Receptor Signal Transduction
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51 terms
Terms | Definitions |
|---|---|
 Which type of receptor is more likely to bind a hydrophillic ligand: cell surface receptor or intracellular? | cell surface receptor |
| Which type of receptor is more likely to bind a hydrophobic ligand: cell surface receptor or intracellular receptor? | intracellular |
| Which type of cell surface receptor have active extracellular domains and intracellular domains that change conformation upon binding? | cell surface recetors |
| What are the 3 forms of ligands that we discussed in class? | 1. signaling by secreted molecules 2. signaling by plasma membrane bound molecules 3. signaling by extracellular matrix molecules |
| What types of cellular responses can occur following receptor activation? | 1. modulation of Ion channels 2. modulation of gene expression 3. modulation of cellular proliferation 4. cell survival vs cell death |
| What are the 2 major classes of cell surface receptors? | 1. G protein linked receptors 2. enzyme linked receptors |
| How do cells communicate with their external environment? | cellular receptors (cell surface or intracellular) |
| What is an example of a signaling by a SECRETED molecule? | TNF-alpha |
| What is an example of signaling by plasma membrane bound molecules? | T cell activation |
| What can happen when a receptor binds a ligand? | 1. activate intracellular enzymes 2. activate enzymatic activity of the receptor itself 3. modulation of ion channels 4. modulation of gene expression |
| T/F: cellular fates are determined by receptor signaling | True |
| How do you cause a cell to divide? | Induction of genes that control cell cycle eg cyclin family |
| What are the 4 forms of signaling mediated by secreted molecules? | 1. paracrine 2. endocrine 3. autocrine 4. synaptic signaling |
| paracrine signaling=? | ligands act in local immediate cellular environment and signal between TWO DIFFERENT cell types |
| autocrine signaling? | local signals that act on similar cell types |
| True/False: G protein linked cell surface receptors can be both inhibitory and stimulatory | True |
| How do G protein linked cell surface receptors work? | via a second messenger |
| Examples of 2nd messengers associated with G protein receptors? | cAMP, cGMP, diacylglyerol, inositol triphosphate, and calcium |
| What do secondary messengers do in regards to G protein linked receptors? | activate other enzymes inside the cell to carry the exctracellular signal |
| True/False: Gs (stimulatory) proteins are trimeric | True |
| What does the Gs protein bind in the inactive state? | GDP |
| Describe how G protein activation of adenylyly cyclase occurs | 1. ligand binds to receptor protein altering the conformation of it, exposing a binding site for Gs protein 2. Gs binds to ligand-receptor complex, which lowers the affinity of Gs for GDP 3. GDP dissociates, allowing GTP to bind 4. GTP bnding causes the alpha subunit to dissociate from the Gs complex, exposing its binding site for adenylyl cyclase 5. The alpha subunit binds to and activates adenyly cyclase to produce molecules of cAMP. 6. ligand dissociates from receptor 7. hydrolysis of the GTP by the alpha subunit returns the subunit to its original conformation, causing it to dissociate from the adenylyl cyclase, inactivating adenylyl cyclase and the alpha subunit recombines with the beta subunit |
| True/False: the alpha s G protein subunit can activate cAMP and Calcium mediated signal transduction | True |
| What does activation of adenylyll cyclase by G protein (s) cause? | increase in cAMP, which activates protein kinase A, which leads to protein phosphorylation which can activate or inactivate protein functions within the cell |
| True/False: the guanyly cyclase pathway is similar to the adenylyl cyclase pathway | True, guanylyl cyclase just produces cGMP |
| T/F: activation of protein kinase A can be either stimulatory or inhibitory to intraceullar enzymatic pathways | True |
| When is protein kinase a causing activation? | when it activates a phosphorylase kinase |
| When is protein kinase A causing inhibition? | when it activates a phosphotase |
| What is kinase C associated with? | G protein-Calcium pathway |
| Describe the calcium activated pathway | 1. Hormone binds to receptor→Activates G protein complex 2. G protein Complex Activates phospholipase C 3. Phospholipase C cleaves PIP 2 into Diaclglycerol and IP3 4. Diacylglycerol activates protein Kinase C 5. IP3 leads to calcium release 6. Calcium activates protein Kinase C as well |
| What activates phospholipase C? | G protein Complex |
| What is function of phospholipase C? | Cleaves PIP2 into Diacylglycerol and IP3 |
| What activates protein kinase c? | Intracellular Calcium release and Diacylglycerol |
| What leads to calcium release? | Ip3 binds to IP3 calcium channel receptor in ER |
| How many receptors are activated in the calcium receptor pathway? | 2-hormone binding receptor and calcium channel receptor |
| Describe how cholera toxin leads to diarrhea | 1. cholera toxin leads to ADP ribosylation of the of the alpha-subunit of the G protein complex 2. This locks G protein alpha in the GTP bound state (cannot release GTP and become inactive) 3. This leads to persistent activation of adenylyl cyclase →Activation of protein Kinase A→stimulates CFTR by phosphorylation→moves chloride into intestinal epithelium (sodium Follows)→water follows→water moves out, causing diarrhea |
| T/F: There are protective effects of being a cystic fibrosis carrier with cholera | True |
| What is endotoxin | lipopolysaccharide (LPS). integral to membranes of gram negative bacteria |
| What does endotoxin induce? | pathways via CD14/ Toll like receptors |
| Describe how NFkB is transcriptionally activated | 1. Activation of LPS receptor complex leads to phosphorylation of IkB kinase (IKK) 2. Phosphorylated IKK phosphorylates IkB 3. Phosphorylation of IkB releases NFkB which is transported to the nucleus 4. NFkB causes TNF alpha to be secreted from the nucleus |
| T/F: endotoxin receptors are enzyme linked receptors | True |
| T/F: unphosphorylated IkB keeps NFkB in cytoplasm | True |
| Describe how inflammation response is both paracrine and autocrine | there is downstream amplification of inflammatory responses via TNF-alpha TNF-alpha can bind to the initial receptor and cause activation of NFkB |
| How do anti-inflammatory agents work? | inhibit NFkB activation and thus the production of TNFalpha |
| Examples of anti inflammatory agents? | glucorticoids (dexamethasone), aspirin |
| How does dexamethasone repress NFkB? | Increases transcription of the IkB-alpha gene which inhibits NFkB |
| How does aspirin repress NFkB activation? | inhibits IKK phosphorylation of IKB alpha |
| T/F: dexamethasone is a glucocorticoid | True |
| Describe sepsis | Bacteria in the blood, endotoxin activates signal transduction pathways such as NFkB, which increases TNFalpha levels, which goes overboard. Too much NFkB, too much TNF alpha |
| How do people usually die from sepsis? | multiple organ dysfunction leading to low vascular resistance and low cardiac output |
| What happens if we ko TNFalpha in mice and give them endotoxins? | 100% survival |
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