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Mouse Anti-KIF5A Recombinant Antibody (D-3) (CBMAB-N0885-WJ)

This product is a Mouse antibody that recognizes KIF5A. The antibody D-3 can be used for immunoassay techniques such as: WB, IP, IF, ELISA.
See all KIF5A antibodies

Summary

Host Animal
Mouse
Specificity
Human, Mouse, Rat
Clone
D-3
Application
WB, IP, IF, ELISA

Basic Information

Specificity
Human, Mouse, Rat
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
kinesin family member 5A
Introduction
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. [provided by RefSeq, Jul 2008]
Entrez Gene ID
Human3798
Mouse16572
Rat314906
UniProt ID
HumanQ12840
MouseP33175
RatQ6QLM7
Alternative Names
Kinesin Family Member 5A; Kinesin Heavy Chain Neuron-Specific 1; Neuronal Kinesin Heavy Chain; NKHC; Spastic Paraplegia 10 (Autosomal Dominant); Kinesin, Heavy Chain, Neuron-Specific; Kinesin Heavy Chain Isoform 5A;
Function
Microtubule-dependent motor required for slow axonal transport of neurofilament proteins (NFH, NFM and NFL). Can induce formation of neurite-like membrane protrusions in non-neuronal cells in a ZFYVE27-dependent manner. The ZFYVE27-KIF5A complex contributes to the vesicular transport of VAPA, VAPB, SURF4, RAB11A, RAB11B and RTN3 proteins in neurons. Required for anterograde axonal transportation of MAPK8IP3/JIP3 which is essential for MAPK8IP3/JIP3 function in axon elongation.
Biological Process
Anterograde axonal protein transportISS:UniProtKB
Anterograde dendritic transport of neurotransmitter receptor complexManual Assertion Based On ExperimentIBA:GO_Central
Axon guidanceManual Assertion Based On ExperimentIBA:GO_Central
Chemical synaptic transmissionManual Assertion Based On ExperimentTAS:ProtInc
Cytoskeleton-dependent intracellular transportManual Assertion Based On ExperimentIBA:GO_Central
Microtubule-based movementManual Assertion Based On ExperimentIBA:GO_Central
Retrograde neuronal dense core vesicle transportISS:ARUK-UCL
Synaptic vesicle transportManual Assertion Based On ExperimentIBA:GO_Central
Vesicle-mediated transportISS:UniProtKB
Cellular Location
Cytoplasm, perinuclear region; Cytoplasm, cytoskeleton; Perikaryon. Concentrated in the cell body of the neurons, particularly in the perinuclear region.
Involvement in disease
Spastic paraplegia 10, autosomal dominant (SPG10):
A form of spastic paraplegia, a neurodegenerative disorder characterized by a slow, gradual, progressive weakness and spasticity of the lower limbs. Rate of progression and the severity of symptoms are quite variable. Initial symptoms may include difficulty with balance, weakness and stiffness in the legs, muscle spasms, and dragging the toes when walking. In some forms of the disorder, bladder symptoms (such as incontinence) may appear, or the weakness and stiffness may spread to other parts of the body.
Myoclonus, intractable, neonatal (NEIMY):
An autosomal dominant neurologic disorder characterized by severe, infantile-onset myoclonic seizures, hypotonia, optic nerve abnormalities, dysphagia, apnea, and early developmental arrest. Brain imaging shows a progressive leukoencephalopathy. Some patients may die in infancy.
Amyotrophic lateral sclerosis 25 (ALS25):
A form of amyotrophic lateral sclerosis, a neurodegenerative disorder affecting upper motor neurons in the brain and lower motor neurons in the brain stem and spinal cord, resulting in fatal paralysis. Sensory abnormalities are absent. The pathologic hallmarks of the disease include pallor of the corticospinal tract due to loss of motor neurons, presence of ubiquitin-positive inclusions within surviving motor neurons, and deposition of pathologic aggregates. The etiology of amyotrophic lateral sclerosis is likely to be multifactorial, involving both genetic and environmental factors. The disease is inherited in 5-10% of the cases. ALS25 is an autosomal dominant form with variable adult onset and incomplete penetrance.

Nakano, J., Chiba, K., & Niwa, S. (2022). An ALS‐associated KIF5A mutant forms oligomers and aggregates and induces neuronal toxicity. Genes to Cells, 27(6), 421-435.

Baron, D. M., Fenton, A. R., Saez-Atienzar, S., Giampetruzzi, A., Sreeram, A., Keagle, P. J., ... & Landers, J. E. (2022). ALS-associated KIF5A mutations abolish autoinhibition resulting in a toxic gain of function. Cell reports, 39(1).

Pant, D. C., Parameswaran, J., Rao, L., Loss, I., Chilukuri, G., Parlato, R., ... & Jiang, J. (2022). ALS‐linked KIF5A ΔExon27 mutant causes neuronal toxicity through gain‐of‐function. EMBO reports, 23(8), e54234.

de Boer, E. M., van Rheenen, W., Goedee, H. S., Kamsteeg, E. J., Brilstra, E. H., Veldink, J. H., ... & van Es, M. A. (2021). Genotype-phenotype correlations of KIF5A stalk domain variants. Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration, 22(7-8), 561-570.

Fukuda, Y., Pazyra-Murphy, M. F., Silagi, E. S., Tasdemir-Yilmaz, O. E., Li, Y., Rose, L., ... & Segal, R. A. (2021). Binding and transport of SFPQ-RNA granules by KIF5A/KLC1 motors promotes axon survival. Journal of Cell Biology, 220(1).

Wang, Q., Tian, J., Chen, H., Du, H., & Guo, L. (2019). Amyloid beta-mediated KIF5A deficiency disrupts anterograde axonal mitochondrial movement. Neurobiology of disease, 127, 410-418.

DuRaine, G., Wisner, T. W., Howard, P., & Johnson, D. C. (2018). Kinesin-1 proteins KIF5A,-5B, and-5C promote anterograde transport of herpes simplex virus enveloped virions in axons. Journal of virology, 92(20), 10-1128.

Nam, D. E., Yoo, D. H., Choi, S. S., Choi, B. O., & Chung, K. W. (2018). Wide phenotypic spectrum in axonal Charcot–Marie–Tooth neuropathy type 2 patients with KIF5A mutations. Genes & genomics, 40, 77-84.

Nicolas, A., Kenna, K. P., Renton, A. E., Ticozzi, N., Faghri, F., Chia, R., ... & Cooper, G. M. (2018). Genome-wide analyses identify KIF5A as a novel ALS gene. Neuron, 97(6), 1268-1283.

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For research use only. Not intended for any clinical use.

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