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Key Documents

HPA018479

Sigma-Aldrich

Anti-AK2 antibody produced in rabbit

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

Synonym(s):

Anti-ATP-AMP transphosphorylase 2, Anti-Adenylate kinase 2, mitochondrial

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About This Item

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

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

rat, mouse, human

technique(s)

immunoblotting: 0.04-0.4 μg/mL
immunohistochemistry: 1:200-1:500

immunogen sequence

LAENFCVCHLATGDMLRAMVASGSELGKKLKATMDAGKLVSDEMVVELIEKNLETPLCKNGFLLDGFPRTVRQAEMLDDLMEKRKEKLDSVIEFSIPDSLLIRR

UniProt accession no.

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... AK2(204)

General description

The gene AK2 (adenylate kinase 2 - mitochondrial) is mapped to human chromosome 1p34. AK2 is expressed in a variety of tissues including liver, kidney, spleen and heart. AK2 is also expressed in the stria vascularis region of the inner ear. The protein is localized in the mitochondrial intermembrane space.

Immunogen

Adenylate kinase 2, mitochondrial 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

Mutation in adenylate kinase 2 - mitochondrial (AK2) is associated with reticular dysgenesis, a severe combined immunodeficiency (SCID). Expression of AK2 in reticular dysgenesis patients overcomes the neutrophil differentiation arrest. AK2 is up-regulated during macrophage and neutrophil differentiation. Knockdown of AK2 particularly inhibits neutrophil differentiation. AK2 is also involved in mitochondrial apoptosis. Presence of AK2 causes activation of caspase-10 via FAS-associated death domain protein (FADD).

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 APREST73806

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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Storage Class

10 - Combustible liquids

wgk_germany

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable

ppe

Eyeshields, Gloves, multi-purpose combination respirator cartridge (US)


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Ayako Tanimura et al.
PloS one, 9(2), e89916-e89916 (2014-03-04)
Adenine nucleotide dynamics in the mitochondrial intermembrane space (IMS) play a key role in oxidative phosphorylation. In a previous study, Drosophila adenylate kinase isozyme 2 (Dak2) knockout was reported to cause developmental lethality at the larval stage in Drosophila melanogaster.
Gene order and localization of enzyme loci on the short arm of chromosome 1.
B Carritt et al.
Annals of human genetics, 46(Pt 4), 329-335 (1982-10-01)
Ho-June Lee et al.
Nature cell biology, 9(11), 1303-1310 (2007-10-24)
Mitochondrial proteins function as essential regulators in apoptosis. Here, we show that mitochondrial adenylate kinase 2 (AK2) mediates mitochondrial apoptosis through the formation of an AK2-FADD-caspase-10 (AFAC10) complex. Downregulation of AK2 attenuates etoposide- or staurosporine-induced apoptosis in human cells, but
Ulrich Pannicke et al.
Nature genetics, 41(1), 101-105 (2008-12-02)
Human severe combined immunodeficiencies (SCID) are phenotypically and genotypically heterogeneous diseases. Reticular dysgenesis is the most severe form of inborn SCID. It is characterized by absence of granulocytes and almost complete deficiency of lymphocytes in peripheral blood, hypoplasia of the
Chantal Lagresle-Peyrou et al.
Nature genetics, 41(1), 106-111 (2008-12-02)
Reticular dysgenesis is an autosomal recessive form of human severe combined immunodeficiency characterized by an early differentiation arrest in the myeloid lineage and impaired lymphoid maturation. In addition, affected newborns have bilateral sensorineural deafness. Here we identify biallelic mutations in

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