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首页> 外文期刊>Journal of Cellular Physiology >Constitutive internalization of murine MHC class I molecules.
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Constitutive internalization of murine MHC class I molecules.

机译：我本构的内化鼠MHC类分子。

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The total number of cell surface glycoprotein molecules at the plasma membrane results from a balance between their constitutive internalization and their egress to the cell surface from intracellular pools and/or biosynthetic pathway. Constitutive internalization is net result of constitutive endocytosis and endocytic recycling. In this study we have compared spontaneous internalization of murine major histocompatibility complex (MHC) class I molecules (K(d), D(d), full L(d), and empty L(d)) after depletion of their egress to the cell surface (Cycloheximide [CHX], brefeldin A [BFA]) and internalization after external binding of monoclonal antibody (mAb). MHC class I alleles differ regarding their cell surface stability, kinetics, and in the way of internalization and degradation. K(d) and D(d) molecules are more stable at the cell surface than L(d) molecules and, thus, constitutively internalized more slowly. Although the binding of mAbs to cell surface MHC class I molecules results in faster internalization than depletion of their egress, it is still slow and, thereby, can serve as a model for tracking of MHC class I endocytosis. Internalization of fully conformed MHC class I molecules (K(d), D(d), and L(d)) was neither inhibited by chlorpromazine (CP) (inhibitor of clathrin endocytosis), nor with filipin (inhibitor of lipid raft dependent endocytosis), indicating that fully conformed MHC class I molecules are internalized via the bulk pathway. In contrast, internalization of empty L(d) molecules was inhibited by filipin, indicating that non-conformed MHC class I molecules require intact cholesterol-rich membrane microdomains for their constitutive internalization. Thus, conformed and non-conformed MHC class I molecules use different endocytic pathways for constitutive internalization.
机译：细胞表面糖蛋白的总数从一个分子在质膜上的结果平衡他们的本构细胞内化和出口从细胞内池和/或表面生物合成途径。内化是本构的最终结果内吞作用和内吞作用的回收。相比我们有自发的学习小鼠主要的内化我组织相容性复合体”(MHC)类后细胞耗竭的出口表面(放线菌酮(CHX) brefeldin(论坛))和内化外部绑定的单克隆抗体(mAb)。关于细胞表面稳定性不同,动力学和内化的退化。稳定在比L (d)细胞表面分子,因此,既定的内化缓慢。我表面类MHC分子导致更快内化比消耗他们的出口,它仍然是缓慢的,从而可以作为MHC类的模型跟踪我内吞作用。我完全符合MHC类的内化分子(K (d)、d (d)和L (d))既不是抑制由氯丙嗪(CP)(抑制剂网格蛋白的内吞作用),也与菲律宾菌素(脂筏相关的内吞作用的抑制剂),我表示完全符合MHC类通过批量通路分子内化。相比之下,内化的空L (d)分子是由菲律宾菌素抑制,表明non-conformed MHC分子类我需要完整的那些高胆固醇膜microdomains他们的本构内化。符合我non-conformed MHC类分子使用不同的本构的内吞作用的途径内化。

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