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KIF5A encodes a member of the kinesin family of proteins. Additionally we are shipping Kinesin Family Member 5A Antibodies (64) and Kinesin Family Member 5A Proteins (8) and many more products for this protein.
Showing 3 out of 9 products:
Deletion of a kinesin I motor unmasks a mechanism of homeostatic axon-branching control by neurotrophin-3 (show NTF3 ELISA Kits).
Our results shed light on Kinesin complexity and reveal determinants of specific Kif5A functions in mitochondrial transport, adaptor binding, and axonal maintenance.
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
Conformations of microtubule-bound human kinesin-5 motor domain were visualised at successive steps in its ATPase (show DNAH8 ELISA Kits) cycle.
A review of the mechanism of pathogenesis involved in spastic paraplegia type 10 when KIF5A is inactivated by mutations.
Data suggest that KIF5 regulates gephyrin sorting by a mechanism that involves GSK3 activity.
KIF5-SNPH (show SNPH ELISA Kits) 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 ELISA Kits) of Comt (catechol-O-methyltransferase (show COMT ELISA Kits)).
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 ELISA Kits)-Kif5A interaction suggesting that the tertiary structure of dystrobrevin (show DTNA ELISA Kits) 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