ArticleNeuroreport2019
Neuronal deletion of phosphatase and tensin homolog results in cerebellar motor learning dysfunction and alterations in intracellular signaling.
Article in Neuroreport, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 13 citations in OpenAlex.
- PTEN variant and genetic backgrounds combine to modify cerebellar neuronal differentiation in autism spectrum disorder.Human molecular genetics · 2026Article
- Altered Primary Somatosensory Neuron Development in a Pten Heterozygous Model for Autism Spectrum Disorder.Autism research : official journal of the International Society for Autism Research · 2025Article
- Altered Expression of MeCP2 and PTEN Genes in the Molecular Basis of Specific Learning Disorder.Journal of molecular neuroscience : MN · 2025Article
- Hippocampal Upregulation of Complement Component C3 in Response to Lipopolysaccharide Stimuli in a Model of Fragile-X Syndrome.Current issues in molecular biology · 2023Article
- Rapamycin improves social and stereotypic behavior abnormalities induced by pre-mitotic neuronal subset specific Pten deletion.Genes, brain, and behavior · 2023Article
- The Cerebellar Involvement in Autism Spectrum Disorders: From the Social Brain to Mouse Models.International journal of molecular sciences · 2022Review
- A vitamin D enriched diet attenuates sex-specific behavioral deficits, increases the lifespan, but does not rescue bone abnormalities in a mouse model of cortical dysplasia.Epilepsy & behavior : E&B · 2021Article
- A Temporal Activity of CA1 Neurons Underlying Short-Term Memory for Social Recognition Altered in PTEN Mouse Models of Autism Spectrum Disorder.Frontiers in cellular neuroscience · 2021Article
- Connecting Genotype with Behavioral Phenotype in Mouse Models of Autism Associated withCold Spring Harbor perspectives in medicine · 2020Review
- Impact of mTOR hyperactive neurons on the morphology and physiology of adjacent neurons: Do PTEN KO cells make bad neighbors?Experimental neurology · 2019Article
- Early Clinical Predictors of Autism Spectrum Disorder in Infants with Tuberous Sclerosis Complex: Results from the EPISTOP Study.Journal of clinical medicine · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
The purpose of this investigation was to examine cerebellar levels of several molecular signaling pathways, including PI3K/AKT/mammalian target of rapamycin (mTOR) signaling and markers of neuronal migration, following loss of the phosphatase and tensin homolog (PTEN) gene in a subset of neurons, as well as the accompanying behavior phenotype in mice. Motor coordination and learning were measured by the sticker removal task and the accelerating rotarod. Western blots were conducted on cerebellar tissue samples. We demonstrated that neuron subset-specific deletion of PTEN in mice led to deficits in motor coordination. These changes were accompanied by alterations in many different proteins, including the PI3K/AKT/mTOR signaling pathway, FMRP, glutamate receptors, and neuronal migration markers. These data firstly support a role for hyperactivation of mTOR in the cerebellum following the loss of PTEN, accompanied by behavioral deficits. Moreover, the results of the current study support a broader role for PTEN signaling in early neuronal migration and organization of the cerebellum, and point to a putative role for PTEN in many neuropsychiatric conditions.
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.