H2 Biology 19 - Cell signalling

LSC

Ligand-receptor interaction

ligand r&b specific binding site of receptor on CSM/within target cell >

ligands complementary in shape to specific binding site of specific receptor protein

Signal transduction

ligand binding induces conformational change in receptor >

relay molecules, various proteins amplify & transduce signal into specific cellular response >

signals could be transmitted through 2nd messengers(cAMP)/phosphorylation cascades via protein kinases

Cellular response

transduced signal triggers specific cellular response, may be change in GE/catalysis by enzyme/rearrangement of cytoskeleton

made up of 1 polypeptide w/ 7 transmembrane a-helices -> allows embedded in & span CSM >

has extracellular region(may be glycosylated) -> serve as specific binding site for ligand >

has intracellular/cytoplasmic region -> serve as specific binding site for G-protein

insulin r&b specific binding site on tyrosine kinase receptor(RTK) on liver/muscle CSM, causes 2 receptor polypeptides to undergo conformational change & dimerise >

dimerisation activates tyrosine kinase region of each polypeptide; each tyrosine kinase phosphorylates tyrosines of other polypeptide >

activated RTK recognised by specific relay proteins, pass signal on, leads to activation of glycogen synthase >

glycogen synthase catalyses glucose -> glycogen conversion(glycogenesis) >

any 1:

insulin also stimulates increase in rate of respiration using glucose as respiratory substrate, broken down & oxidised to CO₂, H₂O ;

increase in plasma membrane permeability of target cells to glucose, increase rate of uptake of glucose from blood by most body cells ;

glucose -> fats conversion for storage in adipose cells/tissues

glucagon r&b specific binding site of GPLR on liver CSM, induces conformational change in receptor >

receptor binds to G protein, activates it; GTP molecule replaces GDP on G protein; activate G protein dissociates from receptor, activates adenyl cyclase >

adenyl cyclase catalyses conversion of ATP to cAMP >

cAMP acts as 2nd messenger, triggers downstream signalling events such that glycogen phosphorylase activated >

glycogen phosphorylase catalyses glycogen -> glucose breakdown(glycogenolysis) >

glucagon also stimulates increase in rate of conversion of amino acids, glycerol to glucose(gluconeogenesis) so that BGC increases, returns to normal

enzyme; catalyses transfer of phosphate groups from phosphate-donating groups(ATP) to specific substrates -> phosphorylation >

phosphorylation activates protein >

active protein in turn activate other proteins, triggers numerous reactions in cell @ once

enzyme; catalyses removal of phosphate groups from proteins by hydrolysis, reverses protein kinase action >

dephosphorylation deactivates protein

small, hydrophilic molecules; usually non protein >

second messengers(cAMP) relay signals received @ surface of cell by GPLR/RTK into cytoplasm/nucleus >

ligand r&b SBS on GPLR, receptor undergoes CC, binds & activates G protein >

G protein activates adenyl cyclase, catalyses conversion of ATP -> cAMP >

cAMP binds & activates another protein; activated protein triggers downstream signalling events(phosphorylation cascade), lead to cellular responses

phosphorylation cascade

activated protein kinase triggers downstream signalling events >

involves sequential phosphorylation of various other proteins/signal transmitted through phosphorylation cascade >

signal amplification

no. of protein molecules phosphorylated increases w/ each level of cascade >

relay molecules, various proteins amplify & transduce signal into specific cellular response

both have extracellular specific binding sites for ligands >

both change conf to trigger downstream signalling pathways/for signal transduction >

both have intracellular regions, interact w/ intracellular proteins >

both have extracellular & intracellular region

receptors need detect signals outside cell >

signals transduced/relayed to molecules inside cell >

receptors span CSM; polar/large ligands cannot pass thru hydrophobic core of transient pores of CSM, remain outside cell >

channels span CSM; transport polar molecules/charged ions, repelled by hydrophobic core of CSM >

channels enable polar molecules/charged ions move across membrane

polar/large ligand which cannot pass thru CSM r&b to receptor on CSM & activate specific protein within cell >

1 ligand molecule stimulate production of more than 1 second messenger, results in signal amplification >

provide diff points @ which cellular response can be regulated(activation of protein, conversion of molecules) >

allows ligand to trigger specific cellular responses due to collection of receptors, specific proteins & second messenger in target cells