Analysis Tools
immune system
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• peritoneal macrophages from homozygous mice secrete normal amounts of type 1 interferon in response to polyI:C, a TLR3-activating ligand
• peritoneal macrophages from homozygous mice secrete nearly normal amounts of type 1 interferon in response to the diacyl peptides MALP-2 and PAM2CSK4, which induce signaling via TLR2 or the TLR2/TLR6 heterodimer
• peritoneal macrophages from homozygous mice normally phosphorylate c-JUN, N-terminal kinase, extracellular signal-regulated kinase, p38, and IkappaB in response to MALP-2 and PAM2CSK4, diacyl peptides that signal via the TLR2/TLR6 heterodimer or TLR2
• following injection with MALP-2, a diacyl lipopeptide that signals via the TLR2/TLR6 heterodimer or TLR2, homozygous mice all died within 12 hours, similarly to wild-type mice, which were all dead within 16 hours
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• immunoblot analysis of lysates of homozygous mutant mouse embryonic fibroblasts (MEFs) using antibody to IkappaB demonstrates failure of these cells to degrade IkappaB in response to interleukin 1 (IL-1)
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• peritoneal macrophages from homozygous mice exhibit no type 1 interferon secretion in response to lipopolysaccharide (LPS), a TLR4-activating ligand, at low doses and a markedly diminished response to LPS at high doses
• peritoneal macrophages from homozygous mice fail to secrete type 1 interferon in response to the TLR1/TLR2-activating lipopeptide PAM3CSK4
• peritoneal macrophages from homozygous mice fail to secrete type 1 interferon in response to the TLR2/TLR6-activating ligand lipoteichoic acid
• peritoneal macrophages from homozygous mice fail to secrete type 1 interferon in response to resiquimod, a TLR7-activating ligand
• peritoneal macrophages from homozygous mice fail to secrete type 1 interferon in response to unmethylated CpG DNA, a TLR9-activating ligand
• immunoblot analysis of lysates of homozygous mutant peritoneal macrophages using antibodies to phosphorylated proteins demonstrates failure of these cells to phosphorylate/activate Ikappa B, JUN N-terminal kinase (JNK) or extracellular signal-related kinase (ERK) in response to the TLR7-activating ligand resiquimod
• homozygous mutant peritoneal macrophages fail to phosphorylate/activate Ikappa B, JUN N-terminal kinase (JNK) or extracellular signal-related kinase (ERK) in response to the TLR1/TLR2-activating lipopeptide PAM3CSK4
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• inocula of Listeria monocytogenes that are easily controlled by wild-type mice are lethal to homozygous mutants
• intradermally inoculated luminescent Streptococcus pyogenes, which are rapidly contained, then cleared by wild-type mice, are able to proliferate in homozygous mutant mice before the infection eventually is controlled
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• inocula of mouse cytomegalovirus (CMV) that are easily controlled by wild-type mice are lethal to homozygous mutants
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hematopoietic system
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• peritoneal macrophages from homozygous mice exhibit no type 1 interferon secretion in response to lipopolysaccharide (LPS), a TLR4-activating ligand, at low doses and a markedly diminished response to LPS at high doses
• peritoneal macrophages from homozygous mice fail to secrete type 1 interferon in response to the TLR1/TLR2-activating lipopeptide PAM3CSK4
• peritoneal macrophages from homozygous mice fail to secrete type 1 interferon in response to the TLR2/TLR6-activating ligand lipoteichoic acid
• peritoneal macrophages from homozygous mice fail to secrete type 1 interferon in response to resiquimod, a TLR7-activating ligand
• peritoneal macrophages from homozygous mice fail to secrete type 1 interferon in response to unmethylated CpG DNA, a TLR9-activating ligand
• immunoblot analysis of lysates of homozygous mutant peritoneal macrophages using antibodies to phosphorylated proteins demonstrates failure of these cells to phosphorylate/activate Ikappa B, JUN N-terminal kinase (JNK) or extracellular signal-related kinase (ERK) in response to the TLR7-activating ligand resiquimod
• homozygous mutant peritoneal macrophages fail to phosphorylate/activate Ikappa B, JUN N-terminal kinase (JNK) or extracellular signal-related kinase (ERK) in response to the TLR1/TLR2-activating lipopeptide PAM3CSK4
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