Dicer ablation affects antibody diversity and cell survival in the B lymphocyte lineage.
By Sergei B Koralov, Stefan A. Muljo, G. Galler, A. Krek, T. Chakraborty, C. Kanellopoulou, Kari Jensen, B. Cobb, Matthias Merkenschlager, Nikolaus Rajewsky and 1 more. Cell, 2008
626 citations recorded by the source corpus.
Subfields: Immunology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/eeb44a9db3af51e7fedc50fbf05e59e3e29d706b
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In Immunology
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In Molecular Biology
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Citations in the corpus
- Unidirectional transfer of microRNA-loaded exosomes from T cells to antigen-presenting cells (2011, background): “In addition, genetic ablation of the whole miRNA machinery or specific miRNAs severely compromises immune development and can lead to autoimmune disorders and cance”
- MicroRNAs in development and disease. (2011, background): “Validated targets of this cluster that potentially mediate its function include the proapoptotic gene Bim (312, 633) and the cell cycle inhibitor CDKN1A/p21waf1/ Cip1 (264). c-Myc enhances the transcription of the miR17 92 gene (459), but suppresses that of miR-15a/16–1, miR-34a, miR-150, miR-195, L”
- MicroRNA control in the immune system: basic principles. (2009, methodology): “When this bioinformatic prediction was tested, Bim and Pten were indeed found to be strongly upregulated in Dicer-deficient B cell progenitors, and, most importantly, B cell development could be partially rescued by transgenic Bcl2 or Bim deficiency (Koralov et al., 2008).”
- Foxp3-dependent microRNA155 confers competitive fitness to regulatory T cells through targeting SOCS1 (2009, background): “…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; Ventura et al., 2008; Xiao et al., 2008).”
- MicroRNAs: new regulators of immune cell development and function (2008, background): “Dicer deficiency in B lymphocytes has been shown to diminish B cell survival and the antibody repertoir”
- Down-regulation of miRNA-200c Links Breast Cancer Stem Cells with Normal Stem Cells (2009, background): “In addition, tissue-specific deletion of Dicer affects selfrenewal of embryonic stem cells, development of B lymphocyte lineage cells, and tissue morphogenesis (Chen et al., 2008; Davis et al., 2008; Koralov et al., 2008).”
- Physiological and pathological roles for microRNAs in the immune system (2010, background): “By contrast, mice with a conditional deletion of Dicer in B cells had a complete block in B cell developmen”
- microRNA regulation of inflammatory responses. (2012, background): “The global importance of miRNAs in B cell development was established by the conditional deletion of Dicer in early B cell development, which led to an arrest of development at the pro-B cell stage (61).”
- The miR-17/92 cluster: a comprehensive update on its genomics, genetics, functions and increasingly important and numerous roles in health and disease (2013, neutral): “Moreover, several novel targets for members of miR-17/92 and miR106b/25 were identified and are also summarized in Figure 4.(25,28) With regard to the miR-106a/363 cluster, it is likely regulated by the microphthalmia-associated transcription factor (MITF) through a binding site at position 133,135,”