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Lecture

OCT 26, 2013 BIO 201.docx

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School
University of Alberta
Department
Biology (Biological Sciences)
Course
BIOL201
Professor
Veugelers P
Semester
Fall

Description
OCT 24 BIO 201: -adrenergic signalling (chp. 14) 2. vs adrenergic receptors, their specific secondary messengers involved. 3. adrenergic receptor on:  smooth muscles of viscera – vasoconstriction effect  …is a G-protein linked receptor (GPLR) – signals with ( ), DAG (NOT a m.) and finally Calcium ( m.)  METABOTROPIC 4. adrenergic receptor on 4 places:  Vasodilatory effect on smooth m. of vasculature (heart, bronchioles) and skeletal m.  Liver – causes glycogen breakdown  releasing stored energy upon demand  …is a G-protein linked receptor (GPLR) – signals with cAMP ( m.) METABOTROPIC 5. FIGURE 14.5 GPLR MECHANISM (do not need to know specific types of G proteins): -heterotrimeric subunits. -inactive state [ -GDP)- ] -active state [( ) + ] Activation: 1. Receptor linked to GP (“R of GPLR”) binds with ligand [in ECF] 2. Receptor now binds with heterotrimeric GP [in ICF, on membrane], causing to RELEASE GDP and acquire a SEPARATE GTP molecule [diff molecules] 3. -GDP)- [trimer]  ) + [monomer + dimer] 4. & are able to direct different pathways(initiate signal transduction events) 5. [In adrenergic receptors, remains bound to receptor and activates adenylyl cyclase (membrane protein enzyme), which proceeds to convert ATP to cAMP] –see slide 10 [In adrenergic receptors, remains bound to receptor and activates phospholipase C (PLC, membrane protein enzyme), which proceeds to breakdown  ] – see slide ____ Note: There are different types of receptors, and G proteins associated with them( – do not need to know). These differences allow for variety in cellular response . Inactivation: 1. has innate ability to hydrolyze its bound GTP GDP [same molecule+. “after its done its job, and no ligand is bound to linked receptor” 2. -GDP)- [trimer] reforms [inactive] 7. Iclicker B – see Inactivation step 1. If GTPase function is halted, then G subunit will continue the response. 10. Adrenergic receptor signalling (ex. Glycogen breakdown in liver [7] steps) [1] Initiation: epi [ligand]  binds to liver receptor [7] Response: phosphorylase a  cleaves glucose-1-phosphate from glycogen terminus end Whats the path from initiation to response?? 12. Figure 14.7 [2] ligand binding  GP activation (see page 1, [1-5]) [3]GPadenylyl cyclase activated (change in conformation by binding of subunit) [4] Adenylyl cyclase  converts ATP cAMP 13. cAMP ( messenger) – do not need to know structure, just know of adenine substituent ATPcAMP [2 steps] [1] 2 phosphates cleaved from ATP *2+ “dangling” phosphate attaches to 3’ carbon (similar to 5’3’ in nucleotides chains) Note: messengers are diffusible molecules, G proteins & adenylyl cyclase are NOT messengers 14. [5] cAMP  PKA (protein kinase A) …kinase – phosphorylating – adds phosphate to a protein AA Note: Do not confuse with phoshotase or phosphorylase 15. pretest question B 18. PKA – dissociation of catalytic domains of PKA by cAMP inactivation of regulatory domains of PKA  Tetrameric protein – 2 pairs of subunits – 1 pair catalytic (do the downstream work), 1 pair regulatory (ON/OFF for catalytic)  Regulatory subunit – has cAMP binding site. When cAMP binds causes regulatory/catalytic  regulatory + catalytic (dissociation). Dissociation of the pairs activates
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