Product Name: Chk2 (65-71) pT68
Product Number: PE-04AJY99
Size: | 200 µg | | Price: | 42.00 |
| 1 mg | | $US | 84.00 |
| 5 mg | | | 185.00 |
Peptide Name: Chk2 (65-71) pT68
Product Use: Services as a blocking peptide for use with the Chk2-pT68 rabbit polyclonal antibody (Cat. No.: AB-PK581) that is also available from Kinexus. This phosphopeptide may also be useful as a substrate for screening the phosphatase activity of protein phosphatases. The peptide sequence is located in the N-terminal portion of the kinase before the FHA domain. T68 phosphorylation stimulates phosphotransferase activity, and induces interactions with Chk2, MDC1, NBS1 and Plk1.
Peptide Production Method: Solid-phase peptide synthesis
Peptide Origin: Homo sapiens
Peptide Sequence: TVS-pT-QEL
Peptide Modifications N Terminus: Free amino
Peptide Modifications C Terminus: βAla-Cys
Peptide Modifications Other: Phosphorylated
Peptide Molecular Mass Calculated: 1031.01 Da
Peptide Purity Percent after Synthesis and Purification: >95
Peptide Appearance: White powder
Peptide Form: Solid
Storage Conditions: -20°C
Related Product 1: Chk2 - pT68 phosphosite-specific antibody (Cat. No.: AB-PK581) Scientific Background: Chk2 (CHEK2) is a protein-serine/threonine kinase of the CAMK group and RAD53 family. It is required for cell cycle arrest, activation of DNA repair, and the promotion of apoptosis in response to double-stranded breaks in DNA. Chk2 is activated through phosphorylation by ATM and ATR at T68. It is activated by phosphorylation at T68 by MLTK in response to replication blocks and DNA damage; the response to DNA damage occurs in an ataxia telangiectasia mutated (ATM)-dependent manner. It is also activated by phosphorylation at S19, T26, S28, S33, S35, T383, T387 and S516. The effects of Chk2 are mediated through the phosphorylation and inhibition of various downstream effectors, including CDC25A, CDC25B, and CDC25C. In addition, Chk2 phosphorylates p53 and BRCA to mediate cell cycle arrest in response to DNA damage. This kinase shows high variability in human tissue distribution with the highest levels detected in spleen and tonsils, and is notably absent in brain and spinal cord. Orthologues of Chk2 are amongst the most highly conserved protein kinases in animals, plants, fungi and unicellular eukaryotes. Expression of wild-type Chk2 leads to increased p53 stabilization after DNA damage, whereas expression of a dominant-negative Chk2 mutant abrogated both phosphorylation of p53 on S20 and p53 stabilization. Chk2 has been linked with the development of Li-Fraumeni Syndrome 2 (LFS2), breast, colon, and prostate cancers, and osteosarcomas.