Project description:To investigate the mechanistic role of NanA and Siglec-5 in this excessive inflammation, we systemically analyzed genes and signaling pathways differentially regulated in macrophages infected with wild type and NanA-deficient pneumococcus.
Project description:In this study, we investigated the transcriptomic response of Streptococcus pneumoniae D39 to sialic acid (N-acetylneuraminic acid: Neu5Ac). Transcriptome comparison of the D39 wild-type grown in M17 medium with and without sialic acid revealed the elevated expression of various genes and operons including the nan gene cluster (nan operon-I and nanA gene). Our microarray analysis and promoter-lacZ fusion studies showed that the transcriptional regulator NanR acts as a transcriptional activator of nan operon-I and the nanA gene in the presence of sialic acid. The putative regulatory site of NanR in the promoter region of nan operon-I is predicted and confirmed by promoter truncation experiments. Furthermore, the role of CcpA in the regulation of the nan gene cluster is demonstrated through microarray analysis and promoter-lacZ fusion studies, suggesting that in the presence of sialic acid and glucose, CcpA represses the expression of nan operon-I while the expression of the nanA gene is CcpA-independent. This SuperSeries is composed of the SubSeries listed below.
Project description:Aberrant DNA methylation is a hallmark of acute myeloid leukemia (AML), often driven by dysregulated DNA methyltransferases. To investigate the epigenomic impact of DNMT3B inhibition, we treated KG1A AML cells with Nanaomycin A (NanA), a selective DNMT3B inhibitor, and performed genome-wide DNA methylation profiling using the Illumina MethylationEPIC v2.0 array. Following 48-hour exposure to NanA (50 nM), differentially methylated CpG sites were identified, with the majority exhibiting moderate hypomethylation (±25% Δβ-value). These changes were enriched in promoter and gene body regions and overlapped with regions of altered chromatin accessibility. The resulting dataset provides a high-resolution view of DNMT3B-dependent methylation dynamics in AML and serves as a resource for understanding the epigenetic consequences of targeted methyltransferase inhibition.
