Evidence map›Paper›PMID 21986207›Full record

ReviewThe Journal of physiology2011

Thyroid iodide efflux: a team effort?

Peying Fong

Abstract readReview
In one paragraph

Review in The Journal of physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

28 citing papers in PubMed.

  1. Review
  2. Review
  3. Substrate for Thyroid Hormone Synthesis: Biochemistry, Evolution, and Physiology.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. Myoinositol in Autoimmune Thyroiditis.Frontiers in endocrinology · 2022
    Review
  8. Cryo-EM: A new dawn in thyroid biology.Molecular and cellular endocrinology · 2021
    Review
  9. Article
  10. Review
  11. Review
  12. The role of thyroglobulin in thyroid hormonogenesis.Nature reviews. Endocrinology · 2019
    Review
  13. Article
  14. Review
  15. Article
  16. Iodide Binding in Sodium-Coupled Cotransporters.Journal of chemical information and modeling · 2017
    Article
  17. Article
  18. Iodide excess regulates its own efflux: a possible involvement of pendrin.American journal of physiology. Cell physiology · 2016
    Article
  19. Review
  20. TAS2R bitter taste receptors regulate thyroid function.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author.

Peying FongDepartment of Anatomy and Physiology, Kansas State University College of Veterinary Medicine, Manhattan, KS 66506, USA. pfong@vet.k-state.edu

Funding

TRANSEPITHELIAL ION TRANSPORT &ITS REGULATIONP20RR017686 · NCRR · KANSAS STATE UNIVERSITY · PI MELGAREJO GARCIA, LUIS TONATIUH · 2002 to 2011
$21.8M
NCRR NIH HHS P20 RR017686NCRR NIH HHS P20-RR017686
6 · The paper itself

Abstract

The thyroid hormones thyroxine (T(4)) and triiodothyronine (T(3)) play key roles in regulating development, growth and metabolism in pre- and postnatal life. Iodide (I(-)) is an essential component of the thyroid hormones and is accumulated avidly by the thyroid gland. The rarity of elemental iodine and I(-) in the environment challenges the thyroid to orchestrate a remarkable series of transport processes that ultimately ensure sufficient levels for hormone synthesis. In addition to actively extracting circulating I(-), thyroid follicular epithelial cells must also translocate I(-) into a central intrafollicular compartment, where thyroglobulin is iodinated to form the protein precursor to T(4) and T(3). In the last decade, several bodies of evidence render questionable the notion that I(-) exits thyrocytes solely via the Cl(-)/I(-) exchanger Pendrin (SLC26A4), therefore necessitating reconsideration of several other candidate I(-) conduits: the Cl(-)/H(+) antiporter, CLC-5, the cystic fibrosis transmembrane conductance regulator (CFTR) and the sodium monocarboxylic acid transporter (SMCT1).

Indexed as

AnimalsChloride ChannelsGoiterHumansIodidesMembrane Transport ProteinsThyroid GlandThyroid HormonesChloride ChannelsCLC5 protein, mouseIodidesMembrane Transport ProteinsThyroid Hormones

Identifiers

PMID21986207
PMCPMC3286676

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.