p53-Independent Elevation of p21 Expression by PMA Results from PKC-Mediated mRNA Stabilization

Authors
Jong-Wook ParkMin-Ah JangYoung Han LeeAntonino PassanitiTaeg Kyu Kwon
Department
Dept. of Immunology (면역학)
Issue Date
2001
Citation
Biochemical and Biophysical Research Communications, Vol.280(1) : 244-248, 2001
ISSN
0006-291X
Abstract
The p21 (cip1/waf1) protein induces cell cycle arrest through inhibition of the activity of cdk (cyclin dependent kinase)/cyclin complexes. Expression of p21 is induced in a p53-dependent manner by DNA damage. p21 can also be induced independently of p53 by phorbol ester or okadaic acid. In this study, we have addressed the role of the PKC (protein kinase C) signaling pathway in the induction of p21 in response to PMA (phorbol myristate acetate) and okadaic acid. Levels of p21 (protein and mRNA) rapidly increased (within ∼4 h) in U937 cells treated with PMA. The PKC-specific inhibitors RO 31-8220 and GF109203X down-regulated PMA or okadaic acid-induced p21 expression. Following persistent PKC activation, p21 mRNA levels remained elevated, indicating an enhanced stability of the mRNA. Using actinomycin D to measure mRNA stability and p21 promoter luciferase assays to measure activity, we provide evidence to support a role for the PKC signaling pathway in p21 mRNA stability. Thus, PKC regulates the amount of p21 in U937 cells at the level of mRNA accumulation and translation.
URI
http://kumel.medlib.dsmc.or.kr/handle/2015.oak/35193
Appears in Collections:
1. Journal Papers (연구논문) > 1. School of Medicine (의과대학) > Dept. of Immunology (면역학)
Keimyung Author(s)
박종욱; 권택규
Full Text
https://linkinghub.elsevier.com/retrieve/pii/S0006291X00941056
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