NF-κB-dependent induction of microRNA miR-146, an inhibitor targeted to signaling proteins of innate immune responses

By K. Taganov, M. Boldin, Kuang-Jung Chang, David Baltimore. Proceedings of the National Academy of Sciences of the United States of America, 2006

4,022 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology

View Paper: https://www.semanticscholar.org/paper/d4fa9963d2005e46262117d461f905f5c80a8c69

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Citations in the corpus

Chondrocyte Apoptosis in the Pathogenesis of Osteoarthritis (2015, background): “miR-146a has gained interest, as a negative correlation between its expression and MMP-13 expression level was observed, and it was found to regulate key signaling intermediates of the pro-inflammatory Toll-like receptor (TLR)-MyD88 pathway [78,79].”
MicroRNA expression alterations are linked to tumorigenesis and non-neoplastic processes in pancreatic ductal adenocarcinoma (2007, background): “Only recently it was shown that nuclear factor kappaB (NF-kB) is able to induce miR-146 expression (Taganov et al., 2006).”
miR-146a is a significant brake on autoimmunity, myeloproliferation, and cancer in mice (2011, methodology): “Previously, we have shown that both genes respond to LPS in human monocytes, but only miR-146a is processed to a mature form, and determined that induction of expression of miR-146a is NF-B dependent (Taganov et al., 2006).”
Aberrant Expression of Oncogenic and Tumor-Suppressive MicroRNAs in Cervical Cancer Is Required for Cancer Cell Growth (2008, background): “. Thus, our finding is important for understanding the mechanisms by which miR-143 and miR-145 are involved in carcinogenesis. Inhibition by miR-143 and miR-145 of HeLa cell growth implies that miR-143 and miR-145 probably need to be downregulated in order for cancer growth. (2) Upregulation of miR-”
Detection of microRNA Expression in Human Peripheral Blood Microvesicles (2008, background): “). Using IPA analysis, miR-484 appears to regulate hematopoiesis, as well as cellular differentiation, proliferation and growth similar to many of the highly expressed miRNAs in the plasma microvesicles. Another of the highly expressed miRNAs, miR-146a is predicted to modulate NK cell signaling and ”
Expression of microRNA-146 in rheumatoid arthritis synovial tissue. (2008, background): “Taganov et al (20) reported that miR-146a/b, miR-132, and miR-155 were identified among 200 microRNA after exposure of the human monocytic THP-1 cell line to LPS.”
Function of miR-146a in controlling Treg cell-mediated regulation of Th1 responses (2010, positive): “In the latter, miR-146a acts as a negative feedback regulator to limit TRAF6 and IRAK1/2-mediated signaling in inflammatory settings (Hou et al., 2009; Taganov et al., 2006), whereas in activated human T cells, miR-146a has been suggested to oppose apoptosis and IL-2 production (Curtale et al., 2010”
MicroRNAs: key players in the immune system, differentiation, tumorigenesis and cell death (2008, background): “…is miR-146a, which has an important function in the innate immune system. miR-146a was found to be upregulated in cells treated with lipopolysaccharide (LPS) through the activation of toll-like receptor (TLR) 4 and concurrent activation of the nuclear factor-kB pathway (Taganov et al., 2006).”
Expression of microRNA-146 suppresses NF-κB activity with reduction of metastatic potential in breast cancer cells (2008, background): “The miR-146b probe showed some cross-hybridization to miR-146a (Figure 1a, right panel) as expected from their sequences (Taganov et al., 2006).”