Previously Previously in Cell Bio A) Fluid Mosaic Model B) Cell Parts: Components and Organelles C)...
-
Upload
lillian-carson -
Category
Documents
-
view
218 -
download
0
Transcript of Previously Previously in Cell Bio A) Fluid Mosaic Model B) Cell Parts: Components and Organelles C)...
PreviouslyPreviously in Cell Bio
A) Fluid Mosaic Model
B) Cell Parts: Componentsand Organelles
C) Introduction to first case study Graves’ disease/ hyperthyroidism
TodaySignaling its roles in Graves’ disease
Thyroid activatorsOur Case Study Thyroid stimulation:
Extracellular signaling and the receptors that mediate it
‘Activating’ Signals:• Hypothalmus: Thyrotropin releasing hormone (TRH)• Pituitary Gland Thyroid stimulating hormone (TSH)• Thyroid
T4 (thyroxine) T3 (triiodothyronine)
How are they all coordinated?
Signaling typesUp close •Direct contact
•AutocrineThrough space
•Paracrine•Endocrine•Synaptic
PM receptorsGap junctionsSecreted ECM
Types of Extracellular Signaling
What types in thyroid regulation?Normal thyroid function
Endocrine signaling:(Intracellular receptorfor T4)
Endocrine signalingPM receptor
Negative feedback loop:What is it and why is it important?
Binding vs. Effector Specificity
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?
Symptoms in Graves’ Disease
Binding vs. effector specificity 2
Different cells make different receptors
Same receptor/ligand complex may trigger different response in a different cell type
Ligand needs to bind with receptor
(Receptors and Ligands? What are they?)
How can thyroid hormone cause different responses in different parts of the body?
Differences between binding specificity and effector specificity
Receptor characteristicsCharacteristics 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)
Types of Receptors
What happens in Graves’?What’s different in a Grave’s disease patient?
(hyperthyroidism=increased thyroid function)
Patients have increased T3 and T4 in bloodstream
HYPOTHESES?
What might make a thyroid put in overtime?
Hypothesis : Thyroid being over-stimulated
Hypothesis: Mutation in signaling within cell leading increase in thyroid hormone production
Normal stimulation results from TSH/receptorinteraction
How does the thyroid know to react?How does a receptor provide specificity
Normal activation is the result of signal transductionsecond messenger cascade
How does signal transduction work?What could have gone wrong?
Testing the hypothesesIF hypothesis is true then what is expected?
What data would suggest the hypothesis needs to be revised?
Tonight: Research Symposium– Gallery 7=9pmNext week: How ‘normal’ signals get in
Lab: Analysis of complementationHow long does response to signal
‘normally’ last