ArticleFrontiers in neuroscience2016
Mechanistic Insights into the Binding of Class IIa HDAC Inhibitors toward Spinocerebellar Ataxia Type-2: A 3D-QSAR and Pharmacophore Modeling Approach.
Article in Frontiers in neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 16 citations in OpenAlex.
- Molecular Mechanisms and Therapeutics for Spinocerebellar Ataxia Type 2.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019Review
- CombinatorialFrontiers in molecular neuroscience · 2017Article
- Recent Developments and Applications of the MMPBSA Method.Frontiers in molecular biosciences · 2017Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Spinocerebellar ataxia (SCA-2) type-2 is a rare neurological disorder among the nine polyglutamine disorders, mainly caused by polyQ (CAG) trinucleotide repeats expansion within gene coding ataxin-2 protein. The expanded trinucleotide repeats within the ataxin-2 protein sequesters transcriptional cofactors i.e., CREB-binding protein (CBP), Ataxin-2 binding protein 1 (A2BP1) leading to a state of hypo-acetylation and transcriptional repression. Histone de-acetylases inhibitors (HDACi) have been reported to restore transcriptional balance through inhibition of class IIa HDAC's, that leads to an increased acetylation and transcription as demonstrated through
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