PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 30910747-6 2019 Neuronal seipin deletion increased activities of GSK3beta and Akt/mTOR signaling, which were corrected by the administration of PPARgamma agonist rosiglitazone for 7 days. Rosiglitazone 146-159 Berardinelli-Seip congenital lipodystrophy 2 (seipin) Mus musculus 9-15 26921684-6 2016 Rosiglitazone treatment significantly reduced the hypercholesterolemia of the Seipin(-/-)Ldlr(-/-) mice, and also alleviated the severity of atherosclerosis. Rosiglitazone 0-13 Berardinelli-Seip congenital lipodystrophy 2 (seipin) Mus musculus 78-84 26818512-6 2016 Rosi treatment in seipin-nKO mice could correct the decrease in expression and activity of AMPA receptor (AMPAR) and was accompanied by recovered synaptic function and LTP induction. Rosiglitazone 0-4 Berardinelli-Seip congenital lipodystrophy 2 (seipin) Mus musculus 18-24 26818512-7 2016 Furthermore, hippocampal ERK2 and CREB phosphorylation in seipin-nKO mice were reduced and this could be rescued by rosi treatment. Rosiglitazone 116-120 Berardinelli-Seip congenital lipodystrophy 2 (seipin) Mus musculus 58-64 26818512-8 2016 Rosi treatment in seipin-nKO mice elevated BDNF concentration. Rosiglitazone 0-4 Berardinelli-Seip congenital lipodystrophy 2 (seipin) Mus musculus 18-24 26818512-9 2016 The MEK inhibitor U0126 blocked rosi-restored AMPAR expression and LTP induction in seipin-nKO mice, but the Trk family inhibitor K252a did not. Rosiglitazone 32-36 Berardinelli-Seip congenital lipodystrophy 2 (seipin) Mus musculus 84-90 26818512-14 2016 The PPARgamma agonist rosiglitazone can ameliorate spatial cognitive deficits and rescue the LTP induction in seipin knock-out mice by restoring AMPA receptor expression and ERK-CREB activities. Rosiglitazone 22-35 Berardinelli-Seip congenital lipodystrophy 2 (seipin) Mus musculus 110-116 26398946-4 2015 We show that the proliferative capability of stem cells in seipin-nKO mice was substantially reduced compared to in wild-type (WT) mice, and that this could be rescued by the PPARgamma agonist rosiglitazone (rosi). Rosiglitazone 193-206 Berardinelli-Seip congenital lipodystrophy 2 (seipin) Mus musculus 59-65 27287266-12 2016 Treatment of the seipin-KO mice with the PPARgamma agonist rosiglitazone (rosi) could prevent Abeta25-35/1-42-induced neuroinflammation and neurotoxicity, which was blocked by the PPARgamma antagonist GW9962. Rosiglitazone 59-72 Berardinelli-Seip congenital lipodystrophy 2 (seipin) Mus musculus 17-23 27287266-12 2016 Treatment of the seipin-KO mice with the PPARgamma agonist rosiglitazone (rosi) could prevent Abeta25-35/1-42-induced neuroinflammation and neurotoxicity, which was blocked by the PPARgamma antagonist GW9962. Rosiglitazone 59-63 Berardinelli-Seip congenital lipodystrophy 2 (seipin) Mus musculus 17-23 27287266-13 2016 In the seipin-KO mice, the level of glycogen synthase kinase-3beta (GSK3beta) phosphorylation at Tyr216 was elevated, while at Ser9, it was reduced compared to the WT mice, which were corrected by the rosi treatment but were unaffected by the Abeta25-35 injection. Rosiglitazone 201-205 Berardinelli-Seip congenital lipodystrophy 2 (seipin) Mus musculus 7-13 26398946-4 2015 We show that the proliferative capability of stem cells in seipin-nKO mice was substantially reduced compared to in wild-type (WT) mice, and that this could be rescued by the PPARgamma agonist rosiglitazone (rosi). Rosiglitazone 193-197 Berardinelli-Seip congenital lipodystrophy 2 (seipin) Mus musculus 59-65 26398946-5 2015 In seipin-nKO mice, neuronal differentiation of progenitor cells was inhibited, with the enhancement of astrogliogenesis; both of these effects were recovered by rosi treatment during early stages of progenitor cell differentiation. Rosiglitazone 162-166 Berardinelli-Seip congenital lipodystrophy 2 (seipin) Mus musculus 3-9 26398946-6 2015 In addition, rosi treatment could correct the decline in hippocampal ERK2 phosphorylation and cyclin A mRNA level in seipin-nKO mice. Rosiglitazone 13-17 Berardinelli-Seip congenital lipodystrophy 2 (seipin) Mus musculus 117-123 26398946-7 2015 The MEK inhibitor U0126 abolished the rosi-rescued cell proliferation and cyclin A expression in seipin-nKO mice. Rosiglitazone 38-42 Berardinelli-Seip congenital lipodystrophy 2 (seipin) Mus musculus 97-103 26398946-8 2015 In seipin-nKO mice, the hippocampal Wnt3 protein level was less than that in WT mice, and there was a reduction of neurogenin 1 (Neurog1) and neurogenic differentiation 1 (NeuroD1) mRNA, levels of which were corrected by rosi treatment. Rosiglitazone 221-225 Berardinelli-Seip congenital lipodystrophy 2 (seipin) Mus musculus 3-9 26398946-9 2015 STAT3 phosphorylation (Tyr705) was enhanced in seipin-nKO mice, and was further elevated by rosi treatment. Rosiglitazone 92-96 Berardinelli-Seip congenital lipodystrophy 2 (seipin) Mus musculus 47-53 26398946-10 2015 Finally, rosi treatment for 10 days could alleviate the depression-like phenotype in seipin-nKO mice, and this alleviation was blocked by the MEK inhibitor U0126. Rosiglitazone 9-13 Berardinelli-Seip congenital lipodystrophy 2 (seipin) Mus musculus 85-91 24651066-10 2014 The PPARgamma agonist rosiglitazone alleviated affective disorders in male seipin-nKO mice. Rosiglitazone 22-35 Berardinelli-Seip congenital lipodystrophy 2 (seipin) Mus musculus 75-81 31776610-10 2020 Treatment of male Seipin+/- mice with rosiglitazone corrected the glucose intolerance. Rosiglitazone 38-51 Berardinelli-Seip congenital lipodystrophy 2 (seipin) Mus musculus 18-24 31776610-11 2020 Male Seipin+/- mice displayed a decrease in islet insulin concentration and GSIS with low expression of Pdx-1, Nkx6.1, Glut2 and proinsulin, and a decline in PDX-1 nuclear translocation; these changes were rescued by rosiglitazone administration. Rosiglitazone 217-230 Berardinelli-Seip congenital lipodystrophy 2 (seipin) Mus musculus 5-11 31776610-12 2020 Male Seipin-/- mice showed obvious, but rosiglitazone-sensitive, increases in islet insulin concentration, islet number and beta cell mass and proliferation, with a notable decline in GSIS. Rosiglitazone 40-53 Berardinelli-Seip congenital lipodystrophy 2 (seipin) Mus musculus 5-11 31776610-13 2020 Ovariectomised female Seipin+/- mice displayed glucose intolerance and deficits in insulin synthesis and secretion, with a decline in islet PPARgamma level; these deleterious effects were reversed by administration of oestradiol or rosiglitazone. Rosiglitazone 232-245 Berardinelli-Seip congenital lipodystrophy 2 (seipin) Mus musculus 22-28 30910747-9 2019 On the other hand, seipin-sKO mice appeared insulin resistance and an increase in phosphorylation of tau at Ser396 and JNK, which were corrected by treatment with rosiglitazone for 30 days rather than 7 days. Rosiglitazone 163-176 Berardinelli-Seip congenital lipodystrophy 2 (seipin) Mus musculus 19-25 29670081-9 2018 In seipin-nKO mice, the phosphorylation of GSK3beta was increased at Tyr216 and was reduced at Ser9, which was corrected by the PPARgamma agonist rosiglitazone. Rosiglitazone 146-159 Berardinelli-Seip congenital lipodystrophy 2 (seipin) Mus musculus 3-9 29670081-10 2018 The increased IL-6 level in seipin-nKO mice was sensitive to rosiglitazone and GSK3beta inhibitor AR-A014418. Rosiglitazone 61-74 Berardinelli-Seip congenital lipodystrophy 2 (seipin) Mus musculus 28-34 29670081-12 2018 The treatment of seipin-nKO mice with rosiglitazone and AR-A014418 rescued the death of dopaminergic neurons, which was accompanied by the improvement of motor coordination. Rosiglitazone 38-51 Berardinelli-Seip congenital lipodystrophy 2 (seipin) Mus musculus 17-23