把门闩上：类发动蛋白基因对癌症的抑制作用
BAR the door: cancer suppression by amphiphysin-like genes.
作者信息
Prendergast George C, Muller Alexander J, Ramalingam Arivudanambi, Chang Mee Young
机构信息
Lankenau Institute for Medical Research, Wynnewood PA, USA.
出版信息
Biochim Biophys Acta. 2009 Jan;1795(1):25-36. doi: 10.1016/j.bbcan.2008.09.001. Epub 2008 Sep 18.
Abstract
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. Bin1 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.
摘要
进化上保守的类发动蛋白基因Bin1和Bin3在膜和肌动蛋白动力学、细胞极性及应激信号传导中发挥作用。近期对小鼠的遗传学研究区分了通常归因于发动蛋白的内吞过程中的非必需作用与癌症抑制中的必需作用。Bin1在原代细胞中由Myc和Raf癌基因触发的凋亡和衰老的默认途径中起作用，并且Bin1基因产物在细胞核中发挥“兼职功能”，在细胞核中还发现了多种其他“内吞”蛋白。总之，酵母、果蝇和小鼠中的遗传学研究表明，类发动蛋白衔接蛋白可能通过帮助整合由肌动蛋白和囊泡动力学产生的细胞极性信号与细胞周期停滞、凋亡和免疫监视的中心调节因子来抑制癌症。
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