resurgent NaV current in cerebellar Purkinje neurons.

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

7. FGF14 regulates presynaptic Ca2+ channels and synaptic transmission in cultured rat neurons.

8. 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.

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

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

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

12. Sodium channels in Fhf1-/-Fhf4-/- granule neurons inactivate at more negative membrane potential, inactivate more rapidly, and are slower to recover from the inactivated state.

13. results suggest that FGF14 is required for normal Nav1.6 expression in Purkinje neurons, and that the loss of FGF14 impairs spontaneous and repetitive firing in Purkinje neurons by altering the expression of Nav1.6 channels