ArticleFrontiers in cellular neuroscience2018
RCAN1 Knockdown Reverts Defects in the Number of Calcium-Induced Exocytotic Events in a Cellular Model of Down Syndrome.
Article in Frontiers in cellular neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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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2 citing papers in PubMed, 6 citations in OpenAlex.
- Gain-of-Function Dynamin-2 Mutations Linked to Centronuclear Myopathy Impair CaInternational journal of molecular sciences · 2022Article
- Down syndrome and Alzheimer's disease: common molecular traits beyond the amyloid precursor protein.Aging · 2020Review
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8 authors at 4 institutions in 2 countries.
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Abstract
In humans, Down Syndrome (DS) is a condition caused by partial or full trisomy of chromosome 21. Genes present in the DS critical region can result in excess gene dosage, which at least partially can account for DS phenotype. Although regulator of calcineurin 1 (RCAN1) belongs to this region and its ectopic overexpression in neurons impairs transmitter release, synaptic plasticity, learning and memory, the relative contribution of RCAN1 in a context of DS has yet to be clarified. In the present work, we utilized an
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