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HPA000888

Sigma-Aldrich

Anti-CCDC22 antibody produced in rabbit

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

Synonym(s):

Anti-Coiled-coil domain-containing protein 22 antibody produced in rabbit

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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

human, mouse, rat

technique(s)

immunoblotting: 0.04-0.4 μg/mL
immunofluorescence: 0.25-2 μg/mL
immunohistochemistry: 1:500-1:1000

immunogen sequence

YQNFLYPSEPDLRDLLLFLAERLPTDASEDADQPAGDSAILLRAIGSQIRDQLALPWVPPHLRTPKLQHLQGSALQKPFHASRLVVPELSSRGEPREFQASPLLLPVPTQVPQPVGRVA

UniProt accession no.

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... CCDC22(28952)

Related Categories

General description

The gene CCDC22 (coiled-coil domain containing 22) is mapped to human chromosome Xp11.23.

Immunogen

Coiled-coil domain-containing protein 22 recombinant protein epitope signature tag (PrEST)

Application

Anti-CCDC22 antibody produced in rabbit, a Prestige Antibody, is developed and validated by the Human Protein Atlas (HPA) project . Each antibody is tested by immunohistochemistry against hundreds of normal and disease tissues. These images can be viewed on the Human Protein Atlas (HPA) site by clicking on the Image Gallery link. The antibodies are also tested using immunofluorescence and western blotting. To view these protocols and other useful information about Prestige Antibodies and the HPA, visit sigma.com/prestige.

Biochem/physiol Actions

Coiled-coil domain containing 22 is a protein encoded by the CCDC22 gene in humans. The protein interacts with the evolutionarily conserved multisubunit WASH complex, which is essential for endosomal deposition of F-actin and the trafficking of cargo. The protein encoded by the gene CCDC22 (coiled-coil domain containing 22) interacts with COMMD (copper metabolism Murr1 domain-containing) proteins and functions in the activation of NF-κB (nuclear factor κ-light-chain-enhancer of activated B cells), a protein that is involved in DNA transcription, production of cytokine, pathogenesis of immune disorders , cell survival and cancer. It is also involved in CCC complex recruitment to endosomes. CCDC22 is a novel candidate gene for syndromic X-linked intellectual disability and is associated with a phenotype similar to RSS/3C syndrome.

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 APREST74055

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 Code

10 - Combustible liquids

WGK

WGK 1

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Personal Protective Equipment

dust mask type N95 (US), Eyeshields, Gloves

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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Christine A Phillips-Krawczak et al.
Molecular biology of the cell, 26(1), 91-103 (2014-10-31)
COMMD1 deficiency results in defective copper homeostasis, but the mechanism for this has remained elusive. Here we report that COMMD1 is directly linked to early endosomes through its interaction with a protein complex containing CCDC22, CCDC93, and C16orf62. This COMMD/CCDC22/CCDC93
Missense variant in CCDC22 causes X-linked recessive intellectual disability with features of Ritscher-Schinzel/3C syndrome.
Mateusz Kolanczyk et al.
European journal of human genetics : EJHG, 23(5), 720-720 (2015-04-17)
Petro Starokadomskyy et al.
The Journal of clinical investigation, 123(5), 2244-2256 (2013-04-09)
NF-κB is a master regulator of inflammation and has been implicated in the pathogenesis of immune disorders and cancer. Its regulation involves a variety of steps, including the controlled degradation of inhibitory IκB proteins. In addition, the inactivation of DNA-bound
Mateusz Kolanczyk et al.
European journal of human genetics : EJHG, 23(5), 633-638 (2014-06-12)
Ritscher-Schinzel syndrome (RSS)/3C (cranio-cerebro-cardiac) syndrome (OMIM#220210) is a rare and clinically heterogeneous developmental disorder characterized by intellectual disability, cerebellar brain malformations, congenital heart defects, and craniofacial abnormalities. A recent study of a Canadian cohort identified homozygous sequence variants in the
CCDC22: a novel candidate gene for syndromic X-linked intellectual disability.
I Voineagu et al.
Molecular psychiatry, 17(1), 4-7 (2011-08-10)

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