Transforming growth factor-β-induced transcription of the Alzheimer β-amyloid precursor protein gene involves interaction between the CTCF-complex and Smads

Burton, Teralee; Liang, Binhua; Dibrov, Alex; Amara, Francis M.

doi:10.1016/s0006-291x(02)00725-8

Cited by 62 publications

(64 citation statements)

References 49 publications

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“…CTCF, in addition to transcriptional silencing or activating in a context-dependent manner, organizes epigenetically controlled chromatin insulators that regulate imprinted genes in soma (Klenova et al, 1993;Filippova et al, 1996;Ohlsson et al, 2001;Klenova et al, 2002). CTCF has been implicated previously in the deregulation of other neuronal-specific genes (Vostrov and Quitschke, 1997;Burton et al, 2002;Vostrov et al, 2002). Our data and model for regulation of the VNTR provides insights into the molecular mechanisms associated with development of neurological disorders in which the 5-HTT gene is implicated.…”

Section: Introductionmentioning

confidence: 68%

YB-1 and CTCF Differentially Regulate the 5-HTT Polymorphic Intron 2 Enhancer Which Predisposes to a Variety of Neurological Disorders

Klenova¹,

Scott²,

Roberts³

et al. 2004

J. Neurosci.

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Section: Introductionmentioning

confidence: 68%

YB-1 and CTCF Differentially Regulate the 5-HTT Polymorphic Intron 2 Enhancer Which Predisposes to a Variety of Neurological Disorders

Klenova¹,

Scott²,

Roberts³

et al. 2004

J. Neurosci.

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“…Nevertheless, dCTCFdependent localization of Smad proteins to specific low occupancy elements is consistent with the CTCF-dependent nature of Smad binding at both the APP and H19 promoters in humans. 7,8 We speculate that dCTCF-dependent Smad localization to low occupancy APBSs within topological domains may represent regulatory elements involved in enhancer-promoter interactions, whereas dCTCF-independent high occupancy APBSs are involved in establishing higher-order chromosome organization. What role Smads might play in establishing or maintaining such long-range interactions relevant to chromosome architecture, or whether Smads and other transcription factors simply localize to high occupancy APBSs due to chromatin accessibility, remains difficult to address.…”

Section: Discussionmentioning

confidence: 98%

“…6 Nevertheless, the mechanisms driving recruitment of Smad proteins to DNA in non-stem cells remain largely unexplored. Studies probing the mammalian Alzheimer amyloid precursor protein (APP) gene promoter 7 and the H19 imprinting control region 8 have identified sites in which Smad recruitment to DNA is mediated by the architectural protein CTCF, previously characterized for its ability to mediate long-range interactions and to function as an insulator. 9 To what degree CTCF recruits Smad proteins to DNA on a global scale, whether these interactions are related to the TGF-b response, and whether CTCF-directed Smad localization is conserved in other organisms remains unknown.…”

Section: Introductionmentioning

confidence: 99%

CTCF-dependent co-localization of canonical Smad signaling factors at architectural protein binding sites in D. melanogaster

et al. 2015

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The transforming growth factor b (TGF-b) and bone morphogenetic protein (BMP) pathways transduce extracellular signals into tissue-specific transcriptional responses. During this process, signaling effector Smad proteins translocate into the nucleus to direct changes in transcription, but how and where they localize to DNA remain important questions. We have mapped Drosophila TGF-b signaling factors Mad, dSmad2, Medea, and Schnurri genome-wide in Kc cells and find that numerous sites for these factors overlap with the architectural protein CTCF. Depletion of CTCF by RNAi results in the disappearance of a subset of Smad sites, suggesting Smad proteins localize to CTCF binding sites in a CTCF-dependent manner. Sensitive Smad binding sites are enriched at low occupancy CTCF peaks within topological domains, rather than at the physical domain boundaries where CTCF may function as an insulator. In response to Decapentaplegic, CTCF binding is not significantly altered, whereas Mad, Medea, and Schnurri are redirected from CTCF to non-CTCF binding sites. These results suggest that CTCF participates in the recruitment of Smad proteins to a subset of genomic sites and in the redistribution of these proteins in response to BMP signaling.

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“…Numerous studies have revealed that TGF-β1 C-509T and T869C polymorphisms are associated with an increased TGF-β1 production. Burton et al (33) reported that the -509T allele was associated with increased transcriptional activity of TGF-β1 compared with the -509C allele. In addition, the polymorphism has been confirmed to be associated with asthma risk (34) and severity (35).…”

Section: Discussionmentioning

confidence: 99%

Associations of genetic variants in ADAM33 and TGF-β1 genes with childhood asthma risk

Zhang

et al. 2014

Biomedical Reports

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Abstract. The aim of the present study was to explore the associations of genetic variants in the ADAM33 and TGF-β1 genes with the risk of childhood asthma. A total of 299 asthmatic children and 311 healthy controls were recruited in the hospital-based case-control study. The asthmatic subjects were further divided into mild and severe groups according to disease severity. Single-nucleotide polymorphisms (SNP) at ADAM33 V4, T2, S2 and T1, and TGF-β1 C-509T and T869C were selected and detected with PCR-RFLP. The associations of the SNPs with asthma risk and severity were analyzed. The associations between the haplotypes of ADAM33 and TGF-β1 were also evaluated. Compared with the GG genotype, the GC and CC genotypes at V4 were associated with an increased asthma risk in children and the ORs were 2.92 and 10.56, respectively. Compared with the CC genotype, the CT/TT genotype at C-509T was associated with an increased asthma risk and the OR was 2.26. Subsequent to stratification by asthma severity, compared with the V4 GG genotype, it was found that the CG and CC genotypes were associated with a mild asthma risk and the ORs were 3.00 and 5.99, respectively. The SNP at C-509T (CT/TT vs. CC) was associated with mild asthma (OR=2.34), whereas a marginally significant association was detected between the SNP (CT/ TT vs. CC) and severe asthma risk (OR=2.19). The haplotype analysis revealed that, compared with the GGCA haplotype of ADAM33, significant associations of the haplotypes of CGCG, CGGA, GACA, GACG and GAGA with asthma risk were observed, and the ORs were 31.12, 12.24, 4.73, 30.85 and 4.83, respectively. No significant association was detected between the TGF-β1 haplotypes and asthma risk. The genetic variants at V4 and C-509T had the potential to modify the childhood asthma risk and the associations showed no notable difference with the disease severity. Thus, ADAM33 haplotypes provided more useful information in the prediction of asthma risk.

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Transforming growth factor-β-induced transcription of the Alzheimer β-amyloid precursor protein gene involves interaction between the CTCF-complex and Smads

Cited by 62 publications

References 49 publications

YB-1 and CTCF Differentially Regulate the 5-HTT Polymorphic Intron 2 Enhancer Which Predisposes to a Variety of Neurological Disorders

YB-1 and CTCF Differentially Regulate the 5-HTT Polymorphic Intron 2 Enhancer Which Predisposes to a Variety of Neurological Disorders

CTCF-dependent co-localization of canonical Smad signaling factors at architectural protein binding sites in D. melanogaster

Associations of genetic variants in ADAM33 and TGF-β1 genes with childhood asthma risk

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