ArticleThe Journal of biological chemistry2004
Identification of a novel cyclic AMP-response element (CRE-II) and the role of CREB-1 in the cAMP-induced expression of the survival motor neuron (SMN) gene.
Article in The Journal of biological chemistry, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 26 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 54 citations in OpenAlex.
- Regulation of Survival Motor Neuron Protein by the Nuclear Factor-Kappa B Pathway in Mouse Spinal Cord Motoneurons.Molecular neurobiology · 2018Article
- Using Systems Biology and Mathematical Modeling Approaches in the Discovery of Therapeutic Targets for Spinal Muscular Atrophy.Advances in neurobiology · 2018Review
- A Role for cAMP and Protein Kinase A in Experimental Necrotizing Enterocolitis.The American journal of pathology · 2017Article
- Synergistic Neuroprotective Effects of Two Herbal Ingredients via CREB-Dependent Pathway.Frontiers in pharmacology · 2016Article
- Salbutamol inhibits ubiquitin-mediated survival motor neuron protein degradation in spinal muscular atrophy cells.Biochemistry and biophysics reports · 2015Article
- IGF-1R Reduction Triggers Neuroprotective Signaling Pathways in Spinal Muscular Atrophy Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Transcription factor decoy: a pre-transcriptional approach for gene downregulation purpose in cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Review
- MiR-1224-5p acts as a tumor suppressor by targeting CREB1 in malignant gliomas.Molecular and cellular biochemistry · 2015Article
- Molecular mechanisms and animal models of spinal muscular atrophy.Biochimica et biophysica acta · 2015Review
- Defects in pancreatic development and glucose metabolism in SMN-depleted mice independent of canonical spinal muscular atrophy neuromuscular pathology.Human molecular genetics · 2014Article
- Advances in therapeutic development for spinal muscular atrophy.Future medicinal chemistry · 2014Review
- Systems biology investigation of cAMP modulation to increase SMN levels for the treatment of spinal muscular atrophy.PloS one · 2014Article
- Shift from extracellular signal-regulated kinase to AKT/cAMP response element-binding protein pathway increases survival-motor-neuron expression in spinal-muscular-atrophy-like mice and patient cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- The canonical nuclear factor-κB pathway regulates cell survival in a developmental model of spinal cord motoneurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- In vivo NMDA receptor activation accelerates motor unit maturation, protects spinal motor neurons, and enhances SMN2 gene expression in severe spinal muscular atrophy mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Effects of 2,4-diaminoquinazoline derivatives on SMN expression and phenotype in a mouse model for spinal muscular atrophy.Human molecular genetics · 2010Article
- DNA plasticity is a key determinant of the energetics of binding of Jun-Fos heterodimeric transcription factor to genetic variants of TGACGTCA motif.Biochemistry · 2009Article
- Spinal muscular atrophy with pontocerebellar hypoplasia is caused by a mutation in the VRK1 gene.American journal of human genetics · 2009Article
- Translational readthrough by the aminoglycoside geneticin (G418) modulates SMN stability in vitro and improves motor function in SMA mice in vivo.Human molecular genetics · 2009Article
- Regulation of SMN protein stability.Molecular and cellular biology · 2009Article
Corrections and comments
- Retraction · 2018-07-19Concerns/Issues about Data · Concerns/Issues about Image · Original Data and/or Images not Provided and/or not Available ·
- Retracted
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Spinal muscular atrophy, an autosomal recessive disorder, is caused by loss of the SMN1 (survival motor neuron) gene while retaining the SMN2 gene. SMN1 produces a majority of full-length SMN transcript, whereas SMN2 generates mostly an isoform lacking exon 7. Here, we demonstrate a novel cAMP-response element, CRE-II, in the SMN promoter that interacts with the cAMP-response element-binding (CREB) family of proteins. In vitro DNase I protection analysis and in vivo genomic footprinting of the SMN promoter using the brain and liver nuclei from SMN2 transgenic mice revealed footprinting at the CRE-II site. Site-directed mutation of the CRE-II element caused a marked reduction in the SMN promoter activity revealed by transient transfection assay. Activation of the cAMP pathway by dibutyryl cAMP (0.5 mm) alone or in combination with forskolin (20 microm) caused a 2-5-fold increase in the SMN promoter activity but had no effect on the CRE-II mutated promoter. Electrophoretic mobility shift assay and a UV-induced DNA-protein cross-linking experiment confirmed that CREB1 binds specifically to the CRE-II site. Transient overexpression of CREB1 protein resulted in a 4-fold increase of the SMN promoter activity. Intraperitoneal injection of epinephrine in mice expressing two copies of the human SMN2 gene resulted in a 2-fold increase in full-length SMN transcript in the liver. Combined treatment with dibutyryl cAMP and forskolin significantly increased the level of both the full-length and exon 7-deleted SMN (exonDelta7SMN) transcript in primary hepatocytes from mice expressing two copies of human SMN2 gene. Similar treatments of type I spinal muscular atrophy mouse and human fibroblasts as well as HeLa cells resulted in an augmented level of SMN transcript. These findings suggest that the CRE-II site in SMN promoter positively regulates the expression of the SMN gene, and treatment with cAMP-elevating agents increases expression of both the full-length and exonDelta7SMN transcript.
Indexed as
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What 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.