Spastin, the most commonly mutated protein in hereditary spastic paraplegia interacts with Reticulon 1 an endoplasmic reticulum protein (Q28306319)

2

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Simone M Sauter

3

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Anne Rauber

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Paula C Byrne

5

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Juergen Neesen

6

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Wolfgang Engel

https://scigraph.springernature.com/pub.10.1007/s10048-006-0034-4

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language of work or name

English

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publication date

May 2006

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published in

Neurogenetics

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volume

7

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issue

2

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page(s)

93-103

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exact match

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cites work

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The cellular and molecular pathology of the motor system in hereditary spastic paraparesis due to mutation of the spastin gene.

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Neuronal differentiation is accompanied by NSP-C expression

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The hereditary spastic paraplegia protein spastin interacts with the ESCRT-III complex-associated endosomal protein CHMP1B.

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Spastin, a new AAA protein, is altered in the most frequent form of autosomal dominant spastic paraplegia

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Classification of the hereditary ataxias and paraplegias

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Hereditary spastic paraplegia caused by mutations in the SPG4 gene

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The hereditary spastic paraplegia gene, spastin, regulates microtubule stability to modulate synaptic structure and function.

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SPG20 is mutated in Troyer syndrome, an hereditary spastic paraplegia.

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Reticulon3 expression in rat optic and olfactory systems.

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Hereditary (familial) spastic paraplegia; further clinical and pathologic observations.

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NIPA1 Gene Mutations Cause Autosomal Dominant Hereditary Spastic Paraplegia (SPG6)

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Spectrum of SPG4 mutations in autosomal dominant spastic paraplegia

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Mutation analysis of the spastin gene (SPG4) in patients with hereditary spastic paraparesis

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A kinesin heavy chain (KIF5A) mutation in hereditary spastic paraplegia (SPG10)

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Reticulon 1-C/neuroendocrine-specific protein-C interacts with SNARE proteins.

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Identification and expression analysis of spastin gene mutations in hereditary spastic paraplegia

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Spastin, the protein mutated in autosomal dominant hereditary spastic paraplegia, is involved in microtubule dynamics

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Cellular Localization, Oligomerization, and Membrane Association of the Hereditary Spastic Paraplegia 3A (SPG3A) Protein Atlastin

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Spastin interacts with the centrosomal protein NA14, and is enriched in the spindle pole, the midbody and the distal axon

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Mutations of SPG4 are responsible for a loss of function of spastin, an abundant neuronal protein localized in the nucleus

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Xenopus embryos regulate the nuclear localization of XMyoD

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Spastin subcellular localization is regulated through usage of different translation start sites and active export from the nucleus

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Maspardin is mutated in mast syndrome, a complicated form of hereditary spastic paraplegia associated with dementia

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The gene encoding alsin, a protein with three guanine-nucleotide exchange factor domains, is mutated in a form of recessive amyotrophic lateral sclerosis

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Human reticulon 1-A and 1-B interact with a medium chain of the AP-2 adaptor complex

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Linking axonal degeneration to microtubule remodeling by Spastin-mediated microtubule severing

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Spastin gene mutation in Japanese with hereditary spastic paraplegia

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Mutations in a newly identified GTPase gene cause autosomal dominant hereditary spastic paraplegia

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Identification of katanin, an ATPase that severs and disassembles stable microtubules

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A 200-amino acid ATPase module in search of a basic function

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