Edward T.H. Yeh
Chairman
Also affiliated: Scripps Research Institute (1997); Brigham and Women's Hospital (2015); Mount Sinai Hospital (2005–2009); Houston Methodist (2014); RELX Group (Netherlands) (2008); Arthritis Foundation (1990); St. Luke's Episcopal Hospital (2000–2014); Texas Medical Center (1997); The University of Texas MD Anderson Cancer Center (2001–2023); Harvard University (1986–2015); University of Miami (1999); The University of Texas System (2000–2004); Duke University (1994); Baylor College of Medicine (1995–2016); China Medical University (2011); University of Toronto (2000–2006); University of Campania "Luigi Vanvitelli" (2007–2013); Lunenfeld-Tanenbaum Research Institute (2005–2009); University of Arkansas Medical Center (2025); University of Missouri Hospital (2016–2018); University of Missouri Health System (2017); Hospital for Sick Children (2000–2001); Lemuel Shattuck Hospital (1988); Canada Research Chairs (2001); Anderson University - Indiana (2011); Massachusetts General Hospital (1990–2015); Newborn Screening Ontario (2015); Mount Sinai Medical Center (1999); St. Luke's Episcopal Hospital (1998–2015); Precision for Medicine (United States) (2017); Temple University Hospital (2013); China Medical University Hospital (2011); Winthrop Rockefeller Foundation (2021–2026); Cardiovascular Research Center (1997); National Taiwan University Hospital (2013); Brown Foundation (1997–2007); Ospedale Monaldi (2011); Toronto Zoo (1995); Institute of Molecular Medicine (1997–2000); Cellular Research (United States) (2023); JR Technology (United Kingdom) (2006); The University of Texas Health Science Center (1997–2005); Arkansas Department of Agriculture (2025); Dana-Farber Brigham Cancer Center (2013); University of Houston (2004–2012); Taipei Medical University (2013); University of Naples Federico II (2007–2013); University of Missouri (2016–2022); University of Pennsylvania (2013); University of Guelph (2008–2009); Temple University (2013); Texas A&M University (2004); The University of Texas Health Science Center at Houston (1993–2011)
Faculty Researcher
Department Chairs, College of Medicine
Research Areas
Biomedical Subjects
Biography and Research Information
OverviewAI-generated summary
Edward T.H. Yeh is a researcher with a significant publication record, indicated by an h-index of 87 and over 28,000 citations. His work has been recognized with a "highly cited researcher" designation. Yeh leads a research group and has a substantial publication history, with 276 total publications. His research interests span several areas, including the molecular mechanisms regulating ion channels and cellular processes like sumoylation and phosphorylation.
Recent publications demonstrate his focus on the role of specific proteins and signaling pathways in physiological and pathological conditions. This includes investigating the regulation of Kv7 potassium channels, which are implicated in hypertension and neurological function. He also studies the involvement of SUMO-specific proteases, such as SENP2, in processes like neurogenesis, adrenal cortex function, and potassium channel regulation. Additionally, his work examines the interplay of signaling pathways, such as TLR4 and TRAF6, in inflammatory responses and disease states like acute lung injury and acute myeloid leukemia.
Yeh collaborates with researchers primarily at the University of Arkansas for Medical Sciences, including Hui‐Ming Chang, with whom he shares 12 co-authored publications. His work involves both animal models, particularly mice, and human health-related topics, as reflected in the MeSH terms associated with his research.
Metrics
- h-index: 88
- Publications: 278
- Citations: 29,126
Selected Publications
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PP4 modulates macrophage-neutrophil crosstalk to restrict CCL5 -driven NETosis in sepsis (2026)
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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 (2025)
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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)
Grants & Funding
As listed on this researcher's institutional profile.
- Doxorubicin-induced Cardiotoxicity: The Role of Topoisomerase 2b NIH/Nat. Heart, Lung & Blood Institute Principal Investigator
- PATHOBIOCHEMISTRY OF ACUTE PROMYELOCYTIC LEUKEMIA NIH 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
- Abstract 12348: Targeted Degradation of Topoisomerase 2b by Dexrazoxane for Prevention of Doxorubicin-Induced Cardiotoxicity: Dose and Time Course Study in Human
Showing 5 of 7 shared publications
- Impaired Kv7 channel activity in the central amygdala contributes to elevated sympathetic outflow in hypertension
- Corticotropin-releasing hormone neurons in the central nucleus of amygdala are required for chronic stress-induced hypertension
- 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
- Corticotropin-releasing hormone neurons in the central nucleus of amygdala are required for chronic stress-induced hypertension
- Dipeptidylpeptidase 4 promotes survival and stemness of acute myeloid leukemia stem cells
- Microglia‐Mediated Synaptic Dysfunction Contributes to Chemotherapy‐Related Cognitive Impairment
- Dependence of Acute Myeloid Leukemia Development on Membrane Protein Dipeptidyl Peptidase 4
- Impaired Kv7 channel activity in the central amygdala contributes to elevated sympathetic outflow in hypertension
- Corticotropin-releasing hormone neurons in the central nucleus of amygdala are required for chronic stress-induced hypertension
- Signaling pathways involved in <scp>NMDA</scp>‐induced suppression of M‐channels in corticotropin‐releasing hormone neurons in central amygdala
- 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 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 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 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 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
- Corticotropin-releasing hormone neurons in the central nucleus of amygdala are required for chronic stress-induced hypertension
- Regulation of TLR4 signaling through the TRAF6/sNASP axis by reversible phosphorylation mediated by CK2 and PP4
- PP4 modulates macrophage-neutrophil crosstalk to restrict CCL5 -driven NETosis in sepsis
- Impaired Kv7 channel activity in the central amygdala contributes to elevated sympathetic outflow in hypertension
- Corticotropin-releasing hormone neurons in the central nucleus of amygdala are required for chronic stress-induced hypertension
- Impaired Kv7 channel activity in the central amygdala contributes to elevated sympathetic outflow in hypertension
- Corticotropin-releasing hormone neurons in the central nucleus of amygdala are required for chronic stress-induced hypertension
- Impaired Kv7 channel activity in the central amygdala contributes to elevated sympathetic outflow in hypertension
- Corticotropin-releasing hormone neurons in the central nucleus of amygdala are required for chronic stress-induced hypertension
- Impaired Kv7 channel activity in the central amygdala contributes to elevated sympathetic outflow in hypertension
- Corticotropin-releasing hormone neurons in the central nucleus of amygdala are required for chronic stress-induced hypertension
- SENP2-PLCβ4 signaling regulates neurogenesis through the maintenance of calcium homeostasis
- The SUMO-specific protease SENP2 plays an essential role in the regulation of Kv7.2 and Kv7.3 potassium channels
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