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A hereditary spastic paraplegia mouse model supports a role of ZFYVE26/SPASTIZIN for the endolysosomal systemFast, multi-dimensional and simultaneous kymograph-like particle dynamics (SkyPad) analysisSpastic paraplegia mutation N256S in the neuronal microtubule motor KIF5A disrupts axonal transport in a Drosophila HSP modelDelving into the complexity of hereditary spastic paraplegias: how unexpected phenotypes and inheritance modes are revolutionizing their nosologyDiabetes alters KIF1A and KIF5B motor proteins in the hippocampusA spastic paraplegia mouse model reveals REEP1-dependent ER shaping.The auto-inhibitory domain and ATP-independent microtubule-binding region of Kinesin heavy chain are major functional domains for transport in the Drosophila germline.Role of kinesin-1-based microtubule sliding in Drosophila nervous system development.Transcriptional evidence for the role of chronic venlafaxine treatment in neurotrophic signaling and neuroplasticity including also Glutamatergic [corrected] - and insulin-mediated neuronal processes.Computer simulation of assembly and co-operativity of hexameric AAA ATPasesRegulation of mitochondrial transport in neurons.Deletion of a kinesin I motor unmasks a mechanism of homeostatic branching control by neurotrophin-3.Mutations in BICD2, which encodes a golgin and important motor adaptor, cause congenital autosomal-dominant spinal muscular atrophyElectrophysiological characterisation of motor and sensory tracts in patients with hereditary spastic paraplegia (HSP).Role of kinesin-1 in the pathogenesis of SPG10, a rare form of hereditary spastic paraplegia.Advances in understanding the role of disease-associated proteins in spinal muscular atrophy.Regulation of long-distance transport of mitochondria along microtubules.KIF5A mutations cause an infantile onset phenotype including severe myoclonus with evidence of mitochondrial dysfunction.Unique function of Kinesin Kif5A in localization of mitochondria in axonsKIF1A mediates axonal transport of BACE1 and identification of independently moving cargoes in living SCG neurons.Elevated copper ion levels as potential cause of impaired kinesin-dependent transport processes.Axonal motor protein KIF5A and associated cargo deficits in multiple sclerosis lesional and normal-appearing white matter.Genome-wide Analyses Identify KIF5A as a Novel ALS Gene.Altered distribution of ATG9A and accumulation of axonal aggregates in neurons from a mouse model of AP-4 deficiency syndrome.
P2860
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P2860
description
2012 nî lūn-bûn
@nan
2012年の論文
@ja
2012年論文
@yue
2012年論文
@zh-hant
2012年論文
@zh-hk
2012年論文
@zh-mo
2012年論文
@zh-tw
2012年论文
@wuu
2012年论文
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2012年论文
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name
Axonal transport deficit in a KIF5A
@nl
Axonal transport deficit in a KIF5A( -/- ) mouse model.
@en
type
label
Axonal transport deficit in a KIF5A
@nl
Axonal transport deficit in a KIF5A( -/- ) mouse model.
@en
prefLabel
Axonal transport deficit in a KIF5A
@nl
Axonal transport deficit in a KIF5A( -/- ) mouse model.
@en
P2860
P1433
P1476
Axonal transport deficit in a KIF5A( -/- ) mouse model.
@en
P2093
Diana Möckel
Kathrin N Karle
P2860
P2888
P304
P356
10.1007/S10048-012-0324-Y
P577
2012-04-01T00:00:00Z