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ChemicalSignaling
HormoneAndChemicalSignaling
| Question | Answer |
|---|---|
| What are the 2 ways that physiological signaling occur? | 1. Electrical signals 2. Chemical signals |
| What are electrical signals? | changes in cell's membrane potential |
| What are chemical signals? | 1. molecules that are secreted into the ECF 2. responsible for most communication |
| What are target cells? | Cells that receive the message REGARDLESS of its chemical or electrical nature |
| What are the 4 methods of cell communication? | 1. gap junctions 2. contact - dependent signals 3. local communication 4. long distance communication |
| When a signal is sent from Point A to Point B, does the distance have to be long? | No |
| Describe gap junctions | 1. controllable (open vs closed) 2. passage of small molecules - amino acid/atp/cAMP/cGMP/ions 3. allow tissues to work as a syncytium |
| What's syncytium? | group of cells working as a functional unit autonomously w/o having a whole lot of control |
| What are examples of syncytium? | Smooth muscle sheets of lower esophagus. when 1 sheet contracts, all others contract |
| What are contact dependent signals? | 2 cells contact each other and ... 1. some type of immune response can start 2. cells know where they are (neurons during growth and dev) 3. platelets can do their thing |
| How do CAMs act as receptors/signalers for contact dependent signals? | Via linkage to intracellular components such as 1. cytoskeletal structures 2. enzymes |
| Give example of contact dependent signals | 1. P-Selectin - stored inside cells when not needed 2. inserted into cell membrane, contact by leukocytes causes their recruitment |
| How do integrins function as contact dependent signals? | Integrins are involved in contact signaling btw platelet formation |
| What is Auto-Crine signaling? | Cell-to-Self 1. cell secretes chemical in response to stimulus 2. chemical binds to receptor on its own membrane |
| What are examples of autocrine signaling and their effects? | 1. IL-1 (Macrophage-Macrophage) - Inflammation 2. IL-1 (Bcell to Bcell) Maturation & Proliferation 3. IL-6 (Bcell to Bcell) differentiation into plasma cells |
| T/F IL-6 acts as autocrine AND paracrine | TRUE |
| What is PARACRINE signaling? | Chemical signals secreted and affect neighboring cells |
| T/F Some chemical signals act as AUTOCRINE and PARACRINE messengers. | TRUE |
| What are some chemical signals for paracrine signaling? | 1. cytokines 2. eicosanoids (prostaglandins, prostacyclins, thromboxane, leukotriences) |
| Give an example of pracrine signaling... | Histamine (cytokine group) 1. act on local area cells, increase p-selectin membrane molecules which attract leukocytes 2. cause phosphorylation of CAM molecules, which causes increased cellular separation (makes them leaky) |
| Describe paracrine, endocrine, and autocrine and the areas that they affect... | 1. paracrine - local (immediate area) 2. endocrine - long distance 3. autocrine - extremely local |
| What are cytokines? | Chemical messenger hybrids - can get into blood stream and go long distance, act as paracrine messengers as well as long dist. messengers but... 1. not hormones cuz they work on many diff cells 2. not produced by endocrine gland |
| T/F Cytokines have no specific targets. | TRUE |
| How does long distance communication occur? | 1. electrical signaling (FAST action potential) 2. Endocrine system 3. Nervous system |
| Describe endocrine system in long distance communication | Hormones: 1. chem. messengers secreted by glands into blood 2. not specific in where they go 3. specificity is due to the receptors 4. slow, long term |
| Describe nervous system in long distance communication | Fast, short term. Chem. released due to electrical signal and becomes: 1. neurocrines (neurotransmitters) - released and binds to target at immediate area 2. neurohormones - released into the blood |
| What are examples of neurocrines | 1. acetylcholine (excitable & inhibitory) 2. GABA (completely inhibitory) |
| What are examples of neurohormones | 1. antidiuretic hormone 2. oxytocin |
| T/F The release of hormones is not specific, but the TARGET is VERY specific | TRUE |
| How do hormones create a reaction in some cells and not others? | Via receptor proteins |
| T/F If a receptor is PRESENT, the effect of binding always initiates a response thru a signal pathway | VERY FUCKING TRUE |
| Where can receptor proteins be located? | 1. Intracellular 2. Cell Membrane |
| Describe intracellular location of receptor protein | 1. chem. messengers must be lipophilic 2. bind to cytosolic receptors or nuclear receptors (effect is to modulate gene activity +/-) 3. increase rate of translation --> increase rate of protein production |
| Describe cell membrane location of receptor protein | 1. lipophobic molecules bind to membrane receptor 2. receptor transfers the signal to ICF (signal transduction) |
| What are benefits of lipophobic? | 1. different rates 2. amplification - bind ligan to effector, create multiple events in cell (takes longer because of more steps) |
| What is lipophilic for signal pathways? | goes right thru plasma membrane |
| What is lipophobic for signal pathways? | bind to membrane receptor |
| What are channel receptors? | 1. ligand binds & elect. signal formed 2. creates a very FAST intracellular response 3. may open via other pathways as well |
| Why do we care about signal transduction? | 1. big payoff with little effort 2. amplification |
| What process does sig. transduction and amplification rely on? | 1. molecule (prim. msgr) in ECF bind to membrane receptor & activates it 2. Membrane receptors ativated 3. Secondary messengers 4. proteins modification (by Ca+2 or PO4-) |
| When membrane proteins are activated in step 2 of signal transduction, what happens? | 1. protein kinases activated 2. Enzymes that create 2ndary msgrs activated |
| What do 2ndary messengers in signal transduction do? | 1. alter ion channel gating resulting in membrane potential change 2. increase intracellular calcium 3. alter enzyme activity of protein kinases (phosphatases) |
| The protein modification (by Ca+2 and PO4-) in signal transduction affects what? | 1. metabolic enzymes 2. motor proteins 3. gene expression (and therefore protein synthesis) 4. membrane transport & receptor proteins |
| What is the key to signal transduction? | AMPLIFICATION - getting LARGE response out of LITTLE stimulus |
| Does amplification always work? | No. IE: diabetic -> lot of insulin -> no cell response -> cell pulls back receptors |
| T/F - The signal transduction pathway is a CASCADING event | TRUE |
| How do you stop the cascading event in signal transduction? | 1. enzymatically tear up ligand bind 2. deactivate G-Protein (now that's GANGSTA!) |
| Explain receptor-enzyme's relationship in signal transduction | 1. Binding of ligand cause activation of active binding site on enzymes & are either: a. protein kinases (xfer phosphates) b. Guanylyl cyclase (convert GTP-cGMP => 2ndary messenger) 2. insulin, cytokines & growth factors bind to recep. enzyme complex |
| What's G-Protein activation? | Most common signal transduction pathway 1. G protein-coupled receptor lined to G-protein (ICF peripheral protein) transducer molecule 2. activated by xchange reaction (GDP->GTP) and a. open ion channel b. activate amplifier enzyme (most common pathw |
| What are the most common amplifier enzymes? | 1. adenylyl cyclase 2. phospholipase C |
| Explain the G-Protein-coupled adenylyl cyclase-cAMP system | 1. most commonly used for protein hormones 2. process figured out in 1905's by Earl Sutherland and he won a Nobel for it |
| Explain the steps of the G protein-coupled adenylyl cyclase-cAMP system | 1. signal molec bind to G prot.-linked receptor, activating G prot. 2. G protein turn on adenylyl cyclase (A.C) 3. A.C. convert ATP to cyclic AMP 4. cAMP activate protein kinase A (k.A) 5. k.A phosphorylates other proteins, leads to cellular respons |
| Explain Step 1 of the G-protein-coupled phospholipase C system | When activated G protein activated phospholipase C, it converts membrane phospholipid (phosphatidyl inositol bisphosphate) into DAG (diacylglycerol) and IP3 (inositol triphosophate) |
| Explain Step 2 of the G-protein-coupled phospholipase C system | DAG is nonpolar and stays in phospholipid bilayer where it activates protein kinase C (PK-C) 1. PK-C phosphorylates cytosolic proteins and furthers the cascade effect |
| Explain Step 3 of the G-protein-coupled phospholipase C system | IP3 is hydrophilic and enters into the cytosol where it beinds to ER and opens Ca+2 channels and acts as a signaling molecule |
| What are examples of 2ndary messengers | 1. Ions - Ca+2 2. Nucleotides - cAMP, cGMP 3. Lipid-Derived - IP3, DAG |
| What are the action and effects of Ca+2 as 2ndary messenger? | 1. Action - binds to calmodulin and other proteins 2. Effects - alters enzyme activity: exocytosis, muscle contraction, cytoskeleton movement, channel opening |
| What are the action and effects of cAMP as 2ndary messenger? | 1. Action - Activates protein kinases, esp. protein kinase A, binds to ion channels 2. Effects - Phoosphorylates proteins, alters channel openings |
| What are the action and effects of cGMP as 2ndary messenger? | 1. Action - Activates protein kinases, esp. protein kinase G, binds to ion channels 2. Effects - Phosphorylates proteins, alters channel openings |
| What are the action and effects of IP3 as 2ndary messenger? | 1. Action - releases Ca+2 from intracellular stores 2. Effects - alters enzyme activity: exocytosis, muscle contraction, cytoskeleton movement, channel opening |
| What are the action and effects of DAG as 2ndary messenger? | 1. Action - activates protein kinase C 2. Effects - phosphorylates proteins |
| What are integrins? | Membrane spanning proteins involved in: 1. hemostasis 2. tissue repair 3. cell adhesion 4. immune processes 5. cell migration during development |
| During integrin receptor signal transduction, when ligan binds to integrin, what happens? | 1. intracellular enzymes are activated 2. cytoskeletal organization changed 3. Quite a few pathways are figured out |
| When integrin membrane receptor is missing and platelet activation does not occur, what happens? | Hemophilia |
| What are the intracellular signal molecules? | 1. Ca+2, NO, CO, H2S 2. 2 important eicosanoids derived from arachadonic acid a. leukotrienes b. prostanoids (prostaglandins & thromboxanes) |
| What are the effects of Ca+2 when intracellular levels increase? | 1. protein activity gets altered 2. exocytosis 3. movement |
| What are NO, CO, and H2S? SHORT ACTING PARACRINE/AUTOCRINE signal molecules | |
| Describe NO | 1. NO acts as a vasodilator by diffusing from the cell that produced it into the surrounding tissue 2. Activates formation of cGMP which can block channels, causing muscle to relax |
| Describe CO | 1. CO is known for its affinity for binding to hemoglobin (thus starving tissues of oxygen) 2. Activates formation of cGMP (works as 2ndary messenger) |
| Describe H2S | 1. acts as a vasodilator 2. IE: Garlic is a good supply of sulfur compounds |
| How do lipids act as paracrine signal molecules? | 1. derived from arachidonic acid (precursor to eicosanoids) 2. phospholipase A2 is responsible for production of arachidonic acid |
| How does arachidonic acid act as a 2ndary messenger? | By influencing ion channels & intracellular enzymes |
| What two other paracrine messengers can arachidonic acid produce? | 1. leukotrienes 2. prostanoids (prostaglandins and thromboxanes) |
| Explain leukotrienes that gets produced by arachidonic acid. | 1. secreted by some leukocytes 2. initiate smooth muscle spasms in bronchioles 3. also involved in anaphylaxis (death unless medical intervention) 4. involved in asthma attacks |
| Explain prostanoids that gets produced by arachidonic acid | Produced as a result of cyclooxygenase (COX) action on arachidonic acid 1. influence sleep, infllamation, pain, fever 2. COX inhibitors (aspirin, ibuprofen) stop the formation of prostaglandins - STOP THE PAIN! |
| T/F - Sphingolipids can also be involved with G protein coupled receptors | TRUE |
| How are pathways controlled? | 1. under homeostasis guidelines 2. receptors are PROTEINS, subject to: a. specificity of binding b. competition for binding site (agonists & antagonists) c. saturation of ligand (up/down regulation of receptors) |
Created by:
lophung
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