Epineptrine dived 2 PKA Glycogen synthase P GS 1 Glycogen Phosphorytise 3 kinase GPK inactive Inhibitory (via medialor 1 Protein P P Glycogen IP GP Synthesis 1 Protein Glycogen phosphatanc degradation Ganagers Insolin Proteinphosphalas IP 11 Gt GS (ii) P GiP GPI: CIPK lactive Glipagen Glijargo degradation du
GPCR -7 transmember receptor N-sexopamic, Adenetyl cyclase. (GAP) deneritization & (GXGDP) a (can) with GTT ATP CAMP 4 GIRCRY B A 2 or a GKGP I' PKA recalilytic c C authonit GGTP agree Execute R R R'Regolatory rubunit trimaic afrlipid thefundtoon Gprotein enchored 2CAMP activate required to 1 PKA The only DOD Amplifications amplification Epinophrin step Adenelyl cylclas 11 only nonamplification PKA PKA PKA PK step. PKA PKA - localized to mentrone AKAP - A kinase Associate Protein Telha memb PKA PM/Nucleal Iltrotata of holds a PDE Phosphodiestelase
Basal PDE sncreased and activation. reduction 2 CAMP PKA activation activity - Resting in CAMP level. 3 1 state mebblic PDE PDE activate no D PDE nucleus C c Transcriptional A activation D P desemity PDE Desensitization Cleave all 4 Return to resting response c C state. CAMP Terminate theresponce P PKA P GPCR Arross recognisedhy airestin Clathrin coatedvesicle formations Cysosomal degradation when GXGTP contacts AC, AC act as GAP GXGDP GKGTP Epineptrine Inaeas heart muscle contraction GPCR GLGTP AC PKA P Ca2+channel ea2t a Ca2+ in extracellular Cytoplasmic Refer side side. muscles] Increase contraction rate.
Gx Trandering Ach cause heart musle relaction GKT muscalinic acetyl chaline a GFCR Stimulatory Inhibitory receptor in heart . GKS GKT heart CK GTTP Br muscle 4 open Kt contraction, Glycogen synthesis channel f Glycagenolegradation ACyclase (effector) Decrease CAMP Relaxation Relaxation Digestive enzyme Release Acetylebdine Pancieas GPCR G2SGTP PLC B PIP2 1P3 DAG openCa2 channel @ ER Ca2+ cyford vesidefurior f enzyme release ca2+ Calmadulin Decrease IP3 responsiveness east HEPATPane pump of channel