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HPA013373

Sigma-Aldrich

Anti-DDRGK1 antibody produced in rabbit

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

Synonym(s):

Anti-DDRGK domain-containing protein 1 Precursor

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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

technique(s)

immunohistochemistry: 1:50- 1:200

immunogen sequence

ASAGQEPLHNEELAGAGRVAQPGPLEPEEPRAGGRPRRRRDLGSRLQAQRRAQRVAWAEADENEEEAVIL

UniProt accession no.

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... DDRGK1(65992)

General description

DDRGK1 (DDRGK domain containing 1) gene is mapped to human chromosome 20p13 and the encoded protein contains a conserved PCI domain (Proteasome, COP9, and initiation factor-3) at the C-terminus that is also called as protein-protein interaction motif. The protein is localized to the endoplasmic reticulum.

Immunogen

DDRGK domain-containing protein 1 Precursor 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

DDRGK1 (DDRGK domain containing 1) gene encodes a member of the DDRGK domain-containing protein family. The expression of this protein is induced by ER stress. It is found to interact with a protein complex containing UFL1 (UFM1-specific ligase 1), the putative tumor suppressor LZAP/C53 and UFM1 (ubiquitin fold modifier 1). UFL1 and LZAP/C53 are involved in the regulation of NF-κB pathway. DDRGK1 interacts with and stabilizes IκBα (inhibitor of NF-κB) and in turn functions in the regulation of transcriptional activity of NF-κB and the expression of its target genes. Loss of DDRGK1 activity is found to inhibit cell proliferation.

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 APREST72393

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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Jian-Xian Lin et al.
World journal of gastroenterology, 24(34), 3898-3907 (2018-09-20)
To investigate the effects of different levels of expression of CDK5RAP3 and DDRGK1 on long-term survival of patients undergoing radical gastrectomy. The expression of CDK5RAP3 and DDRGK1 was detected by immunohistochemistry in 135 patients who received standard gastrectomy were enrolled
Peng Xi et al.
PloS one, 8(5), e64231-e64231 (2013-05-16)
NF-κB is a ubiquitously expressed transcription factor that regulates a large number of genes in response to diverse physiological and pathological stimuli. The regulation of the transcriptional activity of NF-κB is often dependent on its interaction with IκBα. Proteins that
Camille Miller et al.
American journal of physiology. Gastrointestinal and liver physiology, 312(3), G314-G326 (2017-01-21)
Alcoholism causes an imbalance of endoplasmic reticulum (ER) homeostasis in pancreatic acini. In those cells, the ER is involved in the synthesis and folding of pancreatic enzymes. Ubiquitin-fold modifier 1 (Ufm1) is part of a novel ubiquitin-like modification system involved
Jiang Liu et al.
Nature communications, 8, 14186-14186 (2017-01-28)
Disturbance of endoplasmic reticulum (ER) homoeostasis induces ER stress and leads to activation of the unfolded protein response (UPR), which is an adaptive reaction that promotes cell survival or triggers apoptosis, when homoeostasis is not restored. DDRGK1 is an ER
Hong Xie et al.
The Journal of clinical investigation, 128(4), 1300-1316 (2018-01-31)
Myc activation is a primary oncogenic event in many human cancers; however, these transcription factors are difficult to inhibit pharmacologically, suggesting that Myc-dependent downstream effectors may be more tractable therapeutic targets. Here, we show that Myc overexpression induces endoplasmic reticulum

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