ArticlePloS one2014
Disruption of G-protein γ5 subtype causes embryonic lethality in mice.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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.
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
10 citing papers in PubMed, 14 citations in OpenAlex.
- Circular RNA pappalysin-1 enhances glycolysis via microRNA-656-3p targeting G-protein subunit gamma-5 to promote colon cancer progression.Clinics (Sao Paulo, Brazil) · 2025Article
- Subtype-dependent regulation of Gβγ signalling.Cellular signalling · 2021Review
- GNG5 is an unfavourable independent prognostic indicator of gliomas.Journal of cellular and molecular medicine · 2020Article
- GNG5 Controls the Number of Apical and Basal Progenitors and Alters Neuronal Migration During Cortical Development.Frontiers in molecular biosciences · 2020Article
- Mouse Skull Mean Shape and Shape Robustness Rely on Different Genetic Architectures and Different Loci.Frontiers in genetics · 2019Article
- Genetic Analysis of Rare Human Variants of Regulators of G Protein Signaling Proteins and Their Role in Human Physiology and Disease.Pharmacological reviews · 2018Review
- G-protein-coupled receptor signaling and neural tube closure defects.Birth defects research · 2017Review
- Recurrent chimeric fusion RNAs in non-cancer tissues and cells.Nucleic acids research · 2016Article
- Gα(i/o)-coupled receptor-mediated sensitization of adenylyl cyclase: 40 years later.European journal of pharmacology · 2015Review
- Ablation of the GNB3 gene in mice does not affect body weight, metabolism or blood pressure, but causes bradycardia.Cellular signalling · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Heterotrimeric G-proteins modulate many processes essential for embryonic development including cellular proliferation, migration, differentiation, and survival. Although most research has focused on identifying the roles of the various αsubtypes, there is growing recognition that similarly divergent βγ dimers also regulate these processes. In this paper, we show that targeted disruption of the mouse Gng5 gene encoding the γ5 subtype produces embryonic lethality associated with severe head and heart defects. Collectively, these results add to a growing body of data that identify critical roles for the γ subunits in directing the assembly of functionally distinct G-αβγ trimers that are responsible for regulating diverse biological processes. Specifically, the finding that loss of the G-γ5 subtype is associated with a reduced number of cardiac precursor cells not only provides a causal basis for the mouse phenotype but also raises the possibility that G-βγ5 dependent signaling contributes to the pathogenesis of human congenital heart problems.
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Identifiers
What 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.