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10.3389/fimmu.2020.606893 http://scihub22266oqcxt.onion/10.3389/fimmu.2020.606893 33658993!7917126!33658993     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=33658993&cmd=llinks): Failed to open stream: HTTP request failed! 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TRPM7 Kinase Is Essential for Neutrophil Recruitment and Function via Regulation of Akt/mTOR Signaling |pdf=|usr=}}{{33658993}} gab.com Text TRPM7 Kinase Is Essential for Neutrophil Recruitment and Function via Regulation of Akt/mTOR Signaling JO: Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=33658993 #FOAvip During inflammation, neutrophils are one of the first responding cells of innate immunity, contributing to a fast clearance of infection and return to homeostasis. However, excessive neutrophil infiltration accelerates unsolicited disproportionate inflammation for instance in autoimmune diseases such as rheumatoid arthritis. The transient-receptor-potential channel-kinase TRPM7 is an essential regulator of immune system homeostasis. Naive murine T cells with genetic inactivation of the TRPM7 enzyme, due to a point mutation at the active site, are unable to differentiate into pro-inflammatory T cells, whereas regulatory T cells develop normally. Moreover, TRPM7 is vital for lipopolysaccharides (LPS)-induced activation of murine macrophages. Within this study, we show that the channel-kinase TRPM7 is functionally expressed in neutrophils and has an important impact on neutrophil recruitment during inflammation. We find that human neutrophils cannot transmigrate along a CXCL8 chemokine gradient or produce reactive oxygen species in response to gram-negative bacterial lipopolysaccharide LPS, if TRPM7 channel or kinase activity are blocked. Using a recently identified TRPM7 kinase inhibitor, TG100-115, as well as murine neutrophils with genetic ablation of the kinase activity, we confirm the importance of both TRPM7 channel and kinase function in murine neutrophil transmigration and unravel that TRPM7 kinase affects Akt1/mTOR signaling thereby regulating neutrophil transmigration and effector function. Hence, TRPM7 represents an interesting potential target to treat unwanted excessive neutrophil invasion. Twit Text FOAVip TRPM7 Kinase Is Essential for Neutrophil Recruitment and Function via Regulation of Akt/mTOR Signaling ????Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=33658993 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33658993 #FOAvip English Wikipedia <ref>{{Cite pmid|33658993}}</ref> TRPM7 Kinase Is Essential for Neutrophil Recruitment and Function via Regulation of Akt/mTOR Signaling #MMPMID33658993 Nadolni W; Immler R; Hoelting K; Fraticelli M; Ripphahn M; Rothmiller S; Matsushita M; Boekhoff I; Gudermann T; Sperandio M; Zierler S Front Immunol 2020[]; 11 (ä): 606893 PMID33658993show ga During inflammation, neutrophils are one of the first responding cells of innate immunity, contributing to a fast clearance of infection and return to homeostasis. However, excessive neutrophil infiltration accelerates unsolicited disproportionate inflammation for instance in autoimmune diseases such as rheumatoid arthritis. The transient-receptor-potential channel-kinase TRPM7 is an essential regulator of immune system homeostasis. Naive murine T cells with genetic inactivation of the TRPM7 enzyme, due to a point mutation at the active site, are unable to differentiate into pro-inflammatory T cells, whereas regulatory T cells develop normally. Moreover, TRPM7 is vital for lipopolysaccharides (LPS)-induced activation of murine macrophages. Within this study, we show that the channel-kinase TRPM7 is functionally expressed in neutrophils and has an important impact on neutrophil recruitment during inflammation. We find that human neutrophils cannot transmigrate along a CXCL8 chemokine gradient or produce reactive oxygen species in response to gram-negative bacterial lipopolysaccharide LPS, if TRPM7 channel or kinase activity are blocked. Using a recently identified TRPM7 kinase inhibitor, TG100-115, as well as murine neutrophils with genetic ablation of the kinase activity, we confirm the importance of both TRPM7 channel and kinase function in murine neutrophil transmigration and unravel that TRPM7 kinase affects Akt1/mTOR signaling thereby regulating neutrophil transmigration and effector function. Hence, TRPM7 represents an interesting potential target to treat unwanted excessive neutrophil invasion. |*Neutrophil Infiltration[MESH] |Animals[MESH] |Cells, Cultured[MESH] |Disease Models, Animal[MESH] |Humans[MESH] |Mice[MESH] |Mice, Inbred C57BL[MESH] |Mice, Knockout[MESH] |Neutrophils/*enzymology[MESH] |Peritonitis/chemically induced/*enzymology/genetics[MESH] |Protein Serine-Threonine Kinases/genetics/*metabolism[MESH] |Proto-Oncogene Proteins c-akt/*metabolism[MESH] |Reactive Oxygen Species/metabolism[MESH] |Signal Transduction[MESH] |TOR Serine-Threonine Kinases/*metabolism[MESH] |TRPM Cation Channels/genetics/*metabolism[MESH]TRPM7 Kinase Is Essential for Neutrophil Recruitment and Function via (epmc).pdf DeepDyve Pubget Overpricing