2nd messengers
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| Hormones and types: Endocrine Paracrine Autocrine | -secreted into blood by special cells in endocrine glands
-regulate target cells distant from secretion site
Endocrine-hormone signaling
Paracrine-local mediator, diffuse through ECF and act on cell in local area
Autocrine-excreted then target same
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| Hydrophilic *receptor location and action* | -water soluble.bind to plasma membrane receptors and generate intracellular second messenger or activates receptor enzymatic acticity and changes activity of metabolic enzymes
-modulate phosphorylation state
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| G-Proteins | -contain bound GDP (inactive) or GTP (active)
-inactivate themselves
-GDP associate with activated hormone receptors and exchange for GTP
-binding GTP dissociates a-subunit from By dimer
-alter activity of enzymes creating intracellular 2nd messengers
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| Second Messenger | -small intracellular molecules whose abundance changes rapidly in respoinse to hormone action
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| Gs, Gi, and Gq | Gs-activates adenylate cyclase
Gi-inhibit adenylate cyclase
Gq-activates phospholipase C
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| cAMP system: signal transduction plasma membrane-cytosol | -activated receptor protein activates Gs>activates adenylate cyclase
-ATP cleaved from adenylate cyclase > pyrophosphate,PPi
-PPi hydrolyzed to 2 Pi by inorganic pyrophosphatase activity
-PO3 covalently links to 2 sites in ribose (ring)
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| Regulation of cAMP | -increase or decrease in adenylate cyclase control levels of cAMP
-phosphodiester hydrolyze cAMP to AMP
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| IP3-DAG signal transduction system | -Phospholipase C hydrolyzes polar lip head from glycerol backbone of PIP2 > IP3 and DAG
-IP3 binds to receptor, Ca flows out of Ca sequesterin comp. into cytosol activating protein kinase C
-DAG=coactivator of protein kinase C
-PKC phosphorylates proet
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| 1.PIP2 2.Phospholipase C 3.IP3 4.Ca 5.DAG 6.Protein Kinase C | 1.generates IP3 and DAG via hydrolysis of polar lipid head from glycerol backbone
2.catalyzes PIP2 hydrolysis
3.opens IP3 gated Ca channel
4.activates PKC
5.coactivates PKC
6.facilitates recruitment of kinase to plasma membrane
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| How are IP3, DAG, and Ca inactivated? | -dephosphorylated to derivative that doesnt open Ca channel
-phosphorylated>physphatidic acid or hydrolyzed to glycerol and fatty acids
-pumped out of cytosol in sequestering compartments or out of cell
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| NO: Substrate of NO sunthase, affect,enzyme affected, and how is it turned off? | -Arginine
-smooth muscle relaxation, increasing blood flow
-guanylate cyclase
-converted to nitrate or nitrite
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| cGMP | -GTP >guanylate cuclase>cGMP
-activates protein kinase, leading to smooth muschle relaxation
-converted back to GMP by phosphodiesterases
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| How does Nitroglycerin reduce blood pressure? | -converted to NO in the body
-reduces workload of heart, therefore reducing O requirement of workin heart muscle
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| How does viagra work? | -cGMP phosphodiesterase inhibitor
-cGMP levels remain elevated for longer following NO release and relaxation of blood vessels
-cGMP cannot be deactivated and converted back to GMP
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| Catalytic Receptors | -binding leads to activation of latent enzyme activity within receptor
-transmembrane proteins with hormone binding domain (external) and catalytic doman (internal)
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| Catalytic activities of catalytic receptors, which is *most abundant*? | -protein serine kinases
-protein tyrosine phosphatases
-guanylate cyclases
-*protein tyrosine kinases*
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| How does the insulin receptor function? | -tyrosine kinase activity
-insulin binds
-receptor phosphorylates itself on tyrosine residues
-form docking sites to recruit molecules (IRS1)
-phosphorylates molecule
-binding site for molecules that mediate insulin action inside cell
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| Type I vs. Type II Diabetes Mellitus | I: absence of insulin due to autoimmune disorder that destroys insulin-producing B-cells of pancreas. *early onset*
II: deficiency/alteration of insulin receptor
-insulin insensitivity
-can present as insulin deficiency
-some respond to insulin therap
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| Chlorea Toxin | -catalyzes transfer of ADP-ribose of NAD to an arginine res. in Gs protein in intestine.
-high increase of water influx to intestines
-massive diarrhea and dehydration
-frequently fatal if untreated
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| Pertussis Toxin | -catalyzed ADP-ribosylation of G-protein (cysteine res.), inhibiting Gi
-prevents inhibition of adenylate cyclase > increased cAMP
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| YopH protein type | -protein tyrosine phosphatase
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| Glucagon receptor signal transduction mechanism | -glucagon binds to receptor
-activates Gs protein
-activates adenylate cyclase
-elevated cAMP activates protein kinase A
-phosphrylates and activates phosphorylase kinas
-phosphorylates glycogen phosphorylase
-activates glycogen degradation
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| Signal amplification | receptor binds to and activates several g proteins over time
-each can activate adenylate cyclase that will form many cAMP
-2 active protein kinase A subunits/4 cAMP
-enzyme activates multiple copies of next enzyme
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| Lipophilic (hydrophobic) | -fat soluble.pass through plasma membrane and bind to receptor proteins in nucleus or cytosol
-steroidal and bind to regulatory domans in DNA altering transcription rate
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Created by:
MastamikeOD
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