The epitope recognized by the antibody resides within the FHA domain of the Chk2 molecule. This epitope is likely to be masked by protein-protein interactions in vivo.
Immunogen
recombinant human Chk2.
Application
Suitable for immunohistochemistry (formalin-fixed, paraffin-embedded sections) and for immunoblotting at a concentration of 2 to 4 μg/mL using whole extract of cultured 293T cells.
Biochem/physiol Actions
The protein propagates signals from damaged or unreplicated DNA. The protein is expressed throughout the cell cycle. Upon activation it phosphorylates and inhibits CDC25C, which leads to increased inhibitory tyrosine phosphorylation of CDK-cyclin complexes, blocking cell cycle progression. It also regulates apoptosis through the phosphorylation of p53, a tumor suppressor protein. The protein regulates DNA repair through phosphorylation of BRCA2. Mutations in this gene have been linked to Li-Fraumeni syndrome, sarcomas, breast cancer, and brain tumors.
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.
Cyclin-dependent kinase two (Cdk2) is the major regulator of the G1/S transition and the target of an activated G1 checkpoint in somatic cells. In the presence of DNA damage, Cdk2 kinase activity is abrogated by a deficiency of Cdc25A phosphatase
The association between the CHEK2 and breast cancer risk in Chinese women is unknown. Here, we screened the full CHEK2 coding sequence in 118 Chinese familial breast cancer cases who are negative for mutations in BRCA1 and BRCA2, one recurrent
Li Fraumeni Syndrome (LFS) is a multicancer phenotype, most commonly associated with germ-line mutations in TP53. In a kindred with LFS without an inherited TP53 mutation, we have previously reported a truncating mutation (1100delC) in CHK2, encoding a kinase that
The Journal of biological chemistry, 278(35), 33134-33141 (2003-06-18)
The p53 protein is kept labile under normal conditions. This regulation is governed largely by its major negative regulator, Mdm2. In response to stress however, p53 accumulates and becomes activated. For this to occur, the inhibitory effects of Mdm2 have
When exposed to ionizing radiation (IR), eukaryotic cells activate checkpoint pathways to delay the progression of the cell cycle. Defects in the IR-induced S-phase checkpoint cause 'radioresistant DNA synthesis', a phenomenon that has been identified in cancer-prone patients suffering from
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