Figure 1.
Proteomic detection of hepatic FXIII and TG2 levels in APAP-challenged mice. Wild-type mice were challenged with APAP (300 mg/kg) or sterile saline and liver samples were collected 24 hours later. Liquid chromatography–MS/MS-based quantification of the liver proteome was performed as described (see “Materials and methods”). Abundance of Fibα (Fga) (A), Fibβ (Fgb) (B), and Fibγ (Fgg) (C) and FXIII-A (F13a1) (D). (E) Correlation between hepatic levels of F13a1 and Fgg in livers of APAP-challenged mice. (F) Abundance of TG2. Signal intensity for each protein is shown and results from individual mice are plotted and bars represent mean ± standard error of the mean (SEM). (G) Approximate relative of each transglutaminase in the APAP-injured mouse liver as detected by proteomic analysis. ∗P < .05; ∗∗P < .01. Veh, sterile saline.

Proteomic detection of hepatic FXIII and TG2 levels in APAP-challenged mice. Wild-type mice were challenged with APAP (300 mg/kg) or sterile saline and liver samples were collected 24 hours later. Liquid chromatography–MS/MS-based quantification of the liver proteome was performed as described (see “Materials and methods”). Abundance of Fibα (Fga) (A), Fibβ (Fgb) (B), and Fibγ (Fgg) (C) and FXIII-A (F13a1) (D). (E) Correlation between hepatic levels of F13a1 and Fgg in livers of APAP-challenged mice. (F) Abundance of TG2. Signal intensity for each protein is shown and results from individual mice are plotted and bars represent mean ± standard error of the mean (SEM). (G) Approximate relative of each transglutaminase in the APAP-injured mouse liver as detected by proteomic analysis. ∗P < .05; ∗∗P < .01. Veh, sterile saline.

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