Hamartin: An Endogenous Neuroprotective Molecule Induced by Hypoxic Preconditioning

Frontiers in Genetics
Sijie LiGuo Shao

Abstract

Hypoxic/ischemic preconditioning (HPC/IPC) is an innate neuroprotective mechanism in which a number of endogenous molecules are known to be involved. Tuberous sclerosis complex 1 (TSC1), also known as hamartin, is thought to be one such molecule. It is also known that hamartin is involved as a target in the rapamycin (mTOR) signaling pathway, which functions to integrate a variety of environmental triggers in order to exert control over cellular metabolism and homeostasis. Understanding the role of hamartin in ischemic/hypoxic neuroprotection will provide a novel target for the treatment of hypoxic-ischemic disease. Therefore, the proposed molecular mechanisms of this neuroprotective role and its preconditions are reviewed in this paper, with emphases on the mTOR pathway and the relationship between the expression of hamartin and DNA methylation.

References

Sep 24, 1990·Brain Research·K KitagawaK Mikoshiba
Aug 8, 1997·Science·M van SlegtenhorstD J Kwiatkowski
Jun 13, 1998·Human Molecular Genetics·M van SlegtenhorstP van der Sluijs
Feb 23, 1999·Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism·M Shamloo, T Wieloch
Dec 10, 1999·The Journal of Biological Chemistry·M NellistP van der Sluijs
Mar 27, 2001·Modern Pathology : an Official Journal of the United States and Canadian Academy of Pathology, Inc·M W JohnsonH V Vinters
Oct 11, 2003·The Journal of Biological Chemistry·Aristotelis AstrinidisElizabeth Petri Henske
Jan 20, 2004·Trends in Biochemical Sciences·Yong LiKun-Liang Guan
May 22, 2004·Nature Reviews. Genetics·Melissa J Fazzari, John M Greally
Feb 8, 2005·Seminars in Perinatology·Henrik HagbergAlan Leviton
Apr 15, 2005·Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism·Yun S SongPak H Chan
Jun 2, 2005·Neurotoxicology·Stefano BartesaghiBarbara Viviani
Jun 15, 2005·Molecular Neurobiology·Guo-Wei LuCui-Ying Gao
Jul 7, 2005·Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology·Evanthia GalanisUNKNOWN North Central Cancer Treatment Group
Feb 9, 2006·The Journal of Biological Chemistry·Huira Chong-KoperaKun-Liang Guan
Feb 18, 2006·Molecular Cell·Liping LiuM Celeste Simon
Feb 20, 2007·Neurobiology of Disease·Vincent LaudenbachPierre Gressens
Apr 20, 2007·The Journal of Neuroscience : the Official Journal of the Society for Neuroscience·Yi-Bing OuyangRona G Giffard
Jul 7, 2007·Cancer Cell·David A Guertin, David M Sabatini
Jul 25, 2007·Molecular and Cellular Biochemistry·Evan GomesPatricia Rockwell
May 10, 2008·The Biochemical Journal·Jingxiang Huang, Brendan D Manning
May 19, 2009·Journal of Clinical Neuroscience : Official Journal of the Neurosurgical Society of Australasia·Satoshi TaieMasaaki Ueki
Sep 8, 2009·Nature Neuroscience·Hong-Shuo SunMichael Tymianski
Nov 6, 2009·American Journal of Physiology. Endocrinology and Metabolism·Julia KovsanAssaf Rudich
Sep 2, 2010·Journal of Neuroscience Research·Zhi-Yong ChenConstance Tom Noguchi
Sep 18, 2010·Trends in Pharmacological Sciences·Xiaojing YangPeter A Jones
Dec 4, 2010·Science·Joshua D Rabinowitz, Eileen White

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Methods Mentioned

BETA
GTPase
genetic modifications

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