Evidence map›Paper›PMID 20664532›Full record

ReviewNature reviews. Endocrinology2010

The growth hormone receptor: mechanism of activation and clinical implications.

Andrew J Brooks, Michael J Waters

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Endocrinology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 154 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
154citing papers in PubMed, 3 pooled it
11.3field-weighted citation impact, top 1% 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

154 citing papers in PubMed, 3 syntheses or guidelines pooled it, 362 citations in OpenAlex.

  1. Pooled it
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  7. Correlation between umbilical cord concentration of the growth hormone-IGF axis and small for gestational age: A single-center retrospective, observational study.International journal of gynaecology and obstetrics: the official organ of the International Federation of Gynaecology and Obstetrics · 2026
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  17. Prolactin: structure, receptors, and functions.Reviews in endocrine & metabolic disorders · 2024
    Review
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  19. Review
  20. Review

94 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Andrew J BrooksThe University of Queensland, Institute for Molecular Bioscience, St Lucia, Qld 4072, Australia. a.brooks@uq.edu.au
Michael J Waters
University of Queensland · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Growth hormone is widely used clinically to promote growth and anabolism and for other purposes. Its actions are mediated via the growth hormone receptor, both directly by tyrosine kinase activation and indirectly by induction of insulin-like growth factor 1 (IGF-1). Insensitivity to growth hormone (Laron syndrome) can result from mutations in the growth hormone receptor and can be treated with IGF-1. This treatment is, however, not fully effective owing to the loss of the direct actions of growth hormone and altered availability of exogenous IGF-1. Excessive activation of the growth hormone receptor by circulating growth hormone results in gigantism and acromegaly, whereas cell transformation and cancer can occur in response to autocrine activation of the receptor. Advances in understanding the mechanism of receptor activation have led to a model in which the growth hormone receptor exists as a constitutive dimer. Binding of the hormone realigns the subunits by rotation and closer apposition, resulting in juxtaposition of the catalytic domains of the associated tyrosine-protein kinase JAK2 below the cell membrane. This change results in activation of JAK2 by transphosphorylation, then phosphorylation of receptor tyrosines in the cytoplasmic domain, which enables binding of adaptor proteins, as well as direct phosphorylation of target proteins. This model is discussed in the light of salient information from closely related class 1 cytokine receptors, such as the erythropoietin, prolactin and thrombopoietin receptors.

Indexed as

AnimalsHormone AntagonistsHuman Growth HormoneHumansJanus Kinase 2Models, BiologicalModels, MolecularMutationPhosphorylationReceptors, SomatotropinHormone AntagonistsHuman Growth HormoneJanus Kinase 2Receptors, Somatotropin

Identifiers

PMID20664532
OpenAlexW2015846334

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.