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KIF5A encodes a member of the kinesin family of proteins. Additionally we are shipping Kinesin Family Member 5A Antibodies (68) and Kinesin Family Member 5A Kits (13) and many more products for this protein.
Showing 5 out of 8 products:
Deletion of a kinesin I motor unmasks a mechanism of homeostatic axon-branching control by neurotrophin-3 (show NTF3 Proteins).
Our results shed light on Kinesin complexity and reveal determinants of specific Kif5A functions in mitochondrial transport, adaptor binding, and axonal maintenance.
This study identified three pathogenic KIF5A mutations in Korean Charcot-Marie-Tooth neuropathy type 2 patients by whole exome sequencing. Two mutations (p.Arg204Trp and p.Arg280His) were previously reported, but p.Leu558Pro was determined to be a novel de novo mutation.
We conclude that reduced expression of axonal motor KIF5A may have important implications in determining axonal transport deficits and ongoing neurodegeneration in multiple sclerosis
Kinesin family member 5A protein (Kif5A) with hereditary spastic paraplegia (HSP)-causing mutations showed a variety of significantly reduced catalytic and mechanical activities as a result of each mutation, with the shared phenotype from each that motility was significantly reduced.
Variants in SPAST and KIF5A were the most common causes of autosomal dominant hereditary spastic paraplegia in Greece. The first nonsense mutation in KIF5A was identified in HSP patient.
De novo stop-loss frameshift variants in KIF5A result in a novel phenotype that includes severe infantile onset myoclonus, hypotonia, optic nerve abnormalities, dysphagia, apnea, and early developmental arrest.
KIF5A p.Ser974fs de novo mutation associated with myoclonic seizures and neonatal onset progressive leukoencephalopathy.
Zinc ion-mediated inhibition of KIF5A activity might be one molecular cause contributing to impaired transport processes within brain and other organs in cases of zinc dyshomeostasis.
This report describes the first known Asian family with a KIF5A mutation and broadens the clinical and electrophysiological spectrum associated with KIF5A-SPG10 mutations.
study describes 2 Spanish families with an adult onset complicated autosomal dominant hereditary spastic paraplegia with a mild sensory neuropathy; identified 2 novel mutations c.773 C>T and c.833 C>T in the KIF5A gene resulting in the P258L and P278L substitutions; both were located in the highly conserved kinesin motor domain of the protein
Kinesin-14 blocks microtubule nucleation in yeast and reveal that this inhibition is countered by the kinesin-5 protein, Cut7.[Cut7, Pkl1]
Klf5 (show KLF5 Proteins) contributes to adult mouse corneal epithelial homeostasis by promoting (1) permeability barrier function through upregulation of Tjp1 (show TJP1 Proteins), Gkn1 (show GKN1 Proteins), Dsg1a, Lama3 (show LAMA3 Proteins), and Lamb1 (show LAMB1 Proteins), and (2) basal cell proliferation through upregulation of cyclin-D1 (show CCND1 Proteins) and suppression of phospho(Ser (show SIGLEC1 Proteins)-10) p27/Kip1 (show CDKN1B Proteins)
Results from the present study reveal a new system mediated by kinesin-1 sorting in axons that differentially controls stability of arbor terminals.
Data suggest that KIF5 regulates gephyrin sorting by a mechanism that involves GSK3 activity.
KIF5-SNPH (show SNPH Proteins) interaction mediates activity-induced immobilization of axonal mitochondria.
Found a role of KIF5A in process outgrowth and axonal transport of mitochondria, affecting motor neurons more severely than sensory neurons.
Expression of Kif5a in the mouse prefrontal cortex is modulated by a sequence variant (B2 SINE indel) in the 3' UTR of Comt (catechol-O-methyltransferase (show COMT Proteins)).
Data suggest that kinesin-1A is the principal anterograde motor for neurofilaments, that there may be functional redundancy among isoforms in neurofilament transport, and that anterograde and retrograde neurofilament motors are tightly coordinated.
assessement of the kinetics of the dystrobrevin (show DTNA Proteins)-Kif5A interaction suggesting that the tertiary structure of dystrobrevin (show DTNA Proteins) may play a role in regulating its interaction with Kif5a
This gene encodes a member of the kinesin family of proteins. Members of this family are part of a multisubunit complex that functions as a microtubule motor in intracellular organelle transport. Mutations in this gene cause autosomal dominant spastic paraplegia 10.
kinesin family member 5A
, kinesin heavy chain isoform 5A-like
, KIF5A variant protein
, kinesin heavy chain isoform 5A
, kinesin heavy chain neuron-specific 1
, kinesin, heavy chain, neuron-specific
, neuronal kinesin heavy chain
, Kinesin heavy chain