Edward T.H. Yeh
Chairman
faculty
Department Chairs, College of Medicine
Research Areas
Biography and Research Information
OverviewAI-generated summary
Edward T.H. Yeh leads a research group at the University of Arkansas for Medical Sciences, where he serves as Chairman of the Department Chairs in the College of Medicine. His scholarship metrics include an h-index of 87, with 276 total publications and over 28,000 citations, designating him as a highly cited researcher. Yeh's work investigates molecular mechanisms underlying various physiological and pathological processes. Recent publications from his group have focused on the role of SUMO-specific proteases (SENP2) in regulating ion channel function, neurogenesis, and adrenal cortex development. His research also explores the regulation of Toll-like receptor 4 (TLR4) signaling through specific protein interactions and phosphorylation events, with implications for conditions such as acute lung injury. Additionally, his group has examined the involvement of dipeptidylpeptidase 4 in the survival and stemness of acute myeloid leukemia stem cells, and the contribution of Kv7 channel activity in the central amygdala to sympathetic outflow in hypertension. Key collaborators include Hui-Ming Chang and J.C. Hsu, both from the University of Arkansas for Medical Sciences.
Metrics
- h-index: 87
- Publications: 276
- Citations: 28,873
Selected Publications
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PP4 modulates macrophage-neutrophil crosstalk to restrict CCL5 -driven NETosis in sepsis (2026)
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CYLD links the TRAF6/sNASP axis to TLR4 signaling in sepsis-induced acute lung injury (2025)
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Microglia‐Mediated Synaptic Dysfunction Contributes to Chemotherapy‐Related Cognitive Impairment (2025)
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Abstract 12348: Targeted Degradation of Topoisomerase 2b by Dexrazoxane for Prevention of Doxorubicin-Induced Cardiotoxicity: Dose and Time Course Study in Human (2023)
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Lactate: an intracellular metabolite regulates cell cycle progression (2023)
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Corticotropin-releasing hormone neurons in the central nucleus of amygdala are required for chronic stress-induced hypertension (2023)
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Promises and challenges of machine learning for device therapy in heart failure (2023)
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Dipeptidylpeptidase 4 promotes survival and stemness of acute myeloid leukemia stem cells (2023)
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Loss of SUMO-specific protease 2 causes isolated glucocorticoid deficiency by blocking adrenal cortex zonal transdifferentiation in mice (2022)
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Signaling pathways involved in <scp>NMDA</scp>‐induced suppression of M‐channels in corticotropin‐releasing hormone neurons in central amygdala (2022)
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Dependence of Acute Myeloid Leukemia Development on Membrane Protein Dipeptidyl Peptidase 4 (2022)
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PEP-sNASP Peptide Alleviates LPS-Induced Acute Lung Injury Through the TLR4/TRAF6 Axis (2022)
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Loss of SUMO-specific protease 2 causes isolated glucocorticoid deficiency by blocking adrenal cortex zonal transdifferentiation (2022)
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Abstract 9710: Prevention of Doxorubicin-Induced Cardiotoxicity Through Targeted Degradation of Topoisomerase 2b (2021)
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Regulation of TLR4 signaling through the TRAF6/sNASP axis by reversible phosphorylation mediated by CK2 and PP4 (2021)
Grants & Funding
- Doxorubicin-induced Cardiotoxicity: The Role of Topoisomerase 2b NIH/Nat. Heart, Lung & Blood Institute Principal Investigator
- PATHOBIOCHEMISTRY OF ACUTE PROMYELOCYTIC LEUKEMIA NIH Principal Investigator
- Doxorubicin-induced Cardiotoxicity: The Role of Topoisomerase 2b NIH/Nat. Heart, Lung & Blood Institute Principal Investigator
- Prevention of Heart Failure induced by Doxorubicin with Early Administration of Dexrazoxane NIH/Nat. Heart, Lung & Blood Institute Co-Investigator
- Doxorubicin-induced Cardiotoxicity: the Role of Topoisomerase 2b NIH Principal Investigator
- De-SUMOylation and the Hypoxic Response NIH Principal Investigator
- STUDIES OF THE SENTRIN FAMILY OF UBIQUITIN-LIKE PROTEINS NIH Principal Investigator
- PATHOBIOLOGY OF PAROXYSMAL NOCTURNAL HEMOGLOBINURIA NIH Principal Investigator
Collaboration Network
Top Collaborators
- Impaired Kv7 channel activity in the central amygdala contributes to elevated sympathetic outflow in hypertension
- Dipeptidylpeptidase 4 promotes survival and stemness of acute myeloid leukemia stem cells
- Signaling pathways involved in <scp>NMDA</scp>‐induced suppression of M‐channels in corticotropin‐releasing hormone neurons in central amygdala
- Microglia‐Mediated Synaptic Dysfunction Contributes to Chemotherapy‐Related Cognitive Impairment
- Prevention of Heart Failure Induced by Doxorubicin with Early Administration of Dexrazoxane (PHOENIX Study): dose response and time course of dexrazoxane-induced degradation of topoisomerase 2b
Showing 5 of 9 shared publications
- Data from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Methods from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Figure Legends 1-4 from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Figures 1-4 from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Figures 1-4 from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
Showing 5 of 8 shared publications
- Data from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Methods from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Figure Legends 1-4 from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Figures 1-4 from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Figures 1-4 from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
Showing 5 of 8 shared publications
- Data from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Methods from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Figure Legends 1-4 from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Figures 1-4 from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Figures 1-4 from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
Showing 5 of 8 shared publications
- Data from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Methods from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Figure Legends 1-4 from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Figures 1-4 from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Figures 1-4 from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
Showing 5 of 8 shared publications
- Data from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Methods from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Figure Legends 1-4 from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Figures 1-4 from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Figures 1-4 from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
Showing 5 of 8 shared publications
- Data from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Methods from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Figure Legends 1-4 from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Figures 1-4 from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Figures 1-4 from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
Showing 5 of 8 shared publications
- Data from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Methods from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Figure Legends 1-4 from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Figures 1-4 from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Figures 1-4 from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
Showing 5 of 8 shared publications
- Data from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Methods from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Figure Legends 1-4 from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Figures 1-4 from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Figures 1-4 from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
Showing 5 of 8 shared publications
- Data from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Methods from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Figure Legends 1-4 from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Figures 1-4 from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Figures 1-4 from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
Showing 5 of 8 shared publications
- Data from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Methods from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Figure Legends 1-4 from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Figures 1-4 from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Figures 1-4 from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
Showing 5 of 8 shared publications
- Data from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Methods from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Figure Legends 1-4 from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Figures 1-4 from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
- Supplementary Figures 1-4 from Dual Targeting of Tumor Angiogenesis and Chemotherapy by Endostatin–Cytosine Deaminase–Uracil Phosphoribosyltransferase
Showing 5 of 8 shared publications
- Loss of SUMO-specific protease 2 causes isolated glucocorticoid deficiency by blocking adrenal cortex zonal transdifferentiation in mice
- L’excès de SUMOylation altère l’homéostasie postnatale du cortex surrénalien et conduit à un déficit isolé en glucocorticoïde
- Loss of SUMO-specific protease 2 causes isolated glucocorticoid deficiency by blocking adrenal cortex zonal transdifferentiation
- Loss of SUMO-specific protease 2 causes isolated glucocorticoid deficiency by blocking adrenal cortex zonal transdifferentiation
- Loss of SUMO-specific protease 2 leads to adrenal insufficiency limited to glucocorticoids
- Loss of SUMO-specific protease 2 causes isolated glucocorticoid deficiency by blocking adrenal cortex zonal transdifferentiation in mice
- L’excès de SUMOylation altère l’homéostasie postnatale du cortex surrénalien et conduit à un déficit isolé en glucocorticoïde
- Loss of SUMO-specific protease 2 causes isolated glucocorticoid deficiency by blocking adrenal cortex zonal transdifferentiation
- Loss of SUMO-specific protease 2 causes isolated glucocorticoid deficiency by blocking adrenal cortex zonal transdifferentiation
- Loss of SUMO-specific protease 2 leads to adrenal insufficiency limited to glucocorticoids
- Loss of SUMO-specific protease 2 causes isolated glucocorticoid deficiency by blocking adrenal cortex zonal transdifferentiation in mice
- L’excès de SUMOylation altère l’homéostasie postnatale du cortex surrénalien et conduit à un déficit isolé en glucocorticoïde
- Loss of SUMO-specific protease 2 causes isolated glucocorticoid deficiency by blocking adrenal cortex zonal transdifferentiation
- Loss of SUMO-specific protease 2 causes isolated glucocorticoid deficiency by blocking adrenal cortex zonal transdifferentiation
- Loss of SUMO-specific protease 2 leads to adrenal insufficiency limited to glucocorticoids
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