ArticleCell death & disease2024
Heterozygous knockout of Synaptotagmin13 phenocopies ALS features and TP53 activation in human motor neurons.
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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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Who cites it
4 citing papers in PubMed.
- Protein arginine methyltransferases coordinate mitochondrial stress adaptation and neuromuscular function.Experimental & molecular medicine · 2026Review
- Allele specific expression in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Loss of Y chromosome and its implications in male amyotrophic lateral sclerosis: insights from the UK Biobank.BMC medicine · 2025Article
- Intrinsic neuronal resilience as a tool for therapeutic discovery.Brain : a journal of neurology · 2025Article
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Authors and funding
15 authors.
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Abstract
Spinal motor neurons (MNs) represent a highly vulnerable cellular population, which is affected in fatal neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS) and spinal muscular atrophy (SMA). In this study, we show that the heterozygous loss of SYT13 is sufficient to trigger a neurodegenerative phenotype resembling those observed in ALS and SMA. SYT13
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