Based on the microarray data, no inflammatory immune responses were executed.
The transcriptional responses were analysed by microarrays at different time points during activation and repression.
The transcriptomic responses were assayed using microarrays, the proteomic responses were assayed using isotope tags for multiplexed relative and absolute quantification (iTRAQ) and the metabolomic responses were assayed using gas chromatography coupled to time-of-flight mass spectrometry (GC/TOF-MS).
Hepatic transcriptional responses were studied using microarrays in combination with quantitative real-time reverse transcription polymerase chain reaction (qPCR).
Cell molecular network responses were investigated through whole genome microarray analysis of transcript level changes.
Our microarray analysis revealed that genes involved in inflammatory responses were downregulated by RASSF2A.
In this exploratory study, transcriptional gene expression responses were analyzed on a genome-wide scale using RNA microarray technology.
However, it is important that microarrays responses should be validated, at least initially, using real-time quantitative polymerase chain reaction (QPCR).
The over representation of genes involved in defence responses, and specifically SAR is consistent with the observation that AtPNP-A and the correlated genes are most highly expressed in microarray experiments where defence responses are elicited.
Even if we take a different threshold, by considering the result that the microarray profiles of U0126 and wortmannin responses are very close each other as described earlier (correlation coefficients 0.92; Figure 1c ), their combination will remain very close to their original profiles rather than to the gefitinib response.
