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We began analyzing https://www.nature.com/articles/nchembio.496, but it redirected us to https://www.nature.com/articles/nchembio.496. The analysis below is for the second page.

Title[redir]:
Activation of the Raf-MEK-ERK pathway is required for neutrophil extracellular trap formation | Nature Chemical Biology
Description:
A chemical genetics approach identifies the Raf-MEK-ERK signaling system downstream of PKC in formation of the antimicrobial cell structures called neutrophil extracellular traps. The signaling mechanisms leading to the formation of neutrophil extracellular traps (NETs), relevant in infections, sepsis and autoimmune diseases, are poorly understood. Neutrophils are not amenable to studies with conventional genetic techniques. Using a new chemical genetic analysis we show that the Raf-MEK-ERK pathway is involved in NET formation through activation of NADPH oxidase and upregulation of antiapoptotic proteins. We identify potential targets for drugs addressing NET-associated diseases.

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Keywords {🔍}

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nature portfolio permissions reprints privacy policy author information authors nature advertising research hepatic ischemia-reperfusion promotes social media neutrophil extracellular trap single-cell raman microscopy raf-mek-erk pathway automated microscopy data neutrophil extracellular traps permissions springerlink instant access personal data data protection extracellular vesicles produced chemical screen protocol chemical genetic analysis privacy signaling mechanisms leading competing financial interests communication published herbert waldmann translational medicine explore content subscription content european economic area conventional genetic techniques identify potential targets issue learn institutional subscriptions read small-molecule inhibition max planck institute max plank institute hepatocyte sgk1 activated accepting optional cookies article hakkim chemical biology journals search log molecular biology manage preferences drugs addressing net arturo zychlinsky technische universität dortmund content journal publish cell biol

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