ArticleJournal of molecular neuroscience : MN2012
Cyclic AMP response element modulator-1 (CREM-1) involves in neuronal apoptosis after traumatic brain injury.
Article in Journal of molecular neuroscience : MN, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 24 citations in OpenAlex.
- Histone lactylation modification and its role in cerebral ischemia-reperfusion injury (Review).Biomedical reports · 2026Review
- [High expression of CREM is associated with poor prognosis in gastric cancer patients].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- Expression of Transcription FactorThe journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2021Article
- Synaptic Reorganization Response in the Cochlear Nucleus Following Intense Noise Exposure.Neuroscience · 2019Article
- Proteomic Dissection of Nanotopography-Sensitive Mechanotransductive Signaling Hubs that Foster Neuronal Differentiation in PC12 Cells.Frontiers in cellular neuroscience · 2017Article
- Adenosine kinase facilitated astrogliosis-induced cortical neuronal death in traumatic brain injury.Journal of molecular histology · 2016Article
- Upregulation of PRDM5 Is Associated with Astrocyte Proliferation and Neuronal Apoptosis Caused by Lipopolysaccharide.Journal of molecular neuroscience : MN · 2016Article
- Bilateral gene interaction hierarchy analysis of the cell death gene response emphasizes the significance of cell cycle genes following unilateral traumatic brain injury.BMC genomics · 2016Article
- Upregulation of PTP1B After Rat Spinal Cord Injury.Inflammation · 2015Article
- Increased Expression of Mitochondrial Inner-Membrane Protein Mpv17 After Intracerebral Hemorrhage in Adult Rats.Neurochemical research · 2015Article
- Expression of RBMX in the light-induced damage of rat retina in vivo.Cellular and molecular neurobiology · 2015Article
- Up-regulation of Glis2 involves in neuronal apoptosis after intracerebral hemorrhage in adult rats.Cellular and molecular neurobiology · 2015Article
- Upregulation of CREM-1 relates to retinal ganglion cells apoptosis after light-induced damage in vivo.Journal of molecular neuroscience : MN · 2014Article
- (-)-Phenserine attenuates soman-induced neuropathology.PloS one · 2014Article
- Low expression of cyclic AMP response element modulator-1 can increase the migration and invasion of esophageal squamous cell carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013Article
- Increased expression of small heat shock protein αB-crystallin after intracerebral hemorrhage in adult rats.Journal of molecular neuroscience : MN · 2013Article
- Correlated mRNAs and miRNAs from co-expression and regulatory networks affect porcine muscle and finally meat properties.BMC genomics · 2013Article
- Up-regulation of Smurf1 after spinal cord injury in adult rats.Journal of molecular histology · 2013Article
- Expression of RBMX after spinal cord injury in rats.Journal of molecular neuroscience : MN · 2013Article
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cyclic AMP response element-binding protein (CREB) family can regulate biological functions of various types of cells by forming homo- or heterodimers to bind the target DNA sequences; it plays an essential role in individual neuronal function and entire neuronal circuits. One attractive activity of the CREB family is regulating the transcription of apoptosis-suppressor gene bcl-2. Cyclic AMP response element modulator-1 (CREM-1) is one member of the family with limited acquaintance. To investigate whether CREM-1 is involved in central nervous system injury and repair, we performed an acute traumatic brain injury (TBI) model in adult rats. Western blot analysis and immunohistochemistry showed a significant upregulation of CREM-1 in ipsilateral peritrauma cortex. Immunofluorescent labeling indicated that CREM-1 was localized mainly in the nuclei of neurons; co-localization of CREM-1 and active-caspase-3 in the ipsilateral cortex suggested that CREM-1 might participate in neuronal apoptosis. To further investigate the function of CREM-1, a neuronal cell line PC12 was employed to establish an apoptosis model. We analyzed the association of CREM-1 with p-CREB on PC12 cells by Western blot, immunofluorescent labeling, and co-immunoprecipitation. The result implied that the association of CREM-1 with p-CREB was enhanced in apoptotic cells. Additionally, knocking CREM-1 down with siRNA demonstrated the probable pro-apoptotic role played by CREM-1 in neuronal apoptosis. Together with our data, we hypothesized that CREM-1 might play an important role in regulating neuronal death after TBI by interacting with CREB.
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