P.A.L. Wight
Researcher
Also affiliated: University of California, Riverside (1987–1988); The King's College (1961–1980); Scotland's Rural College (1974); University of Arkansas Medical Center (1998); Biotechnology and Biological Sciences Research Council (1965–1987); UCLA Medical Center (1991–1994); Consiglio per la ricerca in agricoltura e l’analisi dell’economia agraria (1961–2010); Moredun Research Institute (1960–1961); King's College Hospital (1969–1975); Poultry CRC (1965–1980)
Faculty Researcher
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
P.A.L. Wight's research focuses on the molecular mechanisms regulating gene expression in the nervous system, particularly concerning myelin production. Recent publications investigate the role of the proteolipid protein 1 (PLP1) gene, examining its splice variants and regulatory elements in both mouse and human systems. One study specifically explores the expression of PLP1 in the enteric nervous system during early postnatal development, identifying a potential intronic enhancer that influences its activity.
Further work by Wight has examined the impact of ethanol exposure on neurodevelopment and myelination in a mouse model of fetal alcohol spectrum disorders, assessing changes in hippocampal neuroinflammation. This research contributes to understanding the cellular and molecular consequences of prenatal substance exposure.
With an h-index of 24 and over 3,500 citations, Wight has a publication record of 114 articles. The researcher has received $321,999 in federal funding from the NIH/National Institute of Neurological Disorders and Stroke for work on elucidating mechanisms controlling human and mouse myelin PLP1 gene expression. Collaborations include shared publications with Pankaj Patyal and Daniel Fil at the University of Arkansas for Medical Sciences.
Metrics
- h-index: 24
- Publications: 114
- Citations: 3,540
Selected Publications
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Detection of a complex chromosomal rearrangement in a novel mouse mutant by optical genome mapping (2026)
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Detection of a complex chromosomal rearrangement in a novel mouse mutant by optical genome mapping (2026)
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Detection of a complex chromosomal rearrangement in a novel mouse mutant by optical genome mapping (2026)
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Detection of a complex chromosomal rearrangement in a novel mouse mutant by optical genome mapping (2026)
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Detection of a complex chromosomal rearrangement in a novel mouse mutant by optical genome mapping (2026)
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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)
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Inside Back Cover, Volume 41, Issue 1 (2019)
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The wmN1 Enhancer Region of the Mouse Myelin Proteolipid Protein Gene (mPlp1) is Indispensable for Expression of an mPlp1-lacZ Transgene in Both the CNS and PNS (2019)
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Xq22 deletions and correlation with distinct neurological disease traits in females: Further evidence for a contiguous gene syndrome (2019)
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A Transgenic Mouse Model to Selectively Identify α3 Na,K-ATPase Expressing Cells in the Nervous System (2018)
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The wmN1 enhancer region in intron 1 is required for expression of human <i>PLP1</i> (2018)
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Effects of Intron 1 Sequences on Human <i>PLP1</i> Expression: Implications for <i>PLP1</i> -Related Disorders (2017)
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Control of Human <i>PLP1</i> Expression Through Transcriptional Regulatory Elements and Alternatively Spliced Exons in Intron 1 (2015)
Federal Grants 1 $321,999 total
Elucidation of Mechanisms Controlling Human and Mouse Myelin PLP1 Gene Expression
Collaboration Network
Top Collaborators
- Detection of a complex chromosomal rearrangement in a novel mouse mutant by optical genome mapping
- Detection of a complex chromosomal rearrangement in a novel mouse mutant by optical genome mapping
- Detection of a complex chromosomal rearrangement in a novel mouse mutant by optical genome mapping
- Detection of a complex chromosomal rearrangement in a novel mouse mutant by optical genome mapping
- 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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