CTCF mediates methylation-sensitive enhancer-blocking activity at the H19/Igf2 locus

By Amy T. Hark, C. Schoenherr, D. Katz, R. Ingram, J. Levorse, S. Tilghman. Nature, 2000

1,588 citations recorded by the source corpus.

Subfields: Genetics, Molecular Biology, Pediatrics, Perinatology and Child Health

View Paper: https://www.semanticscholar.org/paper/54a60012f56cfe3a3545182f517ef31426e694dc

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Citations in the corpus

Insulators: many functions, many mechanisms. (2002, background): “That function is abrogated by CpG methylation of the CTCF-binding sites, allowing Igf2 expression from the paternal allele.”
The fundamental role of epigenetic events in cancer (2002, background): “However, there are examples in which the methylation of individual CpG sites in such promoters can determine the transcriptional status of a gene by blocking the access of certain transcription factors that are sensitive to the methylation of CpG sites in their target binding site”
Inactivation of the apoptosis effector Apaf-1 in malignant melanoma (2001, background): “Only one cell line (11) was Apaf-1-positive and highly resistant to ADR.”
The Evf-2 noncoding RNA is transcribed from the Dlx-5/6 ultraconserved region and functions as a Dlx-2 transcriptional coactivator. (2006, methodology): “Thermal cycler conditions were as follows: 30 min at 48°C, then 15 min at 95°C, followed by 40 cycles of 15 sec at 95°C, 1 min at 59°C. Quantitation of the sample is based on the cycle when the amplicon is first detected, threshold cycle (Ct) as defined by Higuchi et al. (1993).”
Topologically associating domains and chromatin loops depend on cohesin and are regulated by CTCF, WAPL, and PDS5 proteins (2017, positive): “Early work revealed that this enhancerblocking activity is required for imprinted gene expression at the H19-IGF2 locus (Bell & Felsenfeld, 2000; Hark et al, 2000) and indicated that CTCF mediates this function by creating allele-specific chromatin loops (Kurukuti et al, 2006; Splinter et al, 2006).”
CTCF: Master Weaver of the Genome (2009, positive): “…by the same group at the 3′ end of this domain (Saitoh et al., 2000) in parallel with the discovery of four CTCF-binding sites within the imprinted control region (ICR) of the mammalian H19/Igf2 locus (Bell and Felsenfeld, 2000; Hark et al., 2000; Kanduri et al., 2000; Szabo et al., 2000).”
Analysis of the vertebrate insulator protein CTCF-binding sites in the human genome. (2007, positive): “In addition, it has been demonstrated that an insulator in the IGF2/ H19 locus is critical for the imprinting of the locus (Bell and Felsenfeld, 2000; Hark et al., 2000; Kanduri et al., 2000).”
Controlling the double helix (2003, background): “This causes dissociation of a chromatin protein known as CTCF, which normally blocks a downstream enhancer; consequently, the enhancer is then free to activate Igf2 expressio”
CTCF mediates long-range chromatin looping and local histone modification in the beta-globin locus. (2007, positive): “In vivo, CTCF binds to the imprinting control region of the H19 /insulin-like growth factor ( Igf2 ) locus, where it acts as a methylation-sensitive enhancer blocker (Bell and Felsenfeld 2000; Hark et al. 2000).”
Widespread plasticity in CTCF occupancy linked to DNA methylation (2012, background): “…variable CTCF occupancy has been linked with DNA methylation in vivo (Kanduri et al. 2000; Pant et al. 2003), and in vitro studies suggest that methylation may hinder CTCF binding at certain sequence elements (Bell and Felsenfeld 2000; Hark et al. 2000; Filippova et al. 2001; Renda et al. 2007).”