Erratum: Upstream signalling of mTORC1 and its hyperactivation in type 2 diabetes (T2D) [BMB Rep. 50, 12, (2017), 601-609]

Muhammad Ali, Shazia Anwer Bukhari, Han Woong Lee

Research output: Contribution to journalComment/debatepeer-review


Mammalian target of rapamycin complex 1 (mTORC1) plays 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 several 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, the role of telomere attrition is explained. We discuss if chronic inhibition of mTORC1 can reverse adverse effects resulting from hyperactivation. In conclusion, we suggest the regulatory roles of telomerase (TERT) and hexokinase II (HKII) on mTORC1 as possible remedies to treat hyperactivation. The former inhibits mTORC1 under nutrientrich while the latter under starved condition. We provide an idea of TOS (TOR signaling) motifs that can be used for regulation of mTORC1.

Original languageEnglish
Pages (from-to)45-53
Number of pages9
JournalBMB reports
Issue number1
Publication statusPublished - 2018

Bibliographical note

Publisher Copyright:
© 2018 by the The Korean Society for Biochemistry and Molecular Biology.

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology


Dive into the research topics of 'Erratum: Upstream signalling of mTORC1 and its hyperactivation in type 2 diabetes (T2D) [BMB Rep. 50, 12, (2017), 601-609]'. Together they form a unique fingerprint.

Cite this