Ver but preserved IRS2 responsiveness in Tsc2-/-MEFs(A) Influence of TSC2 on PC-TP abundance. MEFs transfected using a green fluorescent protein (GFP) expression vector control or the vector containing TSC2 have been serum starved just before immunoblot analyses. (B) Densitometric quantification of steady state abundance of PC-TP protein and mRNA normalized to the abundance of -Actin and RPL32, respectively. (C) Tsc2-/-MEFs were serum starved and treated with cycloheximide (Chx). (D) Protein abundance in panel (C) quantified by densitometry and normalized to -Actin. (E) Influence of THEM2 abundance on insulin signaling in siRNA-transfected MEFs that had been serum starved ahead of immunoblot analyses. (F) Regulation of IRS2 abundance and Akt phosphorylation by PC-TP and THEM2 in Tsc2-/-MEFs after serum starvation. Inset barplots show densitometric quantification of Akt phosphorylation normalized to total Akt. *P 0.05 and **P 0.025 in comparison with automobile. Immunoblots are representative of 3 independent experiments.Sci Signal. Author manuscript; obtainable in PMC 2014 March 19.L002 Epigenetic Reader Domain Ersoy et al.Lysyl endopeptidase, Achromobacter sp medchemexpress PageNIH-PA Author ManuscriptFig. six. Genetic ablation or pharmacological inhibition of PC-TP promotes insulin signaling in vivo(A) Liver homogenates from chow diet regime fed Pctp+/+ (n = four) and Pctp-/-(n = 4) mice have been had been subjected to immunoblot analyses, and bands have been quantified by densitometry and normalized to (B) -Actin or (C) total protein. *P 0.05 in comparison to Pctp+/+. (D) Effects of compound A1 treatment on IRS2, TSC2, Akt and S6K1 in livers from Pctp+/+ mice on high fat diets. Samples of livers from fasted mice fed a high fat diet plan while getting compound A1 (n = 7) or vehicle (n = 5) as described (7) have been analyzed for IRS2, pAkt(Ser473), Akt, p-S6K1(Thr389), S6K1, p-TSC2(Thr1462) and TSC2. Homogenates were subjected to immunoblot analyses, and bands were quantified by densitometry and normalized to (E) -Actin or (F) total protein. *P 0.05 in comparison with vehicle.NIH-PA Author Manuscript NIH-PA Author ManuscriptSci Signal. Author manuscript; accessible in PMC 2014 March 19.Ersoy et al.PageNIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptSci Signal. Author manuscript; offered in PMC 2014 March 19.Fig. 7. Postulated mechanism by which PC-TP inhibits insulin signalingPC-TP is proposed to serve as a sensor of alterations within the molecular species of membrane phosphatidylcholines. A PC-TP-THEM2 complex limits phosphorylation of Akt by inhibiting IRS2 and that of S6K1 by stabilizing TSC1/TSC2. Dotted lines represent PC-TP binding.PMID:24065671 Arrowheads and blunt ended lines represent activating and inhibitory actions, respectively.
Davtyan et al. Journal of Inflammation 2013, ten:14 http://www.journal-inflammation/content/10/1/RESEARCHOpen AccessThe anti-idiotypic antibody 1F7 stimulates monocyte interleukin-10 production and induces endotoxin toleranceTigran K Davtyan1, David A Poghosyan2, Anna G Sukiasyan3 and Michael D Grant4*AbstractBackground: Pathogens that establish chronic infection elicit immune responses with suppressive cytokines dominating more than pro-inflammatory cytokines. Chronic hepatitis C virus (HCV) infection, human immunodeficiency virus (HIV) infection and simian immunodeficiency virus (SIV) infection are linked to higher levels of antiviral antibodies expressing a common idiotype especially recognized by the 1F7 monoclonal antibody (mAb). The 1F7 mAb is usually a murine IgM antibody raised against immunoglobulin pooled in the plasma of a number of HIV-in.
