ArticleOncotarget2016
Sorting nexin 9 (SNX9) is not essential for development and auditory function in mice.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed, 7 citations in OpenAlex.
- Membrane composition and curvature in SNX9-mediated actin polymerization.Molecular biology of the cell · 2025Article
- Sorting Out Sorting Nexins Functions in the Nervous System in Health and Disease.Molecular neurobiology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sorting nexins are a large family of evolutionarily conserved proteins that play fundamental roles in endocytosis, endosomal sorting and signaling. As an important member of sorting nexin family, sorting nexin 9 (SNX9) has been shown to participate in coordinating actin polymerization with membrane tubulation and vesicle formation. We previously showed that SNX9 is expressed in mouse auditory hair cells and might regulate actin polymerization in those cells. To further examine the physiological role of SNX9, we generated Snx9 knockout mice using homologous recombination method. Unexpectedly, Snx9 knockout mice have normal viability and fertility, and are morphologically and behaviorally indistinguishable from control mice. Further investigation revealed that the morphology and function of auditory hair cells are not affected by Snx9 inactivation, and Snx9 knockout mice have normal hearing threshold. In conclusion, our data revealed that Snx9-deficient mice do not show defects in development as well as auditory function, suggesting that SNX9 is not essential for mice development and hearing.
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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.