Ataxia in Patients With Bi-Allelic NFASC Mutations and Absence of Full-Length NF186-Reference-Cited by-同舟云学术

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Ataxia in Patients With Bi-Allelic NFASC Mutations and Absence of Full-Length NF186

Published:2019-09-24 Issue: Volume:10 Page:
ISSN:1664-8021
Container-title:Frontiers in Genetics
language:
Short-container-title:Front. Genet.

Author:

Kvarnung Malin,Shahsavani Mansoureh,Taylan Fulya,Moslem Mohsen,Breeuwsma Nicole,Laan Loora,Schuster Jens,Jin Zhe,Nilsson Daniel,Lieden Agne,Anderlid Britt-Marie,Nordenskjöld Magnus,Syk Lundberg Elisabeth,Birnir Bryndis,Dahl Niklas,Nordgren Ann,Lindstrand Anna,Falk Anna

Funder

Vetenskapsrådet

Hjärnfonden

Stiftelsen för Strategisk Forskning

Publisher

Frontiers Media SA

Subject

Genetics(clinical),Genetics,Molecular Medicine

Reference28 articles.

1. Loss of neurofascin-186 disrupts alignment of ankyring relative to its binding partners in the axon initial segment;Alpizar;Front. Cell Neurosci.,2019

2. Ankyrin-based subcellular gradient of neurofascin, an immunoglobulin family protein, directs GABAergic innervation at Purkinje axon initial segment;Ango;Cell,2004

3. Slit proteins: key regulators of axon guidance, axonal branching, and cell migration;Brose;Curr. Opin. Neurobiol.,2000

4. Pinceau organization in the cerebellum requires distinct functions of neurofascin in Purkinje and basket neurons during postnatal development;Buttermore;J. Neurosci.,2012

5. Differential stability of PNS and CNS nodal complexes when neuronal neurofascin is lost;Desmazieres;J. Neurosci.,2014

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5. The ataxia protein sacsin is required for integrin trafficking and synaptic organization;2021-08-20

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