Match tier
Listed
Presence
Current · Arkansas
Last published
2026
Sources
OpenAlex · ORCID
Refreshed
2026-08-20
M
Melda Onal
Federal Grant PI
Assistant Professor
Also affiliated: University of Wisconsin–Madison (2014–2019); Central Arkansas Veterans Healthcare System (2011–2016); Institute for Musculoskeletal Health (2025)
Faculty Researcher
Physiology & Cell Biology, College of Medicine
19 h-index
38 pubs
3,205 cited
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Melda Onal investigates the biological mechanisms underlying bone health and skeletal diseases, with a particular focus on the role of autophagy. Her research utilizes genetically engineered mouse models to explore how specific cellular processes, such as chaperone-mediated autophagy and the regulation of RANK Ligand, impact bone density and strength. Her work has explored the effects of deleting regulatory regions involved in RANK Ligand expression and has examined the utility of CRISPR interference as an alternative to the Cre-loxP system for generating genetically modified animal models.
Dr. Onal has received federal funding from the National Institutes of Health (NIH) for two projects. One grant, totaling $162,184 from the National Institute of Arthritis and Musculoskeletal and Skin Diseases, focuses on CRISPR inhibition as an alternative to Cre-loxP. A second grant, for $487,847 from the National Institute on Aging, supports research into the role of autophagy in skeletal diseases. Her scholarship metrics include an h-index of 19 and over 3,191 citations across 38 publications. She actively 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.
Metrics
- h-index: 19
- Publications: 38
- Citations: 3,205
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)
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Effective CRISPR interference of an endogenous gene via a single transgene in mice (2019)
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A Novel Distal Enhancer Mediates Inflammation‐, PTH‐, and Early Onset Murine Kidney Disease‐Induced Expression of the Mouse <i>Fgf23</i> Gene (2017)
Federal Grants 2 $650,031 total
NIH
Contact PI
Jun 2026 - Mar 2031
NIH
Contact PI
Jan 2020 - Dec 2021
Grants & Funding
As listed on this researcher's institutional profile. Federal awards with verified records are shown above.
- 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
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
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