RAIDD mutations underlie the pathogenesis of thin lissencephaly (TLIS)
PLoS ONE, ISSN: 1932-6203, Vol: 13, Issue: 10, Page: e0205042
2018
- 6Citations
- 12Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations6
- Citation Indexes6
- Captures12
- Readers12
- 12
Article Description
Abnormal regulation of caspase-2-mediated neuronal cell death causes neurodegenerative diseases and defective brain development. PIDDosome is caspase-2 activating complex composed of PIDD, RAIDD, and caspase-2. Recent whole-exome sequencing study showed that the RAIDD mutations in the death domain (DD), including G128R, F164C, R170C, and R170H mutations, cause thin lissencephaly (TLIS) by reducing caspase-2- mediated neuronal apoptosis. Given that the molecular structure of the RAIDD DD:PIDD DD complex is available, in this study, we analyzed the molecular mechanisms underlying TLIS caused by the RAIDD TLIS variants by performing mutagenesis and biochemical assays.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85054450034&origin=inward; http://dx.doi.org/10.1371/journal.pone.0205042; http://www.ncbi.nlm.nih.gov/pubmed/30281648; https://dx.plos.org/10.1371/journal.pone.0205042; https://dx.doi.org/10.1371/journal.pone.0205042; https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0205042
Public Library of Science (PLoS)
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