|Tested species reactivity||Human|
|Host / Isotype||Mouse / IgG1|
|Immunogen||Recombinant human protein purified from E.coli(His-Chk2)|
|Storage buffer||HEPES with 0.15M NaCl, 0.01% BSA, 50% glycerol|
|Contains||0.03% sodium azide|
|Tested Applications||Dilution *|
|ELISA (ELISA)||Assay Dependent|
|Immunoprecipitation (IP)||2 µg|
|Western Blot (WB)||0.1 µg/ml|
* Suggested working dilutions are given as a guide only. It is recommended that the user titrate the product for use in their own experiment using appropriate negative and positive controls.
A suggested positive control for this product is HeLa cells.
Both Chk1 and Chk2 are critically important checkpoint kinases. Chk1 is essential for normal development and cell growth and Chk1 deficiency in mouse or in embryonic stem (ES) cells is lethal. Loss of Chk2 is tolerated and has been found to be associated with a subset of Li-Fraumeni cases. Li-Fraumeni syndrome increases greatly the susceptibility to cancer, with particularly high occurrences of breast cancer, brain tumors, acute leukemia, soft tissue sarcomas, bone sarcomas, and adrenal cortical carcinoma. Chk2 regulates cell cycle checkpoints and apoptosis in response to DNA damage, particularly to DNA double-strand breaks. The cell either stops the cell cycle and therefore its proliferation until the damage is repaired, or it destructs itself (apoptosis). The ataxia telangiectasia mutated (ATM) and ATR (ATM and Rad3-related) protein kinases exert cell cycle delay, in part, by phosphorylating Chk1, Chk2, and p53. Phosphorylation on Chk1 and p53 requires ATR, whereas phosphorylation on Chk2 requires ATM. Screening of novel substrates of Chk1 and Ckh2 followed by imunoprecipitation kinase assay and site-directed mutagenesis analysis suggests that HDAC5 and PGC-1 are specific targets for Chk1 and/or Chk2 at least in vitro.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.