Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Activation and invasion of the vascular endothelium by Staphylococcus aureus is a major cause of sepsis and endocarditis. For endothelial cell invasion, S. aureus triggers actin polymerization through Cdc42, N-WASp (also known as WASL) and the Arp2/3 complex to assemble a phagocytic cup-like structure. Here, we show that after stimulating actin polymerization staphylococci recruit Cdc42GAP (also known as ARHGAP1) which deactivates Cdc42 and terminates actin polymerization in the phagocytic cups. Cdc42GAP is delivered to the invading bacteria on recycling endocytic vesicles in concert with the exocyst complex. When Cdc42GAP recruitment by staphylococci was prevented by blocking recycling endocytic vesicles or the exocyst complex, or when Cdc42 was constitutively activated, phagocytic cup closure was impaired and endothelial cell invasion was inhibited. Thus, to complete invasion of the endothelium, staphylococci reorient recycling endocytic vesicles to recruit Cdc42GAP, which terminates Cdc42-induced actin polymerization in phagocytic cups. Analogous mechanisms might govern other Cdc42-dependent cell functions.
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PMID:Staphylococcus aureus recruits Cdc42GAP through recycling endosomes and the exocyst to invade human endothelial cells. 2731 80

We aimed to identify crucial genes relevant to the development of consecutive trauma-induced sepsis.A microarray dataset was used to identify genes differentially expressed between peripheral blood samples from consecutive traumatized patients complicated with sepsis and not complicated with sepsis. The dataset GSE12624 was obtained from Gene Expression Omnibus, containing 34 peripheral blood samples from consecutive traumatized patients complicated by sepsis and 36 consecutive traumatized controls. The differentially expressed genes (DEGs) were identified using Linear Models for Microarray Data package. Then, gene ontology (GO) enrichment analysis for DEGs was performed by Onto-Express. Subsequently, the protein-protein interaction (PPI) network was constructed and pathway enrichment analysis was performed by Search Tool for the Retrieval of Interacting Genes (STRING). Furthermore, protein complexes in the PPI network were predicted by ClusterONE and validated through GO and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses, and protein domain analysis.Totally, 446 upregulated and 447 downregulated DEGs were identified. Some DEGs were related to acyl-CoA binding (eg, ACBD6), chromosome, and centromeric region (eg, CENPN). In the PPI network, some DEGs were enriched in renin-angiotensin system (RAS, eg, AGTR1 and AGTR2). Three predicted protein complexes were validated in the PPI network. Some genes composing protein complex A were associated with cell proliferation (eg, CDC20, CCNB1, MCM4, RPA2, and PRIM2), and several genes composing protein complex F were implicated in regulation of actin cytoskeleton (eg, PFN2, ARPC2, and WASL).The results suggest that those DEGs may be crucial in the etiology of consecutive trauma-induced sepsis, and they are expected to be therapeutic targets.
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PMID:Identification of genes related to consecutive trauma-induced sepsis via gene expression profiling analysis. 2964 83