ArticleCommunicative & integrative biology2013
SIMPLE: A new regulator of endosomal trafficking and signaling in health and disease.
Article in Communicative & integrative biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 10 citations in OpenAlex.
- New evidence for secondary axonal degeneration in demyelinating neuropathies.Neuroscience letters · 2021Review
- The endosomal trafficking regulator LITAF controls the cardiac Nav1.5 channel via the ubiquitin ligase NEDD4-2.The Journal of biological chemistry · 2020Article
- LITAF (Lipopolysaccharide-Induced Tumor Necrosis Factor) Regulates Cardiac L-Type Calcium Channels by Modulating NEDD (Neural Precursor Cell Expressed Developmentally Downregulated Protein) 4-1 Ubiquitin Ligase.Circulation. Genomic and precision medicine · 2019Article
- GILP family: a stress-responsive group of plant proteins containing a LITAF motif.Functional & integrative genomics · 2018Article
- Dysregulation of ErbB Receptor Trafficking and Signaling in Demyelinating Charcot-Marie-Tooth Disease.Molecular neurobiology · 2017Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
SIMPLE, also known as LITAF, EET1 and PIG7, was originally identified based on its transcriptional upregulation by estrogen, p53, lipopolysaccharide or a microbial cell-wall component. Missense mutations in SIMPLE cause Charcot-Marie-Tooth disease (CMT), and altered SIMPLE expression is associated with cancer, obesity and inflammatory bowel diseases. Despite increasing evidence linking SIMPLE to human diseases, the biological function of SIMPLE is unknown and the pathogenic mechanism of SIMPLE mutations remains elusive. Our recent study reveals that SIMPLE is a functional partner of the endosomal sorting complex required for transport (ESCRT) machinery in the regulation of endosome-to-lysosome trafficking and intracellular signaling. Our results indicate that CMT-linked SIMPLE mutants are loss-of-function mutants which act dominantly to impair endosomal trafficking and signaling attenuation. We propose that endosomal trafficking and signaling dysregulation is a key pathogenic mechanism in CMT and other diseases that involve SIMPLE dysfunction.
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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.