Intron 1 Is Required for Cell Type-Specific, But Not Injury-Responsive, Peripherin Gene Expression

Uveges, Thomas E.; Shan, Yuqing; Kramer, Bridget E.; Wight, David C.; Parysek, Linda M.

doi:10.1523/jneurosci.22-18-07959.2002

Cited by 11 publications

(7 citation statements)

References 37 publications

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“…Furthermore, it was observed that one of the target DEGs of SP1 was RAB27A , which is involved in the injury response, suggesting its role in the regulation of injury-associated DEGs after SCI. This agrees with the finding that SP1 or SP1-associated proteins are involved in regulating the expression of peripherin intermediate filament gene, which is activated after nerve injury via binding to the intron 1 site ( 37 ). Thus, whether SP1 functions in the same way in regulating injury-associated genes after SCI should be further validated.…”

Section: Discussionsupporting

confidence: 91%

Regulation of gene expression in rats with spinal cord injury based on microarray data

Chen

Fang

Meng

2015

Molecular Medicine Reports

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The present study aimed to investigate the molecular mechanisms of spinal cord injury (SCI) in rats. First, the differentially expressed genes (DGEs) were screened based on GSE45006 microarray data downloaded from Gene Expression Omnibus using the significant analysis of microarray (SAM) method. Screening was performed for DEGs which were negatively or possibly correlated with time and subsequently subjected to gene ontology (GO) functional annotation. Furthermore, pathway enrichment analysis using the Kyoto Encyclopedia of Genes and Genomes was also performed. In addition, a protein-protein interaction (PPI) network was constructed using the Search Tool for the Retrieval of Interacting Genes/Proteins database. Finally, GeneCodis was used to seek transcription factors and microRNAs that are involved in the regulation of DEGs. A total of 806 DEGs were upregulated and 549 DEGs were downregulated in the rats with SCI. Cholesterol metabolism-associated genes (e.g. HMGCS1, FDFT1 and IDI1) were negatively correlated with time, while injury genes (e.g. SERPING1, C1S and RAB27A) were positively correlated with time after SCI. PCNA, MCM2, JUN and SNAP25 were the hub proteins of the PPI network. The transcription factors LEF1 and SP1 were observed to be associated with the regulation of two DEGs that were involved in the cholesterol-associated metabolism as well as injury responses. A number of microRNAs (e.g. miR210, miR-487b and miR-16) were observed to target cholesterol metabolism-associated DGEs. The hub genes PCNA, MCM2, JUN and SNAP25 presumably have critical roles in rats with SCI, and the transcription factors LEF1 and SP1 may be important for the regulation of cholesterol metabolism and injury responses following SCI.

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Section: Discussionsupporting

confidence: 91%

Regulation of gene expression in rats with spinal cord injury based on microarray data

Chen

Fang

Meng

2015

Molecular Medicine Reports

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“…It was previously established that the 5Ј-flanking sequences of some nerve injury-associated genes such as GAP43, peripherin, and tubulin-␣, have injury-responsive characteristics (2)(3)(4)(5). However, both the detailed transcriptional machinery and the injury-responsive element within those promoters, which are pivotal for the appropriate gene responses to neuronal injury, have not been clarified.…”

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confidence: 99%

Neuronal Injury-inducible Gene Is Synergistically Regulated by ATF3, c-Jun, and STAT3 through the Interaction with Sp1 in Damaged Neurons

Kiryu‐Seo

Kato

Ogawa

et al. 2008

Journal of Biological Chemistry

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Nerve injury requires the expression of large ensembles of genes. The key molecular mechanism for this gene transcription regulation in injured neurons is poorly understood. Among many nerve injury-inducible genes, the gene encoding damageinduced neuronal endopeptidase (DINE) showed most marked expression response to various kinds of nerve injuries in central and peripheral nervous system neurons. This unique feature led us to examine the promoter region of the DINE gene and clarify both the injury-responsive element within the promoter and its related transcriptional machinery. This study showed that DINE promoter was activated by leukemia inhibitory factor and nerve growth factor withdrawal, which were pivotal for the upregulation of DINE mRNA after nerve injury. The injury-inducible transcription factors such as activating transcription factor 3 (ATF3), c-Jun, and STAT3, which were located at the downstream of leukemia inhibitory factor and nerve growth factor withdrawal, seemed to be involved in the activation of the DINE promoter. Surprisingly, these transcription factors did not bind to the DINE promoter directly. Instead, the general transcription factor, Sp1, bound to a GC box within the promoter. ATF3, c-Jun, and STAT3 interacted with Sp1 and are associated with the GC box region of the DINE gene in injured neurons. These findings suggested that Sp1 recruit ATF3, c-Jun, and STAT3 to obtain the requisite synergistic effect. Of these transcription factors, ATF3 may be the most critical, because ATF3 is specifically expressed after nerve injury.

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“…Previous reports have suggested that neuron-specific promoter activity is actualized by neuronal enhancers located upstream of the core promoter, and by non-neuronal repressors within the first intron (Uveges et al 2002, Zhou et al 2005, Kouzmenko et al 1997).…”

Section: Discussionmentioning

confidence: 98%

Transgenic medaka fish which mimic the endogenous expression of neuronal kinesin, KIF5A

et al. 2012

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Intracellular transport is spatiotemporally controlled by microtubule-dependent motor proteins, including kinesins. In order to elucidate the mechanisms controlling kinesin expression, it is important to analyze their genomic regulatory regions. In this study, we cloned the neuronal tissue-specific kinesin in medaka fish and generated transgenic fish which mimic endogenous neuronal kinesin expression in order to elucidate the mechanisms which regulate kinesin expression. Searches for medaka neuronal orthologues by RT-PCR identified a candidate gene expressed only in neuronal tissues. Using BAC clones, we determined the cDNA sequence and the gene structure of the candidate neuronal kinesin. Evolutionary analysis indicated that the candidate gene encoded medaka KIF5Aa. The endogenous medaka orthologue was found to be expressed only in the nervous system, including the brain and spinal cord, while expression of KIF5Ab was not exclusive to neuronal tissues. Transgenic (Tg) medaka that expressed EGFP under the control of the 6.9 kbp 5' and 1.9kbp 3' flanking regions of the KIF5Aa gene showed characteristic expression throughout the nervous system, including the brain, spinal cord, olfactory pit, eye and cranial nerve. Immunohistological analysis showed that EGFP expression in Tg fish co-localized with expression of HuC/D, a neuronal marker. These results demonstrate that the 6.9 kbp 5' and 1.9 kbp 3' flanking regions of medaka KIF5Aa have neuronal-specific promoter activity mimicking endogenous expression of medaka KIF5Ab. This transgenic fish strain will be useful for further functional analysis of the effects of these regulatory regions on gene expression.

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Intron 1 Is Required for Cell Type-Specific, But Not Injury-Responsive, Peripherin Gene Expression

Cited by 11 publications

References 37 publications

Regulation of gene expression in rats with spinal cord injury based on microarray data

Regulation of gene expression in rats with spinal cord injury based on microarray data

Neuronal Injury-inducible Gene Is Synergistically Regulated by ATF3, c-Jun, and STAT3 through the Interaction with Sp1 in Damaged Neurons

Transgenic medaka fish which mimic the endogenous expression of neuronal kinesin, KIF5A

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