PTP1B: a double agent in metabolism and oncogenesis

被引：289

作者：

Yip, Shu-Chin ^{[1
]}

Saha, Sayanti ^{[1
]}

Chernoff, Jonathan ^{[1
]}

机构：

[1] Fox Chase Canc Ctr, Philadelphia, PA 19111 USA

来源：

TRENDS IN BIOCHEMICAL SCIENCES | 2010年 / 35卷 / 08期

关键词：

PROTEIN-TYROSINE-PHOSPHATASE; INCREASED INSULIN SENSITIVITY; HUMAN BREAST-CANCER; ENDOPLASMIC-RETICULUM; 1B DEFICIENCY; IN-VIVO; SIGNALING PATHWAY; MEDIATED ADHESION; CRYSTAL-STRUCTURE; RECEPTOR;

D O I：

10.1016/j.tibs.2010.03.004

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

PTP1B, a non-transmembrane protein tyrosine phosphatase that has long been studied as a negative regulator of insulin and leptin signaling, has received renewed attention as an unexpected positive factor in tumorigenesis. Here, we highlight how views of this enzyme have evolved from regarding it as a simple metabolic off-switch to a more complex view of PTP1B as an enzyme that can play both negative and positive roles in diverse signaling pathways. These dual characteristics make PTP1B a particularly attractive therapeutic target for diabetes, obesity, and perhaps breast cancer.

引用

收藏

页码：442 / 449

页数：8

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