Serine/threonine-protein kinase Chk2; bA444G7; CDS 1; CDS1; Checkpoint kinase 2; Checkpoint like protein CHK2; Chek 2; Chek2; Chk 2; CHK2 checkpoint homolog (S. pombe); CHK2 checkpoint homolog; CHK2_HUMAN; HuCds 1; HuCds1; LFS 2; LFS2; PP1425; RAD 53; RAD53; Rad53 homolog; Serine/threonine protein kinase Chk2; Serine/ threonine-protein kinase Chk2 antibody; checkpoint kinase 2

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

Polyclonal

Immunogen Affinity Purified

Lyophilized. Each vial contains 5mg BSA, 0.9mg NaCl, 0.2mg Na2HPO4, 0.05mg NaN3.

At -20 degree C for one year. After reconstitution, at 4 degree C for one month. It can also be aliquoted and stored frozen at -20 degree C for a longer time. Avoid repeated freezing and thawing.

Manufactured in an ISO 13485:2003 and EN ISO 13485:2012 Certified Laboratory.

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.

Description: Rabbit IgG polyclonal antibody for Serine/threonine-protein kinase Chk2(CHEK2) detection. Tested with WB, IHC-P in Human;Mouse;Rat.

Background: CHK2, a protein kinase that is activated in response to DNA damage, is involved in cell cycle arrest. Mapped on 22q12.1, CHK2 has a potential regulatory region rich in SQ and TQ amino acid pairs. It regulates BRCA1 function after DNA damage by phosphorylating serine-988 of BRCA1. Additionally, CHK2 can be modified by phosphorylation and activated in response to ionizing radiation, and can be also modified in response to hydroxyurea treatment. Furthermore, oligomerization of CHEK2 increases the efficiency of transautophosphorylation, resulting in the release of active CHEK2 monomers that proceed to enforce checkpoint control in irradiated cells. Moreover, CHK2 is a tumor suppressor gene conferring predisposition to sarcoma, breast cancer, and brain tumors, and that their observations provided a link between the central role of p53 inactivation in human cancer and the well-defined G2 checkpoint in yeast. There is a wide expression of small amounts of CHK2 mRNA with larger amounts in human testis, spleen, colon, and peripheral blood leukocytes.

Western Blot (WB), Immunohistochemistry (IHC) Paraffin

Western Blot Concentration: 0.1-0.5ug/ml
Immunohistochemistry (IHC) Paraffin Concentration: 0.5-1ug/ml

Anti- Chk2 Picoband antibody, MBS177969, Western blotting
All lanes: Anti Chk2 (MBS177969) at 0.5ug/ml
Lane 1: Rat Spleen Tissue Lysate at 50ug
Lane 2: Mouse Testis Tissue Lysate at 50ug
Lane 3: SW620 Whole Cell Lysate at 40ug
Predicted bind size: 65KD
Observed bind size: 65KD

Anti- Chk2 Picoband antibody, MBS177969, IHC(P)
IHC(P): Human Lung Cancer Tissue

36,157 Da

checkpoint kinase 2

serine/threonine-protein kinase Chk2

Serine/threonine-protein kinase Chk2

CDS1; CHK2; RAD53; Hucds1; hCds1??[Similar Products]

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

Chromosomal Location of Human Ortholog: 22q12.1

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

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

Biological Process: cell division; cellular protein catabolic process; DNA damage checkpoint; DNA damage induced protein phosphorylation; DNA damage response, signal transduction; DNA damage response, signal transduction by p53 class mediator resulting in cell cycle arrest; DNA damage response, signal transduction resulting in induction of apoptosis; double-strand break repair; G2/M transition of mitotic cell cycle; peptidyl-serine phosphorylation; positive regulation of protein amino acid phosphorylation; positive regulation of transcription, DNA-dependent; protein amino acid autophosphorylation; protein amino acid phosphorylation; protein stabilization; regulation of protein catabolic process; regulation of transcription, DNA-dependent; replicative cell aging; response to DNA damage stimulus; response to gamma radiation; transcription, DNA-dependent

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

1. Ahn, J.-Y.; Li, X.; Davis, H. L.; Canman, C. E. : Phosphorylation of threonine 68 promotes oligomerization and autophosphorylation of the Chk2 protein kinase via the forkhead-associated domain. J. Biol. Chem. 277: 19389-19395, 2002. 2. Bell, D. W.; Varley, J. M.; Szydlo, T. E.; Kang, D. H.; Wahrer, D. C. R.; Shannon, K. E.; Lubratovich, M.; Verselis, S. J.; Isselbacher, K. J.; Fraumeni, J. F.; Birch, J. M.; Li, F. P.; Garber, J. E.; Haber, D. A. : Heterozygous germ line hCHK2 mutations in Li-Fraumeni syndrome. Science 286: 2528-2531, 1999. 3. Brown, A. L.; Lee, C.-H.; Schwarz, J. K.; Mitiku, N.; Piwnica-Worms, H.; Chung, J. H. : A human Cds1-related kinase that functions downstream of ATM protein in the cellular response to DNA damage. Proc. Nat. Acad. Sci. 96: 3745-3750, 1999. 4. Lee, J.-S.; Collins, K. M.; Brown, A. L.; Lee, C.-H.; Chung, J. H. : hCds1-mediated phosphorylation of BRCA1 regulates the DNA damage response. Nature 404: 201-204, 2000.

All of MyBioSource's Products are for scientific laboratory research purposes and are not for diagnostic, therapeutics, prophylactic or in vivo use. Through your purchase, you expressly represent and warrant to MyBioSource that you will properly test and use any Products purchased from MyBioSource in accordance with industry standards. MyBioSource and its authorized distributors reserve the right to refuse to process any order where we reasonably believe that the intended use will fall outside of our acceptable guidelines.

While every efforts were made to ensure the accuracy of the information provided in this datasheet, MyBioSource will not be liable for any omissions or errors contained herein. MyBioSource reserves the right to make changes to this datasheet at any time without prior notice.

It is the responsibility of the customer to report product performance issues to MyBioSource within 30 days of receipt of the product. Please visit our Terms & Conditions page for more information.