1 / 14

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

jasmine
Download Presentation

Graves’ Disease Case: Previously

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. 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’

  2. 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?

  3. 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?

  4. 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?

  5. 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?

  6. Side chains hold the ‘information’ Conventions for writing and speaking about proteins: The N and C termini Polarity of proteins

  7. 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

  8. Adapted from: http://www.bmb.psu.edu/courses/bisci004a/chem/profold.jpg Benjamin Cummings. Ltd. 2001 Levels of Protein Structure Primary Structure Secondary Structure

  9. Levels of Protein Structure Tertiary Structure

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

  11. TSH Receptor: What level of structure? Extracellular Plasma membrane Cytosolic TSH Receptor:from “The Thyroid Manager” Ch16

  12. 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.

  13. 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…….

  14. 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?

More Related