SHP-2 and PTP-pest induction during Rb-E2F associated apoptosis

Cellular & Molecular Biology Letters

Jonathan H. Lieman³  Dae Joon Kim²  Liza D. Morales¹  Karina Pena³ 

[1] Department of Biology, The University of Texas-Pan American, Edinburg, USA$$Edinburg Regional Academic Health Center, Medical Research Division, University of Texas Health Science Center at San Antonio, Edinburg, USA$$;Department of Pharmacology, University of Texas Health Science Center at San Antonio, Edinburg, USA$$Edinburg Regional Academic Health Center, Medical Research Division, University of Texas Health Science Center at San Antonio, Edinburg, USA$$;Department of Biology, The University of Texas-Pan American, Edinburg, USA$$

关键词: Apoptosis;    Focal adhesion kinase;    Rb;    E2F-1;    Phosphatase;    PTP-1B;    SHP-2;    PTP-PEST;    PTPN1;    PTPN11;    PTPN12;    Tumor suppressor;   

DOI  :  10.2478/s11658-012-0020-9

学科分类：分子生物学，细胞生物学和基因

来源: Uniwersytet Wroclawski * Wydzial Biotechnologii / University of Wroclaw, Faculty of Biotechnology

【 摘 要 】

Apoptosis is intimately connected to cell cycle regulation via the Retinoblastoma (Rb)-E2F pathway and thereby serves an essential role in tumor suppression by eliminating aberrant hyperproliferative cells. Upon loss of Rb activity, an apoptotic response can be elicited through both p53-dependent and p53-independent mechanisms. While much of this apoptotic response has been attributed to the p19ARF/p53 pathway, increasing evidence has supported the role of protein tyrosine phosphatases (PTPs) in contributing to the initiation of the Rb-E2F-associated apoptotic response. One protein tyrosine phosphatase, PTP-1B, which is induced by the Rb-E2F pathway, has been shown to contribute to a p53-independent apoptotic pathway by inactivating focal adhesion kinase. This report identifies two additional PTPs, SHP-2 and PTP-PEST, that are also directly activated by the Rb-E2F pathway and which can contribute to signal transduction during p53-independent apoptosis.

【 授权许可】

Unknown