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KIF5A encodes a member of the kinesin family of proteins.
Showing 10 out of 70 products:
Human Polyclonal KIF5A Primary Antibody for ICC, ELISA - ABIN1002704
Hirokawa: mRNA transport in dendrites: RNA granules, motors, and tracks. in The Journal of neuroscience : the official journal of the Society for Neuroscience 2006
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Human Polyclonal KIF5A Primary Antibody for ICC, ELISA - ABIN1002705
Niclas, Navone, Hom-Booher, Vale: Cloning and localization of a conventional kinesin motor expressed exclusively in neurons. in Neuron 1994
Show all 3 Pubmed References
Deletion of a kinesin I motor unmasks a mechanism of homeostatic axon-branching control by neurotrophin-3 (show NTF3 Antibodies).
Our results shed light on Kinesin complexity and reveal determinants of specific Kif5A functions in mitochondrial transport, adaptor binding, and axonal maintenance.
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]
the novel mutation p.Leu259Gln in two siblings affected by Hereditary spastic paraplegia (HSP) complicated by deafness and in their father with a pure form of HSP.
Klf5 (show KLF5 Antibodies) contributes to adult mouse corneal epithelial homeostasis by promoting (1) permeability barrier function through upregulation of Tjp1 (show TJP1 Antibodies), Gkn1 (show GKN1 Antibodies), Dsg1a, Lama3 (show LAMA3 Antibodies), and Lamb1 (show LAMB1 Antibodies), and (2) basal cell proliferation through upregulation of cyclin-D1 (show CCND1 Antibodies) and suppression of phospho(Ser (show SIGLEC1 Antibodies)-10) p27/Kip1 (show CDKN1B Antibodies)
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 Antibodies) 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 (show UTS2R Antibodies) of Comt (catechol-O-methyltransferase (show COMT Antibodies)).
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 Antibodies)-Kif5A interaction suggesting that the tertiary structure of dystrobrevin (show DTNA Antibodies) 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