ArticleTransactions of the American Clinical and Climatological Association2013
Cracking the code for thyroid hormone signaling.
Article in Transactions of the American Clinical and Climatological Association, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
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.
Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- Thyroid hormones and metabolic flexibility: tissue-specific control of energy homeostasis.Frontiers in physiology · 2026Review
- Serine Administration Improves Selenium Status, Oxidative Stress, and Mitochondrial Function in Longissimus Dorsi Muscle of Piglets with Intrauterine Growth Retardation.Biological trace element research · 2023Article
- Use of levothyroxine in the management of hypothyroidism: A historical perspective.Frontiers in endocrinology · 2022Review
- Managing symptoms in hypothyroid patients on adequate levothyroxine: a narrative review.Endocrine connections · 2020Review
- Effects of Dietary Selenium Deficiency or Excess on Selenoprotein Gene Expression in the Spleen Tissue of Pigs.Animals : an open access journal from MDPI · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Cells are not passive bystanders in the process of hormonal signaling and instead can actively customize hormonal action. While diffusing from the plasma membrane to the nucleus, thyroid hormone is modified via the action of thioredoxin fold-containing selenoenzymes known as deiodinases. Whereas the type II deiodinase (D2) converts the prohormone thyroxine (T4) to the biologically active T3, the type III deiodinase (D3) converts it to reverse T3, an inactive metabolite. D3 also inactivates T3 to T2, terminating thyroid hormone action. Therefore, D2 provides cells with the ability to produce extra amounts of T3 and thus enhances thyroid hormone signaling. In contrast, expression of D3 results in the opposite action. In addition, the D2 protein is unique in that it can be switched off and on via an ubiquitin-regulated mechanism, triggered by catalysis of T4. Induction of D2 enhances local thyroid hormone signaling and energy expenditure during activation of brown adipose tissue by cold exposure or high fat diet. On the other hand, induction of D3 in myocardium and brain during ischemia and hypoxia decreases energy expenditure as part of a homeostatic mechanism to slow down cell metabolism in the face of limited O2 supply.
Indexed as
Identifiers
23874007PMC3715916W1504114926What OpenQuestion holds
Registered trials
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.