murine missing in metastasis (mim) mediates cell polarity and regulates the motility response to growth factors小鼠失踪转移(mim)介导细胞极性和调节生长因子的活性反应.pdfVIP

Murine Missing in Metastasis (MIM) Mediates Cell Polarity and Regulates the Motility Response to Growth Factors 1 1 1 1,2 1,2,3 4 Dan Yu , Xiaoguo H. Zhan , Shuqiong Niu , Irina Mikhailenko , Dudley K. Strickland , Jianwei Zhu , Meng Cao1, Xi Zhan1,5,6* 1The Center for Vascular and Inflammatory Diseases, University of Maryland School of Medicine, Baltimore, Maryland, United of States of America, 2 Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland, United of States of America, 3 Department of Surgery, University of Maryland School of Medicine, Baltimore, Maryland, United of States of America, 4 Department of General Surgery, The Affiliated Hospital, Nantong University, The People’s Republic of China, 5 Department of Pathology, University of Maryland School of Medicine, Baltimore, Maryland, United of States of America, 6 University of Maryland Marlene Stewart Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, Maryland, United of States of America Abstract Background: Missing in metastasis (MIM) is a member of the inverse BAR-domain protein family, and in vitro studies have implied MIM plays a role in deforming membrane curvature into filopodia-like protrusions and cell dynamics. Yet, the physiological role of the endogenous MIM in mammalian cells remains undefined. Principal Findings: We have examined mouse embryonic fibroblasts (MEFs) derived from mice in which the MIM locus was targeted by a gene trapping vector. MIM2/ 2 MEFs showed a less polarized architecture characterized by smooth edges and fewer cell protrusions as compared to wild type cells, although the formation of filop