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Merck
CN

MAB1617

Anti-Kinesin Antibody, light chain, clone L2

clone L2, Chemicon®, from mouse

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UNSPSC Code:
12352203
NACRES:
NA.41
eCl@ss:
32160702
Conjugate:
unconjugated
Clone:
L2, monoclonal
Application:
ELISA, IP, RIA, WB
Technique(s):
ELISA: suitable, immunoprecipitation (IP): suitable, radioimmunoassay: suitable, western blot: suitable
Citations:
9
Uniprot accession no.:
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biological source

mouse

conjugate

unconjugated

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

Quality Level

Gene Information

human ... KLC1(3831)

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

Biochem/physiol Actions

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

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.

Immunogen

Bovine brain kinesin.
Epitope: light chain

Other Notes

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

Physical form

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

Preparation Note

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

Legal Information

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

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存储类别

10 - Combustible liquids

wgk

WGK 2

flash_point_f

Not applicable

flash_point_c

Not applicable


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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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