Fig. 7: Adaptive responses in NO/cGMP deficiency. | Communications Biology

Fig. 7: Adaptive responses in NO/cGMP deficiency.

From: Proteomic surveys of the mouse heart unveil cardiovascular responses to nitric oxide/cGMP signaling deficiencies

Fig. 7

a MS and MS/MS extracted ion chromatograms (XIC) for the Mapk3 peptide IADPEHDHTGFLpTEpYVApTR and b for the Mapk1 peptide VADPDHDHTGFLpTEpYVApTR. In both graphs, the top tracings are the MS2, and the bottom are the MS1 XIC. These peptides correspond to the three phosphorylation sites in the Thr-Glu-Tyr-X-X-Thr motif of the activation loops, corresponding to Thr203, Tyr205, and Thr208 in Mapk3, and Thr183, Tyr185, and Thr188 in Mapk1 across all genotypes. c Western blot for phosphorylated and total Mapk3 and Mapk1 in the tNOS and wild-type mouse hearts (n = 3). Quantification of the ratio of phosphorylated to total Mapk3 and Mapk1 from three different mouse hearts (values represent mean ± standard deviation). Total Mapk3 and Mapk1 levels were normalized to GAPDH. *p value = 0.0056 for Mapk3 and p value = 0.0292 for Mapk1. d Representative western blots and quantification of the fold increase in the ratio of phosphorylated to total Mapk3 and Mapk1 in HL-1 cells after inhibition of NOS and sGC. (C) indicates no treatment control, and (I) treatment with the NOS inhibitor L-NAME and the sGC inhibitor ODQ (n = 4 independent cell cultures and treatments, values represent mean ± standard deviation).

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