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The protein encoded by KIF1A is a member of the kinesin family and functions as an anterograde motor protein that transports membranous organelles along axonal microtubules. Additionally we are shipping KIF1A Antibodies (12) and KIF1A Proteins (1) and many more products for this protein.
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these findings support a primary role for KIF1A in the anterograde transport of BACE1 (show BACE ELISA Kits).
propose that KIF1A is essential for the survival and function of sensory neurons.
The Doublecortin specifically enhances binding of the ADP-bound Kif1a motor domain to microtubules. Dcx is essential for the function of Kif1a, a kinesin-3 motor protein that traffics synaptic vesicles.
This study demonstrated that KIF1A is indispensable for BDNF (show BDNF ELISA Kits)-mediated hippocampal synaptogenesis and learning enhancement induced by enrichment.
The KIF1A-microtubule binding free energy is dominated by van (show SLC11A2 ELISA Kits) der (show GDF3 ELISA Kits) Waals interactions and electrostatic interactions.
crystal structures of monomeric KIF1A with three transition-state analogs; structures show that KIF1A uses two microtubule-binding loops in an alternating manner to change its interaction with microtubules during the ATP hydrolysis cycle
propose a model mechanism for microtubule activation of Mg-ADP release from KIF1A
We report a child with a de novo KIF1A gene mutation who was found to have bilateral optic nerve hypoplasia and atrophy.
BORC and Arl8 function upstream of two structurally distinct kinesin types: kinesin-1 (KIF5B (show KIF5B ELISA Kits)) and kinesin-3 (KIF1Bbeta and KIF1A).
De novo missense variant affecting the motor domain of KIF1A was identified as a cause of PEHO syndrome.
Mutations outside the motor domain of the gene can cause (recessive) SPG30 and extends the genotype-phenotype association for KIF1A-related diseases.
This study further delineates clinical features of de novo KIF1A mutations
KIF1A variants in dominant and sporadic forms of hereditary spastic paraparesis.
KIF1A should be considered a candidate gene for hereditary paraplegias regardless of inheritance pattern.
Findings provide evidence that de novo missense mutations in the motor domain of KIF1A cause a more severe phenotype that overlaps with that associated with recessive mutations in the same gene.
Data demonstrated that KIF1A promoter methylation can distinguish breast cancer cases from controls in plasma and was inversely associated with DNA repair capacity.
This study establishes an essential role of the CC1 (show CCL14 ELISA Kits)-FHA dimer for KIF1A/unc-104-mediated neuronal transport.
The protein encoded by this gene is a member of the kinesin family and functions as an anterograde motor protein that transports membranous organelles along axonal microtubules. Mutations at this locus have been associated with spastic paraplegia-30 and hereditary sensory neuropathy IIC. Alternatively spliced transcript variants encoding distinct isoforms have been described.
kinesin family member 1A
, N-3 kinesin
, axonal transporter of synaptic vesicles
, kinesin heavy chain member 1A
, kinesin-like protein KIF1A
, kinesin, heavy chain, member 1A, homolog of mouse
, microtubule-based motor KIF1A
, unc-104- and KIF1A-related protein
, neuron-specific kinesin motor KIF1A