Julie Crawford
Mark van Doren Professor of Humanities
Also affiliated: Crow Canyon Archaeological Center (2006); Target (United States) (2022–2025); United States Fish and Wildlife Service (2017); University of Alaska Fairbanks (2001); University of Phoenix (2021); Phoenix (United States) (2021); Institute for Musculoskeletal Health (2025); Winthrop Rockefeller Foundation (2018); Rocky Mountain Research Station (2001); Rocky Mountain Research (United States) (2001); Grand Canyon National Park (2006); Royal College of Psychiatrists (1965); Columbia University (2015–2024)
Faculty Researcher
Research Areas
Biomedical Subjects
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Biography and Research Information
OverviewAI-generated summary
Julie Crawford, Mark van Doren Professor of Humanities at the University of Arkansas for Medical Sciences, investigates the molecular mechanisms underlying bone metabolism and skeletal health. Her research program focuses on the role of autophagy, a cellular process involving the degradation of damaged components, in bone cells. Crawford's work has explored the impact of specific autophagy regulators, such as Tfeb, on bone mass and strength. She has published studies examining the consequences of autophagy loss in osteoblast lineage cells and its effects on age-related bone loss in mice. Her research also involves utilizing and evaluating genetic engineering tools, including CRISPR interference, for cell type-specific gene manipulation. Crawford has an h-index of 12, with 55 total publications and 758 total citations. She collaborates with researchers at the University of Arkansas for Medical Sciences, including Melda Onal, James A. Hendrixson, A. Gordon James, and Dominique J. Laster.
Metrics
- h-index: 12
- Publications: 55
- Citations: 790
Selected Publications
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Elevation of master autophagy regulator Tfeb in osteoblast lineage cells increases bone mass and strength (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)
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Loss of chaperone-mediated autophagy is associated with low vertebral cancellous bone mass (2022)
Collaboration Network
Top Collaborators
- Loss of chaperone-mediated autophagy is associated with low vertebral cancellous bone mass
- 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
- Loss of chaperone-mediated autophagy is associated with low vertebral cancellous bone mass
- 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
- Loss of chaperone-mediated autophagy is associated with low vertebral cancellous bone mass
- 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
- Loss of chaperone-mediated autophagy is associated with low vertebral cancellous bone mass
- 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
- 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
- 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
- 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
- Loss of chaperone-mediated autophagy is associated with low vertebral cancellous bone mass
- Loss of chaperone-mediated autophagy is associated with low vertebral cancellous bone mass
- Loss of chaperone-mediated autophagy is associated with low vertebral cancellous bone mass
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