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KIF5A encodes a member of the kinesin family of proteins. De plus, nous expédions Kinesin Family Member 5A Kits (11) et Kinesin Family Member 5A Protéines (8) et beaucoup plus de produits pour cette protéine.
Showing 10 out of 65 products:
Human Polyclonal KIF5A Primary Antibody pour ICC, ELISA - ABIN1002705
Hirokawa: mRNA transport in dendrites: RNA granules, motors, and tracks. dans The Journal of neuroscience : the official journal of the Society for Neuroscience 2006
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Human Polyclonal KIF5A Primary Antibody pour ICC, ELISA - ABIN1002704
Niclas, Navone, Hom-Booher, Vale: Cloning and localization of a conventional kinesin motor expressed exclusively in neurons. dans Neuron 1994
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Deletion of a kinesin I motor unmasks a mechanism of homeostatic axon-branching control by neurotrophin-3 (Montrer NTF3 Anticorps).
Our results shed light on Kinesin complexity and reveal determinants of specific Kif5A functions in mitochondrial transport, adaptor binding, and axonal maintenance.
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.
Combining next-generation sequencing and conventional sequencing, study confirms that KIF5A mutations can cause variable phenotypes ranging from hereditary spastic paraplegia to Charcot-Marie-Tooth disease type 2
Klf5 (Montrer KLF5 Anticorps) contributes to adult mouse corneal epithelial homeostasis by promoting (1) permeability barrier function through upregulation of Tjp1 (Montrer TJP1 Anticorps), Gkn1 (Montrer GKN1 Anticorps), Dsg1a, Lama3 (Montrer LAMA3 Anticorps), and Lamb1 (Montrer LAMB1 Anticorps), and (2) basal cell proliferation through upregulation of cyclin-D1 (Montrer CCND1 Anticorps) and suppression of phospho(Ser (Montrer SIGLEC1 Anticorps)-10) p27/Kip1 (Montrer CDKN1B Anticorps)
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 (Montrer GPHN Anticorps) sorting by a mechanism that involves GSK3 (Montrer GSK3b Anticorps) activity.
KIF5-SNPH (Montrer SNPH Anticorps) 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 (Montrer UTS2R Anticorps) of Comt (catechol-O-methyltransferase (Montrer COMT Anticorps)).
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 (Montrer DTNA Anticorps)-Kif5A interaction suggesting that the tertiary structure of dystrobrevin (Montrer DTNA Anticorps) 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