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Graves’ Disease Case: Previously. Normal thyroid signaling requires circuit of signaling: hypothalamus, pituitary, thyroid. Signaling between any cells requires signals and receptors 5 types of extracellular signaling What they are and how they work

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graves disease case previously
Graves’ Disease Case: Previously

Normal thyroid signaling requires circuit of signaling:

hypothalamus, pituitary, thyroid

Signaling between any cells requires signals and receptors

5 types of extracellular signaling

What they are and how they work

4 classes of receptors (only showed list)

Receptors: What are they (describing all of them)

Now: More details on the 4 classes of receptors

Hypothesizing what goes wrong in Graves’

slide2

What’s different in a Grave’s disease patient?

(hyperthyroidism=increased thyroid function)

Patients have increased T3 and T4 in bloodstream

What might make a thyroid put in overtime?

YOUR HYPOTHESES?

slide3

Hypothesis : 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?

testing the hypotheses

Hypothesis : Thyroid being over-stimulated

Known: Normal stimulation results from TSH/receptor

interaction

How does the thyroid ‘know’ to react?

How does a receptor provide specificity?

Testing the hypotheses

IF hypothesis is true then what is expected?

What data would suggest the hypothesis

needs to be revised?

protein structure
Protein structure

Amino acid sequence and folding environment

determine the conformation of a protein

Parts of a protein: amino acids

Amino acids: 5 characteristic parts

If all proteins made of amino acids and all amino

acids have the same parts why do proteins do

different things?

side chains hold the information
Side chains hold the ‘information’

Conventions for writing and speaking about proteins:

The N and C termini

Polarity of proteins

can we predict protein structure
Can we predict protein structure?

Motifs and Domains

How do you change a protein’s shape?

Alter the chain

Change the environment–

what it is floating in or binding with

levels of protein structure

Adapted from: http://www.bmb.psu.edu/courses/bisci004a/chem/profold.jpg Benjamin Cummings. Ltd. 2001

Levels of Protein Structure

Primary Structure

Secondary Structure

levels of protein structure9
Levels of Protein Structure

Tertiary Structure

quaternary structure
Quaternary structure

Protein Kinase C Interacting Protein.http://lectures.molgen.mpg.de/ProteinStructure/Levels/quaternary.gif

tsh receptor what level of structure
TSH Receptor: What level of structure?

Extracellular

Plasma membrane

Cytosolic

TSH Receptor:from “The Thyroid Manager” Ch16

graves hypothesis 1 tsh tsh receptor interaction too strong
Graves’ hypothesis 1: TSH, TSH-Receptorinteraction ‘too strong’

According to this hypothesis and what we

now know about protein binding……

T3 and T4 levels should be _?_ in Graves’

vs. normal.

TSH levels should be __?__ in Graves’ vs.

normal

TSH/TSH receptor interactions should show

__?___ binding constant vs. normal.

blood tests show
Blood tests show

T3 and T4 levels are elevated

TSH levels are decreased

TSH/TSH receptor interactions have same

binding constant vs. normal.

Therefore: Perfectly logical hypothesis…….

now what

Hypothesis 2: Mutation in signaling within

cell leading to 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?

Notsupported by data

Now what?