Volume 11, No 1, Mar 2001

ISSN: 1001-0602 
EISSN: 1748-7838 2018 
impact factor 17.848* 
(Clarivate Analytics, 2019)

Volume 11 Issue 1, March 2001: 55-60

ORIGINAL ARTICLES

p53-independent upregulation of p21^WAF1 in NIH 3T3 cells malignantly transformed by mot-2

TAKANO Syuichi^1,2, Renu WADHWA³, Youji MITSUI^1,2, Sunil C KAUL^1,*

¹National Institute of Bioscience and Human-Technology, AIST, 1-1 Higashi, Tsukuba, Ibaraki 305-8566, Japan
²Institute of Applied Biochemistry, University of Tsukuba, Tsukuba, Ibaraki 305-8577, Japan
³Chugai Research Institute for Molecular Medicine, 153-2 Nagai, Niihari-mura, Ibaraki 300-41, Japan
Correspondence:

Mot-2 protein is shown to interact with
p53 and inhibit its transcriptional activation function. Mot-2 overexpressing
stable clones of NIH 3T3 cells were malignantly transformed, however, they had a
high level of expression of a p53 downstream gene, p21^WAF1. The
present study was undertaken to elucidate possible molecular mechanism(s) of
such upregulation. An increased level of p21^WAF1 expression was
detected in stable transfectants although an exogenous reporter gene driven by
p21^WAF1 promoter exhibited lower activity in these cells suggesting
that some post-transcriptional mechanism contributes to upregulation. Western
analyses of transient and stable clones revealed that upregulation of p21^WAF1
in stable NIH 3T3/mot-2 cells may be mediated by cyclin D1 and cdk-2.

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