Faculty Directory Listing

Julia K. Walker
Tel: (919) 668-0491, (919) 668-3252
Office: 3137 Pearson Building
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Julia K. Walker, PhD


  • Brief Bio

    After receiving a Bachelor of Science degree in Chemistry from Mount Alison University, Dr. Walker pursued a B.Ed. from Ottawa University and was subsequently employed as a board-certified high school chemistry teacher. After teaching for two years she began graduate work focused on cardio-respiratory physiology at Queen’s University in Kingston, Ontario, Canada. Dr. Walker’s postdoctoral training in cell biology at Duke University focused on receptor signaling pathways; in particular those of G protein-coupled receptors. GPCRs are the largest family of cell surface receptors and are the target of more than half of all medically prescribed drugs.

    Dr. Walker’s research, which focuses on understanding the cellular pathophysiological mechanisms that underlie lung disease (in particular asthma) has been independently funded since 2004, and she currently holds the Duke University rank of Associate Professor in Medicine. Currently, Dr. Walker’s research focus has expanded to include the study of novel β-2-adrenoceptor ligands in the treatment of asthma. This research holds great potential to rapidly improve quality of life for asthmatics.

    Dr. Walker has published 33 peer-reviewed basic research and 3 review articles, and has been an invited speaker at various seminar forums within and outside Duke University. She has been recognized by her peers with ATS-sponsored awards such as the Ann Woolcock memorial and ATS Young Investigator awards.

    Academic Program Affiliations

    Doctor of Nursing Practice Program


    Ph.D.Queens University
    M.Sc.Queen's University
    B.Ed.University of Ottawa
    B.Sc.Mount Allison University

    Clinical Interests

    Broadly, my research focuses on the role for G protein-coupled receptors in the pathophysiology of asthma. Asthma is a complex disease characterized by airway inflammation, hyperresponsiveness and remodeling. G protein-coupled receptors figure largely in the pathology and treatment of this disease. For example, beta-agonists, the rescue medication inhaled by asthmatics, act at airway smooth muscle beta2-adrenergic receptors (β2-AR) to relax the airways. However, excessive use of beta-agonists has been associated with clinical worsening of asthma control and increased mortality. β2-ARs can signal through two well characterized and independent signaling pathways; a G protein-dependent pathway and a beta-arrestin-dependent pathway. Previously we showed that mice lacking beta-arrestin-2 do not develop the symptoms of allergic airway inflammatory disease and that T cell and eosinophil migration to the lung is impaired in these mice. Similarly, others have shown that the asthma phenotype is significantly reduced in mice lacking global expression of β2-ARs. Thus, we hypothesize that the beta-arrestin-dependent signaling arm, downstream of the β2-AR, is responsible for promoting the asthma phenotype. The translational relevance of this work is high given that the determination of the signaling pathway that is utilized by β2-ARs can be influenced by the molecular signature of the agonist. Thus, our work could lead to the discovery of a β2-AR ligand that bronchodilates the airways without promoting asthma symptoms. In addition to transducing β2-AR-mediated signaling to promote asthma, we hypothesize that beta-arrestin-2 also mediates chemokine receptor signaling and thus, the inflammatory component of asthma. Chemokines, released in response to allergens, dictate the migration of immune cells to the lung in asthma and chemokine receptors are known to signal via both the G-dependent and beta-arrestin-dependent pathways.