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HPA004469

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Anti-KIF5A antibody produced in rabbit

Prestige Antibodies® Powered by Atlas Antibodies, affinity isolated antibody, buffered aqueous glycerol solution

Synonym(s):

Anti-Kinesin heavy chain isoform 5A antibody produced in rabbit, Anti-Kinesin heavy chain neuron-specific 1 antibody produced in rabbit, Anti-NKHC antibody produced in rabbit, Anti-Neuronal kinesin heavy chain antibody produced in rabbit

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About This Item

UNSPSC Code:
12352203
Human Protein Atlas Number:
NACRES:
NA.41

biological source

rabbit

Quality Level

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

product line

Prestige Antibodies® Powered by Atlas Antibodies

form

buffered aqueous glycerol solution

species reactivity

human, rat, mouse

technique(s)

immunoblotting: 0.04-0.4 μg/mL
immunohistochemistry: 1:50-1:200

immunogen sequence

AQIAKPVRPGHYPASSPTNPYGTRSPECISYTNSLFQNYQNLYLQATPSSTSDMYFANSCTSSGATSSGGPLASYQKANMDNGNATDINDNRSDLPCGYEAEDQAKLFPLHQ

UniProt accession no.

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... KIF5A(3798)

Immunogen

Kinesin heavy chain isoform 5A recombinant protein epitope signature tag (PrEST)

Application

All Prestige Antibodies Powered by Atlas Antibodies are developed and validated by the Human Protein Atlas (HPA) project and as a result, are supported by the most extensive characterization in the industry.

The Human Protein Atlas project can be subdivided into three efforts: Human Tissue Atlas, Cancer Atlas, and Human Cell Atlas. The antibodies that have been generated in support of the Tissue and Cancer Atlas projects have been tested by immunohistochemistry against hundreds of normal and disease tissues and through the recent efforts of the Human Cell Atlas project, many have been characterized by immunofluorescence to map the human proteome not only at the tissue level but now at the subcellular level. These images and the collection of this vast data set can be viewed on the Human Protein Atlas (HPA) site by clicking on the Image Gallery link. We also provide Prestige Antibodies® protocols and other useful information.

Biochem/physiol Actions

KIF5A (kinesin family member 5A) encodes the neuronal kinesis heavy chain (KHC) subunit of kinesin-1 belonging to the kinesin superfamily. It is a two-headed motor protein involved in the axonal transport. It utilizes ATP hydrolysis as energy source for the transportation of intracellular cargo toward the plus-ends of microtubules within axons. Mutation in the KIF5A causes a hereditary disease - spastic paraplegia. Alterations have been reported in the motor domain of the neuronal kinesin heavy chain of the gene KIF5A.

Features and Benefits

Prestige Antibodies® are highly characterized and extensively validated antibodies with the added benefit of all available characterization data for each target being accessible via the Human Protein Atlas portal linked just below the product name at the top of this page. The uniqueness and low cross-reactivity of the Prestige Antibodies® to other proteins are due to a thorough selection of antigen regions, affinity purification, and stringent selection. Prestige antigen controls are available for every corresponding Prestige Antibody and can be found in the linkage section.

Every Prestige Antibody is tested in the following ways:
  • IHC tissue array of 44 normal human tissues and 20 of the most common cancer type tissues.
  • Protein array of 364 human recombinant protein fragments.

Linkage

Corresponding Antigen APREST86857

Physical form

Solution in phosphate-buffered saline, pH 7.2, containing 40% glycerol and 0.02% sodium azide

Legal Information

Prestige Antibodies 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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WGK

WGK 1

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Personal Protective Equipment

dust mask type N95 (US), Eyeshields, Gloves

Regulatory Information

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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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Yo-Tsen Liu et al.
Neurology, 83(7), 612-619 (2014-07-11)
To establish the phenotypic spectrum of KIF5A mutations and to investigate whether KIF5A mutations cause axonal neuropathy associated with hereditary spastic paraplegia (HSP) or typical Charcot-Marie-Tooth disease type 2 (CMT2). KIF5A sequencing of the motor-domain coding exons was performed in
K Hares et al.
Neuropathology and applied neurobiology, 43(3), 227-241 (2016-01-21)
Understanding the causes of axonal pathology remains a key goal in the pursuit of new therapies to target disease progression in multiple sclerosis (MS). Anterograde axonal transport of many proteins vital for axonal viability is mediated by the motor protein
Kenji Kawaguchi
The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry, 19(4), 336-344 (2012-07-13)
Molecular protein motors play key roles in processes such as intracellular cargo transport and brain wiring, and failure of function can give rise to serious diseases. Kinesin-1, a member of the kinesin superfamily (also known as KIFs) is a two-headed
Evan Reid et al.
American journal of human genetics, 71(5), 1189-1194 (2002-10-02)
We have identified a missense mutation in the motor domain of the neuronal kinesin heavy chain gene KIF5A, in a family with hereditary spastic paraplegia. The mutation occurs in the family in which the SPG10 locus was originally identified, at
Kelly Hares et al.
Journal of Alzheimer's disease : JAD, 60(4), 1511-1524 (2017-10-25)
Defects in motor protein-mediated neuronal transport mechanisms have been implicated in a number of neurodegenerative disorders but remain relatively little studied in Alzheimer's disease (AD). Our aim in the present study was to assess the expression of the anterograde kinesin

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