Julie A. 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); Winthrop Rockefeller Foundation (2018); Rocky Mountain Research Station (2001); Rocky Mountain Research (United States) (2001); Grand Canyon National Park (2006); Target PharmaSolutions, Inc. (United States) (2022–2025); Royal College of Psychiatrists (1965); Columbia University (2015–2024)
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Julie A. Crawford is the Mark van Doren Professor of Humanities at the University of Arkansas for Medical Sciences. Her scholarly work primarily focuses on early modern English literature and history, with a particular emphasis on women's roles in literary and political production. Crawford's research investigates how women navigated and contributed to intellectual and cultural life during this period, often examining their engagement with reading, writing, and political discourse. Her publications include "Mediatrix: Women, Politics, and Literary Production in Early Modern England" and "Marvelous Protestantism: Monstrous Births in Post-Reformation England." She has also explored specific historical figures, such as Margaret Hoby, to understand early modern women's reading practices. Crawford's research network includes several collaborators at the University of Arkansas for Medical Sciences, with whom she has co-authored multiple publications. Her academic contributions are reflected in a h-index of 13 and over 790 citations.
Metrics
- h-index: 13
- Publications: 56
- Citations: 794
Positions
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Mark van Doren Professor of Humanities publications 2015–2024Columbia University Department of English and Comparative Literature ORCID
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Mark van Doren Professor of Humanities publications 2022–2025University of Arkansas for Medical Sciences ORCID
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 Tfeb , 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
- Elevation of master autophagy regulator Tfeb 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
- CRISPR activation of Tfeb , 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 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 activation of Tfeb , 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 Tfeb , 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 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
- CRISPR activation of Tfeb , 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 Tfeb , 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 Tfeb , 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 Tfeb , 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 Tfeb , 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