Evidence map›Paper›PMID 31703413›Full record

ArticleInternational journal of molecular sciences2019

The Pathogenic TSH β-subunit Variant C105Vfs114X Causes a Modified Signaling Profile at TSHR.

Laura Kalveram, Gunnar Kleinau, Kamila Szymańska, Patrick Scheerer, Adolfo Rivero-Müller, Annette Grüters-Kieslich, Heike Biebermann

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.5field-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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Cell and Molecular Biology of Thyroid Disorders 2.0.International journal of molecular sciences · 2021
    Article
  3. 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

7 authors at 2 institutions in 2 countries.

Laura KalveramInstitute of Experimental Pediatric Endocrinology, Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, 13353 Berlin, Germany.
Gunnar KleinauInstitute of Medical Physics and Biophysics, Group Protein X-ray Crystallography and Signal Transduction, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, 10117 Berlin, Germany.
Kamila SzymańskaDepartment of Biochemistry and Molecular Biology, Medical University of Lublin, 20-093 Lublin, Poland.
Patrick ScheererInstitute of Medical Physics and Biophysics, Group Protein X-ray Crystallography and Signal Transduction, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, 10117 Berlin, Germany.
Adolfo Rivero-MüllerDepartment of Biochemistry and Molecular Biology, Medical University of Lublin, 20-093 Lublin, Poland.
Annette Grüters-KieslichInstitute of Experimental Pediatric Endocrinology, Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, 13353 Berlin, Germany.
Heike BiebermannInstitute of Experimental Pediatric Endocrinology, Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, 13353 Berlin, Germany.
Humboldt-Universität zu Berlin · DEMedical University of Lublin · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1) Background: Central congenital hypothyroidism (CCH) is a rare endocrine disorder that can be caused by mutations in the β-subunit of thyrotropin (

Indexed as

Congenital HypothyroidismMAP Kinase Signaling SystemMutationReceptors, ThyrotropinSecond Messenger SystemsThyrotropin, beta SubunitCell Line, TumorCyclic AMPExtracellular Signal-Regulated MAP KinasesGTP-Binding Protein alpha Subunits, Gq-G11HEK293 CellsHumansProtein DomainsCyclic AMPExtracellular Signal-Regulated MAP KinasesGTP-Binding Protein alpha Subunits, Gq-G11Receptors, ThyrotropinThyrotropin, beta SubunitTSHR protein, humancentral congenital hypothyroidismG-protein coupled receptorsthyroid-stimulating hormoneTSHR

Identifiers

PMID31703413
PMCPMC6888357
OpenAlexW2987213310

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.