NCBI . NLM . NIH . GOV {
}
We began analyzing https://pmc.ncbi.nlm.nih.gov/articles/PMC4346630/, but it redirected us to https://pmc.ncbi.nlm.nih.gov/articles/PMC4346630/. The analysis below is for the second page.
Title[redir]:
RIPK3 promotes cell death and NLRP3 inflammasome activation in the absence of MLKL - PMC
Description:
RIPK3 and its substrate MLKL are essential for necroptosis, a lytic cell death proposed to cause inflammation via the release of intracellular molecules. Whether and how RIPK3 might drive inflammation in a manner independent of MLKL and cell lysis ...
Title[redir]:
RIPK3 promotes cell death and NLRP3 inflammasome activation in the absence of MLKL - PMC
Description:
RIPK3 and its substrate MLKL are essential for necroptosis, a lytic cell death proposed to cause inflammation via the release of intracellular molecules. Whether and how RIPK3 might drive inflammation in a manner independent of MLKL and cell lysis ...
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- Science
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Custom-built
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Traffic Estimate {📈}
What is the average monthly size of ncbi.nlm.nih.gov audience?
🌠 Phenomenal Traffic: 5M - 10M visitors per month
Based on our best estimate, this website will receive around 6,398,976 visitors per month in the current month.
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How Does Ncbi.nlm.nih.gov Make Money? {💸}
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Keywords {🔍}
ripk, fig, mice, caspase, cell, ilβ, lps, bmdm, activation, tnf, supplementary, mlkl, doi, pubmed, google, scholar, cells, death, iap, arthritis, ciap, nlrp, pmc, secretion, activity, cpa, article, xiap, kinase, min, free, experiments, iaps, inflammatory, macrophages, meansem, inflammasome, disease, necroptosis, apoptosis, data, primed, clysmcrexc, supernatants, levels, serum, loss, stimulation, qvdoph, ripkcaspase,
Topics {✒️}
receptor-interacting kinase-3-mediated pathway tlr–trif–ripk3–il-1β axis tlr–trif–ripk3–caspase-8 signalling pathway directly cleave pro-il-1β cleave pro-il-1β directly propagate pro-survival signals 5 mm edta/phosphate-buffered saline rip1-rip3-drp1 signaling pathway a-induced il-1β secretion a-induced il-1β activation caspase-8-mediated il-1β maturation signal ripk3–caspase-8-mediated apoptosis49 anti-il-1β therapeutic studies facilitate pro-survival responses tnfalpha -induced nf-kappa propagate pro-survival signals3 phenol-red-free dmem a-induced nlrp3–caspase-1 activation pam3cys-induced il-1β secretion tnf-induced il-1β secretion ripk3-dependent il-1β activation calcium-sensing receptor regulates lps-induced nf-κb induce ripk3–mlkl-dependent necroptosis7 lps-induced il-1β secretion lps–tlr4–trif–ripk3 complex lps-induced il-1β activation ice-cold pbs-washed bmdms rhim–rhim homotypic interactions ripk3–mlkl-mediated inflammasome activation promoted il-1β secretion a-mediated il-1β pmc beta search ripk3–mlkl-dependent nlrp3 activation granulocyte-colony stimulating factor granulocyte colony-stimulating factor tnf receptor-mediated necroptosis7 prevent il-1β secretion efficiently activate nf-{kappa} dependent autoantibody-mediated arthritis induce tnfalpha-dependent apoptosis anti-tnf [xt-22] 20 μg ml−1 anti-tnf monoclonal antibody caspase-8 ripk3–mlkl-mediated necroptosis bone marrow-derived macrophages a-triggered caspase-8 activation caused il-1β secretion ripk3-driven inflammatory diseases appreciable il-1β secretion prevent tnf-induced apoptosis
Questions {❓}
- Anti-TNF therapy, from rationale to standard of care: what lessons has it taught us?
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