Richard C. Kurten
Researcher
Also affiliated: Arkansas Children's Hospital (2004–2024); Baylor College of Medicine (1987–1997); Johannes Gutenberg University Mainz (2000); Medical College of Wisconsin (2010); University of Arkansas Medical Center (2004–2022); University of California San Diego (1995–2024); Central Arkansas Veterans Healthcare System (2002); Baylor School (1987); Klinik und Poliklinik für Strahlentherapie und Radioonkologie (2008); La Jolla Bioengineering Institute (2024); Applied BioPhysics (United States) (2015); Arkansas Children's Nutrition Center (2019–2023); Institute of Molecular Biology and Biophysics (2005–2010); Arkansas Department of Agriculture (2008); Heinrich Heine University Düsseldorf (2008); Rogers (United States) (2023); Michigan State University (1987); Texas A&M University (1984–1987); Stanford University (1988)
Faculty Researcher
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Richard C. Kurten's research focuses on understanding the molecular and cellular mechanisms underlying various physiological and pathological processes, with a particular emphasis on respiratory and gastrointestinal diseases. His work has investigated the role of specific proteins and cytokines in conditions such as eosinophilic esophagitis and asthma. For instance, he has studied how mucins are packaged within secretory granules and how the cytokine TNFSF14/LIGHT influences inflammation and remodeling in murine models of eosinophilic esophagitis. His investigations also extend to the function of ORMDL3 in airway smooth muscle, impacting hypertrophy, hyperplasia, and contractility.
Further contributions from Kurten's lab include the development and utilization of research platforms to study infectious diseases. He has been involved in establishing an *ex vivo* human precision-cut lung slice platform to gain insights into SARS-CoV-2 pathogenesis and to evaluate antiviral drug efficacy. His research has also explored the effects of viral infections, such as rhinovirus, on human airways and smooth muscle function. Additionally, his work has examined the impact of neurotransmitter system-targeting drugs on the growth of pathogens like *Coxiella burnetii* in human cells.
Kurten holds a notable scholarly record, with an h-index of 32, reflecting 123 total publications that have garnered 3,640 citations. He is recognized as a highly cited researcher. His collaborative network includes Joshua L. Kennedy, Priyangi A. Malaviarachchi, Duah Alkam, and Srijon K. Banerjee, all affiliated with the University of Arkansas for Medical Sciences, with whom he has co-authored multiple publications.
Metrics
- h-index: 32
- Publications: 123
- Citations: 3,672
Selected Publications
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An <i>ex vivo</i> human precision-cut lung slice platform provides insight into SARS-CoV-2 pathogenesis and antiviral drug efficacy (2024)
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Mechanotransduction-induced interplay between phospholamban and yes-activated protein induces smooth muscle cell hypertrophy (2024)
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Rhinovirus C15 Attenuates Relaxation and cAMP Production in Human Airways and Smooth Muscle (2023)
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An <i>ex vivo</i> human precision-cut lung slice platform provides insight into SARS-CoV-2 pathogenesis and antiviral drug efficacy (2023)
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A Deficiency in the Cytokine TNFSF14/LIGHT Limits Inflammation and Remodeling in Murine Eosinophilic Esophagitis (2022)
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Mucin Expression in Human Precision-Cut Lung Slices (2022)
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Mucins MUC5AC and MUC5B Are Variably Packaged in the Same and in Separate Secretory Granules (2022)
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Reduced AIBP expression in bronchial epithelial cells of asthmatic patients: Potential therapeutic target (2022)
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Esophageal Fibroblasts are the Players in the Interferon Response in Eosinophilic Esophagitis (2022)
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LIGHT controls distinct homeostatic and inflammatory gene expression profiles in esophageal fibroblasts via differential HVEM and LTβR-mediated mechanisms (2021)
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Neurotransmitter System-Targeting Drugs Antagonize Growth of the Q Fever Agent, Coxiella burnetii, in Human Cells (2021)
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ORMDL3 expression in ASM regulates hypertrophy, hyperplasia via TPM1 and TPM4, and contractility (2021)
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Integrative Proteomics and Phosphoproteomics of Asthmatic Airways following RV Infection (2021)
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A unique esophageal extracellular matrix proteome alters normal fibroblast function in severe eosinophilic esophagitis (2021)
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The Yersinia pestis GTPase BipA Promotes Pathogenesis of Primary Pneumonic Plague (2020)
Collaboration Network
Top Collaborators
- A unique esophageal extracellular matrix proteome alters normal fibroblast function in severe eosinophilic esophagitis
- LIGHT controls distinct homeostatic and inflammatory gene expression profiles in esophageal fibroblasts via differential HVEM and LTβR-mediated mechanisms
- A Deficiency in the Cytokine TNFSF14/LIGHT Limits Inflammation and Remodeling in Murine Eosinophilic Esophagitis
- Mechanotransduction-induced interplay between phospholamban and yes-activated protein induces smooth muscle cell hypertrophy
- Esophageal Fibroblasts are the Players in the Interferon Response in Eosinophilic Esophagitis
- A unique esophageal extracellular matrix proteome alters normal fibroblast function in severe eosinophilic esophagitis
- LIGHT controls distinct homeostatic and inflammatory gene expression profiles in esophageal fibroblasts via differential HVEM and LTβR-mediated mechanisms
- Mechanotransduction-induced interplay between phospholamban and yes-activated protein induces smooth muscle cell hypertrophy
- Esophageal Fibroblasts are the Players in the Interferon Response in Eosinophilic Esophagitis
- A unique esophageal extracellular matrix proteome alters normal fibroblast function in severe eosinophilic esophagitis
- LIGHT controls distinct homeostatic and inflammatory gene expression profiles in esophageal fibroblasts via differential HVEM and LTβR-mediated mechanisms
- Mechanotransduction-induced interplay between phospholamban and yes-activated protein induces smooth muscle cell hypertrophy
- Esophageal Fibroblasts are the Players in the Interferon Response in Eosinophilic Esophagitis
- A unique esophageal extracellular matrix proteome alters normal fibroblast function in severe eosinophilic esophagitis
- LIGHT controls distinct homeostatic and inflammatory gene expression profiles in esophageal fibroblasts via differential HVEM and LTβR-mediated mechanisms
- Mechanotransduction-induced interplay between phospholamban and yes-activated protein induces smooth muscle cell hypertrophy
- An <i>ex vivo</i> human precision-cut lung slice platform provides insight into SARS-CoV-2 pathogenesis and antiviral drug efficacy
- An <i>ex vivo</i> human precision-cut lung slice platform provides insight into SARS-CoV-2 pathogenesis and antiviral drug efficacy
- Integrative Proteomics and Phosphoproteomics of Asthmatic Airways following RV Infection
- An <i>ex vivo</i> human precision-cut lung slice platform provides insight into SARS-CoV-2 pathogenesis and antiviral drug efficacy
- An <i>ex vivo</i> human precision-cut lung slice platform provides insight into SARS-CoV-2 pathogenesis and antiviral drug efficacy
- Integrative Proteomics and Phosphoproteomics of Asthmatic Airways following RV Infection
- LIGHT controls distinct homeostatic and inflammatory gene expression profiles in esophageal fibroblasts via differential HVEM and LTβR-mediated mechanisms
- A Deficiency in the Cytokine TNFSF14/LIGHT Limits Inflammation and Remodeling in Murine Eosinophilic Esophagitis
- Esophageal Fibroblasts are the Players in the Interferon Response in Eosinophilic Esophagitis
- LIGHT controls distinct homeostatic and inflammatory gene expression profiles in esophageal fibroblasts via differential HVEM and LTβR-mediated mechanisms
- A Deficiency in the Cytokine TNFSF14/LIGHT Limits Inflammation and Remodeling in Murine Eosinophilic Esophagitis
- Mechanotransduction-induced interplay between phospholamban and yes-activated protein induces smooth muscle cell hypertrophy
- A unique esophageal extracellular matrix proteome alters normal fibroblast function in severe eosinophilic esophagitis
- Mechanotransduction-induced interplay between phospholamban and yes-activated protein induces smooth muscle cell hypertrophy
- ORMDL3 expression in ASM regulates hypertrophy, hyperplasia via TPM1 and TPM4, and contractility
- Reduced AIBP expression in bronchial epithelial cells of asthmatic patients: Potential therapeutic target
- ORMDL3 expression in ASM regulates hypertrophy, hyperplasia via TPM1 and TPM4, and contractility
- Reduced AIBP expression in bronchial epithelial cells of asthmatic patients: Potential therapeutic target
- ORMDL3 expression in ASM regulates hypertrophy, hyperplasia via TPM1 and TPM4, and contractility
- Reduced AIBP expression in bronchial epithelial cells of asthmatic patients: Potential therapeutic target
- LIGHT controls distinct homeostatic and inflammatory gene expression profiles in esophageal fibroblasts via differential HVEM and LTβR-mediated mechanisms
- Esophageal Fibroblasts are the Players in the Interferon Response in Eosinophilic Esophagitis
- LIGHT controls distinct homeostatic and inflammatory gene expression profiles in esophageal fibroblasts via differential HVEM and LTβR-mediated mechanisms
- A Deficiency in the Cytokine TNFSF14/LIGHT Limits Inflammation and Remodeling in Murine Eosinophilic Esophagitis
- LIGHT controls distinct homeostatic and inflammatory gene expression profiles in esophageal fibroblasts via differential HVEM and LTβR-mediated mechanisms
- A Deficiency in the Cytokine TNFSF14/LIGHT Limits Inflammation and Remodeling in Murine Eosinophilic Esophagitis
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