期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 434, 期 4, 页码 735-739出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2013.03.103
关键词
GSK3 beta; Akt; Diabete mellitus; Drug discovery
资金
- National Research Foundation of Korea [2011-0015420]
- National Research Foundation of Korea [2011-0015420] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Abnormal overexpression of GSK3 beta has been implicated in insulin resistance. Although many potent GSK3 beta inhibitors have been developed as drug candidates for anti-insulin resistance, the inhibitors are prone to show side effects because they interfere with normal GSK3 beta function without regulation. Recently, it was reported that the PPPSPxS motifs in the Wnt coreceptor LRP6 were able to directly inhibit GSK3 beta only when the motif was phospholylated. Here, we generated a new GSK3 beta inhibitory peptide that can be activated by Akt by combining the PPPSPxS motif and an Akt target sequence. The peptide exhibited an inhibitory effect on GSK3 beta only when it was phosphorylated by Akt in a purified system and in cells when stimulated by insulin. Thus, our findings provide a novel concept for drugs against diseases that are involved in the abnormal GSK3 beta activity, including type 2 diabetes mellitus. (c) 2013 Elsevier Inc. All rights reserved.
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