Melda Onal

Federal Grant PI

Assistant Professor

University of Arkansas for Medical Sciences

faculty

Physiology & Cell Biology, College of Medicine

19 h-index 38 pubs 3,101 cited

Research Areas

Links

ORCID Lab Website UAMS TRI Profile

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OverviewAI-generated summary

Melda Onal's research focuses on the cellular and molecular mechanisms underlying bone health and aging. Her work investigates the role of autophagy, a cellular degradation process, in maintaining bone mass and strength. She has examined the impact of specific autophagy regulators, such as Tfeb, and the consequences of autophagy loss in osteoblast lineage cells.

Dr. Onal's laboratory also employs and develops novel methods for generating genetically engineered animal models, including the use of CRISPR interference as an alternative to the Cre-loxP system. This work, funded by a $162,184 grant from the NIH/National Institute of Arthritis and Musculoskeletal and Skin Diseases, aims to enhance cell type-specificity in genetic manipulations. Her research has contributed to understanding the identity of mesenchymal cell types involved in bone remodeling and has explored the effects of mitochondrial oxidative stress and autophagy on bone mechanoresponsiveness, particularly in the context of aging.

Metrics

h-index: 19
Publications: 38
Citations: 3,101

Selected Publications

TFEB-mediated autophagy stimulation as an anabolic strategy for bone: insights from TFEB activation in the osteoblast lineage (2025) DOI
The Aging Landscape by <scp>scRNAseq</scp> of Mesenchymal Lineage Cells in Mouse Bone (2025) DOI
Elevation of master autophagy regulator Tfeb in osteoblast lineage cells increases bone mass and strength (2025) DOI
Mitochondrial oxidative stress or decreased autophagy in osteoblast lineage cells is not sufficient to mimic the deleterious effects of aging on bone mechanoresponsiveness (2025) DOI
A new <i>Col1a1</i> conditional knock-in mouse model to study osteogenesis imperfecta (2024) DOI
CRISPR activation of <i>Tfeb</i> , a master regulator of autophagy and lysosomal biogenesis, in osteoblast lineage cells increases bone mass and strength (2024) DOI
Refining the identity of mesenchymal cell types associated with murine periosteal and endosteal bone (2024) DOI
Loss of chaperone‐mediated autophagy does not alter age‐related bone loss in male mice (2024) DOI
A framework for defining mesenchymal cell types associated with murine periosteal and endosteal bone (2023) DOI
CRISPR interference provides increased cell type-specificity compared to the Cre-loxP system (2023) DOI
Novel methods for the generation of genetically engineered animal models (2022) DOI
Loss of chaperone-mediated autophagy is associated with low vertebral cancellous bone mass (2022) DOI
Deletion of a putative promoter-proximal Tnfsf11 regulatory region in mice does not alter bone mass or Tnfsf11 expression in vivo (2021) DOI

Federal Grants 1 $162,184 total

NIH/National Institute of Arthritis and Musculoskeletal and Skin Diseases Contact PI Jan 2020 - Dec 2021

CRISPR inhibition as an alternate for Cre-loxP

National Institute of Arthritis and Musculoskeletal and Skin Diseases $162,184 R21

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