ArticlePloS one2012
Wortmannin reduces insulin signaling and death in seizure-prone Pcmt1-/- mice.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Identification of significant gene expression changes in multiple perturbation experiments using knockoffs.Briefings in bioinformatics · 2023Article
- Human Protein-l-isoaspartateBiochemistry · 2022Article
- Protein Kinase C Theta Modulates PCMT1 through hnRNPL to Regulate FOXP3 Stability in Regulatory T Cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2020Article
- The mechanistic links between insulin and human organic anion transporter 4.International journal of pharmaceutics · 2019Article
- Bi-directional genetic modulation of GSK-3β exacerbates hippocampal neuropathology in experimental status epilepticus.Cell death & disease · 2018Article
- Colorectal cancer lung metastasis treatment with polymer-drug nanoparticles.Journal of controlled release : official journal of the Controlled Release Society · 2018Article
- Brain proteomics supports the role of glutamate metabolism and suggests other metabolic alterations in protein l-isoaspartyl methyltransferase (PIMT)-knockout mice.Journal of proteome research · 2013Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
L-isoaspartyl (D-aspartyl) O-methyltransferase deficient mice (Pcmt1(-/-)) accumulate isomerized aspartyl residues in intracellular proteins until their death due to seizures at approximately 45 days. Previous studies have shown that these mice have constitutively activated insulin signaling in their brains, and that these brains are 20-30% larger than those from age-matched wild-type animals. To determine whether insulin pathway activation and brain enlargement is responsible for the fatal seizures, we administered wortmannin, an inhibitor of the phosphoinositide 3-kinase that catalyzes an early step in the insulin pathway. Oral wortmannin reduced the average brain size in the Pcmt1(-/-) animals to within 6% of the wild-type DMSO administered controls, and nearly doubled the lifespan of Pcmt1(-/-) at 60% survival of the original population. Immunoblotting revealed significant decreases in phosphorylation of Akt, PDK1, and mTOR in Pcmt1(-/-) mice and Akt and PDK1 in wild-type animals upon treatment with wortmannin. These data suggest activation of the insulin pathway and its resulting brain enlargement contributes to the early death of Pcmt1-/- mice, but is not solely responsible for the early death observed in these animals.
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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.