|Application ||WB, IHC-P, FC, IF|
|Calculated MW||H=65,61,57,38,32,26, KDa|
|Antigen Region||111-141 aa|
|Other Names||CHEK2; CDS1; CHK2; RAD53; Serine/threonine-protein kinase Chk2; CHK2 checkpoint homolog; Cds1 homolog; Checkpoint kinase 2|
|Target/Specificity||This CHEK2 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 111-141 amino acids from the N-terminal region of human CHEK2.|
|Format||Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification.|
|Storage||Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||CHEK2 Antibody (N-term) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Synonyms||CDS1, CHK2, RAD53|
|Function||Serine/threonine-protein kinase which is required for checkpoint-mediated cell cycle arrest, activation of DNA repair and apoptosis in response to the presence of DNA double-strand breaks. May also negatively regulate cell cycle progression during unperturbed cell cycles. Following activation, phosphorylates numerous effectors preferentially at the consensus sequence [L-X- R-X-X-S/T]. Regulates cell cycle checkpoint arrest through phosphorylation of CDC25A, CDC25B and CDC25C, inhibiting their activity. Inhibition of CDC25 phosphatase activity leads to increased inhibitory tyrosine phosphorylation of CDK-cyclin complexes and blocks cell cycle progression. May also phosphorylate NEK6 which is involved in G2/M cell cycle arrest. Regulates DNA repair through phosphorylation of BRCA2, enhancing the association of RAD51 with chromatin which promotes DNA repair by homologous recombination. Also stimulates the transcription of genes involved in DNA repair (including BRCA2) through the phosphorylation and activation of the transcription factor FOXM1. Regulates apoptosis through the phosphorylation of p53/TP53, MDM4 and PML. Phosphorylation of p53/TP53 at 'Ser-20' by CHEK2 may alleviate inhibition by MDM2, leading to accumulation of active p53/TP53. Phosphorylation of MDM4 may also reduce degradation of p53/TP53. Also controls the transcription of pro-apoptotic genes through phosphorylation of the transcription factor E2F1. Tumor suppressor, it may also have a DNA damage-independent function in mitotic spindle assembly by phosphorylating BRCA1. Its absence may be a cause of the chromosomal instability observed in some cancer cells.|
|Cellular Location||Isoform 2: Nucleus. Note=Isoform 10 is present throughout the cell Isoform 7: Nucleus. Isoform 12: Nucleus.|
|Tissue Location||High expression is found in testis, spleen, colon and peripheral blood leukocytes. Low expression is found in other tissues|
Thousands of laboratories across the world have published research that depended on the performance of antibodies from Abgent to advance their research. Check out links to articles that cite our products in major peer-reviewed journals, organized by research category.
email@example.com, and receive a free "I Love Antibodies" mug.
Provided below are standard protocols that you may find useful for product applications.
CHEK2 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 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.
Yang, X., et al. J. Biol. Chem. 285(5):3030-3034(2010)
Varmark, H., et al. Cell Cycle 9(2):312-320(2010)
Zhu, H., et al. Neoplasia 11(11):1226-1234(2009)
If you have used an Abgent product and would like to share how it has performed, please click on the "Submit Review" button and provide the requested information. Our staff will examine and post your review and contact you if needed.
If you have any additional inquiries please email technical services at firstname.lastname@example.org.