The GADD45G (growth arrest and DNA damage-inducible gamma) gene is mapped to human chromosome 9q22.2. This gene is highly conserved along evolution. It is found to be localized in various tissues, both in adult and fetus. Anti-GA45G antibody detects endogenous levels of total GA45G protein.
Immunogen
The antiserum was produced against synthesized peptide derived from human GA45G.
Immunogen Range: 101-150
Application
Anti-GA45G antibody produced in rabbit has been used in western blot analysis.
Biochem/physiol Actions
Growth arrest DNA damage-inducible 45 (GADD45G) has its key role in regulating DNA repair, cell cycle and apoptosis. It regulates cellular action in response to physical and environmental stress. GADD45G is considered as a stress-responsive protein. It controls the functions of proliferating cell nuclear antigen (PCNA), p21, Cdk1 (cyclin-dependent kinase 1), cdc2 (cell division cycle protein 2)/cyclin B1, p38 and c-Jun N-terminal kinase (JNK). GADD45G is associated with the disease progression of diffuse large B-cell lymphoma (DLBL). It is known to be hypermethylated in DLBL. Lowered GADD45G gene expression is observed in solid tumors.
Features and Benefits
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Physical form
Rabbit IgG in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.
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.
Post-infarction remodelling is accompanied and influenced by perturbations in mitogen-activated protein kinase (MAPK) signalling. The growth arrest and DNA-damage-inducible 45 (Gadd45) proteins are small acidic proteins involved in DNA repair and modulation of MAPK activity. Little is known about the
Gadd45 gamma regulates cardiomyocyte death and post-myocardial infarction left ventricular remodelling
Lucas A, et al.
Cardiovascular Research, 108(2), 254-267 (2015)
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