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Fig. 4 | BMC Endocrine Disorders

Fig. 4

From: In vitro treatment of 3 T3-L1 adipocytes with recombinant Calcium/calmodulin-dependent Protein Kinase IV (CaMKIV) limits ER stress and improves insulin sensitivity through inhibition of autophagy via the mTOR/CREB signaling pathway

Fig. 4

Effect of CaMKIV on ER stress, insulin signaling, and autophagy in mTOR siRNA transfected adipocytes. Cells were cultured with Tun (2.5 μg/ml) for inducing insulin resistance. Cells were cultured in the presence or absence of CaMKIV with or without 100 nM mTOR siRNA (mTORsi) for 24 h. For insulin signaling, cells were stimulated with 10 nM insulin for 10 min. All indicators were measured at protein levels. The relative quantity of proteins was analyzed using Quantity One Software. a p-mTOR, p-CREB expression and their total protein levels. b IRS-1 tyrosine phosphorylation (pY), Akt serine 473 phosphorylation (p-Akt), and their total protein levels were examined in mice adipocytes either with IP followed by IB or by direct immunoblotting. c ER stress markers including PERK phosphorylation (p-PERK) and cleaved-ATF6 in adipocytes. d Autophagy-related proteins Atg7, p62 and LC3 in adipocytes. Quantitative data are presented as means ± SD from at least 3 independent experiments. * P < 0.05 or ** P < 0.01

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