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15 Cards in this Set
- Front
- Back
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What is signal transduction? |
process by which a cell converts one kind of stimulus into another eg. relay of info from hitting light switch to lights turning off |
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What are the 4 components of signal transduction? |
1) LIGAND - initiates signal transduction pathway, eg. PAMP 2) RECEPTOR- non-covaletntly binds its corresponding ligand, eg. PRR 3) SIGNAL- series of enzymatic events triggered from receptor upon ligand binding 4) RESPONSE- physiological events induced by signatling cascade |
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What is a TRR? |
Toll-Like Receptors -family of PRR -critical for the detection of pathogens and initiation of host defense -activation of TLRs causes the release of antimicrobial peptides, inflammatory cytokines, and other molecules that drive additional immune responses |
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What are adapter proteins? |
Non-enzymatic proteins that assist assembly of signaling complexes |
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What is the signaling complex for TLRs? |
Ligand=microbial PAMP Receptor=member of the TLR family Signal=biochemical pathway activated in response to TLR Response= activation of NF-kB transcription factors |
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What is NF-kB? |
Nuclear Factor-kB -transcription factors that regulate genes involved in immune responses; act as dimers (2 molecules working together) -has 3 domains: dimerization region, DNA binding region, and nuclear localization region |
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What does the dimerization region do in NF-kB? |
-brings 2 molecules together -causes formation of NF-kB dimers |
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What does the DNA binding domain do in NF-kB? |
binds very specific sequences of DNA in a specific neighbourhood -binds upstream of NF-kB responsive genes |
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What does the nuclear localization sequence do in NF-kB? |
-pulls dimers into nucleus for expression of immunities -causes nuclear translocation of NF-kB dimers |
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What processes does NF-kB regulate? |
1) Inflammation 2) Adaptive immunity 3) Proliferation 4) Survival (or growth) |
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How do you keep NF-kB in check? |
-NF-kB should only be turned on in the presence of infection, in absence of infection the inhibitor of kB (I-kB) binds and retains NF-kB in the cytoplasm and masks the NLS on NF-kB (so cannot drive inflammation or cause tissue growth) |
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What are the steps in transcription? |
1) in a resting cell, I-kB retains NF-kB in the cytoplasm 2) PAMP-TLR interactions initiate intracellular signaling 3) Signaling leads to proteolytic destruction of I-kB 4) NF-kB translocates to the nucleus and initiates transcription of immune genes |
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What are some consequences of TLR signaling? (4) |
1. cytokine production: recruits and activates phagocytes and components of the adaptive immune response 2. production of enzymes involved in immune responses 3. growth factor production: resolving damage to tissues 4. activation of adaptive immune cells by innate immune cells |
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What are some advantages of TLR signaling? (3) |
1. speed: very fast 2. economy: small # of TLRs (approx. 10) can detect large # of pathogens 3. amplification: local detection of pathogen but can amplify to other regions |
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What does PRR engagement (with a PAMP) activate? |
-phagocytosis -also boosts the "oxidative burst" (production of reactive O2 and N2 species --> ROIs and RNIs) -signals from PRR also result in the production of cytokines and chemokines (released warnings --> activation) |
