Go to JCI Insight
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Publication ethics
  • Publication alerts by email
  • Advertising
  • Job board
  • Contact
  • Clinical Research and Public Health
  • Current issue
  • Past issues
  • By specialty
    • COVID-19
    • Cardiology
    • Gastroenterology
    • Immunology
    • Metabolism
    • Nephrology
    • Neuroscience
    • Oncology
    • Pulmonology
    • Vascular biology
    • All ...
  • Videos
    • Conversations with Giants in Medicine
    • Video Abstracts
  • Reviews
    • View all reviews ...
    • Complement Biology and Therapeutics (May 2025)
    • Evolving insights into MASLD and MASH pathogenesis and treatment (Apr 2025)
    • Microbiome in Health and Disease (Feb 2025)
    • Substance Use Disorders (Oct 2024)
    • Clonal Hematopoiesis (Oct 2024)
    • Sex Differences in Medicine (Sep 2024)
    • Vascular Malformations (Apr 2024)
    • View all review series ...
  • Viewpoint
  • Collections
    • In-Press Preview
    • Clinical Research and Public Health
    • Research Letters
    • Letters to the Editor
    • Editorials
    • Commentaries
    • Editor's notes
    • Reviews
    • Viewpoints
    • 100th anniversary
    • Top read articles

  • Current issue
  • Past issues
  • Specialties
  • Reviews
  • Review series
  • Conversations with Giants in Medicine
  • Video Abstracts
  • In-Press Preview
  • Clinical Research and Public Health
  • Research Letters
  • Letters to the Editor
  • Editorials
  • Commentaries
  • Editor's notes
  • Reviews
  • Viewpoints
  • 100th anniversary
  • Top read articles
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Publication ethics
  • Publication alerts by email
  • Advertising
  • Job board
  • Contact
Thyroid autoimmunity
Basil Rapoport, Sandra M. McLachlan
Basil Rapoport, Sandra M. McLachlan
Published November 1, 2001
Citation Information: J Clin Invest. 2001;108(9):1253-1259. https://doi.org/10.1172/JCI14321.
View: Text | PDF
Perspective

Thyroid autoimmunity

  • Text
  • PDF
Abstract

Authors

Basil Rapoport, Sandra M. McLachlan

×

Figure 1

Options: View larger image (or click on image) Download as PowerPoint
Schematic representation of the TSHR with its large (397−amino acid resi...
Schematic representation of the TSHR with its large (397−amino acid residue without signal peptide) ectodomain, seven membrane-spanning segments, and short cytoplasmic tail. TSHR intramolecular cleavage into A and B subunits is associated with the loss of a C peptide region that corresponds approximately to a 50−amino acid “insertion” in the TSHR absent in the noncleaving LH and FSH receptors. The C peptide region is not removed intact. Following cleavage at upstream Site 1, the C peptide is rapidly degraded downstream to the Site 2 region. Evidence suggests that N-terminal degradation of the B subunit continues thereafter, leading to loss of the Cys residues tethering the A subunit and to shedding of the latter. The Cys-rich N-terminus of the A subunit is an important component of thyroid-stimulating autoantibodies and is likely to contain two disulfide bonds (hypothetically shown by dotted lines) contributing to a conformationally important portion of the molecule.

Copyright © 2025 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)

Sign up for email alerts