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Cell Signalling

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Question	Answer
Characteristics of hormone receptors	High affinity for hormone Hormone specific Binding is saturatable
Kds	Binding constant 10^-12 to 10^-9 Very little hormone needed for activation
EC50	Conc of hormone that gives 50% response
Receptor classes	Ligand gated ion channels G protein coupled receptors Enzyme linked Intracellular receptors
Ligand gated ion channels	Open in response to NTs Leads to a change in membrane potential due to ion movement Instantaneous response
nACRs	5 protein 2 homodimers and 1 extra protein Blocked by cobra toxins Open in response to ACh binding - non-selective cation channel
Katp channel	Glucose enters beta cells and is metabolised to produce ATP This binds to K channels and blocks them Leads to depolarisation and Ca influx Insulin release triggered ATP acts as a hormone
G protein coupled receptors	Hormone binds to receptor leading to G protein mobilisation They interact with enzymes through a second messenger system Timescale - seconds/minutes
What activates GPCRs	Protein hormones - glucagon Amines - adrenaline Lipids - prostaglandins
Family of GPCRs	Around 820 in the human body All have similar structures - hard to design drugs specific to one, so unwanted effects are common
Structure of GPCRs	7 transmembrane regions Extracellular N-terminus Often post translationally glycosylated and phosphorylated to regulate activity
M2 muscarinic receptors	Found in the heart - slow heart rate QNB - antagonist
G proteins	Get their name from their ability to bind GTP and GDP They exist in an active GTP bound and an inactive GDP bound form Active G proteins bind and activate signalling enzymes causing a specific response Heterotrimeric - alpha, beta and gamma subunits
Types of GPCRs	Gq - activates PLC Gi - inhibits adenylate cyclase Gs - stimulates adenylate cyclase G12/13 - Rho family Gb - activates inwardly rectifying potassium channels
The G protein cycle	Inactive - loosly associated with proteins Ligand binds and recruits G proteins GTP exchange causes dissociation of the protein Subunits have different effects GTP hydrolysis causes reassociation
Downstream effectors of GPCRs	Adenylate cyclase Phospholipase C Ion channels
Adenylate cyclase	Stimulated by Gs and inhibited by Gi Converts ATP into cAMP This activates PKA by releasing its catalytic subunits cAMP degraded by phosphodiesterase
Effects of Cholera	A GPCR agonist Binds to Gs - increased cAMP and PKA Activates CTFR Overactive CTFR causes Cl loss into lumen of gut followed by Na and water Leads to internal dehydration Enkephalin - stimulates Gi to reduce effects
cAMP in steroid synthesis	ACTH stimulates Gs - cAMP produced Immediately upregulated cholesterol synthesis by cholesterol ester hydrolase Over a few hours allows uptake of cholesterol by mitochondria
PLC	Activated by Gq receptors Cleaves PIP2 into DAG and IP3 DAG activates PKC - phosphorylates proteins IP3 activates store operated calcium ion channels leading to Ca efflux from SR - activation of intracellular proteins
Role of Gq/Gs switch in beta cells	Normal B cells us a Gs pathway to secrete insulin involving GIP and GLP-1 Following chronic hyperglycemia and chronic sulfonylurea treatment they switch to Gq
Ion channels in GPCR	Channels phosphorylated - less active e.g. G protein gated inwardly rectifying potassium channels in the heart
Smooth muscle contraction	Uses multiple mechanisms Ligand gated ion channels Voltage gated ion channels Gq proteins - IP3 activates Ryr channels
Amplification	Reaction cascades cause massive signal amplification Proteins made can last a long time, so short activation affects function for longer periods
Enzyme linked channels	Receptor is also the effector enzyme e.g. tyrosine cyclase enzyme activity Receptors dimerise on ligand binding Autophosphorylation at tyrosine and serine residues
Insulin receptor	Tyrosine kinase receptor Leads to insertion of Glut4 into cell membranes Under fasting conditions no insulin = no glucose uptake as no Glut4 channels in membrane
Intracellular receptors	Control of DNA transcription e.g. steroid hormones and Vit D (for Ca uptake) Takes hours for proteins to be produced
Steroid receptor structure	DNA strand contains specific hormone response elements Contains regions for transcriptional regulation, DNA binding and hormone binding
What binds to intracellular receptors	Androgens Estrogen Progesterone Glucocorticoids Mineralocorticoids Thyroid hormone Vit D
Turning off the signal	Removal or degradation of the hormone Desensitisation of the receptor Internalisation of the receptor
Desensitisation of GPCRs	Phosphorylation of certain residues at the C terminus by GRK Arrestin binds to the receptor and prevents G protein interaction
Resensitisation	Phosphatases remove the phosphate from the C terminus Causes arrestin to dissociate
Role of phosphodiesterase's in glucose control	Serves as a connection between glucagon and insulin pathways Insulin drives activation of phosphodiesterase to downregulate the role of glucagon Breaks down cAMP
Receptor internalisation	Receptors taken into the cell by endocytosis Basically receptor mediated endocytosis Dopamine D1 receptors are permanently downregulated due to overuse in addiction - via internalisation and DNA metylation
What causes disease at receptors	Failure of ligand binding Failure of signal transduction Constitutively active signal receptor systems Antibodies to receptor
Inactivating receptor mutations	Receptor does not function despite hormone present
Activating receptor mutations	Receptor continually active without hormone bound
Dwarfism	Due to growth hormone releasing hormone inactivating receptor mutations No signalling - reduced growth hormone release No long bone or muscle growth Treated by administering growth hormone
Activating receptor mutations	Precocious puberty - puberty starting at 5-9 years Constant activation of LH receptors without the presence of the hormone Ovary - estrogen Testes - testosterone
Physiological response to receptor activation	Vesicle fusion Gene transcription Protein production
Types of cell signalling	Depolarisation induced - Ca entry dependant Depolarisation independent - Ca entry dependant