BAR the door: Cancer suppression by amphiphysin-like genes

被引：54

作者：

Prendergast, George C. ^{[1
,2
]}

Muller, Alexander J. ^{[1
,2
]}

Ramalingam, Arivudanambi ^{[1
]}

Chang, Mee Young ^{[1
]}

机构：

[1] Lankenou Inst Med Res, Wynnewood, PA USA

[2] Thomas Jefferson Univ, Kimmel Canc Ctr, Philadelphia, PA 19107 USA

来源：

BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER | 2009年 / 1795卷 / 01期

关键词：

Tumor suppressor; Modifier; Lung cancer; Vesicle trafficking; Indoleamine 2,3-dioxygenase; c-myc; Ras; Rho; C-MYC; TUMOR-SUPPRESSOR; INDOLEAMINE 2,3-DIOXYGENASE; PROTEIN-INTERACTION; CELL-PROLIFERATION; SH3; DOMAIN; FARNESYLTRANSFERASE INHIBITORS; ACTIN CYTOSKELETON; CRYSTAL-STRUCTURE; BIN1; ABLATION;

D O I：

10.1016/j.bbcan.2008.09.001

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The evolutionarily conserved amphiphysin-like genes Bin1 and Bin3 function in membrane and actin dynamics, cell polarity, and stress signaling. Recent genetic studies in mice discriminate non-essential roles in endocytic processes commonly ascribed to amphiphysins from essential roles in cancer suppression. Bin I acts in default pathways of apoptosis and senescence that are triggered by the Myc and Raf oncogenes in primary cells, and Bin1 gene products display a 'moonlighting function' in the nucleus where a variety of other 'endocytic' proteins are also found. Together, genetic investigations in yeast, flies, and mice suggest that amphiphysin-like adapter proteins may suppress cancer by helping integrate cell polarity signals generated by actin and vesicle dynamics with central regulators of cell cycle arrest, apoptosis, and immune surveillance. (C) 2008 Elsevier B.V. All rights reserved.

引用

页码：25 / 36

页数：12

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