Promotional price valid on web orders only. Your contract pricing may differ. Interested in signing up for a dedicated account number?
Learn More

p21 Mouse anti-Human, Clone: DCS-60, Invitrogen™

Mouse Monoclonal Antibody

Manufacturer:  Invitrogen MA112303

Catalog No. 01-670-996


Add to cart

Description

Description

Protein p21 is a tumor suppressor protein which is an inhibitor of Cyclin-dependent kinases (CDK) and is transcriptionally activated by p53. P21 is important in the response of cells to genotoxic stress and a major transcriptional target of p53 protein. The occurrence of p21 in the nucleus executes binding and inhibition activity of cyclin dependent kinases Cdk1 and Cdk2, and blocks the transition from G1 phase into S phase or from G2 phase into mitosis after DNA damage, which enables the repair of damaged DNA. In the cytoplasm, p21 protein has an anti-apoptotic effect. P21 is able to bind to and inhibit caspase 3, as well as the apoptotic kinases ASK1 and JNK. P21 exhibits a dual function in carcinogenesis, and acts as a tumor suppressor, prevents apoptosis, and acts as an oncogene.
Specifications

Specifications

p21
Monoclonal
Unconjugated
CDKN1A
Liquid
CDKN1A
Full length recombit p21protien.
Protein A/G
RUO
Antibody
Monoclonal
Human
Immunohistochemistry, Immunoprecipitation, Western Blot
DCS-60
PBS with 0.08% sodium azide
P38936
CAP20, CDKN1, CDNK1A, MDA-6, SDI1, WAF1, p21CIP1, CDK-interacting protein 1, CDK-interaction protein 1, DNA synthesis inhibitor, cyclin-dependent kinase inhibitor 1, melanoma differentiation associated protein 6, wild-type p53-activated fragment 1
Mouse
IgG2a
100 μg
-20° C, Avoid Freeze/Thaw Cycles
Primary
1026
Documents
Provide Content Correction

We continue to work to improve your shopping experience and your feedback regarding this content is very important to us. Please use the form below to provide feedback related to the content on this product.

Product Title

By clicking Submit, you acknowledge that you may be contacted by Fisher Scientific in regards to the feedback you have provided in this form. We will not share your information for any other purposes. All contact information provided shall also be maintained in accordance with our Privacy Policy.

Cancel Submit