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10.1098/rsob.150155 http://scihub22266oqcxt.onion/10.1098/rsob.150155 C4772804!4772804 !26887408     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26887408 &cmd=llinks): Failed to open stream: HTTP request failed! 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Notch stimulates growth by direct regulation of genes involved in the control of glycolysis and the tricarboxylic acid cycle |pdf=|usr=}}{{26887408 }} gab.com Text Notch stimulates growth by direct regulation of genes involved in the control of glycolysis and the tricarboxylic acid cycle JO: Open Biol http://www.kidney.de/pget.php?&tw=1&pmid=26887408 #FOAvip Glycolytic shift is a characteristic feature of rapidly proliferating cells, such as cells during development and during immune response or cancer cells, as well as of stem cells. It results in increased glycolysis uncoupled from mitochondrial respiration, also known as the Warburg effect. Notch signalling is active in contexts where cells undergo glycolytic shift. We decided to test whether metabolic genes are direct transcriptional targets of Notch signalling and whether upregulation of metabolic genes can help Notch to induce tissue growth under physiological conditions and in conditions of Notch-induced hyperplasia. We show that genes mediating cellular metabolic changes towards the Warburg effect are direct transcriptional targets of Notch signalling. They include genes encoding proteins involved in glucose uptake, glycolysis, lactate to pyruvate conversion and repression of the tricarboxylic acid cycle. The direct transcriptional upregulation of metabolic genes is PI3K/Akt independent and occurs not only in cells with overactivated Notch but also in cells with endogenous levels of Notch signalling and in vivo. Even a short pulse of Notch activity is able to elicit long-lasting metabolic changes resembling the Warburg effect. Loss of Notch signalling in Drosophila wing discs as well as in human microvascular cells leads to downregulation of glycolytic genes. Notch-driven tissue overgrowth can be rescued by downregulation of genes for glucose metabolism. Notch activity is able to support growth of wing during nutrient-deprivation conditions, independent of the growth of the rest of the body. Notch is active in situations that involve metabolic reprogramming, and the direct regulation of metabolic genes may be a common mechanism that helps Notch to exert its effects in target tissues. Twit Text FOAVip Notch stimulates growth by direct regulation of genes involved in the control of glycolysis and the tricarboxylic acid cycle ????Open Biol http://www.kidney.de/pget.php?&tw=1&pmid=26887408 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26887408 #FOAvip English Wikipedia <ref>{{Cite pmid|26887408 }}</ref> Notch stimulates growth by direct regulation of genes involved in the control of glycolysis and the tricarboxylic acid cycle #MMPMID26887408 Slaninova V ; Krafcikova M ; Perez-Gomez R ; Steffal P ; Trantirek L ; Bray SJ ; Krejci A Open Biol 2016[Feb]; 6 (2 ): 150155 PMID26887408 show ga Glycolytic shift is a characteristic feature of rapidly proliferating cells, such as cells during development and during immune response or cancer cells, as well as of stem cells. It results in increased glycolysis uncoupled from mitochondrial respiration, also known as the Warburg effect. Notch signalling is active in contexts where cells undergo glycolytic shift. We decided to test whether metabolic genes are direct transcriptional targets of Notch signalling and whether upregulation of metabolic genes can help Notch to induce tissue growth under physiological conditions and in conditions of Notch-induced hyperplasia. We show that genes mediating cellular metabolic changes towards the Warburg effect are direct transcriptional targets of Notch signalling. They include genes encoding proteins involved in glucose uptake, glycolysis, lactate to pyruvate conversion and repression of the tricarboxylic acid cycle. The direct transcriptional upregulation of metabolic genes is PI3K/Akt independent and occurs not only in cells with overactivated Notch but also in cells with endogenous levels of Notch signalling and in vivo. Even a short pulse of Notch activity is able to elicit long-lasting metabolic changes resembling the Warburg effect. Loss of Notch signalling in Drosophila wing discs as well as in human microvascular cells leads to downregulation of glycolytic genes. Notch-driven tissue overgrowth can be rescued by downregulation of genes for glucose metabolism. Notch activity is able to support growth of wing during nutrient-deprivation conditions, independent of the growth of the rest of the body. Notch is active in situations that involve metabolic reprogramming, and the direct regulation of metabolic genes may be a common mechanism that helps Notch to exert its effects in target tissues. |*Gene Expression Regulation [MESH] |Animals [MESH] |Binding Sites [MESH] |Cell Line [MESH] |Citric Acid Cycle/*genetics [MESH] |Drosophila Proteins/genetics/metabolism [MESH] |Energy Metabolism/genetics [MESH] |Gene Expression [MESH] |Genes, Reporter [MESH] |Glycolysis/*genetics [MESH] |Humans [MESH] |Models, Biological [MESH] |Promoter Regions, Genetic [MESH] |Protein Binding [MESH] |Receptors, Notch/genetics/*metabolism [MESH] |Regulatory Sequences, Nucleic Acid [MESH] |Repressor Proteins/genetics/metabolism [MESH]Notch stimulates growth by direct regulation of genes involved in the (epmc).pdf DeepDyve Pubget Overpricing