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C9108

Sigma-Aldrich

Anti-Chk2 antibody, Mouse monoclonal

clone DCS-273, purified from hybridoma cell culture

Synonym(s):

Monoclonal Anti-Chk2 antibody produced in mouse

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About This Item

MDL number:
MFCD03457550
UNSPSC Code:
12352203
NACRES:
NA.41

biological source

mouse

conjugate

unconjugated

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

DCS-273, monoclonal

form

buffered aqueous solution

mol wt

antigen 61 kDa

species reactivity

human

concentration

~2 mg/mL

technique(s)

immunohistochemistry (formalin-fixed, paraffin-embedded sections): suitable
microarray: suitable
western blot: 2-4 μg/mL using whole extract of cultured 293T (human embryonal kidney) cells

isotype

IgG1

UniProt accession no.

O96017

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... CHEK2(11200)

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Specificity

The epitope recognized by the antibody resides within the FHA domain of the Chk2 molecule. This epitope is likely to be masked by protein-protein interactions in vivo.

Immunogen

recombinant human Chk2.

Application

Suitable for immunohistochemistry (formalin-fixed, paraffin-embedded sections) and for immunoblotting at a concentration of 2 to 4 μg/mL using whole extract of cultured 293T cells.

Biochem/physiol Actions

The protein propagates signals from damaged or unreplicated DNA. The protein is expressed throughout the cell cycle. Upon activation it phosphorylates and inhibits CDC25C, which leads to increased inhibitory tyrosine phosphorylation of CDK-cyclin complexes, blocking cell cycle progression. It also regulates apoptosis through the phosphorylation of p53, a tumor suppressor protein. The protein regulates DNA repair through phosphorylation of BRCA2. Mutations in this gene have been linked to Li-Fraumeni syndrome, sarcomas, breast cancer, and brain tumors.

Physical form

Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 1% BSA and 15 mM sodium azide.

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Yin Liu et al.
Human mutation, 32(9), 1000-1003 (2011-05-28)
The association between the CHEK2 and breast cancer risk in Chinese women is unknown. Here, we screened the full CHEK2 coding sequence in 118 Chinese familial breast cancer cases who are negative for mutations in BRCA1 and BRCA2, one recurrent
Igal Louria-Hayon et al.
The Journal of biological chemistry, 278(35), 33134-33141 (2003-06-18)
The p53 protein is kept labile under normal conditions. This regulation is governed largely by its major negative regulator, Mdm2. In response to stress however, p53 accumulates and becomes activated. For this to occur, the inhibitory effects of Mdm2 have
A L Brown et al.
Proceedings of the National Academy of Sciences of the United States of America, 96(7), 3745-3750 (1999-03-31)
Checkpoints maintain the order and fidelity of the eukaryotic cell cycle, and defects in checkpoints contribute to genetic instability and cancer. Much of our current understanding of checkpoints comes from genetic studies conducted in yeast. In the fission yeast Schizosaccharomyces
Vidar Staalesen et al.
Oncogene, 23(52), 8535-8544 (2004-09-14)
The DNA damage checkpoint kinase, CHK2, promotes growth arrest or apoptosis through phosphorylating targets such as Cdc25A, Cdc25C, BRCA1, and p53. Both germline and somatic loss-of-function CHEK2 mutations occur in human tumours, the former linked to the Li-Fraumeni syndrome, and
Zuzana Koledova et al.
Stem cells (Dayton, Ohio), 28(3), 450-461 (2010-01-28)
Cyclin-dependent kinase two (Cdk2) is the major regulator of the G1/S transition and the target of an activated G1 checkpoint in somatic cells. In the presence of DNA damage, Cdk2 kinase activity is abrogated by a deficiency of Cdc25A phosphatase
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