小鼠巨噬細胞RAW264.7中hnRNP K磷酸化對COX-2 mRNA穩定度的調控

Abstract

當病原體感染發生在生物體中，許多細胞因子或即早基因，應迅速，準確地打開和關閉以進行免疫反應。嚴格地控制這些基因表現對預防免疫系統疾病是非常重要的。而利用RNA結合蛋白參與的轉錄後調控則是細胞用來操縱基因表達的策略之一。異質性核核糖核蛋白K，擁有三個可與RNA結合的KH（K-homology）結構域，並常涉及在調控後轉錄和轉譯的過程。為了研究hnRNP K在免疫反應中可能的功能，在脂多醣（LPS）處理過的小鼠RAW264.7巨噬細胞萃取物中以hnRNP K抗體進行RNA免疫沉澱。兩個即早基因：Tistetraproline（TTP）和腫瘤壞死因子-

When pathogen infection occurrs in organism, many cytokines or immediate genes (IEGs) are rapidly and precisely expressed and/or repressed for performing immune responses. Tight control of these genes is very important for preventing immune disorders. Post-transcriptional regulation involving in trans-acting RNA-binding proteins is one of the favorite strategies of cells to manipulate gene expression. Heterogeneous nuclear ribonucleoprotein K (hnRNP K), containing three KH (K-homology) domains that mediate RNA binding, is involved in the regulation of post-transcription and translation processes. To study the possible functions of hnRNP K in immune response, I performed anti-hnRNP K RNA immunoprecipitation assay with cell extracts from lipopolysaccharide (LPS)-treated mouse RAW264.7 macrophages. Two IEGs, Tistetraproline (TTP) and Tumor necrosis factor