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G6916

Sigma-Aldrich

Anti-GADD153 antibody produced in rabbit

affinity isolated antibody, buffered aqueous solution

Synonym(s):

Anti-CHOP-10

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About This Item

MDL number:
UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

Quality Level

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

antigen 29 kDa

species reactivity

human

technique(s)

immunocytochemistry: 5-10 μg/mL using Hela human cell
microarray: suitable
western blot (chemiluminescent): 1:200-1:400 using whole cell extract of HEK-293 over-expressing GADD 153.

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... DDIT3(1649)
rat ... Ddit3(29467)

General description

Growth arrest and DNA damage inducible protein 153, C/EBP homology protein (GADD153/CHOP10) is a basic region leucine zipper transcription factor, devoid of DNA binding site. Its apparent molecular mass is 29 kDa (or 19 kDa calculated).

Immunogen

peptide corresponding to human GADD153/CHOP10 sequence (amino acids 153-169) with N-terminal lysine added, conjugated to keyhole limpet hemocyanin (KLH). The corresponding sequence in mouse and rat differs by 2 amino acids.

Application

Anti-GADD153 antibody produced in rabbit is suitable as a primary antibody in western blot analysis of:
  • nuclear and cytoplasmic fractions extracted from rat insulinoma (INS) cells to study CHOP Expression in response to ER stress
  • whole cell lysates prepared from ER stress induced rat pancreatic tissues
  • whole cell lysates prepared from ER stress induced pancreatic insulin-producing cells

It is suitable for immunocytochemistry at a working concentration of 5-10μg/mL using Hela human cell and microarray. It is also suitable for western blotting at a working dilution of 1:200-1:400 using whole cell extract of HEK-293 over-expressing GADD 153.

Biochem/physiol Actions

GADD153/CHOP10 (Growth Arrest and DNA Damage Inducible Protein 153, C/EBP Homology Protein) is a leucine zipper transcription factor that lacks a DNA binding site. The protein homodimerizes with members of the CCAAT/enhancer binding protein (C/EBP) family of transcription factors during adipogenesis. Many signals induce the expression of CHOP10. Some of these signals include endoplasmic reticulum stress, hyperosmosis, growth arrest, DNA damage, calcium onophore, nutrient deprivation, hypoxia and hyperoxia. GADD153 heterodimerizes with C/EBPb and inhibits its binding to DNA sequences. Expresssion of this gene induces growth arrest in fibroblasts, inhibits adipocyte differentiation, and is associated with apoptosis in vitro. GADD153 binds to several nuclear proteins as well as the FTE/S3a ribosomal protein and enhances erythroid differentiation. It negatively regulates ATF3, a stress-inducible transcriptional repressor.
Growth arrest and DNA damage inducible protein 153, C/EBP homology protein (GADD153/CHOP10) is also involved in apoptosis in lungs of mice exposed to hyperoxia.

Physical form

Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 1% BSA and 15 mM sodium azide.

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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J D Luethy et al.
The Journal of biological chemistry, 265(27), 16521-16526 (1990-09-25)
A group of five cDNA clones, representing the gadd genes, were recently isolated from Chinese hamster ovary (CHO) cells as genes induced upon growth arrest and after DNA damage (Fornace, A. J., Jr., Nebert, D. W., Hollander, M. C., Luethy
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M A O'Reilly et al.
American journal of physiology. Lung cellular and molecular physiology, 278(3), L552-L559 (2000-03-11)
Previous studies have shown that lungs of adult mice exposed to >95% oxygen have increased terminal deoxyribonucleotidyltransferase dUTP nick end-label staining and accumulate p53, the expression of which increases in cells exposed to DNA-damaging agents. The present study was designed

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