“…Expression for TPPP3 (tubulin polymerization-promoting protein family member 3), ATP1B1 (ATPase, Na+/K+ transporting, beta 1 polypeptide), BTG2 (BTG family, member 2), KDM2B (lysine-specific demethylase 2B), RGCC (regulator of cell cycle), KLF2 (Kruppel-like factor 2), VIMP (VCP-interacting membrane protein), CD93 (CD93 molecule), SORD (sorbitol dehydrogenase), LMCD1 (LIM and cysteine-rich domains 1), ITIH5 (inter-alpha-trypsin inhibitor heavy chain family, member 5), and CTNNA1 [catenin (cadherin-associated protein), alpha 1, 102 kDa] were increased in PeM compared to BPR, while expression of SLC7A2 [solute carrier family 7 (cationic amino acid transporter, y + system), member 2], ELL2 (elongation factor, RNA polymerase II, 2), NRIP1 (nuclear receptor interacting protein 1) and UGP2 (UDP-glucose pyrophosphorylase 2) were decreased by PRKAG3 in PeM. All of these downstream molecules of PRKAG3 are involved in either a) glucose metabolism (SORD [37], UGP2 [38], VIMP [39]), b) cytoskeletal formation (TPPP3 [40], CD93 [41], CTNNA1 [42]), c) cell cycle regulation (BTG2 [43], CD93 [41], RGCC [44]), d) transcription (ELL2 [45], KLF2 [46], LMCD1 [47]), e) transporters in cell/mitochondrial membranes (ATP1B1 [48], SLC7A2 [49]), f) hormone dependent nuclear receptor (NRIP1 [50]), g) ubiquitination (KDM2B [51], BTG2 [43]), or h) inflammatory response (VIMP [39]). The PRKAG3 associated interactions were derived from a list of DE genes identified by microarray assay that was performed with skeletal muscle tissues of PRKAG3 transgenic mice including missense point mutation and knock-out genotypes [52].…”