Title: Previously
1Previously
Previously in Cell Bio
A) Fluid Mosaic Model
B) Cell Parts Components and Organelles
C) Introduction to first case study Graves
disease/ hyperthyroidism
Today
Signaling its roles in Graves disease
2Thyroid activators
How are they all coordinated?
Our Case Study ? Thyroid stimulation Extracellula
r signaling and the receptors that mediate it
3Signaling types
Types of Extracellular Signaling
PM receptors Gap junctions Secreted ECM
- Through space
- Paracrine
- Endocrine
- Synaptic
4Compare
Compare synaptic signaling endocrine signaling
Carried how?
Relative rate
5What types in thyroid regulation?
Normal thyroid function
Negative feedback loop What is it and why is it
important?
6Binding vs. Effector Specificity
Symptoms in Graves Disease
- Increase in circulating thyroid hormone causes
- Increase in secretion by sweat glands
- Increase in rate and force of heart
contractions - Decrease in muscle strength
How can this happen?
7Binding vs. effector specificity 2
How can thyroid hormone cause different
responses in different parts of the body?
Ligand needs to bind with receptor
Different cells make different receptors
Same receptor/ligand complex may trigger
different response in a different cell type
Differences between binding specificity and
effector specificity
(Receptors and Ligands? What are they?)
8Receptor characteristics
Characteristics of a receptor What does it need
to have to do its job?
Ribbon diagram of Thyroid hormone bound to
Thyroid hormone receptor
Diagram of isoproterenol bound to B2 adrengergic
receptor (Fig20-1 Molecular Cell Biology)
9Types
Types of Receptors
G-protein linked receptors (G protein coupled
receptors/GPCR)
Ion Channel receptors
Enzyme linked receptors (Receptor S/T kinases,
Receptor Y kinases Receptor guanylyl cyclases,
Protein Y phosphatases, Y-kinase associated
receptors H-kinase associated receptors)
Intracellular receptors
10What happens in Graves?
Whats different in a Graves disease
patient? (hyperthyroidismincreased thyroid
function)
Patients have increased T3 and T4 in bloodstream
What might make a thyroid put in overtime?
HYPOTHESES?
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12Hypothesis Thyroid being over-stimulated
Normal stimulation results from
TSH/receptor interaction How does the thyroid
know to react? How does a receptor provide
specificity
Hypothesis Mutation in signaling within cell
leading increase in thyroid hormone production
Normal activation is the result of signal
transduction second messenger cascade How does
signal transduction work? What could have gone
wrong?