ArticleMolecular neurobiology2016
SMAD Transcription Factor, Sma-9, Attunes TGF-β Signaling Cascade Towards Modulating Amyloid Beta Aggregation and Associated Outcome in Transgenic C. elegans.
Article in Molecular neurobiology, 2016. 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, 17 citations in OpenAlex.
- TGF-β pathways in aging and immunity: lessons fromFrontiers in genetics · 2023Review
- Deconstructing Alzheimer's Disease: How to Bridge the Gap between Experimental Models and the Human Pathology?International journal of molecular sciences · 2021Review
- Resolvin E1-ChemR23 Axis Regulates the Hepatic Metabolic and Inflammatory Transcriptional Landscape in Obesity at the Whole Genome and Exon Level.Frontiers in nutrition · 2021Article
- Functional Characterization of Novel Circular RNA Molecule, circzip-2 and Its Synthesizing Gene zip-2 in C. elegans Model of Parkinson's Disease.Molecular neurobiology · 2018Article
- The Aβ Containing Brain Extracts Having Different Effects in Alzheimer's Disease TransgenicFrontiers in aging neuroscience · 2018Article
- Modulation of Alpha-synuclein Expression and Associated Effects by MicroRNA Let-7 in TransgenicFrontiers in molecular neuroscience · 2017Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The considerable roles of transcription factors, and the associated signaling molecules that activate them, are well deciphered in the context of various biological processes. One of the important transcription factors, the transforming growth factor-β (TGF-β) pathway, has a profound role in neuronal cell survival-a process that gets awry in multiple conditions which include various neurological ailments. Alzheimer's disease (AD) is one such condition wherein toxic buildup of misfolded proteins occurs, cellular signaling gets disrupted, and neuronal cell death ensues. We endeavored to study whether the transcriptional cofactors, associated with the TGF-β pathway, have a role to play in modulating the disease outcome. Employing transgenic C. elegans model, we studied β-amyloid aggregation, acetylcholine levels, and associated endpoints and figured that SMAD transcriptional cofactor, Sma-9, modulates the outcome associated with AD. Our studies conclude that Sma-9, a subset of the TGF-β-mediated signaling pathway, can be a potential target in neurodegenerative AD as it can influence neuronal, and organismal, survival and play crucial role in limiting adverse effects of AD.
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