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MAB1617

Sigma-Aldrich

Anti-Kinesin Antibody, light chain, clone L2

clone L2, Chemicon®, from mouse

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About This Item

UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41

biological source

mouse

Quality Level

antibody form

purified antibody

antibody product type

primary antibodies

clone

L2, monoclonal

species reactivity (predicted by homology)

mammals

manufacturer/tradename

Chemicon®

technique(s)

ELISA: suitable
immunoprecipitation (IP): suitable
radioimmunoassay: suitable
western blot: suitable

isotype

IgG2a

NCBI accession no.

UniProt accession no.

shipped in

wet ice

target post-translational modification

unmodified

Gene Information

human ... KLC1(3831)

Specificity

Reacts with the light chain of kinesin near the C-terminal.

Immunogen

Bovine brain kinesin.
Epitope: light chain

Application

Anti-Kinesin Antibody, light chain, clone L2 is an antibody against Kinesin for use in ELISA, IP, RIA & WB.
Immunoblotting

Immunoprecipitation

EIA/RIA

Optimal working dilutions must be determined by the end user.

Note: Does not work for immunohistochemistry and works only marginally for immunocytochemistry.
Research Category
Cell Structure
Research Sub Category
Cytoskeleton

Physical form

Format: Purified
Liquid in 0.02 M Phosphate buffer, 0.25 M NaCl with 0.1% sodium azide.

Storage and Stability

Maintain at 2-8°C in undiluted aliquots for up to 6 months.

Other Notes

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.

Legal Information

CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Storage Class Code

10 - Combustible liquids

WGK

WGK 2

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Kyoko Okada et al.
Nature communications, 14(1), 5833-5833 (2023-09-21)
Processive transport by the microtubule motor cytoplasmic dynein requires the regulated assembly of a dynein-dynactin-adapter complex. Interactions between dynein and dynactin were initially ascribed to the dynein intermediate chain N-terminus and the dynactin subunit p150Glued. However, recent cryo-EM structures have
Yanpeng Zheng et al.
FEBS letters, 590(7), 1028-1037 (2016-03-19)
Although the exact etiology and pathogenesis of Alzheimer's disease (AD) are still unclear, amyloid-β (Aβ) generated by the proteolytic processing of amyloid-β precursor protein (APP) aggregate to form toxic amyloid species. Kinesin-1 is the first identified ATP-dependent axonal transport motor
Hao Wu et al.
The Journal of biological chemistry, 295(19), 6605-6628 (2020-03-01)
Motor protein-based active transport is essential for mRNA localization and local translation in animal cells, yet how mRNA granules interact with motor proteins remains poorly understood. Using an unbiased yeast two-hybrid screen for interactions between murine RNA-binding proteins (RBPs) and
Anuttama Kulkarni et al.
FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 31(3), 965-974 (2016-12-07)
Acetylcholinesterase (AChE), which is implicated in the pathophysiology of neurological disorders, is distributed along the axon and enriched at the presynaptic basal lamina. It hydrolyses the neurotransmitter acetylcholine, which inhibits synaptic transmission. Aberrant AChE activity and ectopic axonal accumulation of
Ping Shi et al.
Biochimica et biophysica acta, 1802(9), 707-716 (2010-06-01)
Transport of material and signals between extensive neuronal processes and the cell body is essential to neuronal physiology and survival. Slowing of axonal transport has been shown to occur before the onset of symptoms in amyotrophic lateral sclerosis (ALS). We

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