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Julia K. Walker, PhD

Professor
Phone: 
(919) 668-0491, (919) 668-3252
Office: 
3137 Pearson Building

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

Education

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

Awards and Honors

  • 2009 || ATS-Appointed Young Investigator to the 49th Annual Japanese Respiratory Society Meeting, American Thoracic Society
  • 2004 || Ann Woolcock Memorial Award, ATS - American Thoracic Society
  • 1999 || Fellowship, Medical Council of Canada
  • 1997 || Fellowship, Canadian Lung Association/Medical Research Council
  • 1996 || Abrahams’ Prize in Physiology, Queen’s University
  • 1995 || Ontario Graduate Student Award
  • 1995 || Queen's Graduate Award, Queen’s University
  • 1994 || Dean's Award, Queen's University
  • 1994 || Queen's Graduate Fellowship, Queen’s University
  • 1993 || Fellowship, Ontario Thoracic Society
  • 1992 || Ontario Graduate Student Award
  • 1991 || Dean's Award, Queen’s University
  • 1991 || Fellowship, Ontario Thoracic Society
  • 1987 || Murray Sears Memorial Prize in Chemistry, Mount Allison University
  • 1985 || Dean's Scholarship, Academic, Mount Allison University
  • 1985 || Dean's Scholarship, Athletic Achievement, Mount Allison University
  • 1984 || Ralph Pickard Bell Entrance Scholarship, Mount Allison University
  • 1983 || Carleton Board of Education Bursary for Gifted Students

Areas of Interest

Physiology

Representative Publications

  • 2015 -- PubMed # : 26103985 Pera, T. and Hegde, A. and Deshpande, D. A. and Morgan, S. J. and Tiegs, B. C. and Theriot, B. S. and Choi, Y. H. and Walker, J. K. and Penn, R. B. Specificity of arrestin subtypes in regulating airway smooth muscle G protein-coupled receptor signaling and function. FASEB J. October, 2015 29(10); 4227-35 PMC4566941
  • 2015 -- PubMed # : 25569510 Chen, M. and Hegde, A. and Choi, Y. H. and Theriot, B. S. and Premont, R. T. and Chen, W. and Walker, J. K. Genetic Deletion of β-Arrestin-2 and the Mitigation of Established Airway Hyperresponsiveness in a Murine Asthma Model. Am J Respir Cell Mol Biol. 53(3); 346-54 PMC4566063
  • 2015 -- PubMed # : 25658948 Hegde, A. and Strachan, R. T. and Walker, J. K. Quantification of Beta adrenergic receptor subtypes in Beta-arrestin knockout mouse airways. PLoS One. February 6, 2015 10(2); e0116458
  • 2014 -- PubMed # : 24907413 Walker, J. K. and DeFea, K. A. Role for β-arrestin in mediating paradoxical β2AR and PAR2 signaling in asthma. Curr Opin Pharmacol. 16C 142-147
  • 2014 -- PubMed # : 24888515 Walker, J. K. and Fisher, J. T. Editorial overview: Respiratory: GPCR signaling and the lung. Curr Opin Pharmacol. 16 iv-vi
  • 2014 -- PubMed # : 24292841 Penn, R. B. and Bond, R. A. and Walker, J. K. GPCRs and Arrestins in Airways: Implications for Asthma. Handb Exp Pharmacol. 2014 219 387-403
  • 2013 -- PubMed # : 23991664 Forkuo, G. S. and Thanawala, V. J. and Al-Sawalha, N. and Bond, R. A. and Walker, J. K. Reply: Adverse effects of long-acting beta-agonists on airway hyperresponsiveness. Am J Respir Cell Mol Biol. September, 2013 49(3); 502
  • 2013 -- PubMed # : 23408785 Walker, J. K. and Kraft, M. and Fisher, J. T. Assessment of murine lung mechanics outcome measures: alignment with those made in asthmatics. Front Physiol. February, 2013 3(491); PMC3569663
  • 2013 -- PubMed # : 23204390 Thanawala, V. J. and Forkuo, G. S. and Al-Sawalha, N. and Azzegagh, Z. and Nguyen, L. P. and Eriksen, J. L. and Tuvim, M. J. and Lowder, T. W. and Dickey, B. F. and Knoll, B. J. and Walker, J. K. and Bond, R. A. β2-Adrenoceptor agonists are required for development of the asthma phenotype in a murine model. Am J Respir Cell Mol Biol. February, 2013 48(2); 220-9
  • 2012 -- PubMed # : 23012429 Nichols, H. L. and Saffeddine, M. and Theriot, B. S. and Hegde, A. and Polley, D. and El-Mays, T. and Vliagoftis, H. and Hollenberg, M. D. and Wilson, E. H. and Walker, J. K. and DeFea, K. A. β-Arrestin-2 mediates the proinflammatory effects of proteinase-activated receptor-2 in the airway. Proc Natl Acad Sci U S A. October, 2012 109(41); 16660-5 PMC3478622

Pages

Grant Funding (Selected)

  • Optimizing Beta-Adrenoceptor Signaling Bias in Asthma

    National Institutes of Health
    1R01-AI110007-01A1
    06/2014 to 05/2019
    Role: Principal Investigator

    Project Goals: We propose studies to solve the “beta-2 adrenoceptor paradox” in asthma by establishing the cell-specific role of beta-2 adrenoceptor signaling pathways in regulating the asthma phenotype, and identifying from among current and newly generated beta-2 adrenoceptor ligands or modulators those with biased signaling properties that are optimal in their ability to antagonize pathogenic beta-2 adrenoceptor signaling via arrestins, yet promote beneficial G protein signaling.

  • Host Factors in Regulation of Inflammatory and Fibroproliferative Lung Disease

    Cedars Sinai Medical Center
    001073456
    06/2014 to 05/2015
    Role: PI
  • Mechanisms of Beta-blocker Induced Improvements in Asthma

    NIH-NHLBI
    AI079236-03
    06/2013 to 05/2018
    Role: Co-Principal Investigator

    Project Goals: The primary goal of this project is to determine the mechanism of the proasthmatic effect of β2AR signaling.

  • Host factors in regulation of inflammatory and fibroproliferative lung disease

    NIH-NHLBI
    08/2012 to 07/2017
    Role: Animal Core Principal Investigator

    Project Goals: The primary goal of this project is to determine the mechanism by which host factors interact with lung injury or allergen exposure to promote lung inflammation and fibrosis.

  • Modeling beta2-adrenergic receptor desensitization in mouse airway smooth muscle

    Aerie Pharmaceuticals
    03/2012 to 02/2013
    Role: Principal Investigator

    Project Goals: The overall goal of this research is to evaluate the immediate and prophylactic effects of Aerie Pharmaceutical compounds (rho-kinase super inhibitors) on asthmatic inflammation and associated airway hyperresponsiveness in mice.

  • Arrestin selectivity for GPCRs in airway smooth muscle

    NIH-NHLBI
    R01-HL093103-01A2
    04/2010 to 03/2014
    Role: Co-Principal Investigator

    Project Goals: The primary goal of this project is to delineate the functional selectivity of β arrestin-mediated desensitization of pro-and anti-contractile GPCRs in airway smooth muscle.

  • T cell metabolism as a determinant of differentiation in allergic asthma

    NIH-NHLBI
    R01-HL108006-01
    04/2010 to 03/2015
    Role: Collaborator Investigator

    Project Goals: The primary goal of this project is to delineate the mechanism by which glucose transporter function influences T cell metabolism and function in allergic asthma.

  • T cell function in asthma depends on a novel signaling pathway

    NIH-NHLBI
    R01-HL084123
    02/2008 to 01/2013
    Role: Principal Investigator

    Project Goals: The primary goal of this project is to delineate the mechanism by which beta arrestin-2 regulates T cell chemotaxis in asthma.

  • Modeling beta2-adrenergic receptor desensitization in mouse airway smooth muscle

    Sepracor, Inc.
    10/2005 to 12/2007
    Role: Principal Investigator

    Project Goals: The overall goal of this research is to develop a mouse model of beta2-adrenergic receptor desensitization in airway smooth muscle and to test the effects of levalbuterol in this model. 2-adrenergic receptor dysfunction occurs in human asthmatics precipitating morbidity and mortality.

  • Mouse Models of Heart, Lung and Blood Diseases

    NIH-NHLBI
    U01 HL66611 renewal
    09/2004 to 08/2008
    Role: Principal Investigator (subcontract: David A. Schwartz)

    Project Goals: The overall goal of this research is to provide new resources for identifying the genes underlying lung disorders by examining the physiologic and biologic response of the lung to complementary challenges in ENU mutagenized mice.

Pages

Thursday, April 7, 2016

Julia Walker published an article entitled "PDE4 Inhibitors Attenuate the Asthma Phenotype Produced by β2-adrenoceptor Agonists in PNMT-KO Mice" in the February issue of the American Journal of Respiratory Cell and Molecular Biology.

Wednesday, June 18, 2014

Julia Walker has received an award for her NIH R01 proposal entitled "Optimizing Beta-Adrenoceptor Signaling Bias in Asthma." This award is for a five-year period, awarded June 18, 2014 to May 31, 2019. This project was awarded at $2,820,445 for the five-year project period.

Monday, November 18, 2013

Kudos to Julia Walker and her entire team for the resubmission of their NIH R01 application entitled "Optimizing Beta-Adrenoceptor Signaling Bias in Asthma." This proposal requests funding for a five-year period with a start date of July 1, 2014.