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Mouse Anti-KIF1A Recombinant Antibody (16/KIF1A) (CBMAB-K0849-LY)

This product is antibody recognizes KIF1A. The antibody 16/KIF1A immunoassay techniques such as: WB.
See all KIF1A antibodies

Summary

Host Animal
Mouse
Specificity
Mouse, Rat
Clone
16/KIF1A
Antibody Isotype
IgG1
Application
WB

Basic Information

Immunogen
Mouse KIF1A aa. 902-1015
Specificity
Mouse, Rat
Antibody Isotype
IgG1
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!]

Format
Liquid
Concentration
0.25 mg/mL
Purity
> 95% Purity determined by SDS-PAGE.
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freezethaw cycles.

Target

Full Name
kinesin family member 1A
Introduction
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. [provided by RefSeq, Apr 2012]
Entrez Gene ID
Mouse16560
Rat363288
UniProt ID
MouseP33173
RatF1M4A4
Alternative Names
ATSV; C630002N23Rik; Gm1626; Kns1
Function
Motor for anterograde axonal transport of synaptic vesicle precursors. Also required for neuronal dense core vesicles (DCVs) transport to the dendritic spines and axons. The interaction calcium-dependent with CALM1 increases vesicle motility and interaction with the scaffolding proteins PPFIA2 and TANC2 recruits DCVs to synaptic sites.
Biological Process
Anterograde axonal transportManual Assertion Based On ExperimentTAS:ProtInc
Anterograde neuronal dense core vesicle transportISS:ARUK-UCL
Cytoskeleton-dependent intracellular transportManual Assertion Based On ExperimentIBA:GO_Central
Dense core granule cytoskeletal transportISS:UniProtKB
Microtubule-based movementManual Assertion Based On ExperimentIBA:GO_Central
Regulation of dendritic spine developmentISS:UniProtKB
Regulation of dendritic spine morphogenesisISS:UniProtKB
Retrograde neuronal dense core vesicle transportISS:ARUK-UCL
Vesicle-mediated transportManual Assertion Based On ExperimentIBA:GO_Central
Cellular Location
Cytoplasm, cytoskeleton; Cell projection, neuron projection; Cell projection, axon; Cytoplasm, perinuclear region; Cell junction, synapse; Cytoplasmic vesicle, secretory vesicle, neuronal dense core vesicle membrane. Within neuronal cells concentrated in the axon, with smaller amounts in the perinuclear and synaptic regions (By similarity).
Expressed in distal regions of neurites
Involvement in disease
Spastic paraplegia 30 (SPG30):
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. Some SPG30 patients have a pure form of the disorder, limited to spastic paraplegia, whereas others may have a complicated form that includes additional features such as cognitive dysfunction, learning disabilities, peripheral sensorimotor neuropathy, urinary sphincter problems, and/or cerebellar atrophy. SPG30 is characterized by onset in the first or second decades of unsteady spastic gait and hyperreflexia of the lower limbs. Inheritance can be autosomal dominant or autosomal recessive.
Neuropathy, hereditary sensory, 2C (HSN2C):
A neurodegenerative disorder characterized by onset in the first decade of progressive distal sensory loss leading to ulceration and amputation of the fingers and toes. Affected individuals also develop distal muscle weakness, primarily affecting the lower limbs.
NESCAV syndrome (NESCAVS):
A neurodegenerative disorder characterized by onset in the first decade of progressive distal sensory loss leading to ulceration and amputation of the fingers and toes. Affected individuals also develop distal muscle weakness, primarily affecting the lower limbs.
NESCAV syndrome (NESCAVS):
An autosomal dominant neurodegenerative disorder with variable manifestations. Main features are delayed psychomotor development, progressive spasticity, intellectual disability, speech delay, and learning disabilities. Some patients never achieve ambulation. Additional variable features are cortical visual impairment, often associated with optic atrophy, axonal peripheral neuropathy, seizures, dysautonomia, ataxia, and dystonia. Brain imaging often shows progressive cerebellar atrophy and thin corpus callosum. Disease onset is in infancy or early childhood.

Zaniewski, T. M., & Hancock, W. O. (2023). Positive charge in the K-loop of the kinesin-3 motor KIF1A regulates superprocessivity by enhancing microtubule affinity in the one-head–bound state. Journal of Biological Chemistry, 299(2).

Pyrpassopoulos, S., Gicking, A. M., Zaniewski, T. M., Hancock, W. O., & Ostap, E. M. (2023). KIF1A is kinetically tuned to be a superengaging motor under hindering loads. Proceedings of the National Academy of Sciences, 120(2), e2216903120.

Budaitis, B. G., Jariwala, S., Rao, L., Yue, Y., Sept, D., Verhey, K. J., & Gennerich, A. (2021). Pathogenic mutations in the kinesin-3 motor KIF1A diminish force generation and movement through allosteric mechanisms. Journal of Cell Biology, 220(4), e202004227.

Kaur, S., Van Bergen, N. J., Verhey, K. J., Nowell, C. J., Budaitis, B., Yue, Y., ... & Christodoulou, J. (2020). Expansion of the phenotypic spectrum of de novo missense variants in kinesin family member 1A (KIF1A). Human mutation, 41(10), 1761-1774.

Mahase, V., Sobitan, A., Johnson, C., Cooper, F., Xie, Y., Li, L., & Teng, S. (2020). Computational analysis of hereditary spastic paraplegia mutations in the kinesin motor domains of KIF1A and KIF5A. Journal of Theoretical and Computational Chemistry, 19(06), 2041003.

Lessard, D. V., Zinder, O. J., Hotta, T., Verhey, K. J., Ohi, R., & Berger, C. L. (2019). Polyglutamylation of tubulin's C-terminal tail controls pausing and motility of kinesin-3 family member KIF1A. Journal of Biological Chemistry, 294(16), 6353-6363.

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

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