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| Catalog | Product Name | EC No. | CAS No. | Source | Price |
|---|---|---|---|---|---|
| NATE-0122 | Checkpoint Kinase 2, Active Human, Recombinant | E. coli | Inquiry |
Checkpoint kinases (Chek) are protein kinases involved in cell cycle regulation. Two isoforms of checkpoint kinases have been identified: Chek1 and Chek2. Chek1 is a central component of the genomic surveillance pathway and is a key regulator of the cell cycle and cell survival. Chek1 is required for initiation of the DNA damage checkpoint and has recently been shown to play a role in the normal (undisturbed) cell cycle. Chek2 is a protein kinase that is activated in response to DNA damage and is involved in cell cycle arrest. In response to DNA damage and replication arrest, cell cycle progression is halted by the control of cell cycle regulators. The protein encoded by this gene is a cell cycle checkpoint regulator and putative tumor suppressor.
The CHEK2 gene encodes the CHEK2 protein, a serine threonine kinase. The protein consists of 543 amino acids and the following structural domains.
The SCD structural domain contains multiple SQ/TQ motifs that serve as phosphorylation sites in response to DNA damage. The most prominent and most frequently phosphorylated site is Thr68.
Since autophagy-associated proteins play an important role in autophagy, the investigators selected five autophagy-associated proteins for immunoprecipitation experiments with Chek2, with significant binding between Chek2 and Beclin l. The activation of Chek2T68 site was enhanced with the prolongation of stimulation time, thus it is speculated that the binding between Beclin 1 and Ch.2 is regulated by the phosphorylation of T68 site. After the addition of Chek2 small molecule inhibitor, the activation of Ch.2T68 site was reduced, and the binding strength with Beclin 1 was also significantly weakened.
The serine kinase CHEK2 (checkpoint kinase 2) is a key mediator in the DNA damage response and is involved in promoting cell cycle arrest, cell death and DNA repair. Overall the cell cycle checkpoint zymase CHEK2 plays an important role in the DNA damage response. Studies have shown that d NTP homeostasis is important for maintaining accurate DNA replication and efficient DNA damage repair when: when NTP supply is insufficient, the replication machinery will not be able to maintain normal efficiency and sustained replication capacity, leading to DNA damage and genomic instability; in addition, when the dNTP pool is abnormally increased, it induces base mismatches during DNA replication and reduces replication fidelity, resulting in The increase of gene mutation rate leads to the development of cancer.
Chek2 plays a central role in orchestrating the DNA damage response and is therefore an important area of oncology and cancer therapeutic drug development. Initially, Chek2 was considered a tumor suppressor because of its regulatory role in cells with DNA damage. Chek2 has been shown to be overexpressed in many tumors, including breast, colon, liver, gastric, and nasopharyngeal cancers. Chek2 expression is positively correlated with tumor grade and disease recurrence, suggesting that Chek2 may promote tumor growth. Chek2 is essential for cell survival, and by being expressed at high levels in tumors, its function may be to induce tumor cell proliferation.
