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Merck

HPA042669

Anti-TMEM259 antibody produced in rabbit

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

Synonyme(s) :

Anti-Asbabp1, Anti-Chromosome 19 open reading frame 6, Anti-Mbrl, Anti-Mgc4022

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A propos de cet article

UNSPSC Code:
12352203
NACRES:
NA.41
Human Protein Atlas Number:
Conjugate:
unconjugated
Clone:
polyclonal
Application:
IHC
Citations:
2
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biological source

rabbit

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

technique(s)

immunoblotting: 0.04-0.4 μg/mL, immunohistochemistry: 1:20-1:50

immunogen sequence

IKFELDIEPKVFKPPSSTEALNDSQEFPFPETPTKVWPQDEYIVEYSLEYGFLRLSQATRQRLSIPVMVVTL

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

Quality Level

Gene Information

human ... C19orf6(91304)

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Immunogen

chromosome 19 open reading frame 6 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.

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.

Physical form

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

Other Notes

Corresponding Antigen APREST83778

Legal Information

Prestige Antibodies is a registered trademark of Merck KGaA, Darmstadt, Germany

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Classe de stockage

10 - Combustible liquids

wgk

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable


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Lot/Batch Number

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Retrouvez la documentation relative aux produits que vous avez récemment achetés dans la Bibliothèque de documents.

Consulter la Bibliothèque de documents

Bing Zhu et al.
Nature communications, 8(1), 1472-1472 (2017-11-15)
Endoplasmic-reticulum-associated degradation (ERAD) is an important protein quality control system which maintains protein homeostasis. Constituents of the ERAD complex and its role in neurodegeneration are not yet fully understood. Here, using proteomic and FRET analyses, we demonstrate that the ER
Lu-Lin Jiang et al.
The Journal of clinical investigation, 129(8), 3103-3120 (2019-05-22)
Mechanisms underlying motor neuron degeneration in amyotrophic lateral sclerosis (ALS) are yet unclear. Specific deletion of the ER-component membralin in astrocytes manifested postnatal motor defects and lethality in mice, causing the accumulation of extracellular glutamate through reducing the glutamate transporter

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