ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1997
Identification of a novel repressive element that contributes to neuron-specific gene expression.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 47 citations in OpenAlex.
- GAP-43 and BASP1 in Axon Regeneration: Implications for the Treatment of Neurodegenerative Diseases.Frontiers in cell and developmental biology · 2020Review
- Systematic discovery of novel eukaryotic transcriptional regulators using sequence homology independent prediction.BMC genomics · 2017Article
- A Shift from a Pivotal to Supporting Role for the Growth-Associated Protein (GAP-43) in the Coordination of Axonal Structural and Functional Plasticity.Frontiers in cellular neuroscience · 2017Review
- hnRNP-Q1 represses nascent axon growth in cortical neurons by inhibiting Gap-43 mRNA translation.Molecular biology of the cell · 2016Article
- Transcriptional regulatory regions of gap43 needed in developing and regenerating retinal ganglion cells.Developmental dynamics : an official publication of the American Association of Anatomists · 2010Article
- Two non-homologous brain diseases-related genes, SERPINI1 and PDCD10, are tightly linked by an asymmetric bidirectional promoter in an evolutionarily conserved manner.BMC molecular biology · 2007Article
- Molecular mechanisms, biological actions, and neuropharmacology of the growth-associated protein GAP-43.Current neuropharmacology · 2006Article
- Hypoxia induces a functionally significant and translationally efficient neuronal NO synthase mRNA variant.The Journal of clinical investigation · 2005Article
- Protein kinase A-dependent derepression of the human prodynorphin gene via differential binding to an intragenic silencer element.Molecular and cellular biology · 1998Article
- Transcriptional regulation of the GluR2 gene: neural-specific expression, multiple promoters, and regulatory elements.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1998Article
- The activity of a highly promiscuous AP-1 element can be confined to neurons by a tissue-selective repressive element.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1998Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Multiple signaling pathways are thought to control the selective expression of genes over the course of neuronal differentiation. One approach to elucidating these pathways is to identify specific cis-acting elements that serve as the final targets for these signaling pathways in neural-specific genes. We now identify a novel repressive element from the growth-associated protein 43 (GAP-43) gene that can contribute to neuron-specific gene expression by inhibiting transcription in a wide range of non-neuronal cell types. This repressive element is located downstream of the GAP-43 TATA box and is highly position-dependent. When transferred to viral promoters this element preferentially inhibits transcription in non-neuronal cells. Electrophoretic mobility shift assays show that the repressive element comprises at least two protein recognition sites. One of these is a novel sequence motif that we designate the SNOG element, because it occurs downstream of the TATA boxes of the synaptosomal-associated protein of 25 kDa and neuronal nitric oxide synthase genes, as well as the GAP-43 gene. The GAP-43 repressive element is distinct in sequence and position dependence from the repressor element 1/neuron-restrictive silencer element previously described in other neural genes and therefore is a likely target for a distinct set of signaling pathways involved in the control of neuronal differentiation.
Indexed as
Identifiers
9315881PMC6793915W2110727504What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.