Global mapping of H3K4me3 and H3K27me3 reveals specificity and plasticity in lineage fate determination of differentiating CD4+ T cells.
By Gang Wei, Lai Wei, Jinfang Zhu, Chongzhi Zang, J. Hu‐Li, Zhengju Yao, Kairong Cui, Y. Kanno, Tae-Young Roh, W. Watford and 6 more. Immunity, 2009
1,191 citations recorded by the source corpus.
Subfields: Immunology
View Paper: https://www.semanticscholar.org/paper/e750dc963a781a87c621c7ad5ad44350384d8131
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Immunology
- Shizuo Akira
- Dan R. Littman
- O. Takeuchi
- Y. Belkaid
- W. E. Paul
- Jinfang Zhu
- J. O’Shea
- Shimon Sakaguchi
Citations in the corpus
- Decrease of Foxp3+ Treg cell number and acquisition of effector cell phenotype during lethal infection (2009, background): “Recent evidence also supports the idea that Treg cells can become unstable after exposure to defined stimulatory signals or in lymphopenic environments (Degauque et al., 2008; Duarte et al., 2009; Wei et al., 2009; Xu et al., 2007).”
- Fast gene set enrichment analysis (2016, methodology): “As the example ranking Th0 vs Th1 comparison was used from dataset GSE14308 [4].”
- The Jmjd3-Irf4 axis regulates M2 macrophage polarization and host responses against helminth infection (2010, background): “In the case of histone modification, trimethylation of H3K4 is associated with active gene transcription, whereas trimethylation of H3K9, H3K27 and H4K20 is linked to silencing of gene expressio”
- Phenotypic and functional specialization of FOXP3+ regulatory T cells (2011, result): “Together, these studies suggest that highly polarized inflammatory environments can subvert T Reg cell function by converting them to FOXP3 − effector T cells in vivo , and are consistent with a recent epigenetic analysis demonstrating that the loci encoding the key transcription factors and cyto”
- Opposing regulation of the Il17 locus through direct, reciprocal actions of STAT3 and STAT5 (2011, background): “For efficient and stable gene transcription, the locus must be held in an open conformation, which can be monitored by the presence of characteristic histone modification”
- Diverse Targets of the Transcription Factor STAT3 Contribute to T Cell Pathogenicity and Homeostasis (2010, methodology): “and then processed for ChIP-Seq as previously described (Wei et al., 2009).”
- Plasticity of CD4+ T cell lineage differentiation. (2009, background): “The experiments described above, using in vitro polarization or adoptive transfer, are representative of current approaches for studying Th17 cell stability (Lee et al., 2009; Croxford et al., 2009; Wei et al., 2009; Bending et al., 2009).”
- Peripheral CD4 T cell differentiation regulated by networks of cytokines and transcription factors (2010, background): “The NF-jB family member c-Rel is highly expressed in both nTregs and iTregs (94).”
- T-bet controls regulatory T cell homeostasis and function during type-1 inflammation (2009, background): “Indeed, genome-wide histone-methylation analyses indicate that Tbx21 exists in a poised epigenetic state in T reg cells and can readily be upregulated in T H 1-polarizing conditions in vitro”
- T cell receptor stimulation-induced epigenetic changes and Foxp3 expression are independent and complementary events required for Treg cell development. (2012, methodology): “We therefore checked possible nTreg-specific histone modifications by using available chromatin databases of T cell subsets (Wei et al., 2009).”
- Genome-wide mapping of HATs and HDACs reveals distinct functions in active and inactive genes (2009, background): “…mapping has revealed numerous combinatorial patterns of histone modifications in human CD4+ T cells (Barski et al., 2007; Wang et al., 2008) and suggested that modification patterns can indicate differentiation potential of cells (Cui et al., 2009; Wei et al., 2009; reviewed in Wang et al., 2009).”
- Development and maintenance of regulatory T cells. (2013, background): “In addition, enhanced H3K4me3 histone modification of the Treg cell signature genes detected in nTreg cells is easily primed in Tconv cells under a Th1-, Th2-, or Th17-cell-polarizing or iTreg-cell-inducing condition (Wei et al., 2009) (Figure 1).”