Ezh2 controls B cell development through histone H3 methylation and Igh rearrangement

By I. Su, A. Basavaraj, A. Krutchinsky, O. Hobert, A. Ullrich, Brian T. Chait, A. Tarakhovsky. Nature Immunology, 2003

645 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/25052b86ab7ff8c155042510bba6d46f891d9ef6

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Citations in the corpus

Pax5: the guardian of B cell identity and function (2007, background): “The recombination of distal V H genes is also specifically impaired in the absence of the histone methyltransferase Ezh2 (ref”
EZH2 is required for germinal center formation and somatic EZH2 mutations promote lymphoid transformation (2013, background): “Conditional Ezh2 knockout mice (loxPflanked EZH2 allele, EZH2fl/fl) were a generous gift of Dr. Alexander Tarakhovsky, The Rockefeller University (Su et al., 2003).”
EZH1 mediates methylation on histone H3 lysine 27 and complements EZH2 in maintaining stem cell identity and executing pluripotency. (2008, background): “…development, PRC2 is required for diverse physiological functions including B lymphoid development, myogenic differentiation, imprinted X chromosome inactivation, and reprogramming of migrating primordial germ cells (Caretti et al., 2004; Kalantry et al., 2006; Seki et al., 2007; Su et al., 2003).”
An epigenetic road map for histone lysine methylation (2003, background): “…histone lysine methylation probably affects most chromatintemplated processes – from cell proliferation and tumorigenesis (Varambally et al., 2002) to imprinting, X-inactivation, lineage commitment (Su et al., 2003), aging, stem cell plasticity and the epigenetic reprogramming of the genome.”
Somatic mutations at EZH2 Y641 act dominantly through a mechanism of selectively altered PRC2 catalytic activity, to increase H3K27 trimethylation. (2011, background): “2 M biotinylated peptide substrate (ie, peptide mimicking the H3 tail, H3(21-44)), which has been unmethylated (H3K27me0, open bar or me0), monomethylated (H3K27me1, gray bar or me1) or dimethylated (H3K27me2, black bar or me2) at Lys-27.”
Mechanism and control of V(D)J recombination at the immunoglobulin heavy chain locus. (2006, background): “In addition to elements of the IL-7 signaling cascade, B-cellspecific deletion of Ezh2, a histone methyltransferase, results in a decrease in VHJ558 rearrangement (again as measured by PCR on pro-B cell DNA), but in the presence of normal germline transcripts and histone acetylation; instead, methyl”
Ezh1 and Ezh2 maintain repressive chromatin through different mechanisms (2008, background): “Interestingly, whereas deletion of Ezh2 in pro-B cells resulted in a dramatic decrease in H3K27 methylation (Su et al., 2003), we did not observe a clear correlation between Ezh2 expression and H3K27me3 in kidney from aging mice or in adult tissues (data not shown).”
The Polycomb Ezh2 methyltransferase regulates muscle gene expression and skeletal muscle differentiation. (2004, background): “Pertinent to its putative role in cell differentiation are the findings that conditional inactivation of Ezh2 results in selectively impaired formation of pre-B and immature B cells but an unaltered development of pro-B cells (Su et al. 2003).”
Ezh2 Orchestrates Gene Expression for the Stepwise Differentiation of Tissue-Specific Stem Cells (2009, methodology): “Mice harboring the floxed Ezh2 allele (Su et al., 2003) were bred to mice expressing Cre recombinase under the keratin 14 (K14) promoter in embryonic epidermal progenitors (Vasioukhin et al.”