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10.1073/pnas.1707929115 http://scihub22266oqcxt.onion/10.1073/pnas.1707929115 C5866536!5866536 !29507229     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 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 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\29507229 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Proc+Natl+Acad+Sci+U+S+A 2018 ; 115 (12 ): E2801-E2810 Nephropedia Template TP {{tp|p=29507229 |t=2018. Myeloid ERK5 deficiency suppresses tumor growth by blocking protumor macrophage polarization via STAT3 inhibition |pdf=|usr=}}{{29507229 }} gab.com Text Myeloid ERK5 deficiency suppresses tumor growth by blocking protumor macrophage polarization via STAT3 inhibition JO: Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=29507229 #FOAvip Owing to the prevalence of tumor-associated macrophages (TAMs) in cancer and their unique influence upon disease progression and malignancy, macrophage-targeted interventions have attracted notable attention in cancer immunotherapy. However, tractable targets to reduce TAM activities remain very few and far between because the signaling mechanisms underpinning protumor macrophage phenotypes are largely unknown. Here, we have investigated the role of the extracellular-regulated protein kinase 5 (ERK5) as a determinant of macrophage polarity. We report that the growth of carcinoma grafts was halted in myeloid ERK5-deficient mice. Coincidentally, targeting ERK5 in macrophages induced a transcriptional switch in favor of proinflammatory mediators. Further molecular analyses demonstrated that activation of the signal transducer and activator of transcription 3 (STAT3) via Tyr705 phosphorylation was impaired in erk5-deleted TAMs. Our study thus suggests that blocking ERK5 constitutes a treatment strategy to reprogram macrophages toward an antitumor state by inhibiting STAT3-induced gene expression. Twit Text FOAVip Myeloid ERK5 deficiency suppresses tumor growth by blocking protumor macrophage polarization via STAT3 inhibition ????Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=29507229 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29507229 #FOAvip English Wikipedia <ref>{{Cite pmid|29507229 }}</ref> Myeloid ERK5 deficiency suppresses tumor growth by blocking protumor macrophage polarization via STAT3 inhibition #MMPMID29507229 Giurisato E ; Xu Q ; Lonardi S ; Telfer B ; Russo I ; Pearson A ; Finegan KG ; Wang W ; Wang J ; Gray NS ; Vermi W ; Xia Z ; Tournier C Proc Natl Acad Sci U S A 2018[Mar]; 115 (12 ): E2801-E2810 PMID29507229 show ga Owing to the prevalence of tumor-associated macrophages (TAMs) in cancer and their unique influence upon disease progression and malignancy, macrophage-targeted interventions have attracted notable attention in cancer immunotherapy. However, tractable targets to reduce TAM activities remain very few and far between because the signaling mechanisms underpinning protumor macrophage phenotypes are largely unknown. Here, we have investigated the role of the extracellular-regulated protein kinase 5 (ERK5) as a determinant of macrophage polarity. We report that the growth of carcinoma grafts was halted in myeloid ERK5-deficient mice. Coincidentally, targeting ERK5 in macrophages induced a transcriptional switch in favor of proinflammatory mediators. Further molecular analyses demonstrated that activation of the signal transducer and activator of transcription 3 (STAT3) via Tyr705 phosphorylation was impaired in erk5-deleted TAMs. Our study thus suggests that blocking ERK5 constitutes a treatment strategy to reprogram macrophages toward an antitumor state by inhibiting STAT3-induced gene expression. |Animals [MESH] |Antigens, CD/metabolism [MESH] |Antigens, Differentiation, Myelomonocytic/metabolism [MESH] |CD163 Antigen [MESH] |Cell Polarity [MESH] |Humans [MESH] |Macrophages/*metabolism/pathology [MESH] |Mice, Inbred C57BL [MESH] |Mice, Transgenic [MESH] |Mitogen-Activated Protein Kinase 7/genetics/*metabolism [MESH] |Neoplasms/*metabolism/*pathology [MESH] |Phosphorylation [MESH] |Receptors, Cell Surface/metabolism [MESH] |STAT3 Transcription Factor/genetics/*metabolism [MESH] |Tyrosine/metabolism [MESH]Myeloid ERK5 deficiency suppresses tumor growth by blocking protumor m(epmc).pdf DeepDyve Pubget Overpricing