LIF/STAT3 controls ES cell self-renewal and pluripotency by a Myc-dependent mechanism

By P. Cartwright, C. McLean, A. Sheppard, D. Rivett, K. Jones, S. Dalton. Development, 2005

789 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/35f369e11b7e8ea34df6fd3cf368652484302871

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Citations in the corpus

Module map of stem cell genes guides creation of epithelial cancer stem cells. (2008, background): “…c-Myc promotes self-renewal and blocks differentiation in ESCs and cancer but, conversely, promotes differentiation with depletion of stem cells in hair bulge and bone marrow (Arnold and Watt, 2001; Arvanitis and Felsher, 2006; Cartwright et al., 2005; Waikel et al., 2001; Wilson et al., 2004).”
Daedalus: a robust, turnkey platform for rapid production of decigram quantities of active recombinant proteins in human cell lines using novel lentiviral vectors (2011, positive): “The recombinant LIF was also functionally tested in its ability to maintain mouse ES cells in an undifferentiated state, as measured by maintenance of the cell-surface marker SSEA1 in culture (Supplementary Figure S4B) (50); there was no difference compared to commercial LIF.”
Quantitative interaction proteomics and genome-wide profiling of epigenetic histone marks and their readers. (2010, background): “Because c-Myc plays key roles in ES cell self-renewal and proliferation (Cartwright et al., 2005) and can bind the pause-release factor P-TEFb in tumor cells (Eberhardy and Farnham, 2001, 2002; Gargano et al.”
c-Myc regulates transcriptional pause release (2010, background): “Because c-Myc is a key ES cell transcription factor required for self-renewal and proliferation (Cartwright et al., 2005), which occupies a third of active genes (see below), we investigated whether c-Myc plays a role in P-TEFb-depen-dent pause release at the genes it occupies in ES cells.”
How is pluripotency determined and maintained? (2007, background): “These findings suggest that the regulation of the G1-S transition may contribute to the maintenance of pluripotency, which is promoted by the Lif-Stat3 pathway in mouse ES cells (Burdon et al., 2002).”
Targeting cancer stem cell pathways for cancer therapy (2020, background): “113 The expression of the three members of the MYC family is different in different tumors, such as C-MYC in leukemia and tongue SCC stem cells 114, 115 and N-MYC in small-cell lung cancer, prostate cancer, neuroblastoma, and medulloblastoma.”
Induction of pluripotent stem cells from mouse embryonic and adult fibroblast cultures by defined factors. (2006, background): “…genes that are frequently upregulated in tumors, such as Stat3 (Matsuda et al., 1999; Niwa et al., 1998), E-Ras (Takahashi et al., 2003), c-myc (Cartwright et al., 2005), Klf4 (Li et al., 2005), and b-catenin (Kielman et al., 2002; Sato et al., 2004), have been shown to contribute to the…”
Myc's broad reach. (2008, background): “Although stabilization of Myc has been shown to be important in both normal and neoplastic settings (Kenney et al. 2003; Welcker et al. 2004a; Yeh et al. 2004; Cartwright et al. 2005; Hemann et al. 2005), the “stabilized” Myc protein nonetheless still possesses a measurable, and often quite rapid, r”
Integration of external signaling pathways with the core transcriptional network in embryonic stem cells. (2008, background): “Klf4 and Myc TFs are reprogramming factors that are also implicated in the maintenance of the undifferentiated state of ES cells (Cartwright et al., 2005; Jiang et al., 2008).”
Functional redundancy of GSK-3α and GSK-3β in wnt/β-catenin signaling shown by using an allelic series of embryonic stem cell lines (2007, background): “The transcripts for axin2, brachyury, and cdx1 are all elevated in DKO ESCs when compared with WT ESCs maintained in standard ESC culture conditions with LIF supplementation (Fig.”
Mechanisms of stem cell self-renewal. (2009, background): “The targets of the JAK/Stat3 pathway are largely unknown but have been suggested to include c-myc, a known promoter of pluripotency (Cartwright et al. 2005, Takahashi & Yamanaka 2006).”
Activin/Nodal and FGF pathways cooperate to maintain pluripotency of human embryonic stem cells (2005, background): “Interestingly, it has recently been proposed that GSK3 inhibition was necessary for pluripotency of mouse ESCs with increased stability of cMyc (Cartwright et al., 2005).”
Control of Embryonic Stem Cell State (2011, background): “…2008; Marson et al., 2008b); 5 (Niwa et al., 1998); 6 (Ying et al., 2003); 7 (Beattie et al., 2005; James et al., 2005; Vallier et al., 2005), 8 (Cartwright et al., 2005); 9 (Ivanova et al., 2006; Zhang et al., 2008); 10 (Wu et al., 2006; Zhang et al., 2006); 11 (Han et al.; Ivanova et al.,…”