Signalling, cell cycle and pluripotency in embryonic stem cells.
By T. Burdon, Austin G Smith, P. Savatier. Trends in Cell Biology, 2002
713 citations recorded by the source corpus.
Subfields: Developmental Neuroscience, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/29643e5e5715f05ea5e14b9dab01dde09d99c978
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In Developmental Neuroscience
- H. Niwa
- Shenghui He
- S. Morrison
- M. D. Bettess
- Konstantinos Kaloulis
- Austin G Smith
- H. Macdonald
- C. Knabenhans
In Molecular Biology
- S. Yamanaka
- Austin G Smith
- José C. R. Silva
- Kazutoshi Takahashi
- H. Niwa
- C. D. Allis
- T. Jenuwein
- Shenghui He
Citations in the corpus
- Dicer-deficient mouse embryonic stem cells are defective in differentiation and centromeric silencing. (2005, background): “DCR / cells also showed no evidence of aneuploidy or genomic instability, suggesting that ES cells use different mechanisms for maintaining genomic stability than differentiated cells (Burdon et al. 2002).”
- FGF stimulation of the Erk1/2 signalling cascade triggers transition of pluripotent embryonic stem cells from self-renewal to lineage commitment (2007, background): “Presence of the self-renewal cytokine LIF, which activates Erk in addition to Stat3 (Burdon et al., 2002; Burdon et al., 1999), only partially restored pErk levels in the null cells and did not further augment pErk in the heterozygous cells.”
- The homeoprotein Nanog is required for maintenance of pluripotency in mouse epiblast and ES cells. (2003, background): “…showed that mobility of consensus oligonucleo- Prior to this study, LIF/gp130/Stat3 was the only known biochemical pathway that could maintain self-renewaltides was retarded by extracts of F9 embryonic carcinoma cells (Figure 7B) and RF8 ES cells (data not of mouse ES cells (Burdon et al., 2002).”
- Distinct factors control histone variant H3.3 localization at specific genomic regions (2010, background): “We speculate that Hira / ESCs may be rescued by the replicationcoupled deposition of histones during the frequent S phases of rapidly dividing ESCs (Burdon et al., 2002).”
- Adaptation to culture of human embryonic stem cells and oncogenesis in vivo (2007, background): “In MESCs, GRB2 has been implicated in ERK signaling that encourages differentiatio”
- Capture of authentic embryonic stem cells from rat blastocysts. (2008, positive): “Propidium iodide staining revealed that more than 50% of cells are in S phase, a cell-cycle profile shared with mouse ES cells (Figure 5C) and distinct from most somatic cells that tend to reside in G1 (Burdon et al., 2002).”
- Cell-cycle control and cortical development (2007, background): “It is tempting to speculate that shortening of the G1 phase might shield stem cells from signals that induce differentiatio”
- Mechanisms of stem cell self-renewal. (2009, background): “Mouse ES cells have a very short G1 phase of the cell cycle, marked by little or no hypophosphorylated Rb (Burdon et al. 2002, Stead et al. 2002).”
- How is pluripotency determined and maintained? (2007, background): “During self-renewal, most ES cells are in the S phase of the cell cycle, with only a few in G1 (Burdon et al., 2002).”
- Multiple Roles of the PI3K/PKB (Akt) Pathway in Cell Cycle Progression (2003, background): “The G(2) DNA damage checkpoint targets both Wee1 and Cdc25.”
- Embryonic Stem Cell Specific MicroRNAs Regulate the G1/S Transition and Promote Rapid Proliferation (2008, background): “The rapid proliferation of ES cells is thought to be due to their unique cell cycle structure, especially their shortened G1 phas”
- Cdks, cyclins and CKIs: roles beyond cell cycle regulation (2013, background): “It is well-established that pluripotent embryonic stem cells (ESCs) possess a distinctive mode of cell cycle regulation characterized by rapidly alternating rounds of S and M phases that are interspersed by short gap phases (Becker et al., 2006; Burdon et al., 2002; Singh and Dalton, 2009).”