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BAR the door: Cancer suppression by amphiphysin-like genes

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出版社

ELSEVIER
DOI: 10.1016/j.bbcan.2008.09.001

关键词

Tumor suppressor; Modifier; Lung cancer; Vesicle trafficking; Indoleamine 2,3-dioxygenase; c-myc; Ras; Rho

资金

  1. NATIONAL CANCER INSTITUTE [R01CA100123, R01CA109542] Funding Source: NIH RePORTER
  2. NCI NIH HHS [R01 CA100123-01, R01 CA100123, R01 CA109542, R01 CA109542-02] Funding Source: Medline

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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.

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