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http://dx.doi.org/10.1038/s41392-021-00464-z | DOI Listing |
Nat Commun
October 2023
Centro Andaluz de Biología Molecular y Medicina Regenerativa CABIMER, Universidad de Sevilla-CSIC-Universidad Pablo de Olavide, 41092, Seville, Spain.
Genome instability is a feature of cancer cells, transcription being an important source of DNA damage. This is in large part associated with R-loops, which hamper replication, especially at head-on transcription-replication conflicts (TRCs). Here we show that TRCs trigger a DNA Damage Response (DDR) involving the chromatin network to prevent genome instability.
View Article and Find Full Text PDFSignal Transduct Target Ther
April 2021
State Key Laboratory of Medicinal Chemical Biology and College of Pharmacy, Nankai University, Tianjin, China.
Front Immunol
June 2019
Rudolf Buchheim Institute of Pharmacology, Justus Liebig University Giessen, Giessen, Germany.
The potent proinflammatory cytokine interleukin (IL)-1 triggers gene expression through the NF-κB signaling pathway. Here, we investigated the cofactor requirements of strongly regulated IL-1 target genes whose expression is impaired in p65 NF-κB-deficient murine embryonic fibroblasts. By two independent small-hairpin (sh)RNA screens, we examined 170 genes annotated to encode nuclear cofactors for their role in mRNA expression and identified 22 factors that modulated basal or IL-1-inducible levels.
View Article and Find Full Text PDFSci Rep
September 2016
Laboratory of Epileptogenesis, Department of Molecular and Cellular Neurobiology, Nencki Institute of Experimental Biology of Polish Academy of Sciences, Warsaw, Poland.
The aim of the present study was to examine involvement of MBD3 (methyl-CpG-binding domain protein 3), a protein involved in reading DNA methylation patterns, in epileptogenesis and epilepsy. We used a well-characterized rat model of temporal lobe epilepsy that is triggered by status epilepticus, evoked by electrical stimulation of the amygdala. Stimulated and sham-operated animals were sacrificed 14 days after stimulation.
View Article and Find Full Text PDFJpn J Clin Oncol
August 2015
Department of Thoracic Surgery, Second Affiliated Hospital Zhejiang University College of Medicine, Hangzhou, China
Objective: Metastasis-associated protein 2 is considered as an intrinsic subunit of the nucleosome remodelling and histone deacetylase complex, which contributes to the epigenetic silencing genes. More and more evidence suggests that metastasis-associated protein 2 is required to maintain the malignant phenotype, but the role of metastasis-associated protein 2 function in mediating tumour metastasis in non-small-cell lung cancer has not been explored.
Methods: Bioinformatics was used to detect the GEO 3141 database, the online tool of Kmplot was used to confirm the high expression of metastasis-associated protein 2 in influencing 5-year overall survival.
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