ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007
Characterization of an enhancer region of the galanin gene that directs expression to the dorsal root ganglion and confers responsiveness to axotomy.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 28 citations in OpenAlex.
- Neurons Are Not All the Same: Diversity in Neuronal Populations and Their Intrinsic Responses to Spinal Cord Injury.ASN neuro · 2025Review
- Involvement of Scratch2 in GalR1-mediated depression-like behaviors in the rat ventral periaqueductal gray.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Injury-specific promoters enhance herpes simplex virus-mediated gene therapy for treating neuropathic pain in rodents.The journal of pain · 2015Article
- Plasticity of DNA methylation in a nerve injury model of pain.Epigenetics · 2015Article
- Galanin negatively modulates opiate withdrawal via galanin receptor 1.Psychopharmacology · 2012Article
- Role of transcription factors in peripheral nerve regeneration.Frontiers in molecular neuroscience · 2012Article
- Proto-oncogene PBF/PTTG1IP regulates thyroid cell growth and represses radioiodide treatment.Cancer research · 2011Article
- Differential activity by polymorphic variants of a remote enhancer that supports galanin expression in the hypothalamus and amygdala: implications for obesity, depression and alcoholism.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2011Article
- gp130 cytokines are positive signals triggering changes in gene expression and axon outgrowth in peripheral neurons following injury.Frontiers in molecular neuroscience · 2011Article
- Characterisation of the nociceptive phenotype of suppressible galanin overexpressing transgenic mice.Molecular pain · 2010Article
- The expression of ELK transcription factors in adult DRG: Novel isoforms, antisense transcripts and upregulation by nerve damage.Molecular and cellular neurosciences · 2010Article
- 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
- Axotomy-induced Smad1 activation promotes axonal growth in adult sensory neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Effects of norepinephrine on galanin expression in dorsal root ganglion neurons in vitro.Current therapeutic research, clinical and experimental · 2009Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Galanin expression markedly increases in the dorsal root ganglion (DRG) after sciatic nerve axotomy and modulates pain behavior and regeneration of sensory neurons. Here, we describe transgenic mice expressing constructs with varying amounts of sequence upstream of the murine galanin gene marked by LacZ. The 20 kb region upstream of the galanin gene recapitulates the endogenous expression pattern of galanin in the embryonic and adult intact DRG and after axotomy. In contrast, 1.9 kb failed to drive LacZ expression in the intact DRG or after axotomy. However, the addition of an additional 2.7 kb of 5' flanking DNA (4.6 kb construct) restored the expression in the embryonic DRG and in the adult after axotomy. Sequence analysis of this 2.7 kb region revealed unique 18 and 23 bp regions containing overlapping putative Ets-, Stat-, and Smad-binding sites, and adjacent putative Stat- and Smad-binding sites, respectively. Deletion of the 18 and 23 bp regions from the 4.6 kb construct abolished the upregulation of LacZ expression in the DRG after axotomy but did not affect expression in the embryonic or intact adult DRG. Also, a bioinformatic analysis of the upstream regions of a number of other axotomy-responsive genes demonstrated that the close proximity of putative Ets-, Stat-, and Smad-binding sites appears to be a common motif in injury-induced upregulation in gene expression.
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