Integration of external signaling pathways with the core transcriptional network in embryonic stem cells.
By X. Chen, Han Xu, P. Yuan, Fang Fang, M. Huss, V. Vega, Eleanor Wong, Y. Orlov, Weiwei Zhang, Jianming Jiang and 13 more. Cell, 2008
2,639 citations recorded by the source corpus.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/0586680ad2cd22583f9f2e9b7f727a27e1cac01e
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In Molecular Biology
- Richard A. Young
- K. Hochedlinger
- David P. Bartel
- R. Weinberg
- Tong Ihn Lee
- R. Jaenisch
- M. Stadtfeld
- S. Yamanaka
Citations in the corpus
- DIDO as a Switchboard that Regulates Self-Renewal and Differentiation in Embryonic Stem Cells (2017, background): “…cell growth, and differentiation, as well as genes whose function is largely unknown or remains to be validated in the context of stem cell biology, including the Dido (death inducer obliterator) gene (Kim et al., 2008; Kidder et al., 2008; Chen et al., 2008; Brandenberger et al., 2004).”
- Transcriptional Amplification in Tumor Cells with Elevated c-Myc (2012, positive): “Previous studies have shown that c-Myc tends to occupy the promoter regions of protein-coding genes (Chen et al., 2008; Fernandez et al., 2003; Guccione et al., 2006; Kidder et al., 2008; Li et al., 2003; Rahl et al., 2010; Zeller et al., 2006), so we focused our initial analysis on the 2 kb…”
- Simple combinations of lineage-determining transcription factors prime cis-regulatory elements required for macrophage and B cell identities (2010, background): “This model offers an explanation for the extensive genome-wide and cell typespecific colocalization of transcription factors observed in various previous studies (Chen et al., 2008; MacArthur et al., 2009) and provides insights into how simple combinations of lineage-restricted transcription factors”
- Master Transcription Factors Determine Cell-Type-Specific Responses to TGF-β Signaling (2011, positive): “Examination of binding data at individual genes such as that encoding Max (Figure 2A) revealed that Smad3 co-occupied sites with Oct4 as well as Sox2 and Nanog, which are key ESC transcription factors that occupy the genome together (Boyer et al., 2005; Chen et al., 2008; Marson et al., 2008).”
- A Myc rather than core pluripotency module accounts for the shared signatures of embryonic stem and cancer cells (2010, neutral): “between Embryonic Stem and Cancer”
- Somatic cell reprogramming and transitions between pluripotent states: facts, hypotheses, unresolved issues (2010, neutral): “These factors also coactivate redundant target genes and cooperate with secondary transcription factors that provide further stability to the ESC state (Chen et al., 2008).”
- Nanog Is the Gateway to the Pluripotent Ground State (2009, neutral): “Information is accumulating on the molecular composition and inferred regulatory circuitry of the pluripotent state (Chen et al., 2008; Jaenisch and Young, 2008; Kim et al., 2008a).”
- Transcriptional Regulation and its Misregulation in Disease (2013, positive): “Enhancers can be identified by profiling the locations of key transcriptional regulators genome-wide and testing whether these DNA elements are active in enhancer-reporter vectors, and a large population of embryonic stem cell (ESC) enhancers has been identified in this manner (Chen et al., 2008).”
- ChIPBase: a database for decoding the transcriptional regulation of long non-coding RNA and microRNA genes from ChIP-Seq data (2012, background): “A click on linc1428, a known ES-cellsassociated lncRNA, launches a deepView genome browser view that also recapitulates the published TFBSs of E2F1, n-Myc and Klf4 (25) (Figure 5).”
- c-Myc is a universal amplifier of expressed genes in lymphocytes and embryonic stem cells (2012, neutral): “These complex patterns of binding, expression, and function, typical for studies of this oncogene (Chen et al., 2008; Dang, 2010; Eilers and Eisenman, 2008; Ji et al., 2011), failed to illuminate a principle for Myc action.”
- oPOSSUM-3: Advanced Analysis of Regulatory Motif Over-Representation Across Genes or ChIP-Seq Datasets (2012, methodology): “The cMyc and Sox2 ChIP-Seq datasets [mouse embryonic stem cells (mES)] (Chen et al. 2008) were obtained as BED files from Gene Expression Omnibus (GEO accession GSE11431) (Edgar et al. 2002) and processed into peaks (putative TF bound regions) using the FindPeaks algorithm (Fejes et al. 2008) with…”
- Transcriptional regulation of macrophage polarization: enabling diversity with identity (2011, background): “Data that have accumulated from chromatin immunoprecipitation followed by high-throughput sequencing (ChIP–seq) in recent years indicate that many transcription factors can bind to thousands of sites in the genome, most often concentrated in 'hotspots' that are associated with multiple transcripti”
- DNA-binding specificities of human transcription factors. (2013, neutral): “Similar approaches can also be applied to analysis of human transcriptional networks important for particular processes, using methods such as classical genetics, chromatin immunoprecipitation followed by sequencing (ChIP-seq), and RNAi (see, for example, Balaskas et al., 2012; Chen et al., 2008; Ch”
- Master Transcription Factors and Mediator Establish Super-Enhancers at Key Cell Identity Genes (2013, positive): “Previous studies have noted that many different ESC transcription factors can bind to sites called multiple transcription factor-binding loci (Chen et al., 2008; Kim et al., 2008), but these loci differ from super-enhancers and are associated with different genes.”
- Control of Embryonic Stem Cell State (2011, background): “The p300 cofactor occupies most active promoters in ESCs (Chen et al., 2008b).”