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. 2019 Jan 16;6:424. doi: 10.3389/fped.2018.00424

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Copyright © 2019 Nicolescu, Al-Khawaga, Minassian and Hussain.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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(A) Glycogen metabolism, degradation, and glycogen-metabolizing protein interactions. Both insulin and exercise increase glucose uptake via GLUT4. Increased Glucose-6-phosphate (G6P) levels provide feedforward activation of glycogen synthase (GS). HK, hexokinase; G6Pase, glucose-6-phosphatase; GNG, gluconeongenesis; PGM, phosphoglucomutase; GAA, lysosomal α-glucosidase; BE, branching enzyme; PH, glycogen phosphorylase; UP, UPD-glucose pyrophosphorylase; UGPPase, UDP-glucose pyrophosphatase; GN, glycogenin; GS, glycogen synthase; DBE, debranching enzyme; PKA, protein kinase A; LB, Lafora bodies (10). (B) A schematic illustration of Lamin structure with patient's mutation (p.Pro129His) in the NHL domain. Malin contains a RING domain and six NHL repeats.