ArticleBMC molecular biology2015
RE1 silencing transcription factor (REST) negatively regulates ALL1-fused from chromosome 1q (AF1q) gene transcription.
Article in BMC molecular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 5 citations in OpenAlex.
- AF1q is a universal marker of neuroblastoma that sustains N-Myc expression and drives tumorigenesis.Oncogene · 2024Article
- Mllt11 Regulates Migration and Neurite Outgrowth of Cortical Projection Neurons during Development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Dual-specificity tyrosine phosphorylation-regulated kinase 1A ameliorates insulin resistance in neurons by up-regulating IRS-1 expression.The Journal of biological chemistry · 2019Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundALL1-fused from chromosome 1q (AF1q), originally considered as an oncogenic factor, has been implicated in neuronal development; however, its upstream regulatory mechanisms in neural system remained elusive.
resultsOur study showed that REST (RE1 silencing transcription factor), a key transcription factor in neurodevelopment, could down-regulate the gene expression of AF1q. The promoter assay identified a neuron-restrictive silencer element at -383 to -363 bp of human AF1q promoter. Electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation (CHIP) confirmed the binding of REST to the NRSE in AF1q gene promoter. Additionally, the negative correlation between the expression levels of Af1q and Rest in mice neurodevelopment supported the negative regulation of AF1q by REST and the potential functions of AF1q in neurodevelopment.
conclusionThese results demonstrate that REST regulates AF1q gene transcription through directly binding to a NRSE at -383 to -363 bp of AF1q promoter.
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