ArticleNeuromolecular medicine2007
Brain tumor formation in tuberous sclerosis depends on Erk activation.
Article in Neuromolecular medicine, 2007. 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, 21 citations in OpenAlex.
- Hyperactivation of mTORC1 in a double hit mutant zebrafish model of tuberous sclerosis complex causes increased seizure susceptibility and neurodevelopmental abnormalities.Frontiers in cell and developmental biology · 2022Article
- Tuberous sclerosis complex-associated CNS abnormalities depend on hyperactivation of mTORC1 and Akt.The Journal of clinical investigation · 2018Article
- Article
- Activation of extracellular regulated kinase and mechanistic target of rapamycin pathway in focal cortical dysplasia.Neuropathology : official journal of the Japanese Society of Neuropathology · 2016Article
- Subependymal giant cell astrocytoma: current concepts, management, and future directions.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2014Review
- Novel proteins regulated by mTOR in subependymal giant cell astrocytomas of patients with tuberous sclerosis complex and new therapeutic implications.The American journal of pathology · 2010Article
- The pathogenesis and imaging of the tuberous sclerosis complex.Pediatric radiology · 2008Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tuberous sclerosis (TS) is an autosomal dominant disease associated with the formation of usually benign tumors or hamartomas. The disease is connected with upregulation of mammalian target of rapamycin, central regulator of protein translation, which is usually regarded to be activated by Akt kinase. Here, we show for the first time that in all four brain lesions and one angiomyolipoma from TS patients both extracellular signal-regulated kinase (Erk) and p90 ribosomal S6 kinase 1 activation as well as Erk-dependent phosphorylation of p70 ribosomal S6 kinase 1 are markedly elevated whereas Akt, participating in the classical pathway of mammalian target of rapamycin activation is not always activated. Erk activation is also present in TS-derived cell lines. Importantly, Erk inhibition leads to the decrease of proliferation potential of such lines. These results show that Erk is specifically implicated in the pathogenesis of hamartomas.
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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.