mRNA 编辑：C 到 U 转换
中文名称
通路描述
肠道apolipoprotein B转录本中C到U编辑的最佳已知案例，该编辑事件产生提前终止密码子，从而导致蛋白质缩短。在肝脏中，C到U编辑对于apolipoprotein B酶特定异构体的表达很重要。ApoB mRNA编辑是一种转录后、核内过程，可在剪接后、多聚腺苷酸化时启动，并在pre-mRNA完全成熟前完成（参考Blanc和Davidson, 2003）。该编辑事件是简单的胞苷脱氨作用转化为尿嘧啶，由Apobec-1酶及其互补因子ACF执行。ApoB mRNA的编辑涉及(C6666到U)的特异性胞苷脱氨作用，将密码子2153从谷氨酰胺密码子CAA转换为提前终止密码子UAA。由于ACF在多种组织中分布，且这些基因包含多个家族成员，因此可能在其他靶点上发现编辑事件。C到U编辑的顺式作用调控元件包括：ApoB mRNA内的22 nt编辑位点，5'三叶草结构域及其相邻的增强子元件，以及位于胞苷3'侧的间隔序列和锚定序列（参考Smith等, 1997）。
英文描述
Role of LAT2/NTAL/LAB on calcium mobilization The lipid raft resident adaptor molecules LAT1 and Non-T cell activation linker (NTAL), also known as linker for activation of B cells (LAB)/LAT2 are known participants in the regulation of mast cell calcium responses. Both LAT and NTAL are expressed and phosphorylated following engagement of FCERI on mast cells. NTAL is functionally and topographically different from LAT. There is a considerable debate on the role of NTAL in mast cell. Depending on the circumstances, NTAL appears to have a dual role as positive and negative regulator of MC responses elicited via FCERI. Studies conducted in bone marrow-derived mast cells (BMMCs) of mice lacking NTAL displayed enhanced FCERI-mediated tyrosine phosphorylation of several substrates, calcium response, degranulation, and cytokine production. This indicated that NTAL negatively regulates FCERI-mediated degranulation. However, in mice lacking both LAT and NTAL showed severe block in FCERI-mediated signaling than BMMCs deficient in LAT alone, suggesting that NTAL also shares a redundant function with LAT to play a positive role (Draberova et al. 2007, Orr & McVicar. 2011, Zhu et al. 2004, Volna et al. 2004). The major steps in NTAL mediated Ca+2 influx involves NTAL--> GAB2--> PI3K
所含基因
24 个基因