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P.A.L. Wight's research investigates the molecular mechanisms controlling gene expression, with a particular focus on the myelin proteolipid protein 1 (PLP1) gene in both human and mouse models. This work has been supported by a $321,999 grant from the NIH/National Institute of Neurological Disorders and Stroke for the "Elucidation of Mechanisms Controlling Human and Mouse Myelin PLP1 Gene Expression." Publications examine the role of PLP1 splice variants, including those with "human-specific" exons, and identify regulatory elements, such as an intronic enhancer, that influence PLP1 expression during early postnatal brain development. The research also explores the expression of PLP1 in the enteric nervous system, specifically noting its presence as the DM20 splice variant during early postnatal development in mice.
Further research extends to the impact of ethanol on neuroinflammation, myelination, and neurodevelopment in a postnatal mouse model relevant to fetal alcohol spectrum disorders. This work contributes to understanding the consequences of prenatal substance exposure on neurological development. With an h-index of 24 and over 3,500 citations across 113 publications, Wight is recognized as a highly cited researcher. Key collaborators include Pankaj Patyal, Daniel Fil, Paul D. Drew, and Victoria M. Niedzwiedz‐Massey, all from the University of Arkansas for Medical Sciences, with whom shared publications have been co-authored.
Metrics
- h-index: 24
- Publications: 113
- Citations: 3,515
Selected Publications
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Plp1 in the enteric nervous system is preferentially expressed during early postnatal development in mouse as DM20, whose expression appears reliant on an intronic enhancer (2023)
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PLP1-lacZ transgenic mice reveal that splice variants containing “human-specific” exons are relatively minor in comparison to the archetypal transcript and that an upstream regulatory element bolsters expression during early postnatal brain development (2023)
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Ethanol modulation of hippocampal neuroinflammation, myelination, and neurodevelopment in a postnatal mouse model of fetal alcohol spectrum disorders (2021)
Federal Grants 1 $321,999 total
Elucidation of Mechanisms Controlling Human and Mouse Myelin PLP1 Gene Expression
Collaboration Network
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- Plp1 in the enteric nervous system is preferentially expressed during early postnatal development in mouse as DM20, whose expression appears reliant on an intronic enhancer
- PLP1-lacZ transgenic mice reveal that splice variants containing “human-specific” exons are relatively minor in comparison to the archetypal transcript and that an upstream regulatory element bolsters expression during early postnatal brain development
- Plp1 in the enteric nervous system is preferentially expressed during early postnatal development in mouse as DM20, whose expression appears reliant on an intronic enhancer
- PLP1-lacZ transgenic mice reveal that splice variants containing “human-specific” exons are relatively minor in comparison to the archetypal transcript and that an upstream regulatory element bolsters expression during early postnatal brain development
- Ethanol modulation of hippocampal neuroinflammation, myelination, and neurodevelopment in a postnatal mouse model of fetal alcohol spectrum disorders
- Ethanol modulation of hippocampal neuroinflammation, myelination, and neurodevelopment in a postnatal mouse model of fetal alcohol spectrum disorders
- Ethanol modulation of hippocampal neuroinflammation, myelination, and neurodevelopment in a postnatal mouse model of fetal alcohol spectrum disorders
- Ethanol modulation of hippocampal neuroinflammation, myelination, and neurodevelopment in a postnatal mouse model of fetal alcohol spectrum disorders
- Ethanol modulation of hippocampal neuroinflammation, myelination, and neurodevelopment in a postnatal mouse model of fetal alcohol spectrum disorders
- PLP1-lacZ transgenic mice reveal that splice variants containing “human-specific” exons are relatively minor in comparison to the archetypal transcript and that an upstream regulatory element bolsters expression during early postnatal brain development
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