Missense Mutation of Pro387Leu in Protein Tyrosine Phosphatase-1B (PTP-1B) Is Not Associated With Type 2 Diabetes in a Chinese Han Population
- Jianping Weng, MD, PHD,
- Jinhua Yan, MD,
- Zhimin Huang, MD,
- Yi Sui, MD and
- Lingling Xiu, MD, PHD
- Department of Endocrinology, the First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China
- Address correspondence to Prof. Jianping Weng, Department of Endocrinology, the First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong, China 510080. E-mail: gzwengjp{at}pub.guangzhou.gd.cn
Type 2 diabetes is both a phenotypically and geneotypically heterogeneous disease. It is caused by defective insulin secretion and action. Protein tyrosine phosphatases (PTPases) play important roles in insulin cascade signal transduction and have been suggested to be related to insulin resistance (1,2). PTP-1B, a member of the PTP family, is expressed widely in many tissues, acting as a negative regulator in the insulin receptor signal transduction pathway (3–5). The PTP-1B gene is located on the long arm of human chromosome 20, in the region of q13.1–q13.2, which has been linked to quantitative trait loci of obesity and insulin (6,7). A recent study by Echwald S.M. et al. (8) demonstrated that a Pro387Leu variation of the …
