ArticleMolecular neurobiology2015
Endoplasmic Reticulum Protein 29 Protects Axotomized Neurons from Apoptosis and Promotes Neuronal Regeneration Associated with Erk Signal.
Article in Molecular neurobiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- The PI3K/AKT signalling pathway in inflammation, cell death and glial scar formation after traumatic spinal cord injury: Mechanisms and therapeutic opportunities.Cell proliferation · 2022Review
- Proteins involved in the endoplasmic reticulum stress are modulated in synovitis of osteoarthritis, chronic pyrophosphate arthropathy and rheumatoid arthritis, and correlate with the histological inflammatory score.Scientific reports · 2020Article
- Protein Degradome of Spinal Cord Injury: Biomarkers and Potential Therapeutic Targets.Molecular neurobiology · 2020Review
- Article
- ERp29 counteracts the suppression of malignancy mediated by endoplasmic reticulum stress and promotes the metastasis of colorectal cancer.Oncology reports · 2019Article
- ERp29 downregulation enhances lung adenocarcinoma cell chemosensitivity to gemcitabine by upregulating HSP27 phosphorylation.Experimental and therapeutic medicine · 2019Article
- Protein profiling of infected human gastric epithelial cells with an IranianGastroenterology and hepatology from bed to bench · 2017Article
- Neuroprotective effects of cold-inducible RNA-binding protein during mild hypothermia on traumatic brain injury.Neural regeneration research · 2016Article
- Friend or foe: Endoplasmic reticulum protein 29 (ERp29) in epithelial cancer.FEBS open bio · 2015Review
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spinal cord injury (SCI) results in a series of severe dysfunction of sensory and motor functions, while the molecular mechanisms that cause these dysfunctions remain elusive. Using proteomics technology, Western blot (WB), and immunohistochemistry (IHC), we found endoplasmic reticulum protein 29 (ERp29) was substantially downregulated in the motor cortex 3 days postoperation (dpo) after spinal cord transection (SCT, T10) followed by a gradual recovery 28 dpo. IHC showed that ERp29 is expressed in cortical neurons. In order to investigate the role of ERp29 in axotomized cortical neurons, we developed an in vitro axotomy injury model. ERp29 overexpression in cortical neurons after axotomy protected them from apoptosis; prevented the reduction of the number of neurons, and prevented reduction of neurite length. Moreover, we found that ERp29 overexpression increased neuronal regeneration assessed by neurite number and length. Furthermore, overexpression of ERp29 in cortical neurons after axotomy increased expression of Erk-1 and PI3K while decreasing the expression of caspase-3 expression. The present data therefore provides evidence to address the role of ERp29 in axotomized cortical neurons and identifies new therapeutic targets for the treatment of SCI.
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Registered trials
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