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10.1038/srep11046 http://scihub22266oqcxt.onion/10.1038/srep11046 C4468580!4468580 !26078204     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26078204 &cmd=llinks): Failed to open stream: HTTP request failed! 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Suppression of cell division-associated genes by Helicobacter pylori attenuates proliferation of RAW264 7 monocytic macrophage cells |pdf=|usr=}}{{26078204 }} gab.com Text Suppression of cell division-associated genes by Helicobacter pylori attenuates proliferation of RAW264 7 monocytic macrophage cells JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=26078204 #FOAvip Helicobacter pylori at multiplicity of infection (MOI ? 50) have been shown to cause apoptosis in RAW264.7 monocytic macrophage cells. Because chronic gastric infection by H. pylori results in the persistence of macrophages in the host's gut, it is likely that H. pylori is present at low to moderate, rather than high numbers in the infected host. At present, the effect of low-MOI H. pylori infection on macrophage has not been fully elucidated. In this study, we investigated the genome-wide transcriptional regulation of H. pylori-infected RAW264.7 cells at MOI 1, 5 and 10 in the absence of cellular apoptosis. Microarray data revealed up- and down-regulation of 1341 and 1591 genes, respectively. The expression of genes encoding for DNA replication and cell cycle-associated molecules, including Aurora-B kinase (AurkB) were down-regulated. Immunoblot analysis verified the decreased expression of AurkB and downstream phosphorylation of Cdk1 caused by H. pylori infection. Consistently, we observed that H. pylori infection inhibited cell proliferation and progression through the G1/S and G2/M checkpoints. In summary, we suggest that H. pylori disrupts expression of cell cycle-associated genes, thereby impeding proliferation of RAW264.7 cells, and such disruption may be an immunoevasive strategy utilized by H. pylori. Twit Text FOAVip Suppression of cell division-associated genes by Helicobacter pylori attenuates proliferation of RAW264 7 monocytic macrophage cells ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=26078204 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26078204 #FOAvip English Wikipedia <ref>{{Cite pmid|26078204 }}</ref> Suppression of cell division-associated genes by Helicobacter pylori attenuates proliferation of RAW264 7 monocytic macrophage cells #MMPMID26078204 Tan GM ; Looi CY ; Fernandez KC ; Vadivelu J ; Loke MF ; Wong WF Sci Rep 2015[Jun]; 5 (ä): 11046 PMID26078204 show ga Helicobacter pylori at multiplicity of infection (MOI ? 50) have been shown to cause apoptosis in RAW264.7 monocytic macrophage cells. Because chronic gastric infection by H. pylori results in the persistence of macrophages in the host's gut, it is likely that H. pylori is present at low to moderate, rather than high numbers in the infected host. At present, the effect of low-MOI H. pylori infection on macrophage has not been fully elucidated. In this study, we investigated the genome-wide transcriptional regulation of H. pylori-infected RAW264.7 cells at MOI 1, 5 and 10 in the absence of cellular apoptosis. Microarray data revealed up- and down-regulation of 1341 and 1591 genes, respectively. The expression of genes encoding for DNA replication and cell cycle-associated molecules, including Aurora-B kinase (AurkB) were down-regulated. Immunoblot analysis verified the decreased expression of AurkB and downstream phosphorylation of Cdk1 caused by H. pylori infection. Consistently, we observed that H. pylori infection inhibited cell proliferation and progression through the G1/S and G2/M checkpoints. In summary, we suggest that H. pylori disrupts expression of cell cycle-associated genes, thereby impeding proliferation of RAW264.7 cells, and such disruption may be an immunoevasive strategy utilized by H. pylori. |*Genome [MESH] |Animals [MESH] |Aurora Kinase B/genetics/immunology [MESH] |Bacterial Load [MESH] |CDC2 Protein Kinase/genetics/immunology [MESH] |Cell Cycle Checkpoints/*genetics/immunology [MESH] |Cell Cycle Proteins/*genetics/immunology [MESH] |Cell Line, Transformed [MESH] |Cell Proliferation [MESH] |DNA Replication/genetics/immunology [MESH] |Gene Expression Profiling [MESH] |Gene Expression Regulation [MESH] |Helicobacter pylori/*immunology/pathogenicity [MESH] |Immune Evasion [MESH] |Macrophages/*metabolism/microbiology [MESH] |Mice [MESH] |Oligonucleotide Array Sequence Analysis [MESH]Suppression of cell division-associated genes by Helicobacter pylori a(epmc).pdf DeepDyve Pubget Overpricing