丝氨酸/苏氨酸蛋白激酶在结核分枝杆菌致病机制中的作用  

The role of serine/threonine protein kinases in Mycobacterium tuberculosis pathogenesis

作　　者：康涵[1] 吴文娟[1] 

机构地区：[1]上海市(复旦大学附属)公共卫生临床中心,上海201508

出　　处：《微生物与感染》2012年第1期56-61,共6页Journal of Microbes and Infections

基　　金："十一五"国家科技重大专项(2009ZX10004-505)

摘　　要：丝氨酸/苏氨酸蛋白激酶(STPK)是一类真核细胞样的蛋白激酶,是分枝杆菌生长和代谢的重要调节因子,参与其多种细胞活动(如细胞和菌落形态、葡萄糖和谷氨酰胺转运、吞噬体-溶酶体融合、转录因子活性等)的调节。结核分枝杆菌编码产生11种STPK(PknA、PknB、PknD～PknL),可分为5群(ABL群、HED群、FIJ群、PknG和PknK)。ABL群STPK中的PknA和PknB主要与细胞形态有关;PknL可磷酸化DNA结合蛋白Rv2175c。HED群参与细菌的多种重要生理活动并与致病性密切相关。FIJ群的PknF可能与葡萄糖转运和细菌分裂有关;PknI可能参与调节有害环境中的细菌生长;PknJ可磷酸化多种功能蛋白,进而影响细菌代谢活动。PknG参与谷氨酸盐/谷氨酰胺代谢,并与致病性有关。PknK可能对调节体内环境压力下的生长起重要作用。综上所述,STPK可能参与结核分枝杆菌致病过程中的多个环节,但详细机制还不清楚,仍需进一步研究。Mycobacteria-produced serine/threonine protein kinases （STPKs） are eukaryotic-like regulatory proteins involved in various cellular processes, including cell shape and morphology, glucose and glutamine transport, phagosome-lysosome fusion, and/or activity of transcription factors. Mycobacterium tuberculosis encodes 11 STPKs （PknA, PknB, PknD to PknL）, which are divided into five clusters （ABL, HED, FIJ, PknG and PknK）. PknA and PknB of the ABL cluster may play a role in morphology and cell division, and PknL can phosphorylate a DNA-binding protein Rv2175c. The HED cluster may be associated with several physiological processes and pathogenesis. PknF of the FU cluster may participate in glucose transport and cell division, PknI may regulate bacterial growth against hostile environments, and Pkrd may regulate bacterial metabolism by phosphorylating many functional proteins. PknG may play a role in glutamate/ glutamine metabolism and pathogenesis. PknK may be associated with regulating bacterial growth in hostile environment in vivo. In general, STPKs may participate in many steps in the pathogenesis of Mycobacterium tuberculosis, but details of the mechanisms involved remain unclear. Thus further investigations are required.

关 键 词：结核分枝杆菌 丝氨酸/苏氨酸蛋白激酶 发病机制 

分 类 号：R52[医药卫生—内科学]