ArticleFrontiers in cellular neuroscience2022
Conditional deletion of MAD2B in forebrain neurons enhances hippocampus-dependent learning and memory in mice.
Article in Frontiers in cellular neuroscience, 2022. 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, 4 citations in OpenAlex.
- NCOA3 as a Key Regulator in Diabetic Cognitive Dysfunction.Molecular neurobiology · 2026Article
- Targeting MAD2B as a strategy for ischemic stroke therapy.Journal of advanced research · 2025Article
- Tirzepatide ameliorates spatial learning and memory impairment through modulation of aberrant insulin resistance and inflammation response in diabetic rats.Frontiers in pharmacology · 2023Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
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Abstract
Mitotic arrest deficient 2-like protein 2 (MAD2B) is not only a DNA damage repair agent but also a cell cycle regulator that is widely expressed in the hippocampus and the cerebral cortex. However, the functions of MAD2B in hippocampal and cerebral cortical neurons are poorly understood. In this study, we crossed
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Registered trials
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