ArticleBrain, behavior, & immunity - health2020
The SMYD1 and skNAC transcription factors contribute to neurodegenerative diseases.
Article in Brain, behavior, & immunity - health, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 9 citations in OpenAlex.
- Developmental manganese exposure, but not concurrent lead, alters social processing selectively in male mice.iScience · 2026Article
- Histone methyltransferase SMYD1: playing a crucial role in disease progression.Frontiers in molecular biosciences · 2026Review
- Epigenetic Modifiers: Exploring the Roles of Histone Methyltransferases and Demethylases in Cancer and Neurodegeneration.Biology · 2024Review
- Article
- Targeting Epigenetic Changes Mediated by Members of the SMYD Family of Lysine Methyltransferases.Molecules (Basel, Switzerland) · 2023Review
- Sex and diet-dependent gene alterations in human and rat brains with a history of nicotine exposure.Frontiers in psychiatry · 2023Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
SMYD1 and the skNAC isoform of the NAC transcription factor have both previously been characterized as transcription factors in hematopoiesis and cardiac/skeletal muscle. Here we report that comparative analysis of genes deregulated by SMYD1 or skNAC knockdown in differentiating C2C12 myoblasts identified transcripts characteristic of neurodegenerative diseases, including Alzheimer's, Parkinson's and Huntington's Diseases (AD, PD, and HD). This led us to determine whether SMYD1 and skNAC function together or independently within the brain. Based on meta-analyses and direct experimentation, we observed SMYD1 and skNAC expression within cortical striata of human brains, mouse brains and transgenic mouse models of these diseases. We observed some of these features in mouse myoblasts induced to differentiate into neurons. Finally, several defining features of Alzheimer's pathology, including the brain-specific, axon-enriched microtubule-associated protein, Tau, are deregulated upon SMYD1 loss.
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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.