Besides tumor suppression, what’s p53 busy for during embryogenesis?
Besides tumor suppression, what’s p53 busy for during embryogenesis?
p53 is well known as a tumor suppressor by inducing cell cycle arrest and apoptosis. Inactivation of p53 inhibitors Mdm2 and Mdm4 leads to embryonic lethality. However, the regulation of p53 activity is not fully understood. A recent article published on Nature Communications by Dr. Riascos-Bernal and his colleagues shows that β-catenin promotes vascular SMC (smooth muscle cell) proliferation and survival during artery formation by inhibiting p53 activity. Loss of SMC β-catenin causes impaired arterial maturation and embryonic lethality. The vascular phenotype caused by loss of β-catenin is suppressed when lacking p53. Moreover, the authors proved that β-catenin C-terminal indirect interactions are required for repression of p53 activity. This study is the first report to demonstrate that SMC β-catenin is essential for developmental vascular maturation and p53 is involved in this process. For further related study, arigo’s antibodies and reagents are ready for you!
p53 and β-catenin antibody available for identification of associated protein complex
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Endothelial marker CD31 and SMC markers Sm22α and α-SMA
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Endothelial marker CD31 | Endothelial marker CD31 | SMC marker α-SMA | ||
Human tonsil. | Paraffin-embedded human colon carcinoma. | Human heart. |
Reference:
Riascos-Bernal et al. (2016) Nat Commun. 7:12389.