To test this model, we measured expression of immune and metabolic MEF2 targets in uninfected and infected animals inducibly expressing wild-type Mef2, Mef2T20E, Mef2T20A, or driver-only controls.
Using the Enterococcus faecalis alkaline phosphatase gene, phoZ, we measured expression of C. difficile genes using a colorimetric alkaline phosphatase assay.
Using newly designed and validated qRT-PCR primers, we measured expression of these genes in C. elegans exposed to the sequenced TT01 strain of P. luminescens, on two different media types.
To understand the molecular basis of lipid reduction in liver, we measured expression of SREBP1, SREBP2, ChREBP and FAS.
We measured expression of Comt across multiple tissues in over 100 strains of mice and several large F2 intercrosses using four microrray platforms.
To validate Messina's results, we measured expression of S100A2 protein by immunohistochemistry upon a separate patient cohort from that used in the microarray data [8].
We also measured expression of CD62 ligand (CD62L) and CD44 on tetramer+ cells to distinguish between naive (CD44lowCD62Lhigh), central memory (CD44highCD62Lhigh), and effector memory cells (CD44highCD62Llow).
We also measured expression of TNFα, to evaluate if the different therapeutic regimens had a direct effect on the inflammatory response of effector CD4+CD25− cells.
To examine the involvement of IRF-5P68 in the IRF-5-mediated transactivation activity, we measured expression of luciferase reporter gene driven by the IL12p40 promoter IL12p40-lucc) in HEK293 and RAW264.7 cells.
Based on GSEA, we also measured expression of genes involved in Notch signaling (Notch1/4 and Jag1) and matrix remodeling/fibrinolysis (Mmp9 and Timp4) and found them to be regulated by UAG (Fig. 3G).
Third, we measured expression of TLR-2, TLR-4, and HLA-DR because these receptors are integral components of the host response to infection and are involved in activating the inflammatory and coagulant response to infection [52], [53], [54].
