机译:水痘带状疱疹病毒糖蛋白B中基于免疫受体酪氨酸的抑制基序调节细胞融合和皮肤发病机理
Departments of Pediatrics , Stanford University School of Medicine, Stanford, CA 94305;
Departments of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305;
Departments of Pediatrics, Stanford University School of Medicine, Stanford, CA 94305;
Departments of Pediatrics, Stanford University School of Medicine, Stanford, CA 94305,Pathology Core Labs Electron Microscopy, Genentech, South San Francisco, CA 94080;
Departments of Pediatrics, Stanford University School of Medicine, Stanford, CA 94305;
Departments of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305;
Departments of Pediatrics, Stanford University School of Medicine, Stanford, CA 94305,Departments of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305;
fusogenicity; mutagenesis; polykaryocyte; virulence;
机译:IRF-1调节乳腺癌上皮细胞中癌胚抗原相关细胞粘附分子1(CEACAM1)的替代性mRNA剪接,产生包含同种型的基于免疫酪氨酸的抑制基序(ITIM)
机译:VariCella-Zoster病毒糖蛋白M的C-末端含有贩运的基序,其在VZV发病机制的SCID - 人模型中介导皮肤毒力
机译:水痘带状疱疹病毒糖蛋白H的胞质域调节合胞体形成和皮肤发病机理。
机译:水痘-带状疱疹病毒感染的宿主细胞核和PML笼的3D重建通过连续切片阵列-SEM和TEM断层扫描
机译:Syk串联SH2域与基于免疫受体酪氨酸的激活基序相互作用的变构调节机制的生物物理研究。
机译:水痘带状疱疹病毒糖蛋白B中基于免疫受体酪氨酸的抑制基序调节细胞融合和皮肤发病机理
机译:水痘-带状疱疹病毒糖蛋白B的诱变:假定的融合环残留物对于病毒复制是必不可少的,并且弗林蛋白酶切割基序有助于体内皮肤组织的发病机理。
机译:以色列农业住区居民和海外志愿者中肠道病毒和水痘 - 带状疱疹病毒抗体的流行