Organisation of the Body
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show | High affinity for hormone
Hormone specific
Binding is saturatable
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Kds | show 🗑
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show | Conc of hormone that gives 50% response
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Receptor classes | show 🗑
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Ligand gated ion channels | show 🗑
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show | 5 protein
2 homodimers and 1 extra protein
Blocked by cobra toxins
Open in response to ACh binding - non-selective cation channel
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show | 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
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G protein coupled receptors | show 🗑
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What activates GPCRs | show 🗑
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show | Around 820 in the human body
All have similar structures - hard to design drugs specific to one, so unwanted effects are common
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show | 7 transmembrane regions
Extracellular N-terminus
Often post translationally glycosylated and phosphorylated to regulate activity
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show | Found in the heart - slow heart rate
QNB - antagonist
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show | 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
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Types of GPCRs | show 🗑
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show | 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
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Downstream effectors of GPCRs | show 🗑
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Adenylate cyclase | show 🗑
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show | 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
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show | ACTH stimulates Gs - cAMP produced
Immediately upregulated cholesterol synthesis by cholesterol ester hydrolase
Over a few hours allows uptake of cholesterol by mitochondria
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show | 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
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show | 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
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show | Channels phosphorylated - less active
e.g. G protein gated inwardly rectifying potassium channels in the heart
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Smooth muscle contraction | show 🗑
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show | Reaction cascades cause massive signal amplification
Proteins made can last a long time, so short activation affects function for longer periods
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Enzyme linked channels | show 🗑
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show | 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
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show | Control of DNA transcription
e.g. steroid hormones and Vit D (for Ca uptake)
Takes hours for proteins to be produced
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show | DNA strand contains specific hormone response elements
Contains regions for transcriptional regulation, DNA binding and hormone binding
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What binds to intracellular receptors | show 🗑
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show | Removal or degradation of the hormone
Desensitisation of the receptor
Internalisation of the receptor
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Desensitisation of GPCRs | show 🗑
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Resensitisation | show 🗑
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show | Serves as a connection between glucagon and insulin pathways
Insulin drives activation of phosphodiesterase to downregulate the role of glucagon
Breaks down cAMP
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show | 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
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show | Failure of ligand binding
Failure of signal transduction
Constitutively active signal receptor systems
Antibodies to receptor
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show | Receptor does not function despite hormone present
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Activating receptor mutations | show 🗑
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Dwarfism | show 🗑
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Activating receptor mutations | show 🗑
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Physiological response to receptor activation | show 🗑
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Types of cell signalling | show 🗑
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