MiR-150 controls B cell differentiation by targeting the transcription factor c-Myb.

By Changchun Xiao, D. Calado, G. Galler, T. Thai, H. C. Patterson, Jing Wang, Nikolaus Rajewsky, T. Bender, K. Rajewsky. Cell, 2007

892 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/8be86920b263cd5aa1f64ca7d53910a57d31a5c1

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Citations in the corpus

Metazoan MicroRNAs (2018, background): “miR-150 (1) miR-150 Increased B1 cells and enhanced humoral immune response (Xiao et al., 2007); impaired maturation of natural killer T cells (Bezman et al.”
microRNA regulation of inflammatory responses. (2012, positive): “Indeed, examining transgenic mice with differing levels of expression of miR-150, Xiao and colleagues (66, 67) demonstrated a dosage effect on both c-Myb levels and the ensuing phenotype.”
Non-coding RNAs in disease: from mechanisms to therapeutics (2023, positive): “Cellular overexpression of miR-150 was sufficient to inhibit the pre-pro-B cell to pro-B cell transition by targeting MYB and FOXP1, respectively 184,185 .”
Foxp3-dependent microRNA155 confers competitive fitness to regulatory T cells through targeting SOCS1 (2009, positive): “…miR150 has been shown to profoundly affect early B cell differentiation and mature B cell responses by targeting the transcription factor c-Myb (Xiao et al., 2007), whereas the miR17–92 cluster can limit apoptosis through downregulation of the proapoptotic protein Bim (Koralov et al., 2008;…”
Extracellular miRNAs: From Biomarkers to Mediators of Physiology and Disease (2019, positive): “Incubation of microvascular endothelial cells with these EVs downregulates the miR-150 target gene c-Myb, a transcription factor involved in endothelial cell migration (Kopecki et al., 2007; Xiao et al., 2007; Zhang et al., 2010; Zhang et al., 2010b).”
MicroRNAs in development and disease. (2011, neutral): “In contrast, miR-150 knockout mice developed normally, including a typical T-cell, follicular and marginal zone B-cell populations, except for an increase in peritoneal and splenic B1a cells, known for recognizing self-antigens (675).”
MicroRNA miR-326 regulates TH-17 differentiation and is associated with the pathogenesis of multiple sclerosis (2009, neutral): “, whereas miR-150, the hematopoiesis-specific microRNA, controls embryonic development and B cell differentiation by regulating a key target, c-My”
An overview of microRNAs (2015, background): “miRNAs have been linked to the function of many hematopoietic lineages including neutrophils, lymphocytes, erythrocytes, megakaryocytes, an hematopoetic stem cells [17, 150-161].”
Hematopoiesis: an evolving paradigm for stem cell biology. (2008, positive): “For example, miR-150 impinges on B cell differentiation by targeting c-myb mRNA (Xiao et al., 2007), whereas miR-155 is required for T helper cell generation and germinal center activity (Rodriguez et al., 2007; Thai et al., 2007).”