Retooling of the beta 4 integrin in tumor cells--ligands lost and kinase gained.
作者信息
Hemler M E
机构信息
Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA.
出版信息
Dev Cell. 2001 Dec;1(6):728-30. doi: 10.1016/s1534-5807(01)00102-2.
Abstract
In carcinoma cells, the beta 4 integrin functions in a ligand-independent manner to promote proliferation, migration, and invasion. An interesting new paper describes a mechanism whereby the beta 4 integrin cytoplasmic tail becomes an integrin ligand-independent adaptor protein for the Met receptor tyrosine kinase, thereby enhancing the mitogenic, morphogenic, and motogenic properties of Met.
摘要
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