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Centromere protein J is overexpressed in human glioblastoma and promotes cell proliferation and migration
AbstractGlioblastoma is the most common and malignant type of primary brain tumor. Previous studies have shown that alterations in centrosome amplification and its components are frequently found in treatment-resistant tumors and may be associated with tumor progression. A centrosome protein essential for centrosome biogenesis is the centromere protein J (CENPJ), known to control the proliferation of neural progenitors and hepatocarcinoma cells, and also neuronal migration. However, it remains unknown the role of CENPJ in glioblastoma. Here we show that CENPJ is overexpressed in human glioblastoma cell lines in comparison ...
Source: Journal of Neurochemistry - July 7, 2022 Category: Neuroscience Authors: Gabriella P. A. de Freitas, Luiz Henrique M. Geraldo, Bruna M. Faria, Soniza Vieira Alves ‐Leon, Jorge Marcondes de Souza, Vivaldo Moura‐Neto, Bruno Pontes, Luciana F. Romão, Patrícia P. Garcez Tags: ORIGINAL ARTICLE Source Type: research

Pro ‐inflammatory role of high‐mobility group box‐1 on brain mast cells via the RAGE/NF‐κB pathway
In this study, we used P815 cells to study the activating role of HMGB‐1 on MCs and to explore its potential mechanismin vitro. In anin vivo study, adult male Sprague ‐Dawley rats receivedi.c.v. injection of sterile saline or cromoglycate (stabilizer of MCs) 30  min prior toi.p. injection of HMGB ‐1. Increased levels of tumor necrosis factor and IL‐1β were observed in the P815 cells, as well as in the rats’ brains, after HMGB‐1 treatment. Pretreatment with the receptor of advanced glycation endproducts (RAGE)‐siRNA inhibited the HMGB‐1‐induced inflammatory process in the P815 cells. Activation of the RA...
Source: Journal of Neurochemistry - October 26, 2019 Category: Neuroscience Authors: Qing ‐Qing Qian, Xiang Zhang, Yi‐Wei Wang, Jia‐Wen Xu, Hong‐Quan Dong, Na‐Na Li, Yan‐Ning Qian, Bo Gui Tags: Original Article Source Type: research

Tumor necrosis factor receptor ‐associated factor 6 participates in early brain injury after subarachnoid hemorrhage in rats through inhibiting autophagy and promoting oxidative stress
This study was designed to explore changes of expression level and potential roles and mechanisms of TRAF6 in early brain injury (EBI) after SAH using a Sprague–Dawley rat model of SAH induced in 0.3 mL non‐heparinized autologous arterial blood injected into the pre‐chiasmatic cistern. First, compared with the sham group, we found that the expression levels of TRAF6 increased gradually and peaked at 24 h after SAH. Second, the results showed that application of TRAF6 over‐expression plasmid and genetic silencing siRNA could increase or decrease expression of TRAF6, respectively, and severely exacerbate or relieve...
Source: Journal of Neurochemistry - June 20, 2017 Category: Neuroscience Authors: Yang Dou, Haitao Shen, Dongxia Feng, Haiying Li, Xiaodi Tian, Jian Zhang, Zhong Wang, Gang Chen Tags: Original Article Source Type: research