丝氨酸/苏氨酸蛋白激酶（STPK）是一类真核细胞样的蛋白激酶，是生长和代谢的重要调节因子，参与分枝杆菌多种细胞活动（如细胞及菌落形态、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。

Serine-threonine protein kinases (STPKs) are eukaryotic-like protein kinases, which are important regulator of bacterial growth and metabolism, involved in various cellular processes of mycobacteria, including cell shape and morphology, glucose and glutamine transport, phagosome-lysosome fusion, and/or activity of transcription factors. Mycobacterium tuberculosis encodes 11 eukaryotic-like STPKs (PknA, PknB, PknD to PknL), which are divided into five clusters, ABL cluster, HED cluster, FIJ cluster, PknG and PknK. PknA and PknB of ABL cluster may play a role in morphology and cell division, and PknL can phosphorylate a DNA-binding protein Rv2175c. HED cluster may be associated with several physiological process and pathogenesis. PknF of FIJ cluster may participate in glucose transport and cell division, PknI may regulate bacterial growth against hostile environment, and PknJ may regulate bacterial metabolism by phosphorylating many functional protein. 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 more details of the mechanisms involved remain unclear to further investigation. Thus further studies are needed to uncover the mystery.