A. Gordon James
Graduate Student
Also affiliated: European Bioinformatics Institute (2013); Unilever (United Kingdom) (2004–2023); University of Strathclyde (1994); The Ohio State University Wexner Medical Center (1960); The Ohio State University (1960); Wellcome Trust (2013)
Graduate Student Researcher
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
A. Gordon James's research investigates the molecular mechanisms underlying bone aging and strength, with a particular focus on the role of autophagy.
His work has explored the impact of the master autophagy regulator Tfeb in osteoblast lineage cells, demonstrating that its activation can increase bone mass and strength. James has also examined the effects of mitochondrial oxidative stress and decreased autophagy on bone mechanoresponsiveness in the context of aging, finding that these factors alone do not fully replicate the age-related decline in bone properties. His research further includes studies on the contribution of chaperone-mediated autophagy to age-related bone loss in male mice.
Additionally, James has contributed to research on axillary odor variation and the application of CRISPR technology for enhanced cell type specificity in genetic studies. He collaborates with researchers at the University of Arkansas for Medical Sciences, including Melda Onal and Maria Almeida.
Metrics
- h-index: 11
- Publications: 21
- Citations: 685
Selected Publications
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The Aging Landscape by <scp>scRNAseq</scp> of Mesenchymal Lineage Cells in Mouse Bone (2025)
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Elevation of master autophagy regulator Tfeb in osteoblast lineage cells increases bone mass and strength (2025)
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Mitochondrial oxidative stress or decreased autophagy in osteoblast lineage cells is not sufficient to mimic the deleterious effects of aging on bone mechanoresponsiveness (2025)
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CRISPR activation of <i>Tfeb</i> , a master regulator of autophagy and lysosomal biogenesis, in osteoblast lineage cells increases bone mass and strength (2024)
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Loss of chaperone‐mediated autophagy does not alter age‐related bone loss in male mice (2024)
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CRISPR interference provides increased cell type-specificity compared to the Cre-loxP system (2023)
Collaboration Network
Top Collaborators
- CRISPR interference provides increased cell type-specificity compared to the Cre-loxP system
- Elevation of master autophagy regulator Tfeb in osteoblast lineage cells increases bone mass and strength
- Mitochondrial oxidative stress or decreased autophagy in osteoblast lineage cells is not sufficient to mimic the deleterious effects of aging on bone mechanoresponsiveness
- Loss of chaperone‐mediated autophagy does not alter age‐related bone loss in male mice
- The Aging Landscape by <scp>scRNAseq</scp> of Mesenchymal Lineage Cells in Mouse Bone
Showing 5 of 6 shared publications
- CRISPR interference provides increased cell type-specificity compared to the Cre-loxP system
- Elevation of master autophagy regulator Tfeb in osteoblast lineage cells increases bone mass and strength
- Loss of chaperone‐mediated autophagy does not alter age‐related bone loss in male mice
- CRISPR activation of <i>Tfeb</i> , a master regulator of autophagy and lysosomal biogenesis, in osteoblast lineage cells increases bone mass and strength
- CRISPR interference provides increased cell type-specificity compared to the Cre-loxP system
- Elevation of master autophagy regulator Tfeb in osteoblast lineage cells increases bone mass and strength
- Loss of chaperone‐mediated autophagy does not alter age‐related bone loss in male mice
- CRISPR activation of <i>Tfeb</i> , a master regulator of autophagy and lysosomal biogenesis, in osteoblast lineage cells increases bone mass and strength
- Elevation of master autophagy regulator Tfeb in osteoblast lineage cells increases bone mass and strength
- Mitochondrial oxidative stress or decreased autophagy in osteoblast lineage cells is not sufficient to mimic the deleterious effects of aging on bone mechanoresponsiveness
- The Aging Landscape by <scp>scRNAseq</scp> of Mesenchymal Lineage Cells in Mouse Bone
- CRISPR activation of <i>Tfeb</i> , a master regulator of autophagy and lysosomal biogenesis, in osteoblast lineage cells increases bone mass and strength
- CRISPR interference provides increased cell type-specificity compared to the Cre-loxP system
- Elevation of master autophagy regulator Tfeb in osteoblast lineage cells increases bone mass and strength
- The Aging Landscape by <scp>scRNAseq</scp> of Mesenchymal Lineage Cells in Mouse Bone
- Elevation of master autophagy regulator Tfeb in osteoblast lineage cells increases bone mass and strength
- Mitochondrial oxidative stress or decreased autophagy in osteoblast lineage cells is not sufficient to mimic the deleterious effects of aging on bone mechanoresponsiveness
- CRISPR activation of <i>Tfeb</i> , a master regulator of autophagy and lysosomal biogenesis, in osteoblast lineage cells increases bone mass and strength
- Elevation of master autophagy regulator Tfeb in osteoblast lineage cells increases bone mass and strength
- Mitochondrial oxidative stress or decreased autophagy in osteoblast lineage cells is not sufficient to mimic the deleterious effects of aging on bone mechanoresponsiveness
- The Aging Landscape by <scp>scRNAseq</scp> of Mesenchymal Lineage Cells in Mouse Bone
- CRISPR interference provides increased cell type-specificity compared to the Cre-loxP system
- Loss of chaperone‐mediated autophagy does not alter age‐related bone loss in male mice
- CRISPR interference provides increased cell type-specificity compared to the Cre-loxP system
- Loss of chaperone‐mediated autophagy does not alter age‐related bone loss in male mice
- CRISPR interference provides increased cell type-specificity compared to the Cre-loxP system
- Loss of chaperone‐mediated autophagy does not alter age‐related bone loss in male mice
- CRISPR interference provides increased cell type-specificity compared to the Cre-loxP system
- The Aging Landscape by <scp>scRNAseq</scp> of Mesenchymal Lineage Cells in Mouse Bone
- The Aging Landscape by <scp>scRNAseq</scp> of Mesenchymal Lineage Cells in Mouse Bone
- CRISPR activation of <i>Tfeb</i> , a master regulator of autophagy and lysosomal biogenesis, in osteoblast lineage cells increases bone mass and strength
- Elevation of master autophagy regulator Tfeb in osteoblast lineage cells increases bone mass and strength
- CRISPR activation of <i>Tfeb</i> , a master regulator of autophagy and lysosomal biogenesis, in osteoblast lineage cells increases bone mass and strength
- Elevation of master autophagy regulator Tfeb in osteoblast lineage cells increases bone mass and strength
- CRISPR activation of <i>Tfeb</i> , a master regulator of autophagy and lysosomal biogenesis, in osteoblast lineage cells increases bone mass and strength
- Elevation of master autophagy regulator Tfeb in osteoblast lineage cells increases bone mass and strength
- CRISPR activation of <i>Tfeb</i> , a master regulator of autophagy and lysosomal biogenesis, in osteoblast lineage cells increases bone mass and strength
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