|Application ||WB, IHC-P, IF, FC, E|
|Calculated MW||18119 Da|
|Antigen Region||134-164 aa|
|Other Names||Cyclin-dependent kinase inhibitor 1, CDK-interacting protein 1, Melanoma differentiation-associated protein 6, MDA-6, p21, CDKN1A, CAP20, CDKN1, CIP1, MDA6, PIC1, SDI1, WAF1|
|Target/Specificity||This p21 (CDKN1A) antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 134-164 amino acids from the C-terminal region of human p21 (CDKN1A).|
|Format||Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis against PBS.|
|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||p21 (CDKN1A) Antibody (C-term) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Synonyms||CAP20, CDKN1, CIP1, MDA6, PIC1, SDI1, WA|
|Function||May be involved in p53/TP53 mediated inhibition of cellular proliferation in response to DNA damage. Binds to and inhibits cyclin-dependent kinase activity, preventing phosphorylation of critical cyclin-dependent kinase substrates and blocking cell cycle progression. Functions in the nuclear localization and assembly of cyclin D-CDK4 complex and promotes its kinase activity towards RB1. At higher stoichiometric ratios, inhibits the kinase activity of the cyclin D-CDK4 complex. Inhibits DNA synthesis by DNA polymerase delta by competing with POLD3 for PCNA binding (PubMed:11595739).|
|Cellular Location||Cytoplasm. Nucleus.|
|Tissue Location||Expressed in all adult tissues, with 5-fold lower levels observed in the brain|
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Provided below are standard protocols that you may find useful for product applications.
CDKN1A is a potent cyclin-dependent kinase inhibitor. It binds to and inhibits the activity of cyclin-CDK2 or -CDK4 complexes, and thus functions as a regulator of cell cycle progression at G1. Expression is tightly controlled by the tumor suppressor protein p53, through which this protein mediates the p53-dependent cell cycle G1 phase arrest in response to a variety of stress stimuli. This protein can interact with proliferating cell nuclear antigen (PCNA), a DNA polymerase accessory factor, and plays a regulatory role in S phase DNA replication and DNA damage repair. This protein was reported to be specifically cleaved by CASP3-like caspases, which thus leads to a dramatic activation of CDK2, and may be instrumental in the execution of apoptosis following caspase activation.
Fukuchi, K., et al., Biochim. Biophys. Acta 1642(3):163-171 (2003).
Frouin, I., et al., J. Biol. Chem. 278(41):39265-39268 (2003).
Dupont, J., et al., J. Biol. Chem. 278(39):37256-37264 (2003).
Di Padova, M., et al., J. Biol. Chem. 278(38):36496-36504 (2003).
Bai, Y.Q., et al., Oncogene 22(39):7942-7949 (2003).
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