crim1 complexes with ?-catenin and cadherins, stabilizes cell-cell junctions and is critical for neural morphogenesiscrim1复合物连环蛋白和钙粘蛋白,稳定和信息枢纽和对神经形态发生至关重要.pdfVIP
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crim1 complexes with ?-catenin and cadherins, stabilizes cell-cell junctions and is critical for neural morphogenesiscrim1复合物连环蛋白和钙粘蛋白,稳定和信息枢纽和对神经形态发生至关重要
CRIM1 Complexes with ß-catenin and Cadherins, Stabilizes Cell-Cell Junctions and Is Critical for Neural Morphogenesis Virgilio G. Ponferrada1,2, Jieqing Fan1,2,5, Jefferson E. Vallance1,2, Shengyong Hu1,3, Aygun 1,3 3 3 3 1,3 Mamedova , Scott A. Rankin , Matthew Kofron , Aaron M. Zorn , Rashmi S. Hegde *, Richard A. Lang1,2,3,4,5* 1The Visual Systems Group, Cincinnati Children’s Hospital Medical Center, University of Cincinnati, Cincinnati, Ohio, United States of America, 2 Divisions of Pediatric Ophthalmology, Cincinnati Children’s Hospital Medical Center, University of Cincinnati, Cincinnati, Ohio, United States of America, 3 Divisions of Developmental Biology, Cincinnati Children’s Hospital Medical Center, University of Cincinnati, Cincinnati, Ohio, United States of America, 4 Department of Ophthalmology, University of Cincinnati, Cincinnati, Ohio, United States of America, 5 Molecular and Developmental Biology Graduate Program, University of Cincinnati, Cincinnati, Ohio, United States of America Abstract In multicellular organisms, morphogenesis is a highly coordinated process that requires dynamically regulated adhesion between cells. An excellent example of cellular morphogenesis is the formation of the neural tube from the flattened epithelium of the neural plate. Cysteine-rich motor neuron protein 1 (CRIM1) is a single-pass (type 1) transmembrane protein that is expressed in neural structures beginning at the neural plate stage. In the frog Xenopus laevis, loss of function studies using CRIM1 antisense morpholino oligonucleotides resulted in a failure of neural development. The CRIM1 knockdown phenotype was, in some cases,
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