Nükhet Aykin‐Burns Data-verified
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Associate Professor
faculty
Research Areas
Biography and Research Information
OverviewAI-generated summary
Nükhet Aykin‐Burns' research focuses on the biological mechanisms underlying bone loss, aging, and the impact of oxidative stress on cellular function. She investigates the role of mitochondria, specifically Sirtuin 3 (Sirt3), in age-related and estrogen deficiency-induced bone loss, as well as the effects of ionizing radiation and simulated galactic cosmic rays on osteoclast function and bone integrity in mice. Her work also explores how iron uptake through the transferrin receptor 1 influences bone mass by affecting osteoclast mitochondria and cytoskeleton. Aykin‐Burns has examined chemotherapy-induced oxidative stress in the ovary and its potential interventions, and the mechanisms of ferroptosis in hepatocellular carcinoma cells induced by parthenolide. She also studies the role of curcumin in mitigating acrolein-induced alveolar epithelial apoptosis through Keap1 cysteine conjugation. Aykin‐Burns leads a research group and has a significant publication record with 111 publications and over 7,281 citations, achieving an h-index of 36. She has a network of key collaborators at the University of Arkansas for Medical Sciences, including Kimberly J. Krager, Francesca V. LoBianco, Ha‐Neui Kim, and Brian Koss, with whom she has co-authored numerous publications.
Metrics
- h-index: 36
- Publications: 112
- Citations: 7,383
Selected Publications
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SIRT3–IDH2 axis is a target of dietary fructose: implication of IDH2 as a key player in dietary carcinogen toxicity in mice colon (2025)
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Sirtuin-3 promotes osteoclast maturation and bone loss by regulating mitochondrial ROS production during ionizing radiation exposure (2025)
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Enhancing Rectal Cancer Radiosensitivity and Gut Protection through Methionine Restriction (2025)
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SIRT3-IDH2 axis is a target of dietary fructose: implication of IDH2 as a key player in dietary carcinogen toxicity in mice colon (2025)
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Tocotrienols Provide Radioprotection to Multiple Organ Systems through Complementary Mechanisms of Antioxidant and Signaling Effects (2023)
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The Role of Cytochrome P450 3A4-Mediated Metabolism in Sorafenib and Lapatinib Hepatotoxicity (2023)
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466 Development of a novel tocotrienol analogue, tocoflexol, as a radiomitigator (2023)
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Abstract 2839: Methionine restriction radiosensitizes KRAS mutant rectal cancer (2023)
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Effect of Sirt3 on hippocampal MnSOD activity, mitochondrial function, physiology, and cognition in an aged murine model (2023)
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Effect of Sirt3 on Hippocampal MnSOD Activity, Mitochondrial Function, Physiology, And Cognition in an Aged Murine Model (2022)
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Effect of Sirt3 on Hippocampal MnSOD Activity, Mitochondrial Function, Physiology, and Cognition in an Aged Murine Model (2022)
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Hematopoietic cytoplasmic adaptor protein Hem1 promotes osteoclast fusion and bone resorption in mice (2022)
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Chemotherapy induced oxidative stress in the ovary: drug-dependent mechanisms and potential interventions (2022)
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Parthenolide induces rapid thiol oxidation that leads to ferroptosis in hepatocellular carcinoma cells (2022)
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Author response: Transferrin receptor 1-mediated iron uptake regulates bone mass in mice via osteoclast mitochondria and cytoskeleton (2022)
Collaboration Network
Top Collaborators
- Mitochondrial Sirt3 contributes to the bone loss caused by aging or estrogen deficiency
- Transferrin receptor 1-mediated iron uptake regulates bone mass in mice via osteoclast mitochondria and cytoskeleton
- Ionizing Radiation Activates Mitochondrial Function in Osteoclasts and Causes Bone Loss in Young Adult Male Mice
- Parthenolide induces rapid thiol oxidation that leads to ferroptosis in hepatocellular carcinoma cells
- Simulated Galactic Cosmic Rays Modify Mitochondrial Metabolism in Osteoclasts, Increase Osteoclastogenesis and Cause Trabecular Bone Loss in Mice
Showing 5 of 24 shared publications
- Mitochondrial Sirt3 contributes to the bone loss caused by aging or estrogen deficiency
- Ionizing Radiation Activates Mitochondrial Function in Osteoclasts and Causes Bone Loss in Young Adult Male Mice
- Simulated Galactic Cosmic Rays Modify Mitochondrial Metabolism in Osteoclasts, Increase Osteoclastogenesis and Cause Trabecular Bone Loss in Mice
- Mitochondrial protein deacetylation by SIRT3 in osteoclasts promotes bone resorption with aging in female mice
- Hematopoietic cytoplasmic adaptor protein Hem1 promotes osteoclast fusion and bone resorption in mice
Showing 5 of 7 shared publications
- Parthenolide induces rapid thiol oxidation that leads to ferroptosis in hepatocellular carcinoma cells
- The Role of Cytochrome P450 3A4-Mediated Metabolism in Sorafenib and Lapatinib Hepatotoxicity
- Effect of Sirt3 on hippocampal MnSOD activity, mitochondrial function, physiology, and cognition in an aged murine model
- Abstract No. 584 Parthenolide induces thiol oxidation inducing ferroptosis in human hepatocellular carcinoma cells
- Overcoming the Restricted Therapy Options and Monitoring Challenges in Metastatic Breast Cancer
Showing 5 of 7 shared publications
- Transferrin receptor 1-mediated iron uptake regulates bone mass in mice via osteoclast mitochondria and cytoskeleton
- Transferrin receptor 1-mediated iron uptake regulates bone mass in mice via osteoclast mitochondria and cytoskeleton
- Author response: Transferrin receptor 1-mediated iron uptake regulates bone mass in mice via osteoclast mitochondria and cytoskeleton
- Data from Epigenetic Control of <i>Cdkn2a.Arf</i> Protects Tumor-Infiltrating Lymphocytes from Metabolic Exhaustion
- Supplementary Materials from Epigenetic Control of <i>Cdkn2a.Arf</i> Protects Tumor-Infiltrating Lymphocytes from Metabolic Exhaustion
Showing 5 of 7 shared publications
- Mitochondrial Sirt3 contributes to the bone loss caused by aging or estrogen deficiency
- Ionizing Radiation Activates Mitochondrial Function in Osteoclasts and Causes Bone Loss in Young Adult Male Mice
- Simulated Galactic Cosmic Rays Modify Mitochondrial Metabolism in Osteoclasts, Increase Osteoclastogenesis and Cause Trabecular Bone Loss in Mice
- Mitochondrial protein deacetylation by SIRT3 in osteoclasts promotes bone resorption with aging in female mice
- Hematopoietic cytoplasmic adaptor protein Hem1 promotes osteoclast fusion and bone resorption in mice
Showing 5 of 6 shared publications
- Ionizing Radiation Activates Mitochondrial Function in Osteoclasts and Causes Bone Loss in Young Adult Male Mice
- Mitochondrial protein deacetylation by SIRT3 in osteoclasts promotes bone resorption with aging in female mice
- Data from Epigenetic Control of <i>Cdkn2a.Arf</i> Protects Tumor-Infiltrating Lymphocytes from Metabolic Exhaustion
- Supplementary Materials from Epigenetic Control of <i>Cdkn2a.Arf</i> Protects Tumor-Infiltrating Lymphocytes from Metabolic Exhaustion
- Supplementary Materials from Epigenetic Control of <i>Cdkn2a.Arf</i> Protects Tumor-Infiltrating Lymphocytes from Metabolic Exhaustion
Showing 5 of 6 shared publications
- Mitochondrial Sirt3 contributes to the bone loss caused by aging or estrogen deficiency
- Ionizing Radiation Activates Mitochondrial Function in Osteoclasts and Causes Bone Loss in Young Adult Male Mice
- Simulated Galactic Cosmic Rays Modify Mitochondrial Metabolism in Osteoclasts, Increase Osteoclastogenesis and Cause Trabecular Bone Loss in Mice
- Mitochondrial protein deacetylation by SIRT3 in osteoclasts promotes bone resorption with aging in female mice
- Hematopoietic cytoplasmic adaptor protein Hem1 promotes osteoclast fusion and bone resorption in mice
- Data from Epigenetic Control of <i>Cdkn2a.Arf</i> Protects Tumor-Infiltrating Lymphocytes from Metabolic Exhaustion
- Supplementary Materials from Epigenetic Control of <i>Cdkn2a.Arf</i> Protects Tumor-Infiltrating Lymphocytes from Metabolic Exhaustion
- Supplementary Materials from Epigenetic Control of <i>Cdkn2a.Arf</i> Protects Tumor-Infiltrating Lymphocytes from Metabolic Exhaustion
- Data from Epigenetic Control of <i>Cdkn2a.Arf</i> Protects Tumor-Infiltrating Lymphocytes from Metabolic Exhaustion
- Enhancing Rectal Cancer Radiosensitivity and Gut Protection through Methionine Restriction
- Mitochondrial Sirt3 contributes to the bone loss caused by aging or estrogen deficiency
- Mitochondrial protein deacetylation by SIRT3 in osteoclasts promotes bone resorption with aging in female mice
- Hematopoietic cytoplasmic adaptor protein Hem1 promotes osteoclast fusion and bone resorption in mice
- Hem1 promotes osteoclast fusion and bone resorption in mice
- Mitochondrial Sirt3 contributes to the bone loss caused by aging or estrogen deficiency
- Mitochondrial protein deacetylation by SIRT3 in osteoclasts promotes bone resorption with aging in female mice
- Hematopoietic cytoplasmic adaptor protein Hem1 promotes osteoclast fusion and bone resorption in mice
- Hem1 promotes osteoclast fusion and bone resorption in mice
- Parthenolide induces rapid thiol oxidation that leads to ferroptosis in hepatocellular carcinoma cells
- Chemotherapy induced oxidative stress in the ovary: drug-dependent mechanisms and potential interventions
- Simulated Galactic Cosmic Rays Modify Mitochondrial Metabolism in Osteoclasts, Increase Osteoclastogenesis and Cause Trabecular Bone Loss in Mice
- Effect of Sirt3 on hippocampal MnSOD activity, mitochondrial function, physiology, and cognition in an aged murine model
- Data from Epigenetic Control of <i>Cdkn2a.Arf</i> Protects Tumor-Infiltrating Lymphocytes from Metabolic Exhaustion
- Supplementary Materials from Epigenetic Control of <i>Cdkn2a.Arf</i> Protects Tumor-Infiltrating Lymphocytes from Metabolic Exhaustion
- Supplementary Materials from Epigenetic Control of <i>Cdkn2a.Arf</i> Protects Tumor-Infiltrating Lymphocytes from Metabolic Exhaustion
- Data from Epigenetic Control of <i>Cdkn2a.Arf</i> Protects Tumor-Infiltrating Lymphocytes from Metabolic Exhaustion
- Data from Epigenetic Control of <i>Cdkn2a.Arf</i> Protects Tumor-Infiltrating Lymphocytes from Metabolic Exhaustion
- Supplementary Materials from Epigenetic Control of <i>Cdkn2a.Arf</i> Protects Tumor-Infiltrating Lymphocytes from Metabolic Exhaustion
- Supplementary Materials from Epigenetic Control of <i>Cdkn2a.Arf</i> Protects Tumor-Infiltrating Lymphocytes from Metabolic Exhaustion
- Data from Epigenetic Control of <i>Cdkn2a.Arf</i> Protects Tumor-Infiltrating Lymphocytes from Metabolic Exhaustion
- Data from Epigenetic Control of <i>Cdkn2a.Arf</i> Protects Tumor-Infiltrating Lymphocytes from Metabolic Exhaustion
- Supplementary Materials from Epigenetic Control of <i>Cdkn2a.Arf</i> Protects Tumor-Infiltrating Lymphocytes from Metabolic Exhaustion
- Supplementary Materials from Epigenetic Control of <i>Cdkn2a.Arf</i> Protects Tumor-Infiltrating Lymphocytes from Metabolic Exhaustion
- Data from Epigenetic Control of <i>Cdkn2a.Arf</i> Protects Tumor-Infiltrating Lymphocytes from Metabolic Exhaustion
- Data from Epigenetic Control of <i>Cdkn2a.Arf</i> Protects Tumor-Infiltrating Lymphocytes from Metabolic Exhaustion
- Supplementary Materials from Epigenetic Control of <i>Cdkn2a.Arf</i> Protects Tumor-Infiltrating Lymphocytes from Metabolic Exhaustion
- Supplementary Materials from Epigenetic Control of <i>Cdkn2a.Arf</i> Protects Tumor-Infiltrating Lymphocytes from Metabolic Exhaustion
- Data from Epigenetic Control of <i>Cdkn2a.Arf</i> Protects Tumor-Infiltrating Lymphocytes from Metabolic Exhaustion
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