Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Antiretroviral restriction factors may play an essential role in the safety of xenotransplantation. Therefore, the present study focused on investigation of the changes in the tripartite motif-containing family (TRIM) gene expression in normal human dermal fibroblasts with and without lipopolysaccharide stimulation in response to porcine endogenous retrovirus infection. Analysis of the expression profile of TRIMs was performed using oligonucleotide microarrays and QRT-PCR. Nine (TRIM1, TRIM2, TRIM5, TRIM14, TRIM16, TRIM18, TRIM22, TRIM27 and TRIM31) statistically significantly differentially expressed genes were found (P < 0.05, one-way ANOVA). In conclusion, comprehensive analysis of retroviral restriction factor gene expression in human dermal fibroblasts before and after porcine endogenous retrovirus infection with and without LPS stimulation may suggest association of the selected TRIMs with antiretroviral activity.
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PMID:Differential expression of tripartite motif-containing family in normal human dermal fibroblasts in response to porcine endogenous retrovirus infection. 2505 37

Autophagy is responsible for the bulk degradation of cytosolic constituents and plays an essential role in the intestinal epithelium by controlling beneficial host-bacterial relationships. Atg5 and Atg7 are thought to be critical for autophagy. However, Atg5- or Atg7-deficient cells still form autophagosomes and autolysosomes, and are capable of removing proteins or bacteria. Here, we report that human TRIM31 (tripartite motif), an intestine-specific protein localized in mitochondria, is essential for promoting lipopolysaccharide-induced Atg5/Atg7-independent autophagy. TRIM31 directly interacts with phosphatidylethanolamine in a palmitoylation-dependent manner, leading to induction of autolysosome formation. Depletion of endogenous TRIM31 significantly increases the number of intestinal epithelial cells containing invasive bacteria. Crohn's disease patients display TRIM31 downregulation. Human cytomegalovirus-infected intestinal cells show a decrease in TRIM31 expression as well as a significant increase in bacterial load, reversible by the introduction of wild-type TRIM31. We provide insight into an alternative autophagy pathway that protects against intestinal pathogenic bacterial infection.
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PMID:TRIM31 promotes Atg5/Atg7-independent autophagy in intestinal cells. 2721 61