ArticleInternational journal of clinical and experimental pathology2013
Involvement of GMRP1, a novel mediator of Akt pathway, in brain damage after intracerebral hemorrhage.
Article in International journal of clinical and experimental pathology, 2013. 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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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Identification of Potential Feature Genes in CRSwNP Using Bioinformatics Analysis and Machine Learning Strategies.Journal of inflammation research · 2024Article
- BTBD10 inhibits glioma tumorigenesis by downregulating cyclin D1 and p-Akt.Open life sciences · 2022Article
- The emerging role of the KCTD proteins in cancer.Cell communication and signaling : CCS · 2021Review
- KCTD: A new gene family involved in neurodevelopmental and neuropsychiatric disorders.CNS neuroscience & therapeutics · 2019Review
- Up-regulation of Vps4A promotes neuronal apoptosis after intracerebral hemorrhage in adult rats.Metabolic brain disease · 2017Article
- Effects of that ATRA inhibits Nrf2-ARE pathway on glial cells activation after intracerebral hemorrhage.International journal of clinical and experimental pathology · 2015Article
- Heme oxygenase 1 plays role of neuron-protection by regulating Nrf2-ARE signaling post intracerebral hemorrhage.International journal of clinical and experimental pathology · 2015Article
- Astrocytes require insulin-like growth factor I to protect neurons against oxidative injury.F1000Research · 2014Article
- KCTD20, a relative of BTBD10, is a positive regulator of Akt.BMC biochemistry · 2013Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
GMRP1, also known as BTBD10, has been reported to inhibit apoptosis of neuronal and islet beta cells via Akt pathway. The present study attempted to investigate whether GMRP1 and its mediated Akt pathway were involved in brain injury of rats after intracerebral hemorrhage (ICH). Rat models of ICH had been established successfully. Western blotting was used to investigate the levels of GMRP1 protein in caudate nuclei tissues of hemorrhagic and contralateral sides at 6 h, day 1, day 3, day 5, day 7 after ICH. Phosphorylation of Akt was determined in caudate nuclei mentioned above. TUNEL assay was used to measure the cell apoptosis. GMRP1 protein levels, as well as phosphorylations of Akt, significantly decreased in caudate nuclei of hemorrhagic side, compared with those of contralateral side at day 1, day 3 after ICH. Enhanced cell apoptosis was observed in hemorrhagic side by TUNEL assay. We presented here evidence that decreased GMRP1-mediated Akt pathway contributed to cell apoptosis in hemorrhagic side, suggesting that GMRP1 played an important role in brain damage after ICH.
Indexed as
Identifiers
23330007PMC3544232W169353224What 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.