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Upstream Signalling of mTORC1 and Its Hyperactivation in Type 2 Diabetes (T2D)
Muhammad Ali1, Shazia Anwer Bukhari1, Muhammad Ali1, Han-Woong Lee1,*
1Department of Biochemistry and 2Department of Zoology, Government College University, Faisalabad, 38000 Pakistan,
3Department of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul 120-749, Republic of Korea
Abstract
Mammalian target of rapamycin complex 1 (mTORC1) is known to play a major role in cell growth, proliferation, polarity, differentiation, development, and controls transitioning between anabolic and catabolic states of the cell. It collects almost all extracellular and intracellular signals from growth factors, nutrients, and maintains cellular homeostasis, and is involved in a number of pathological conditions including, neurodegeneration, type 2 diabetes (T2D), obesity, and cancer. In this review, we summarize current knowledge of upstream signaling of mTORC1 to explain etiology of T2D and hypertriglyceridemia, in which state, a role of telomere attrition is explained. We also discuss if the chronic inhibition of mTORC1 can reverse adverse effects resulting from its hyperactivation. In conclusion, we suggest the regulatory role of telomerase (TERT) and hexokinase II (HKII) on mTORC1 as a possible remedy to treat its hyperactivation. The former inhibits mTORC1 under nutrient-rich while the latter under starved condition. We also provide an idea of TOS (TOR signaling) motifs that can be utilized for the regulation of mTORC1.
Abstract, Accepted Manuscript [Submitted on October 30, 2017, Accepted on October 30, 2017]
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