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10.1038/s41419-018-0761-0 http://scihub22266oqcxt.onion/10.1038/s41419-018-0761-0 C6030166!6030166!29970880     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Death+Dis 2018 ; 9 (7): ä Nephropedia Template TP {{tp|p=29970880|t=2018. Consequences of blunting the mevalonate pathway in cancer identified by a pluri-omics approach |pdf=|usr=}}{{29970880}} gab.com Text Consequences of blunting the mevalonate pathway in cancer identified by a pluri-omics approach JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=29970880 #FOAvip We have previously shown that the combination of statins and taxanes was a powerful trigger of HGT-1 human gastric cancer cells? apoptosis1. Importantly, several genes involved in the ?Central carbon metabolism pathway in cancer?, as reported in the Kyoto Encyclopedia of Genes and Genomes, were either up- (ACLY, ERBB2, GCK, MYC, PGM, PKFB2, SLC1A5, SLC7A5, SLC16A3,) or down- (IDH, MDH1, OGDH, P53, PDK) regulated in response to the drug association. In the present study, we conducted non-targeted metabolomics and lipidomics analyses by complementary methods and cross-platform initiatives, namely mass spectrometry (GC-MS, LC-MS) and nuclear magnetic resonance (NMR), to analyze the changes resulting from these treatments. We identified several altered biochemical pathways involved in the anabolism and disposition of amino acids, sugars, and lipids. Using the Cytoscape environment with, as an input, the identified biochemical marker changes, we distinguished the functional links between pathways. Finally, looking at the overlap between metabolomics/lipidomics and transcriptome changes, we identified correlations between gene expression modifications and changes in metabolites/lipids. Among the metabolites commonly detected by all types of platforms, glutamine was the most induced (6?7-fold), pointing to an important metabolic adaptation of cancer cells. Taken together, our results demonstrated that combining robust biochemical and molecular approaches was efficient to identify both altered metabolic pathways and overlapping gene expression alterations in human gastric cancer cells engaging into apoptosis following blunting the cholesterol synthesis pathway. Twit Text FOAVip Consequences of blunting the mevalonate pathway in cancer identified by a pluri-omics approach ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=29970880 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29970880 #FOAvip English Wikipedia <ref>{{Cite pmid|29970880}}</ref> Consequences of blunting the mevalonate pathway in cancer identified by a pluri-omics approach #MMPMID29970880 Goulitquer S; Croyal M; Lalande J; Royer AL; Guitton Y; Arzur D; Durand S; Le Jossic-Corcos C; Bouchereau A; Potin P; Akoka S; Antignac JP; Krempf M; Ferchaud-Roucher V; Giraudeau P; Corcos L Cell Death Dis 2018[Jul]; 9 (7): ä PMID29970880show ga We have previously shown that the combination of statins and taxanes was a powerful trigger of HGT-1 human gastric cancer cells? apoptosis1. Importantly, several genes involved in the ?Central carbon metabolism pathway in cancer?, as reported in the Kyoto Encyclopedia of Genes and Genomes, were either up- (ACLY, ERBB2, GCK, MYC, PGM, PKFB2, SLC1A5, SLC7A5, SLC16A3,) or down- (IDH, MDH1, OGDH, P53, PDK) regulated in response to the drug association. In the present study, we conducted non-targeted metabolomics and lipidomics analyses by complementary methods and cross-platform initiatives, namely mass spectrometry (GC-MS, LC-MS) and nuclear magnetic resonance (NMR), to analyze the changes resulting from these treatments. We identified several altered biochemical pathways involved in the anabolism and disposition of amino acids, sugars, and lipids. Using the Cytoscape environment with, as an input, the identified biochemical marker changes, we distinguished the functional links between pathways. Finally, looking at the overlap between metabolomics/lipidomics and transcriptome changes, we identified correlations between gene expression modifications and changes in metabolites/lipids. Among the metabolites commonly detected by all types of platforms, glutamine was the most induced (6?7-fold), pointing to an important metabolic adaptation of cancer cells. Taken together, our results demonstrated that combining robust biochemical and molecular approaches was efficient to identify both altered metabolic pathways and overlapping gene expression alterations in human gastric cancer cells engaging into apoptosis following blunting the cholesterol synthesis pathway. äConsequences of blunting the mevalonate pathway in cancer identified b(epmc).pdf DeepDyve Pubget Overpricing