Immunology Group, International Centre for Genetic Engineering and Biotechnology, Aruna Asaf Ali Marg, New Delhi, 110067, India.
Mol Cell Biochem. 2018 Mar;440(1-2):127-138. doi: 10.1007/s11010-017-3161-3. Epub 2017 Aug 29.
The success of Mycobacterium tuberculosis (Mtb) as a pathogen stems from its ability to manipulate the host macrophage towards increased lipid biogenesis and lipolysis inhibition. Inhibition of lipolysis requires augmented uptake of glucose into the host cell causing an upregulation of the glucose transporters GLUT1 and GLUT3 on the cell surface. Mechanism behind this upregulation of the GLUT proteins during Mtb infection is hitherto unknown and demands intensive investigation in order to understand the pathways linked with governing them. Our endeavor to investigate some of the key proteins that have been found to be affected during Mtb infection led us to investigate host molecular pathways such as Akt and PPAR-γ that remain closely associated with the survival of the bacilli by modulating the localization of glucose transporters GLUT1 and GLUT3.
结核分枝杆菌（Mtb）作为病原体的成功源于其能够操纵宿主巨噬细胞，促进脂质生物发生和脂解抑制。脂解抑制需要增加葡萄糖进入宿主细胞，导致葡萄糖转运蛋白 GLUT1 和 GLUT3 在细胞表面的上调。在 Mtb 感染过程中 GLUT 蛋白上调的背后机制尚不清楚，需要深入研究以了解与调控它们相关的途径。我们努力研究在 Mtb 感染过程中发现的一些关键蛋白，这使我们研究了 Akt 和 PPAR-γ 等宿主分子途径，这些途径通过调节葡萄糖转运蛋白 GLUT1 和 GLUT3 的定位，与细菌的存活密切相关。
