ArticleJournal of molecular neuroscience : MN2012
Expression of the newly identified gene CAC1 in the hippocampus of Alzheimer's disease patients.
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 6 papers.
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Who cites it
6 citing papers in PubMed, 14 citations in OpenAlex.
- Investigating aberrantly expressed microRNAs in peripheral blood mononuclear cells from patients with treatment‑resistant schizophrenia using miRNA sequencing and integrated bioinformatics.Molecular medicine reports · 2020Article
- CAC1 knockdown reverses drug resistance through the downregulation of P-gp and MRP-1 expression in colorectal cancer.PloS one · 2019Article
- Vanillin improves scopolamine‑induced memory impairment through restoration of ID1 expression in the mouse hippocampus.Molecular medicine reports · 2018Article
- Effects of chronic scopolamine treatment on cognitive impairment and neurofilament expression in the mouse hippocampus.Molecular medicine reports · 2018Article
- Effects of Chronic Scopolamine Treatment on Cognitive Impairments and Myelin Basic Protein Expression in the Mouse Hippocampus.Journal of molecular neuroscience : MN · 2016Article
- CACUL1/CAC1 Regulates the Antioxidant Response by Stabilizing Nrf2.Scientific reports · 2015Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
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Abstract
Alzheimer's disease (AD), the most common form of senile dementia, is associated with neurodegeneration. The development of Alzheimer's disease is related to abnormalities of cell cycle regulation. Preliminary work showed that a novel gene, CAC1, was highly expressed in tumors and had an oncogene-like function related to cell cycle regulation. The pathogenesis of AD is still incompletely understood. In this study, we measured the expression level of CAC1 in the hippocampus of AD patients to explore the involvement of CAC1 in the development of AD. Our findings showed that the expression level of CAC1 in the hippocampus of AD patients was significantly lower than that of normal controls. The reduction of CAC1 expression did not affect tau/p-tau-396, amyloid precursor protein or apolipoprotein E4 in the in vitro model. A reduction of cyclin E was detected after a CAC1-knockdown. Interestingly, we found that the knockdown of CAC1 by RNAi led to an increase in oxidative stress and the level of p53 protein in SHSY-5Y cells. The expression of CAC1 in SHSY-5Y cells protected the cells from apoptosis induced by Aβ toxicity or oxidative stress. These results established that CAC1 is an important factor for the protection of cells against Aβ toxicity and oxidative stress.
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