Evidence map›Paper›PMID 19009345›Full record

ReviewHeart failure reviews2010

Physiological consequences of the TRalpha1 aporeceptor state.

Jens Mittag, Karin Wallis, Björn Vennström

Abstract readReview
PubMed Publisher
In one paragraph

Review in Heart failure reviews, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.3field-weighted citation impact, top 35% of its field
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

5 citing papers in PubMed, 19 citations in OpenAlex.

  1. Thyroid Hormone Receptor α Mutations Cause Heart Defects in Zebrafish.Thyroid : official journal of the American Thyroid Association · 2021
    Article
  2. Review
  3. Article
  4. Review
  5. 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

3 authors at 1 institution in 1 country.

Jens MittagDepartment of Cell & Molecular Biology, Karolinska Institute, von Eulers väg 3, 17177 Stockholm, Sweden. jens.mittag@ki.se
Karin Wallis
Björn Vennström
Karolinska Institutet · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Many patients have been characterized harboring a mutation in thyroid hormone receptor (TR) beta. Surprisingly none has yet been identified carrying a mutation in TRalpha1. To facilitate the identification of such patients, several animal models with a mutant TRalpha1 have been generated. While some phenotypic characteristics, such as an adult euthyroidism, are similar in the mutant mice, other aspects such as metabolism are quite variable. This review summarizes the most important consequences of a mutation in TRalpha1 in mice focusing on the TRalpha1-R384C mutation, and projects the insights from the animal models to a putative phenotype of patients with a mutated TRalpha1.

Indexed as

Disease Models, AnimalMutationAnimalsHumansMiceMice, TransgenicPhenotypeThyroid Hormone Receptors alphaThyroid Hormone Resistance SyndromeThyroid HormonesThyroid Hormone Receptors alphaThyroid Hormones

Identifiers

PMID19009345
OpenAlexW2028803932

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.