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. 2014 Dec 3;1(12):1024–1035. doi: 10.1002/acn3.149

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© 2014 The Authors. Annals of Clinical and Translational Neurology published by Wiley Periodicals, Inc on behalf of American Neurological Association.

This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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PTRH2 mediates cell survival and cell size. Simplified schematic drawing indicates model of putative role of PTRH2 in control of cell survival and cell size pathways. PTRH2, peptidyl-tRNA hydrolase 2; AES, amino-terminal enhancer of split; FAK, focal adhesion kinase; PI3K, phosphatidylinositide 3-kinase; AKT, serine/threonine-specific kinase or protein kinase B; ERK, extracellular signal-regulated kinase; NFκB, nuclear factor kappa-light-chain-enhancer of activated B cells; Bcl2, B-cell lymphoma 2; mTOR, mechanistic target of rapamycin (serine/threonine kinase); S6K, ribosomal protein S6 kinase; 4EBP, eukaryotic initiation factor-4E-binding protein. Modified according to Jan et al.3 and Griffiths et al.4