ArticleNeurochemical research2015
Up-Regulation of CCT8 Related to Neuronal Apoptosis after Traumatic Brain Injury in Adult Rats.
Article in Neurochemical research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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
3 citing papers in PubMed, 6 citations in OpenAlex.
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- Retraction Note: CD109 Mediates Cell Survival in Hepatocellular Carcinoma Cells.Digestive diseases and sciences · 2019Article
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Traumatic brain injury (TBI) initiates a series of neurochemical and signaling changes that could eventually lead to neuronal apoptosis. Recent studies indicated that mature neurons cell cycle re-enter played a crucial role in neuronal apoptosis. In this study, we identified that the chaperonin containing TCP-1, subunit 8 (CCT8), as a member of class II chaperonins, was significantly upregulated following TBI. Moreover, double immunofluorescence staining revealed that CCT8 was co-expressed with neuronal nuclei (NeuN). Besides, co-localization of CCT8/active caspase 3 was detected in NeuN. We also examined the expression profiles of active caspase 3 whose changes were correlated with the expression of CCT8. All our findings suggested that CCT8 might be involved in the pathophysiology of brain after TBI.
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