M
Melda Onal
Federal Grant PI
Assistant Professor
faculty
Physiology & Cell Biology, College of Medicine
19 h-index
38 pubs
3,170 cited
Research Areas
Links
Biography and Research Information
OverviewAI-generated summary
Melda Onal's research program investigates the biological mechanisms underlying bone health and development, with a particular focus on the role of cellular processes like autophagy and the regulation of osteoblast and osteoclast activity. Her work utilizes genetically engineered mouse models to study the in vivo consequences of specific genetic alterations on bone mass, density, and strength.
Onal has received federal funding from the NIH/National Institute of Arthritis and Musculoskeletal and Skin Diseases for her project "CRISPR inhibition as an alternate for Cre-loxP," totaling $162,184. This grant supports her investigation into novel methods for generating genetically engineered animal models, exploring the specificity and efficacy of CRISPR interference compared to traditional Cre-loxP systems.
Her publications address topics such as the identity of mesenchymal cell types in bone, the impact of chaperone-mediated autophagy loss on bone mass, and the effects of altering autophagy regulators like Tfeb in osteoblast lineage cells. She also examines the role of mitochondrial oxidative stress and decreased autophagy in age-related bone changes. Onal collaborates with researchers at the University of Arkansas for Medical Sciences, including Jinhu Xiong, Charles A. O’Brien, Maria Almeida, and A. Gordon James, with whom she has co-authored multiple publications. Her scholarship metrics include an h-index of 19, 38 total publications, and over 3,100 citations.
Metrics
- h-index: 19
- Publications: 38
- Citations: 3,170
Selected Publications
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TFEB-mediated autophagy stimulation as an anabolic strategy for bone: insights from TFEB activation in the osteoblast lineage (2025)
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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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A new <i>Col1a1</i> conditional knock-in mouse model to study osteogenesis imperfecta (2024)
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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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Refining the identity of mesenchymal cell types associated with murine periosteal and endosteal bone (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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A framework for defining mesenchymal cell types associated with murine periosteal and endosteal bone (2023)
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CRISPR interference provides increased cell type-specificity compared to the Cre-loxP system (2023)
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Novel methods for the generation of genetically engineered animal models (2022)
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Loss of chaperone-mediated autophagy is associated with low vertebral cancellous bone mass (2022)
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Deletion of a putative promoter-proximal Tnfsf11 regulatory region in mice does not alter bone mass or Tnfsf11 expression in vivo (2021)
Federal Grants 1 $162,184 total
NIH/National Institute of Arthritis and Musculoskeletal and Skin Diseases
Contact PI
Jan 2020 - Dec 2021
Grants & Funding
- CRISPR inhibition as an alternate for Cre-loxP NIH/Nat. Inst. of Arthritis & Musculoskeletal & Skin Diseases Principal Investigator
- Center for Musculoskeletal Disease Research (CMDR) NIH/Nat. Inst. of General Medical Sciences Principal Investigator
- DEAP Awards - P. Drew - UAMS VCRI - FY26 Role of Oligodendrocyte-Lineage Cells in FASD UAMS Division of Research and Innovation Principal Investigator
- Center for Musculoskeletal Disease Research (CMDR) NIH/Nat. Inst. of General Medical Sciences Principal Investigator
Collaboration Network
Top Collaborators
Jinhu Xiong
University of Arkansas for Medical Sciences
6 shared publications
In database
- Refining the identity of mesenchymal cell types associated with murine periosteal and endosteal bone
- Deletion of a putative promoter-proximal Tnfsf11 regulatory region in mice does not alter bone mass or Tnfsf11 expression in vivo
- 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
Showing 5 of 6 shared publications
Charles A. O’Brien
University of Arkansas for Medical Sciences
6 shared publications
In database
- Refining the identity of mesenchymal cell types associated with murine periosteal and endosteal bone
- Deletion of a putative promoter-proximal Tnfsf11 regulatory region in mice does not alter bone mass or Tnfsf11 expression in vivo
- 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
- A framework for defining mesenchymal cell types associated with murine periosteal and endosteal bone
Showing 5 of 6 shared publications
Maria Almeida
University of Arkansas for Medical Sciences
6 shared publications
In database
- Refining the identity of mesenchymal cell types associated with murine periosteal and endosteal 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
- The Aging Landscape by <scp>scRNAseq</scp> of Mesenchymal Lineage Cells in Mouse Bone
- A framework for defining mesenchymal cell types associated with murine periosteal and endosteal bone
Showing 5 of 6 shared publications
Julie Crawford
Institute for Musculoskeletal Health
5 shared publications
In database
- 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
Intawat Nookaew
University of Arkansas for Medical Sciences
5 shared publications
In database
- Refining the identity of mesenchymal cell types associated with murine periosteal and endosteal bone
- 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
- A framework for defining mesenchymal cell types associated with murine periosteal and endosteal bone
A. Gordon James
University of Arkansas for Medical Sciences
5 shared publications
In database
- 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
- CRISPR activation of <i>Tfeb</i> , a master regulator of autophagy and lysosomal biogenesis, in osteoblast lineage cells increases bone mass and strength
Qiang Fu
University of Arkansas for Medical Sciences
4 shared publications
In database
- Refining the identity of mesenchymal cell types associated with murine periosteal and endosteal bone
- Loss of chaperone-mediated autophagy is associated with low vertebral cancellous bone mass
- Mitochondrial oxidative stress or decreased autophagy in osteoblast lineage cells is not sufficient to mimic the deleterious effects of aging on bone mechanoresponsiveness
- A framework for defining mesenchymal cell types associated with murine periosteal and endosteal bone
James A. Hendrixson
University of Arkansas for Medical Sciences
4 shared publications
In database
- 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
Jeff D. Thostenson
University of Arkansas for Medical Sciences
3 shared publications
In database
- Deletion of a putative promoter-proximal Tnfsf11 regulatory region in mice does not alter bone mass or Tnfsf11 expression in vivo
- CRISPR interference provides increased cell type-specificity compared to the Cre-loxP system
- A new <i>Col1a1</i> conditional knock-in mouse model to study osteogenesis imperfecta
Nisreen Akel
University of Arkansas for Medical Sciences
3 shared publications
In database
- 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
Stuart B. Berryhill
University of Arkansas for Medical Sciences
3 shared publications
In database
- 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
Dominique J. Laster
University of Arkansas for Medical Sciences
3 shared publications
In database
- 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
Visanu Wanchai
Institute for Musculoskeletal Health
3 shared publications
In database
- Refining the identity of mesenchymal cell types associated with murine periosteal and endosteal bone
- Elevation of master autophagy regulator Tfeb in osteoblast lineage cells increases bone mass and strength
- A framework for defining mesenchymal cell types associated with murine periosteal and endosteal bone
Ha‐Neui Kim
University of Arkansas for Medical Sciences
3 shared publications
In database
- Refining the identity of mesenchymal cell types associated with murine periosteal and endosteal bone
- The Aging Landscape by <scp>scRNAseq</scp> of Mesenchymal Lineage Cells in Mouse Bone
- A framework for defining mesenchymal cell types associated with murine periosteal and endosteal bone
Ilham Kadhim
University of Arkansas for Medical Sciences
3 shared publications
In database
- 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
Similar Researchers
Based on overlapping research topics
A. Gordon James
University of Arkansas for Medical Sciences
Bone Metabolism and Diseases
CRISPR and Genetic Engineering
Jacob Laster
University of Arkansas for Medical Sciences
Bone Metabolism and Diseases
CRISPR and Genetic Engineering
James A. Hendrixson
University of Arkansas for Medical Sciences
Bone Metabolism and Diseases
CRISPR and Genetic Engineering
Julie Crawford
University of Arkansas for Medical Sciences
Bone Metabolism and Diseases
CRISPR and Genetic Engineering
Dominique J. Laster
University of Arkansas for Medical Sciences
Bone Metabolism and Diseases
Animal Models in Research
Nisreen Akel
University of Arkansas for Medical Sciences
Bone Metabolism and Diseases
CRISPR and Genetic Engineering