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10.3389/fgene.2020.582368 http://scihub22266oqcxt.onion/10.3389/fgene.2020.582368 33193709!7556298!33193709     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=33193709&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Front+Genet 2020 ; 11 (?): 582368 Nephropedia Template TP {{tp|p=33193709|t=2020. Hamartin: An Endogenous Neuroprotective Molecule Induced by Hypoxic Preconditioning |pdf=|usr=}}{{33193709}} gab.com Text Hamartin: An Endogenous Neuroprotective Molecule Induced by Hypoxic Preconditioning JO: Front Genet http://www.kidney.de/pget.php?&tw=1&pmid=33193709 #FOAvip 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. Twit Text FOAVip Hamartin: An Endogenous Neuroprotective Molecule Induced by Hypoxic Preconditioning ????Front Genet http://www.kidney.de/pget.php?&tw=1&pmid=33193709 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33193709 #FOAvip English Wikipedia <ref>{{Cite pmid|33193709}}</ref> Hamartin: An Endogenous Neuroprotective Molecule Induced by Hypoxic Preconditioning #MMPMID33193709 Li S; Ren C; Stone C; Chandra A; Xu J; Li N; Han C; Ding Y; Ji X; Shao G Front Genet 2020[]; 11 (?): 582368 PMID33193709show ga 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. ?Hamartin: An Endogenous Neuroprotective Molecule Induced by Hypoxic P(epmc).pdf DeepDyve Pubget Overpricing