Search results for CTCF

Showing 13 results out of 13

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Protein (1 results from a total of 1)

Identifier: R-HSA-3782562
Species: Homo sapiens
Compartment: nucleoplasm
Primary external reference: UniProt: CTCF: P49711

Complex (5 results from a total of 5)

Identifier: R-HSA-5617873
Species: Homo sapiens
Compartment: nucleoplasm
Identifier: R-HSA-5617651
Species: Homo sapiens
Compartment: nucleoplasm
Identifier: R-HSA-5617645
Species: Homo sapiens
Compartment: nucleoplasm
Identifier: R-HSA-6810160
Species: Homo sapiens
Compartment: nucleoplasm
Identifier: R-HSA-5617876
Species: Homo sapiens
Compartment: nucleoplasm

Reaction (7 results from a total of 7)

Identifier: R-HSA-6810161
Species: Homo sapiens
Compartment: nucleoplasm
In human fibroblasts (Lan et al. 2007) and human embryonic carcinoma cells (Lee et al. 2007, Sessa et al. 2007) treated with retinoic acid HOXA3 chromatin is activated by loss of methylation at lysine-27 of histone H3 (H3K27me3) and gain of H3K4me3. KDM6A (UTX) binds near HOXA3 (Lan et al. 2007, Lee et al. 2007) but does not appear to participate in the loss of H3K27me3. KDM6A forms complexes with the histone methyltransferases KMT2C,D (MLL2,3) which may participate in methylating H3K4 (Lee et al. 2007). Polycomb repressive complex 2 (PRC2), which binds H3K27me3, is also lost during activation of HOXA3 (Lan et al. 2007, Lee et al. 2007, Sessa et al. 2007). The change in chromatin at HOXA3 may result from euchromatin spreading from distant 3' retinoic acid response elements. The chromosomal conformation of the entire HOXA cluster changes during activation (Rousseau et al. 2014).
Identifier: R-HSA-5617862
Species: Homo sapiens
Compartment: nucleoplasm
As inferred from mouse embryos, retinoic acid initially activates expression of the HOXA4 gene in rhombomere 7 (r7) by binding RARB or RARA in dimeric RAR:RXR complexes located at retinoic acid response elements (RAREs) in the 5' flanking region of the HOXA4 promoter (also observed in human teratocarcinoma cells in Doerksen et al. 1996, Sessa et al. 2007), correlating dissociation of corepressors and recruitment of coactivators. In mouse embryos Hoxa4 itself maintains later expression in an autoregulatory loop.
In human fibroblasts (Lan et al. 2007) and teratocarcinoma cells (Sessa et al 2007) activation of HOXA4 chromatin is accompanied by loss of methylation at lysine-27 of histone H3 (H3K27me3) and gain of H3K4me3. The polycomb repressive complex 2 (PRC2), which binds H3K27me3, is also reduced at active HOXA4 chromatin (Lan et al. 2007, Sessa et al. 2007).
Identifier: R-HSA-9011997
Species: Homo sapiens
Compartment: nucleoplasm
MYC gene expression is estrogen-responsive and expression of MYC and CCND1 contribute to the proliferative response stimulated by estrogen treatment (Dubnik et al, 1987; Dubnik et al, 1988; Dubnik and Shu, 1992; Prall et al, 1998). Estrogen-responsive MYC expression appears to depend at least in part on a distal enhancer element 67 kb from the transcriptional start site that contains a half ERE and an AP-1 site (Denardo et al, 2005; Carroll et al, 2006; Wang et al, 2011). Upon estrogen stimulation, these sites are occupied by ESR1 and a JUND:FOSB heterodimer, respectively (Wang et al, 2011). Estrogen-responsive MYC expression also depends on the cohesin complex, as depletion of the RAD21 cohesin subunit abrogates expression (Stedman et al, 2008; Schmidt et al, 2010; McEwan et al, 2011; Antony et al, 2015). Genome-wide studies have shown that RAD21 and ESR1 binding sites overlap in a fraction of estrogen-responsive genes, including MYC (Schmidt et al, 2010). Cohesin may contribute to target gene expression by promoting chromatin looping structures between distal enhancers and the target gene promoters or through other mechanisms that remain to be elucidated (Li et al, 2012; Antony et al, 2015; reviewed Rhodes et al, 2011; Losada, 2014). Overexpression of histone isoform HIST1H2AC in breast cancer has been shown to contribute to MYC gene expression by promoting the formation of activating chromatin loops and facilitating the recruitment of ESR1, EP300 and RNA polymerase II (Su et al, 2014).
Identifier: R-HSA-9011975
Species: Homo sapiens
Compartment: nucleoplasm
MYC gene expression is estrogen-responsive and expression of MYC and CCND1 contribute to the proliferative response stimulated by estrogen treatment (Dubnik et al, 1987; Dubnik et al, 1988; Dubnik and Shu, 1992; Prall et al, 1998). Estrogen-responsive MYC expression appears to depend at least in part on a distal enhancer element 67 kb from the transcriptional start site that contains a half ERE and an AP-1 site (Denardo et al, 2005; Carroll et al, 2006; Wang et al, 2011). Upon estrogen stimulation, these sites are occupied by ESR1 and a JUND:FOSB heterodimer, respectively (Wang et al, 2011). Estrogen-responsive MYC expression also depends on the cohesin complex, as depletion of the RAD21 cohesin subunit abrogates expression (Stedman et al, 2008; Schmidt et al, 2010; McEwan et al, 2011; Antony et al, 2015). Genome-wide studies have shown that RAD21 and ESR1 binding sites overlap in a fraction of estrogen-responsive genes, including MYC (Schmidt et al, 2010). Cohesin may contribute to target gene expression by promoting chromatin looping structures between distal enhancers and the target gene promoters or through other mechanisms that remain to be elucidated (Li et al, 2012; Antony et al, 2015; reviewed Rhodes et al, 2011; Losada, 2014). Overexpression of histone isoform HIST1H2AC in breast cancer has been shown to contribute to MYC gene expression by promoting the formation of activating chromatin loops and facilitating the recruitment of ESR1, EP300 and RNA polymerase II (Su et al, 2014).
Identifier: R-HSA-5617471
Species: Homo sapiens
Compartment: nucleoplasm, cytosol
CNOT6 (CCR4) and ZNF335 (NIF-1) directly associate and indirectly enhance the transcription of HOXA1 produced by activation by retinoic acid (Garapaty et al. 2008)
After activation by retinoic acid, the HOXA1 gene is transcribed to yield mRNA (inferred from mouse embryos, also demonstrated in human cancer cells, Chariot et al. 1995, Xu et al. 2014). The mRNA is a target of the microRNAs miR-10a in megakaryocytes (Garzon et al. 2006), miR210 in tumors (Huang et al. 2009), let-7c in non-small cell lung cancer cells (Zhan et al. 2013), miR-99 in epithelial cells (Chen et al. 2013), and miR-100 in tumor cells (Chen et al. 2014), however it is unknown if these play a role in embryogenesis. Opposite strand intergenic transcripts are also observed in adult tissues and placenta (Sessa et al. 2007).
In mouse embryos, expression of Hoxa1 occurs in the neural tube, adjacent mesenchyme, paraxial mesoderm, somites, and gut epithelium from rhombomere 4 to the caudal-most region of the embryo. (Rhombomeres are transiently formed segments in the neural tube that will eventually form the hindbrain.)
Regulation of HOXA1 by retinoic acid is inferred from mouse embryos (Frasch et al. 1995, Dupe et al. 1997, Paschaki et al. 2013) and cell lines (Langston and Gudas 1992, Langston et al. 1997, Gillespie and Gudas 2007).
RQCD1 (RCD1) enhances transcription of the HOXA1 in response to activation by retinoic acid (Garapaty et al. 2008).
Identifier: R-HSA-9612440
Species: Homo sapiens
Compartment: nucleoplasm
The intracellular fragment of the cyt1 isoform of ERBB4, ERBB4jmAcyt1s80, binds the promoter region of the MXD4 gene. The ERBB4 binding site overlaps with MYC and CTCF binding elements (Wali et al. 2014).
Identifier: R-HSA-6810139
Species: Homo sapiens
Compartment: nucleoplasm
In human cell lines and tissues activation of HOXA2 chromatin by retinoic acid occurs through loss of methylation at lysine-27 of histone H3 (H3K27), dissociation of polycomb repressive complexes, and gain of methylation at H3K4 (Lee et al. 2007 Supplementary, Sakamoto et al. 2007, Sessa et al. 2007). The change in chromatin may be produced by euchromatin spreading from distant 3' retinoic acid response elements. DNA methylation and MBD1 also appear to play a role in maintaining repression at HOXA2 in HeLa cells (Sakamoto et al. 2007). The histone demethylase KDM6A binds HOXA2 (Lee et al. 2007 Supplementary) and may participate in removing H3K27 methylation. KDM6A associates with histone methyltransferases KMT2C,D (MLL2,3) which may participate in methylating H3K4 in embryonal carcinoma cells (Lee et al. 2007, also observed at other HOXA genes in Lan et al. 2007). The conformation of the entire HOXA cluster in the nucleus changes during differentiation of a myeloid leukemia cell line and the conformation changes correlate with gene activity, H3K27me2,3 occurence, and proximity to CTCF binding sites (Rousseau et al. 2014, see also Lonfat and Duboule 2015).
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