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Stuart Maudsley

  • Odysseus Professor
  • Vice-Chair, Department of Biomedical Research
  • University of Antwerp
  • 45h-indexImpact measure calculated using publication and citation counts. Updated daily.
  • 9055CitationsNumber of citations received by Stuart's publications. Updated daily.

Other IDs

Research interests

Drug Discovery and DesignProteomicsBioinformaticsReceptor Pharmacology

About

Professor Maudsley received his Ph.D. in 1997 in Pharmacology from the Department of Pharmacology at the University of Leeds where he studied the molecular mechanisms of tachykinin receptor activation and desensitization. With a Howard Hughes Medical Institute Fellowship, he moved to Duke University to work with Professor Robert J. Lefkowitz (2012 Nobel Laureate in Chemistry) on the connectivity of G protein-coupled receptor (GPCR) signaling to tyrosine kinase pathways. During this period Dr. Maudsley developed new theories of GPCR signaling based upon the creation of higher order multi-protein superstructures. Dr. Maudsley then accepted an Investigator position at the Medical Research Council at the University of Edinburgh in the United Kingdom. There he furthered the development of his concepts of the organization of GPCRs into discrete signaling structures for specific physiological functions. This work forms the basis of his research into the alteration of the GPCR signaling structures during healthy and pathological aging. Research Interests: For the majority of its experimental lifetime, information flow through G protein-coupled receptors (GPCRs) has been envisioned as unidirectional, i.e., changes in receptor conformation produced by extracellular agonist binding promotes the transfer of information from outside the cell inwards. Recent experimentation however, has demonstrated that receptor conformation is also controlled by protein-protein interactions occurring inside the cell. Receptor dimerization and interactions with intracellular scaffolding and signaling proteins can modify receptor structure and ligand selectivity and predetermine, from a menu of available options, which intracellular responses will predominate. In essence, the influences on receptor conformation are bi-directional; internal factors change the conformation of the receptor to reflect the status of the intracellular milieu, while extracellular factors, i.e., agonists, convey information to the cell about the external environment. This concept has critical implications for receptor theory and the design of therapeutics. Thus in complex physiological processes, e.g., aging or neurodegenerative disease, in which multiple proteins expression patterns are changed it is more likely than previously thought that GPCR signal conditioning could be affected. Therefore if indeed there is an alteration of GPCR pharmacology in these states then perhaps drug design should be targeted toward this new pharmacology rather than the standard models previously used.

Groups

Co-authors (526)

  • Abdul Majeed
  • Techavera noida
  • Cristian Randieri -Looking for international partners contact me by social@randieri.com
  • ASHOK KUMAR DWIVEDI
  • karnika joshi

Publications (5)

  • GIT2—A keystone in ageing and age-related disease

    • van Gastel J
    • Boddaert J
    • Jushaj A
    • et al.
    N/AReaders
    0Citations
    Get full text
  • Intelligent and effective informatic deconvolution of “Big Data” and its future impact on the quantitative nature of neurodegenerative disease therapy

    • Maudsley S
    • Devanarayan V
    • Martin B
    • et al.
    N/AReaders
    0Citations
    Get full text
  • Inhibitory actions of the NRG-1/ErbB4 pathway in macrophages during tissue fibrosis in the heart, skin, and lung

    • Vermeulen Z
    • Hervent A
    • Dugaucquier L
    • et al.
    N/AReaders
    1Citations
    Get full text
  • Human Obesity Associated with an Intronic SNP in the Brain-Derived Neurotrophic Factor Locus

    • Mou Z
    • Hyde T
    • Lipska B
    • et al.
    N/AReaders
    17Citations
    Get full text
  • Recessive mutations in SLC13A5 result in a loss of citrate transport and cause neonatal epilepsy, developmental delay and teeth hypoplasia

    • Hardies K
    • De Kovel C
    • Weckhuysen S
    • et al.
    N/AReaders
    18Citations
    Get full text

Editorships

American Journal of Alzheimer's Disease

Editor in Chief

2013 - Present

Frontiers in Endocrinology

Associate Editor

2013 - Present

Professional experience

Vice-Chair, Department of Biomedical Research

University of Antwerp

September 2016 - Present

Head, Receptor Pharmacology Unit

National Institutes of Health

February 2004 - January 2014(10 years)

Principal Investigator

Medical Research Council

January 2000 - February 2004(4 years)

Howard Hughes Medical Institute Research Scholar

Duke University

December 1997 - December 2000(3 years)

Education

Howard Hughes Research Fellowship

Duke University

December 1997 - December 2000(3 years)

Ph.D.

University of Leeds

October 1993 - October 1996(3 years)

B.Sc.

University of Leeds

October 1990 - July 1993(3 years)