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KIF5A encodes a member of the kinesin family of proteins. Additionally we are shipping Kinesin Family Member 5A Antibodies (67) and Kinesin Family Member 5A Kits (7) and many more products for this protein.
Showing 8 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.
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 cycle.
A review of the mechanism of pathogenesis involved in spastic paraplegia type 10 when KIF5A is inactivated by mutations.
Data suggest that the impairment of the microtubule-kinesin function by alpha-synuclein oligomers drives early neurite pathology.
This study extends the phenotype of SPG10 and argues for abnormalities in the axonal vesicular transport.
These results provide an insight into the molecular mechanisms of KIF5A, which regulate inhibitory neural transmission and KIF5A deletion causes epilepsy.
The results obtained indicate a KIF5A mutation frequency of 8.8% in the Italian HSP population and identify a region of the kinesin protein (show KIF2B Proteins), the stalk domain, as a novel target for mutation.
Molecular genetic analysis identified a new missense mutation of KIF5A gene causing hereditary spastic paraplegia
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