For Research Use Only. Not for use in diagnostic procedures.

Polyclonal

Rabbit

Chk2 (Ab-68) antibody detects endogenous levels of total Chk2 protein.

The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.

Liquid

1ug/ul (lot specific)

This product is stable for several weeks at 4 degree C as an undiluted liquid. Dilute only prior to immediate use. For extended storage, aliquot contents and freeze at -20 degree C or below. Avoid cycles of freezing and thawing. Expiration date is one (1) year from date of receipt.

Small volumes of anti-Chk2 antibody vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

Western Blot (WB), Immunohistochemistry (IHC)

WB: 1:500~1:1000
IHC: 1:50~1:100

36,157 Da

checkpoint kinase 2

serine/threonine-protein kinase Chk2; CHK2 checkpoint homolog; cds1 homolog; checkpoint-like protein CHK2

Serine/threonine-protein kinase Chk2

CHK2_HUMAN

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 this 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 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 this 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. [provided by RefSeq, Apr 2012]

Chk2: a CAMK protein kinase of the Rad53 family. 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. Phosphorylates and inhibits CDC25C, preventing entry into mitosis, p53, leading to cell cycle arrest in G1, and BRCA1, restoring survival after DNA damage. Twelve splice variant isoforms have been described for human Chk2. LOF mutants cause Li-Fraumeni syndrome, a highly penetrant familial cancer phenotype also caused by p53 mutations. Familial mutations also associated with prostate and breast cancer, and mutations also seen in a variety of sporadic cancers and cell lines.

Protein type: Protein kinase, CAMK; Protein kinase, Ser/Thr (non-receptor); Kinase, protein; EC 2.7.11.1; Tumor suppressor; CAMK group; RAD53 family

Chromosomal Location of Human Ortholog: 22q12.1

Cellular Component: nucleoplasm; Golgi apparatus; PML body; chromosome, telomeric region

Molecular Function: identical protein binding; protein serine/threonine kinase activity; protein binding; protein homodimerization activity; ubiquitin protein ligase binding; metal ion binding; protein kinase binding; ATP binding

Biological Process: transcription, DNA-dependent; protein stabilization; DNA damage induced protein phosphorylation; positive regulation of transcription, DNA-dependent; protein amino acid autophosphorylation; DNA damage response, signal transduction; protein amino acid phosphorylation; regulation of transcription, DNA-dependent; DNA damage response, signal transduction resulting in induction of apoptosis; cell division; cellular protein catabolic process; double-strand break repair; DNA damage checkpoint; response to gamma radiation; regulation of protein catabolic process; G2/M transition of mitotic cell cycle; response to DNA damage stimulus

Disease: Li-fraumeni Syndrome 2; Breast Cancer; Prostate Cancer; Osteogenic Sarcoma

Bhoumik A, et al. (2005) Mol Cell; 18(5): 577-87.
Gorgoulis VG, et al. (2005) Nature; 434(7035): 907-13.
Falck J, et al. (2005) Nature; 434(7033): 605-11.
Jin ZH, et al. (2005) Oncogene; 24(12): 1973-81.
Li J, et al. (2005) J Biol Chem; 280(12): 12041-50.

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