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| http://dx.doi.org/10.1080/15384101.2015.1035968 | DOI Listing |
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Super-enhancer-driven lncRNA Snhg7 aggravates cardiac hypertrophy via Tbx5/GLS2/ferroptosis axis.
Eur J Pharmacol
August 2023
Department of Pharmacology, Harbin Medical University-Daqing, Daqing, 163319, China. Electronic address:
Long non-coding RNAs (lncRNAs) are expressed aberrantly in cardiac disease, but their roles in cardiac hypertrophy are still unknown. Here we sought to identify a specific lncRNA and explore the mechanisms underlying lncRNA functions. Our results revealed that lncRNA Snhg7 was a super-enhancer-driven gene in cardiac hypertrophy by using chromatin immunoprecipitation sequencing (ChIP-seq).
View Article and Find Full Text PDFp73 regulates serine biosynthesis in cancer.
Oncogene
October 2014
1] Medical Research Council, Toxicology Unit, Leicester University, Leicester, UK [2] Department of Experimental Medicine and Surgery, University of Rome 'Tor Vergata', Rome, Italy.
Activation of serine biosynthesis supports growth and proliferation of cancer cells. Human cancers often exhibit overexpression of phosphoglycerate dehydrogenase (PHGDH), the metabolic enzyme that catalyses the reaction that diverts serine biosynthesis from the glycolytic pathway. By refueling serine biosynthetic pathways, cancer cells sustain their metabolic requirements, promoting macromolecule synthesis, anaplerotic flux and ATP.
View Article and Find Full Text PDFGLS2 is transcriptionally regulated by p73 and contributes to neuronal differentiation.
Cell Cycle
November 2013
Medical Research Council; Toxicology Unit; Leicester University; Leicester, UK; Institute of Health Sciences; Shanghai Institutes for Biological Sciences; Chinese Academy of Sciences & Shanghai Jiao Tong University School of Medicine; Shanghai, China.
The amino acid Glutamine is converted into Glutamate by a deamidation reaction catalyzed by the enzyme Glutaminase (GLS). Two isoforms of this enzyme have been described, and the GLS2 isoform is regulated by the tumor suppressor gene p53. Here, we show that the p53 family member TAp73 also drives the expression of GLS2.
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