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SKU: PKSH030433_50μg-ES
Recombinant Human CHK2/CHEK2 Protein (GST Tag), 50 μg
In response to DNA damage and replication blocks, cell cycle progression is halted through the control of critical cell cycle regulators. The protein encoded by CHEK2 gene is a cell cycle checkpoint regulator and putative tumor suppressor. It contains a forkhead-associated protein interaction domain essential for activation in response to DNA damage and is rapidly phosphorylated in response to replication blocks and DNA damage. When activated, the encoded CHEK2 protein is known to inhibit CDC25C phosphatase, preventing entry into mitosis, and has been shown to stabilize the tumor suppressor protein p53, leading to cell cycle arrest in G1. In addition, this protein interacts with and phosphorylates BRCA1, allowing BRCA1 to restore survival after DNA damage. Mutations in this gene have been linked with Li-Fraumeni syndrome, a highly penetrant familial cancer phenotype usually associated with inherited mutations in TP53. Also, mutations in CHEK2s gene are thought to confer a predisposition to sarcomas, breast cancer, and brain tumors. This nuclear protein is a member of the CDS1 subfamily of serine/threonine protein kinases. Several transcript variants encoding different isoforms have been found for this gene.
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Product Specification
Basic Information
Brands:Elabscience
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Place of Origin:China
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Reconstitution:Not Applicable
Shipping:This product is provided as liquid. It is shipped at frozen temperature with blue ice/gel packs. Upon receipt, store it immediately at < - 20°C.
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Calculated Molecular Weight:88.1 kDa
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Purity: > 95 % as determined by reducing SDS-PAGE.
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Storage:Store at < -20°C, stable for 6 months. Please minimize freeze-thaw cycles.
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Calculated Molecular Weight:88.1 kDa
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Endotoxin: < 1.0 EU per μg of the protein as determined by the LAL method.
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Research Areas:Cancer;epigenetics and nuclear signal
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Bio-activity:Not validated for activity
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Formulation:Supplied as sterile 50 mM Tris, 150 mM NaCl, 25 %glycerol, pH 7.5, 0.1 mM EDTA, 0.5 mM TCEP.
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