ArticleCommunicative & integrative biology2009
Mouse models to investigate the function of spermine.
Article in Communicative & integrative biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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.
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
8 citing papers in PubMed, 21 citations in OpenAlex.
- Spermine synthase in Snyder-Robinson syndrome and cancer.Molecular biology reports · 2025Review
- Polyamines and Their Metabolism: From the Maintenance of Physiological Homeostasis to the Mediation of Disease.Medical sciences (Basel, Switzerland) · 2022Review
- Introduction to the Thematic Minireview Series: Sixty plus years of polyamine research.The Journal of biological chemistry · 2018Review
- Mitochondrial nicotinamide adenine dinucleotide reduced (NADH) oxidation links the tricarboxylic acid (TCA) cycle with methionine metabolism and nuclear DNA methylation.PLoS biology · 2018Article
- Functions of Polyamines in Mammals.The Journal of biological chemistry · 2016Review
- Article
- Current status of the polyamine research field.Methods in molecular biology (Clifton, N.J.) · 2011Review
- Spermine synthase.Cellular and molecular life sciences : CMLS · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Many functions have been ascribed to polyamines, but there has been no clear identification of a unique role for spermine. The Gy mouse has a deletion of part of the X chromosome that includes the SMS gene encoding spermine synthase. Tissues from male Gy mice have no spermine but increased spermidine. They have multiple abnormalities including a tendency to sudden death, small size, circling behavior and other neurological symptoms, sterility and deafness. These changes are reversed by breeding with mice expressing a spermine synthase transgene. Detailed studies of hearing in Gy mice show that the absence of spermine synthase leads to loss of the endocochlear potential. Since this potential requires the cochlear lateral wall-specific Kir4.1 channel, regulation by spermine of transport via these channels appears to be an essential function. A similar spermine-related defect in the functioning of cardiac Kir channels could account for arrhythmias leading to sudden death. The effect of the absence of spermine on glutamate receptor ion channels in the brain may account for the neurological symptoms and could contribute to the lack of fertility and normal growth but more direct effects on gene expression are also possible. Advantages and limitations of the Gy model are discussed.
Indexed as
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.