Modulation of miR-155 and miR-125b Levels following Lipopolysaccharide/TNF-α Stimulation and Their Possible Roles in Regulating the Response to Endotoxin Shock1
By E. Tili, J. Michaille, Amelia Cimino, S. Costinean, C. Dumitru, Brett Adair, M. Fabbri, H. Alder, C. Liu, George A. Calin and 1 more. Journal of Immunology, 2007
1,409 citations recorded by the source corpus.
Subfields: Cancer Research, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/0571b25693395b49455002b98f768e679bd0ab53
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In Cancer Research
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Citations in the corpus
- MicroRNA control in the immune system: basic principles. (2009, result): “The functional importance of LPS-induced miR-155 expression in myeloid cells was further supported by the work of Tili et al. (2007), and the myeloproliferative disorder that develops in mice reconstituted with bone marrow progenitors that had been retrovirally transduced to express miR-155…”
- MicroRNAs in development and disease. (2011, background): “miR-155 is one of the most substantially upregulated miRNA after stimulation of macrophages with IFN- (458) or TNF(614).”
- MicroRNA-155 modulates the interleukin-1 signaling pathway in activated human monocyte-derived dendritic cells (2009, background): “In murine macrophages, miR-155 over-expression has also been postulated to increase TNF- translation and to render mice hypersensitive to LPS/d-galactosamine-induced septic shock (18).”
- miR-155 gene: a typical multifunctional microRNA. (2009, background): “challenged with LPS and are hypersensitive to LPS/D-galactosamine induced septic shock [33] with respect to their normal counterparts.”
- MicroRNAs in cancer: small molecules with a huge impact. (2009, background): “44,45 Moreover, miR-155 could represent the connection between inflammation, immunity, and cancer, because its expression can be induced by mediators of inflammation and is involved in response to endotoxic shock.(46) He et al(12) reported that miR-17-92 polycistron was upregulated in 65% of patient”
- Macrophage phenotypes in atherosclerosis (2014, background): “The miR-125 family is composed of miR-125a, miR125b1, and miR125b2, all being expressed in macrophages, in which they are differentially regulated by LPS, with an induction of miR-125a and a reduction in miR-125b expression (134, 135).”
- Induction and regulatory function of miR-9 in human monocytes and neutrophils exposed to proinflammatory signals (2009, methodology): “Recently, activation of the innate immune response also has been associated with changes in the expression of selected miRNAs [namely miR-146 (9, 10), miR-155 (11, 12), miR-132 (10), and miR-125b (12)].”
- microRNA regulation of inflammatory responses. (2012, background): “Both miR-125b and let7 are downregulated by LPS stimulation of macrophages; miR-125b targets TNF-α mRNA, whereas let-7 targets IL-6 mRNA (42, 43).”
- Heterogeneity of Microglial Activation in the Innate Immune Response in the Brain (2009, background): “Recently, noncoding RNA oligonucleotides (microRNA or miRNA) have been shown to regulate gene expression by binding to 3′ untranslated regions of specific target genes (Tili et al. 2007; Valencia-Sanchez et al. 2006).”
- Akt1 controls macrophage response to LPS by regulating microRNAs (2009, background): “LPS-generated signals in macrophages regulate miRNAs that control the expression of molecules involved in TLR signaling (O’Connell et al., 2007; Tili et al., 2007).”
- MicroRNAs: key players in the immune system, differentiation, tumorigenesis and cell death (2008, background): “, 2007) and immunoglobulin heavy chain enhancer (Em-miR-155 transgenic mice were hypersensitive to LPS/D-galactosamineinduced septic shock; Tili et al., 2007).”