Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The host mechanisms responsible for protection against malaria remain poorly understood, with only a few protective genetic effects mapped in humans. Here, we characterize a host-specific genome-wide signature in whole-blood transcriptomes of Plasmodium falciparum-infected West African children and report a demonstration of genotype-by-infection interactions in vivo. Several associations involve transcripts sensitive to infection and implicate complement system, antigen processing and presentation, and T-cell activation (i.e., SLC39A8, C3AR1, FCGR3B, RAD21, RETN, LRRC25, SLC3A2, and TAPBP), including one association that validated a genome-wide association candidate gene (SCO1), implicating binding variation within a noncoding regulatory element. Gene expression profiles in mice infected with Plasmodium chabaudi revealed and validated similar responses and highlighted specific pathways and genes that are likely important responders in both hosts. These results suggest that host variation and its interplay with infection affect children's ability to cope with infection and suggest a polygenic model mounted at the transcriptional level for susceptibility.
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PMID:Evidence for additive and interaction effects of host genotype and infection in malaria. 2294 51

We aimed to investigate significant genes associated with diabetic nephropathy (DN), and their potential mechanisms in the process of DN pathogenesis. We downloaded the microarray data of GSE111154 from gene expression omnibus (GEO) database. First, we analyzed differentially expressed genes (DEGs) between early diabetic nephropathy (EDN) samples and nondiabetic control samples. Functional and pathway enrichment analysis was carried out. Disease-related gene sets were analyzed. Then, we constructed the protein-protein interaction (PPI) network and predicted the relation. Finally, transcriptional regulation analyses of microRNA and transcription factors were performed. Totally 554 DEGs between EDN samples and nondiabetic control samples were obtained. Enrichment analysis of disease-related gene sets showed that transforming growth factor beta 1 (TGFB1) was significantly enriched in DN. TGFB1 was involved in more pathways, such as proteoglycans in cancer, malaria, and amebiasis. Furthermore, TGFB1 had the highest degree in PPI network. In addition, TGFB1 was correlated with miR-21-5p, miR-146a-5p, and RAD21. TGFB1, miR-146a-5p, and miR-21-5p are important for DN development. Furthermore, TGFB1 may be involved in DN progression through the regulation of miR-21-5p, miR-146a-5p, and RAD21.
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PMID:Key Genes Involved in Diabetic Nephropathy Investigated by Microarray Analysis. 3135 12