Chapter 13: Signal Transduction

Signal

ligand binds to receptor

Reception

conformational change occurs

Transduction

message is relayed + molecules amplify

Response

cell changes

Termination

pathway turned off

Glucagon/ Epinephrine/Adrenaline Hormone

fasting/stress state

GPCR receptor

glucose release

Insulin Hormone

Fed state

RTK receptor type

glucose storing

GDP

off state

GTP

on state

CAMP activating PKA

CAMP binds to R subunits on PKA

R subunits disassociate

C subunits become activated

C subunits continue to phosphorylate GPCR function

Pathway Termination

G proteins hydrolyze bound GTP to GDP switching off through GTPase activity

Protein phosphotases remove PKA-added phosphotates from target proteins

Phosphodiesterases hydrolyze CAMP to AMP

Ligand (epi/glycogen/adenaline) disassociated from receptor

Phosphodiesterase

turns OFF the second messenger (cAMP); removes signal that activates PKA

Protein Phosphotase

remove phosphate group from PKA (protein kinase A) making it dysfunctional

Cholera

bacterial disease caused by choleragen that produces life-threatening diarrhea

Choleragen

bacterial toxin thay causes Cholera; modifies G protein to be stuck in active GTP form that causes overstimulation of PKA which causes excessive loss of NaCL and water into intestine

Gq (smooth muscles)

activates phospholipase C (which goes on to cleave PIP2 into second messengers)

Phospholipase C

Cleave PIP2 into DAG and IP3

IP3

binds to ion channel receptor causing influx of Ca+ ions into cytoplasm

DAG

works with Ca+ influx from IP3 and activated protein kinase C (serine/threonine kinase)

Insulin Receptor

insulin binds which causes conformational change to RTK (autophosphorylation)

IRS protein binds and get phosphorylated

phosphoinositide 3-kinase comes in, binds to IRS, and gets activated

PIP₂ → PIP₃ conversion

PIP3 brings AKt to membrane which releases GLUT4

Type 2 Diabetes

insulin resistance

signaling is impaired; GLUT gets impaired so there is less glucose uptake, pancrease compensated by producing more insuline and becomes exhausted

treatment: boost insulin sensitivity or supply insulin