Acetyl-CoA is further converted to malonyl-CoA by ACC, the rate-limiting step in de novo fatty acid synthesis. Malonyl-CoA is then used as the substrate of fatty acid synthase for fatty acid synthesis. This increase in detection sensitivity appears to be a reflection of higher signal intensity and lower signal to noise importantly, the basis of sample segregation appears to be dependent on sample types rather than the biological nature of the samples suggestingthatPAX and PAX -GR evenafter globindepletionhavea unique expression profile compared to PBMCs and this could be attributed to the presence of cells other than mononuclear cells in the whole blood RNA. The improvement in detection sensitivity after globin depletion also permitted detection of several genes that were masked by globins in the original PAX samples. ratio as evidenced by the transformation of an absent call to a present call as shown in Table. 2. Interestingly, even after globin reduction the PAX and PAX-GR samples by principal component analysis clustered together rather than clustering with the PBMCs. Recently, TWS119 adipose tissue lipogenesis has been shown to be controlled by leptin via STAT3-independent central mechanisms ; whereas a liporegulatory role of hyperleptinemia has been implicated in non-adipose tissues, affecting lipogenesis and fatty acid oxidation. There are increasing evidences that nucleolin expression on the cell surface is implicated in growth of tumor cells. Inhibition of nucleolin activity results in cell growth inhibition. It was demonstrated in several studies that AS1411, a quadruplex-forming oligonucleotide aptamer, targets nucleolin and inhibits cancer cells growth. In addition, ErbB receptor tyrosine kinases are major contributors to malignant transformation and they are frequently overexpressed in a variety of human carcinomas. In the present study, we demonstrated that infection of primary human monocytes with EBV leads to the inhibition of the IFNa signal transduction pathway and hence, to an impairment in the amplification of IFNa secretion. Based on our results, we propose a hypothetical model of EBV-mediated negative regulation of IFN response and secretion in monocytes. According to this model, virion entry into the cell activates IRF3 and IRF7 leading to a first wave of type I IFN production. At the same time, EBV modulates SOCS3 expression in order to inhibit IFN receptormediated intracellular signaling through the JAK/STAT pathway. The latter results in a marked attenuation of the amplification loop initiated by the binding of type I IFNs to their cognate receptor. As a consequence, interferon-stimulated genes and IRF7 are negatively regulated and the second wave of IFNa secretion is impaired. Thus, our results may suggest that the significance of nucleolin expression on the cell surface of tumor cell lines is to increase receptor-mediated activities.