Evidence map›Paper›PMID 42290866›Full record

ArticleFrontiers in endocrinology2026

GH-resistant (Laron) mice: gene therapy with a liver-specific GH receptor causes unbalanced upregulation of female-biased and growth-related genes.

Joshua K Tay, Kian Chuan Sia, Siti Humairah Mohd Rodhi, Shu Uin Gan, Zhen Ying Fu, Maxim Pyatkov, John J Kopchick, Michael J Waters, David J Waxman, Kok-Onn Lee

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In one paragraph

Article in Frontiers in endocrinology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

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.

2 · The registry

The trial behind it

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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

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0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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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

10 authors.

Joshua K Tay *Department of Otolaryngology-Head & Neck Surgery, National University of Singapore, Singapore, Singapore.
Kian Chuan Sia *Department of Surgery, National University of Singapore, Singapore, Singapore.
Siti Humairah Mohd RodhiDepartment of Surgery, National University of Singapore, Singapore, Singapore.
Shu Uin GanDepartment of Surgery, National University of Singapore, Singapore, Singapore.
Zhen Ying FuDepartment of Surgery, National University of Singapore, Singapore, Singapore.
Maxim PyatkovDepartment of Biology and Bioinformatics Program, Boston University, Boston, MA, United States.
John J KopchickInstitute of Molecular Medicine and Aging, Ohio University, Athens, OH, United States.
Michael J WatersInstitute for Molecular Bioscience, The University of Queensland, Brisbane, QLD, Australia.
David J WaxmanDepartment of Biology and Bioinformatics Program, Boston University, Boston, MA, United States.
Kok-Onn LeeDepartment of Medicine, National University of Singapore, Singapore, Singapore.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Growth hormone (GH) receptor (GHR) mutations give rise to GH-resistance (Laron syndrome). We previously treated GH-resistant Ghr-/- mice (Laron mice) with adeno-associated virus (AAV) delivering mouse (m)Ghr controlled by a constitutively active liver-specific promoter (HLP). A single injection of AAV-HLP-mGHR resulted in a significant but limited increase in body length and weight, consistent with studies of IGF-1 treatment in humans and mice. Here, we performed RNA-seq on male and female mouse livers comprising the following groups: GHR+/+ (wild-type), GHR-/- (Laron), AAV-HLP-mGHR-treated GHR-/- (treatment group), and AAV-HLP-Luc (Luciferase)-treated GHR-/- (control group). Only four genes showed significant differential expression in GHR -/- mouse liver following Luciferase vector treatment, indicating minimal effect of the AAV-HLP vector. AAV-HLP-mGHR stimulated significant expression changes in 448 genes compared to AAV-HLP-Luc control, substantially fewer than the 2781 genes whose expression was altered in GHR-/- compared to GHR+/+. AAV-HLP-mGHR treatment induced the GH-responsive IGF signaling genes

Indexed as

Genetic TherapyGrowth HormoneLaron SyndromeLiverReceptors, SomatotropinAnimalsDependovirusFemaleGenetic VectorsInsulin-Like Growth Factor IMaleMiceMice, KnockoutUp-RegulationGrowth HormoneInsulin-Like Growth Factor IReceptors, Somatotropinadeno-associated virus (AAV)differential gene expressiongrowth hormone receptor (GHR)IGF-1 signalingLaron syndromeoncogenesRNA-Seqsex-biased genes

Identifiers

PMID42290866
PMCPMC13253266

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