MicroRNA-155 is induced during the macrophage inflammatory response

By Ryan M. O’Connell, K. Taganov, M. Boldin, G. Cheng, David Baltimore. Proceedings of the National Academy of Sciences of the United States of America, 2007

1,970 citations recorded by the source corpus.

Subfields: Cancer Research

View Paper: https://www.semanticscholar.org/paper/1666353387d0cc207e8985b49d2271d91b283db0

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In Cancer Research

Citations in the corpus

miR-155 gene: a typical multifunctional microRNA. (2009, background): “Furthermore, pharmacological inhibition of the c-Jun N-terminal kinase (JNK) blocks induction of miR-155, suggesting that miR-155-inducing signals use the JNK pathway [26].”
Inositol phosphatase SHIP1 is a primary target of miR-155 (2009, methodology): “Northern blotting was performed as described (19) using a probe reverse complementary to the human miR-155 seed mutant (see Table S1).”
Function of miR-146a in controlling Treg cell-mediated regulation of Th1 responses (2010, neutral): “…(cancer-associated micro-RNA), is constitutively expressed in high amounts in Treg cells in a Foxp3-dependent manner, whereas T cells lacking Foxp3, B cells, and myeloid cells transiently upregulate miR-155 upon activation (Androulidaki et al., 2009; O’Connell et al., 2007; Thai et al., 2007).”
Negative regulation of TLR4 via targeting of the proinflammatory tumor suppressor PDCD4 by the microRNA miR-21 (2010, background): “Studies have shown considerable upregulation of miR-155 in macrophage”
MicroRNAs: key players in the immune system, differentiation, tumorigenesis and cell death (2008, background): “Another TLR-responsive gene, miR-155, was identified to respond to the stimulation of TLR3 on macrophages (O’Connell et al., 2007) and immunoglobulin heavy chain enhancer (Em-miR-155 transgenic mice were hypersensitive to LPS/D-galactosamineinduced septic shock; Tili et al., 2007).”
Small non-coding RNAs in animal development (2008, background): “BIC/miR-155 expression is increased in activated B and T cells, macrophages and dendritic cell”
MicroRNA-155 promotes autoimmune inflammation by enhancing inflammatory T cell development (2010, background): “Specific miRNAs, such asmiR-146a,miR-155, andmiR-132, were initially shown to be upregulated during the macrophage inflammatory response (O’Connell et al., 2007; Taganov et al., 2006).”
Induction and regulatory function of miR-9 in human monocytes and neutrophils exposed to proinflammatory signals (2009, methodology): “by both LPS and TNF- , we tested whether TLR4 induction of miR-9 required a TNF- autocrine signaling as previously reported for miR-155 (11).”
Diversity, Mechanisms and Significance of Macrophage Plasticity (2019, background): “This hypothesis is supported by the demonstration that miR-146a and miR-146b isoforms are induced by different transcription factors (i.e. NF-κB and STAT3, respectively) at different moments in the same cell type.”
MicroRNAs and complex diseases: from experimental results to computational models (2019, positive): “Function on viral infection When viruses attack human body, host cells use miRNAs to target viral functions and defend against RNA and DNA viruses [48, 58, 59].”
microRNA-155 Regulates the Generation of Immunoglobulin Class-Switched Plasma Cells (2007, background): “Bic is also expressed by macrophages following Toll-like receptor and type-I interferon stimulation (O’Connell et al., 2007); and in B cells following treatment with antibodies to surface IgM (van den Berg et al., 2003).”