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Arrest defective 1 autoacetylation is a critical step in its ability to stimulate cancer cell proliferation

Title
Arrest defective 1 autoacetylation is a critical step in its ability to stimulate cancer cell proliferation
Authors
Seo J.H.Cha J.-H.Park J.-H.Jeong C.-H.Park Z.-Y.Lee H.-S.Oh S.H.Kang J.-H.Suh S.W.Kim K.H.Ha J.Y.Han S.H.Kim S.-H.Lee J.-W.Park J.A.Jeong J.-W.Lee K.-J.Oh G.T.Lee M.-N.Kwon S.W.Lee S.-K.Chun K.-H.Lee S.-J.Kim K.-W.
Ewha Authors
이공주오구택이미니
SCOPUS Author ID
이공주scopus; 오구택scopus; 이미니scopusscopus
Issue Date
2010
Journal Title
Cancer Research
ISSN
0008-5472JCR Link
Citation
vol. 70, no. 11, pp. 4422 - 4432
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
The N-acetyltransferase arrest defective 1 (ARD1) is an important regulator of cell growth and differentiation that has emerged recently as a critical molecule in cancer progression. However, the regulation of the enzymatic and biological activities of human ARD1 (hARD1) in cancer is presently poorly understood. Here, we report that hARD1 undergoes autoacetylation and that this modification is essential for its functional activation. Using liquid chromatography-tandem mass spectrometry and site-directed mutational analyses, we identified K136 residue as an autoacetylation target site. K136R mutation abolished the ability of hARD1 to promote cancer cell growth in vitro and tumor xenograft growth in vivo. Mechanistic investigations revealed that hARD1 autoacetylation stimulated cyclin D1 expression through activation of the transcription factors β-catenin and activator protein-1. Our results show that hARD1 autoacetylation is critical for its activation and its ability to stimulate cancer cell proliferation and tumorigenesis. ©2010 AACR.
DOI
10.1158/0008-5472.CAN-09-3258
Appears in Collections:
약학대학 > 약학과 > Journal papers
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