ArticleJournal of biomedical science2019
Promyelocytic leukemia zinc finger is involved in the formation of deep layer cortical neurons.
Article in Journal of biomedical science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Region and Cell-Selective Induction of Zbtb16/Plzf by Multiple Stressors in the Adult Murine Hypothalamus.The European journal of neuroscience · 2026Article
- Integrated analysis of molecular atlases unveils modules driving developmental cell subtype specification in the human cortex.Nature neuroscience · 2025Article
- Zbtb16 mediates a switch between Fgf signalling regimes in the developing hindbrain.Development (Cambridge, England) · 2023Article
- Functional modular networks identify the pivotal genes associated with morphine addiction and potential drug therapies.BMC anesthesiology · 2023Article
- Sex-specific transcriptomic and epitranscriptomic signatures of PTSD-like fear acquisition.iScience · 2022Article
- Prenatal Environment and Neurodevelopmental Disorders.Frontiers in endocrinology · 2022Review
- Zbtb16 regulates social cognitive behaviors and neocortical development.Translational psychiatry · 2021Article
- Zinc Finger Transcription Factor Zbtb16 Coordinates the Response to Energy Deficit in the Mouse Hypothalamus.Frontiers in neuroscience · 2020Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
backgroundPromyelocytic leukemia zinc finger (Plzf), a transcriptional regulator involved in a lot of important biological processes during development, has been implied to maintain neural stem cells and inhibit their differentiation into neurons. However, the effects of Plzf on brain structures and functions are still not clarified.
resultsWe showed that Plzf expression was detected as early as embryonic day (E) 9.5 in Pax6
conclusionsPlzf is expressed at early stages of brain development and involved in the formation of deep layer cortical neurons. Loss of Plzf results in dysregulation of Mash1, microcephaly with reduced numbers of early-born neurons, and impairment of recognition memory.
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