亨廷顿病(huntington’s disease,HD)是一种遗传性神经退化性疾病,其发生癌症的危险性明显低于其一级亲属及一般人群,预示着HD患者体内应该存在某些可以抑制肿瘤发生发展的生物活性物质。近些年来亨廷顿相关蛋白1(huntingtin-associated...亨廷顿病(huntington’s disease,HD)是一种遗传性神经退化性疾病,其发生癌症的危险性明显低于其一级亲属及一般人群,预示着HD患者体内应该存在某些可以抑制肿瘤发生发展的生物活性物质。近些年来亨廷顿相关蛋白1(huntingtin-associated protein 1,HAP1)因与亨廷顿蛋白相互作用并直接或间接影响了HD的发病机制从而倍受关注,论文就HAP1近些年的研究进展作一概括阐述,以期为预测肿瘤发生发展提供一种功能性分子标志物。展开更多
Post-translational modifications are rapid, effective and reversible ways to regulate protein stability, localization, function, and their interactions with other molecules. Post-translational modifications usually oc...Post-translational modifications are rapid, effective and reversible ways to regulate protein stability, localization, function, and their interactions with other molecules. Post-translational modifications usually occur as chemical modifications at amino acid residues, including SUMOylation, phosphorylation, palmitoylation, acetylation, etc. These complex biochemical modifications tightly regulate and control a variety of cellular processes. Several forms of post-translational modifications of huntingtin （Htt） have been described. These modifications affect Htt metabolism, protein-protein interactions and cellular toxicity. Cleavage and clearance of mutant Htt, and the interactions between mutant Htt and other cellular proteins are important biochemical events leading to Huntington＇s disease （HD）. Therefore, identifying signaling pathways of Htt modification and evaluating the significance of Htt modifications would lead to a better understanding of the normal function of wild-type Htt and the pathogenic mechanisms of mutant Htt.展开更多
文摘亨廷顿病(huntington’s disease,HD)是一种遗传性神经退化性疾病,其发生癌症的危险性明显低于其一级亲属及一般人群,预示着HD患者体内应该存在某些可以抑制肿瘤发生发展的生物活性物质。近些年来亨廷顿相关蛋白1(huntingtin-associated protein 1,HAP1)因与亨廷顿蛋白相互作用并直接或间接影响了HD的发病机制从而倍受关注,论文就HAP1近些年的研究进展作一概括阐述,以期为预测肿瘤发生发展提供一种功能性分子标志物。
基金supported by grants from the National Natural Science Foundation of China (No.30600197)
文摘Post-translational modifications are rapid, effective and reversible ways to regulate protein stability, localization, function, and their interactions with other molecules. Post-translational modifications usually occur as chemical modifications at amino acid residues, including SUMOylation, phosphorylation, palmitoylation, acetylation, etc. These complex biochemical modifications tightly regulate and control a variety of cellular processes. Several forms of post-translational modifications of huntingtin （Htt） have been described. These modifications affect Htt metabolism, protein-protein interactions and cellular toxicity. Cleavage and clearance of mutant Htt, and the interactions between mutant Htt and other cellular proteins are important biochemical events leading to Huntington＇s disease （HD）. Therefore, identifying signaling pathways of Htt modification and evaluating the significance of Htt modifications would lead to a better understanding of the normal function of wild-type Htt and the pathogenic mechanisms of mutant Htt.
