Kinesin heavy chain Antibody [C20E5]

Application: Reactivity: Sea urchin, Rat, Chicken, Squid, Human, Mouse

Usage Information

Dilution
WB1:500

Application
WB, IP, IHC, IF, ELISA

Reactivity
Sea urchin, Rat, Chicken, Squid, Human, Mouse

Source
Mouse Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW
124 kDa

Positive Control	Mouse Brain
Negative Control

Datasheet & SDS

Biological Description

Specificity
Kinesin heavy chain Antibody [C20E5] detects endogenous levels of total Kinesin heavy chain protein.

Clone
C20E5

Synonym(s)
Kinesin-1 heavy chain; Conventional kinesin heavy chain; Ubiquitous kinesin heavy chain (UKHC); KIF5B; KNS; KNS1

Background
Kinesin heavy chain, KHC, is the catalytic core of the canonical kinesin-1 heterotetramer consisting of two heavy and two light chains, and is a plus-end-directed microtubule-based motor protein of about 963 amino acids in the KIF5B isoform, essential for anterograde cargo transport, axonal logistics, and mitotic spindle dynamics. The protein comprises an N-terminal motor domain of approximately 340 amino acids that forms a globular head with six beta-strands flanked by alpha-helices, containing Switch I and II loops for ATP and microtubule coordination, and a conserved P-loop GxxxxGK[T/S] nucleotide pocket. This is followed by a neck linker of about 15 amino acids, which acts as a beta-strand docking against the microtubule upon ATP hydrolysis for 8 nm hand-over-hand stepping, a stalk coiled-coil domain of about 400 amino acids providing a dimerization hinge for the autoinhibited folded state, and a C-terminal KLC-binding tail of about 150 amino acids, a globular domain with tetratricopeptide repeats for adaptor and cargo specificity. KHC acts as a processive ATP-fueled motor, where ATP binding triggers neck linker docking that biases forward head rotation by about 16 nm per step, and hydrolysis advances the trailing head to the leading position, enabling more than 100 steps per encounter at about 800 amino acids per second in vitro, transporting vesicles, organelles, RNA, and proteins along polarized microtubules. Autoinhibition is mediated via a tail-motor clasp and relieved by binding of cargo, KLC, or JIP1. KHC powers axonal transport in neurons, synaptic vesicle delivery, lysosome positioning, and chromosome congression, with Drosophila khc mutants showing paralysis despite normal mitosis. KIF5A mutations cause SPG10 hereditary spastic paraplegia due to axonal degeneration, while KIF5B overexpression drives cancer metastasis through Golgi scattering and microtubule reorganization.

Background

Kinesin heavy chain, KHC, is the catalytic core of the canonical kinesin-1 heterotetramer consisting of two heavy and two light chains, and is a plus-end-directed microtubule-based motor protein of about 963 amino acids in the KIF5B isoform, essential for anterograde cargo transport, axonal logistics, and mitotic spindle dynamics. The protein comprises an N-terminal motor domain of approximately 340 amino acids that forms a globular head with six beta-strands flanked by alpha-helices, containing Switch I and II loops for ATP and microtubule coordination, and a conserved P-loop GxxxxGK[T/S] nucleotide pocket. This is followed by a neck linker of about 15 amino acids, which acts as a beta-strand docking against the microtubule upon ATP hydrolysis for 8 nm hand-over-hand stepping, a stalk coiled-coil domain of about 400 amino acids providing a dimerization hinge for the autoinhibited folded state, and a C-terminal KLC-binding tail of about 150 amino acids, a globular domain with tetratricopeptide repeats for adaptor and cargo specificity. KHC acts as a processive ATP-fueled motor, where ATP binding triggers neck linker docking that biases forward head rotation by about 16 nm per step, and hydrolysis advances the trailing head to the leading position, enabling more than 100 steps per encounter at about 800 amino acids per second in vitro, transporting vesicles, organelles, RNA, and proteins along polarized microtubules. Autoinhibition is mediated via a tail-motor clasp and relieved by binding of cargo, KLC, or JIP1. KHC powers axonal transport in neurons, synaptic vesicle delivery, lysosome positioning, and chromosome congression, with Drosophila khc mutants showing paralysis despite normal mitosis. KIF5A mutations cause SPG10 hereditary spastic paraplegia due to axonal degeneration, while KIF5B overexpression drives cancer metastasis through Golgi scattering and microtubule reorganization.

References
https://pubmed.ncbi.nlm.nih.gov/20566873/ https://pubmed.ncbi.nlm.nih.gov/20930137/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%