p53 tumor suppressor gene mutations are one of the most common genetic alterations in human tumors, including lymphomas.
Altering or inactivating p53 by mutation or reaction with oncogenes or viruses may cause depletion of p53, or conversion of p53 from a tumor suppressor gene to a transforming oncogene.
The nuclear protein p53 is associated with cell transformation and proliferation, with definitive possibilities as a marker in malignant lymphoma progression.
p53's role in the multistep process leading to cancer is still being investigated, with an emphasis on its relation and control over additional tumor suppressors.
Expression correlates with poor prognosis in breast cancer.
In colonic cancer p53 expression seen in 47% of tumors and 9% of colonomas.
The p53 tumor suppressor protein plays a major role in cellular response to DNA damage and other genomic aberrations.
Activation of p53 can lead to either cell cycle arrest and DNA repair or apoptosis.
p53 is phosphorylated at multiple sites in vivo and by several different protein kinases in vitro.
DNA damage induces phosphorylation of p53 at Ser15 and Ser20 and leads to reduced interaction of p53 with its negative regulator, oncoprotein MDM2.
MDM2 inhibits the accumulation of p53 by targeting it for ubiquitination and proteasomal degradation.
p53 can apparently be phosphorylated by ATM, ATR and DNA-PK at Ser15 and Ser37; the phosphorylations impair the ability of MDM2 to bind p53, promoting both the accumulation and functional activation of p53 in response to DNA damage.
Chk2 and Chk1 can phosphorylate p53 at Ser20, enhancing its tetramerization, stability and activity.
p53 is phosphorylated at Ser392 in vivo and by CAK in vitro.
Phosphorylation of p53 at Ser392 is altered in human tumors and has been reported to influence the growth suppressor function, DNA binding and transcriptional activation of p53.
p53 is phosphorylated at Ser6 and Ser9 by ck1delta and ck1epsilon both in vitro and in vivo).
Phosphorylation of p53 at Ser46 is important in regulating the ability of p53 to induce apoptosis.
Applications:Suitable for use in Western Blot and Immunoprecipitation.
Other applications not tested.
Recommended Dilution:Western Blot: 0.5-2ug/ml.
Raji cell lysate was resolved by electrophoresis, transferred to nitrocellulose and probed with P1001-30 (1ug/ml).
Proteins were visualized using a goat anti-mouse secondary antibody conjugated to HRP and a chemiluminescence detection system.
Optimal dilutions to be determined by the researcher.
