P.A.L. Wight
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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)
Research Areas
Biomedical Subjects
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Biography and Research Information
OverviewAI-generated summary
P.A.L. Wight's research has focused on the molecular mechanisms controlling gene expression, particularly in the context of myelin development and neurological disorders. A significant portion of this work involved the use of transgenic mouse models to study the function and regulation of the myelin proteolipid protein (PLP1) gene. This research was supported by a $321,999 grant from the NIH/National Institute of Neurological Disorders and Stroke, for which Wight served as Principal Investigator. The project aimed to elucidate the mechanisms controlling human and mouse PLP1 gene expression.
Wight's publications also include investigations into animal physiology and disease, with studies on the Harderian gland of chickens, mast cells in domestic fowl, and the effects of zinc oxide on chicks and laying hens. Early work explored X chromosome-linked muscular dystrophy (mdx) in mice. Collaborations include shared publications with Pankaj Patyal, Daniel Fil, and Gretchen Holtgrefe, all from the University of Arkansas for Medical Sciences.
With an h-index of 24 and over 114 publications accumulating more than 3,500 citations, Wight is recognized as a highly cited researcher. The researcher maintains an active lab website and has been recently active, with publications extending into 2026.
Metrics
- h-index: 24
- Publications: 114
- Citations: 3,562
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 PLP1 (2018)
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Effects of Intron 1 Sequences on Human PLP1 Expression: Implications for PLP1 -Related Disorders (2017)
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Control of Human PLP1 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
- Dual Luminescence-Based Reporter Gene Assay for Luciferase andβ-Galactosidase
- The first intron of the myelin proteolipid protein gene confers cell type-specific expression by a transcriptional repression mechanism in non-expressing cell types
- Expression of myelin genes: Comparative analysis of Oli‐neu and N20.1 oligodendroglial cell lines
- Characterization of an intronic enhancer that regulates myelin proteolipid protein (Plp) gene expression in oligodendrocytes
- Proteomic analysis of nuclear factors binding to an intronic enhancer in the myelin proteolipid protein gene
Showing 5 of 12 shared publications
- Xq22 deletions and correlation with distinct neurological disease traits in females: Further evidence for a contiguous gene syndrome
- A Transgenic Mouse Model to Selectively Identify α3 Na,K-ATPase Expressing Cells in the Nervous System
- The wmN1 enhancer region in intron 1 is required for expression of human PLP1
- 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
- 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
Showing 5 of 7 shared publications
- A Transgenic Mouse Model to Selectively Identify α3 Na,K-ATPase Expressing Cells in the Nervous System
- The wmN1 enhancer region in intron 1 is required for expression of human PLP1
- Targeted deletion of the antisilencer/enhancer (ASE) element from intron 1 of the myelin proteolipid protein gene (Plp1) in mouse reveals that the element is dispensable for Plp1 expression in brain during development and remyelination
- Control of Human PLP1 Expression Through Transcriptional Regulatory Elements and Alternatively Spliced Exons in Intron 1
- 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
- Enhanced Gastrointestinal Expression of Cytosolic Malic Enzyme (ME1) Induces Intestinal and Liver Lipogenic Gene Expression and Intestinal Cell Proliferation in Mice
- Expression of myelin genes: Comparative analysis of Oli‐neu and N20.1 oligodendroglial cell lines
- The wmN1 enhancer region in intron 1 is required for expression of human PLP1
- Control of Human PLP1 Expression Through Transcriptional Regulatory Elements and Alternatively Spliced Exons in Intron 1
- 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
- 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
- Detection of a complex chromosomal rearrangement in a novel mouse mutant by optical genome mapping
- Characterization of an intronic enhancer that regulates myelin proteolipid protein (Plp) gene expression in oligodendrocytes
- Functional Characterization of a cis‐Acting DNA Antisilencer Region that Modulates Myelin Proteolipid Protein Gene Expression
- Potentiation of myelin proteolipid protein (Plp) gene expression is mediated through AP‐1‐like binding sites
- Repression of myelin proteolipid protein gene expression is mediated through both general and cell type‐specific negative regulatory elements in nonexpressing cells
- Myelin proteolipid protein (Plp) intron 1 DNA is required to temporally regulate Plp gene expression in the brain
- Leydig cells express the myelin proteolipid protein gene and incorporate a new alternatively spliced exon
- Repression of myelin proteolipid protein gene expression is mediated through both general and cell type‐specific negative regulatory elements in nonexpressing cells
- Expression of myelin genes: Comparative analysis of Oli‐neu and N20.1 oligodendroglial cell lines
- Leydig cells express the myelin proteolipid protein gene and incorporate a new alternatively spliced exon
- Targeted deletion of the antisilencer/enhancer (ASE) element from intron 1 of the myelin proteolipid protein gene (Plp1) in mouse reveals that the element is dispensable for Plp1 expression in brain during development and remyelination
- Characterization of an intronic enhancer that regulates myelin proteolipid protein (Plp) gene expression in oligodendrocytes
- Leydig cells express the myelin proteolipid protein gene and incorporate a new alternatively spliced exon
- Targeted deletion of the antisilencer/enhancer (ASE) element from intron 1 of the myelin proteolipid protein gene (Plp1) in mouse reveals that the element is dispensable for Plp1 expression in brain during development and remyelination
- Regulation of murine myelin proteolipid protein gene expression
- Expression of a Myelin Proteolipid Protein (Plp)-lacZ Transgene is Reduced in both the CNS and PNS of Plp jp Mice
- Characterization of an intronic enhancer that regulates myelin proteolipid protein (Plp) gene expression in oligodendrocytes
- YY1 Negatively Regulates Mouse Myelin Proteolipid Protein ( PLP1 ) Gene Expression in Oligodendroglial Cells
- Xq22 deletions and correlation with distinct neurological disease traits in females: Further evidence for a contiguous gene syndrome
- Inside Back Cover, Volume 41, Issue 1
- Xq22 deletions and correlation with distinct neurological disease traits in females: Further evidence for a contiguous gene syndrome
- Inside Back Cover, Volume 41, Issue 1
- Xq22 deletions and correlation with distinct neurological disease traits in females: Further evidence for a contiguous gene syndrome
- Inside Back Cover, Volume 41, Issue 1
- Xq22 deletions and correlation with distinct neurological disease traits in females: Further evidence for a contiguous gene syndrome
- Inside Back Cover, Volume 41, Issue 1
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