Cindy Knall, PhD - University of Alaska System

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Cindy Knall, PhD
Education: Dr. Knall received her bachelor’s degree in zoology with minors in biological
anthropology and American literature from The George Washington University in 1985.
She completed her doctorate in microbiology and immunology in 1994 at the University of
Colorado Health Sciences Center. Dr. Knall completed her training as a post-doctoral
research fellow from 1994-1999 at National Jewish Medical and Research Center.
Professional Experience: Dr. Knall is beginning her fourth decade of work in health
care research and training, and basic and clinical-translational biomedical research. While
an undergraduate student, Dr. Knall worked for four years as a research assistant in the
GWU Department of Family Medicine and Heath Plan. Following a year of graduate study in
cellular-molecular biology at Roswell Park Cancer Institute, she spent two years working in
the Laboratory of Immunobiology at Dana-Faber Cancer Institute, a teaching affiliate of
Harvard Medical School and a participating institution of the Harvard Cancer. In 1999
following graduate school and post-doctoral training, Dr. Knall joined the Lovelace
Respiratory Research Institute as an Associate Scientist in Pulmonary Immunology. At that
time, she also was appointed an Adjunct Assistant Professor of Pathology in the School of
Medicine, and a Clinical Assistant Professor in the College of Pharmacy at the University of
New Mexico Health Sciences Center. During her time at LRRI, Dr. Knall was the founding
Director of the Lovelace Science Academy, a pre-college minority outreach program,
funded by the Howard Hughes Medical Institute. In 2005, Dr. Knall joined the faculty of the
WWAMI School of Medical Education at the University of Alaska Anchorage where she
currently holds the rank of Associate Professor with tenure. Dr. Knall is also Affiliate
Associate Professor of Immunology in the Department of Immunology at the University of
Washington, School of Medicine.
Honors & Awards: Dr. Knall attended George Washington University on an academic
scholarship and earned the James McBride Sterrett, Jr. Award in Physics as a sophomore. In
graduate school, Dr. Knall was appointed to an institutional National Institutes of Health
(NIH) National Research Service Award (NRSA) in cellular immunology and won the
Department of Cellular and Structural Biology Award in 1991. As a post-doctoral fellow, Dr.
Knall was awarded an individual NIH-NRSA, an American Cancer Society-IRG fellowship
and was named the Helen Wohlberg and Herman Lambert Fellow in Cancer Biology. In
2010, Dr. Knall was a Keynote Speaker for Science for Alaska.
Research: Since her post-doctoral days, Dr. Knall's research has focused on aspects of
innate immunity and inflammation relevant to tobacco exposures. Tobacco use causes
inflammation which is associated with the development of tobacco related diseases such as
leukoplakia, head-neck and lung cancers and chronic obstructive pulmonary disease. Dr.
Knall’s research has targeted three cell populations with roles in tobacco mediated disease
development. These cell populations are lung epithelial cells, targets of tobacco smoke, oral
epithelial cells, targets of chewing tobacco, and neutrophils, mediators of acute
inflammation. In each of these cell types, Dr. Knall’s research investigates the signal
transduction pathways activated within these cells in response to direct tobacco exposure
or the inflammatory chemical mediators produced as a result of tobacco exposure. The goal
of Dr. Knall’s research is to understand the mechanisms by which tobacco alters the cells
before irreversible disease develops. The knowledge gained from these studies will identify
new targets for therapeutic interventions to control the initial cellular changes brought on
by tobacco use.
Selected Publications:
Olivera, D., Knall, C., Boggs, S.E. & Seagrave, J. 2010. Cytoskeletal Modulation and
Tyrosine Phosphorylation of Tight Junction Proteins Are Associated with Mainstream
Cigarette Smoke Induced Permeability of Airway Epithelium. Experimental and Toxicologic
Pathology 62:133–143.
Otten, A., Salter, D., & Knall, C. 2009. Cell Culture Forensics of Calu-3 – A Human Lung
Epithelial Cell Line. Ethnicity and Disease. 19(2) suppl. 3:78-79.
Alakayak, J. & Knall, C. 2008. Mentholated and Non-mentholated Cigarettes Alter
Transepithelial Electrical Resistance (TER) of CALU3 Human Bronchial Epithelial Cells.
Ethnicity and Disease. 18(2) suppl. 1: 45- 46.
Olivera, D.S., Boggs, S.E., Beenhouwer, C., Aden, J. & Knall, C. 2007. Cellular Mechanisms
of Mainstream Cigarette Smoke-Induced Lung Epithelial Tight Junction Permeability
Changes In Vitro. Inhal. Toxicol. 19:13–22.
Razani-Boroujerdi, S., Singh, S.P., Knall, C., Hahn, F.F., Philippides, J.C., Kalra, R., Langley,
R.J. & Sopori, M. 2004. Chronic nicotine inhibits inflammation and promotes influenza
infection. Cell. Immunol. 230:1-9.
Ambruso, D.R., Knall, C., Abell, A.N., Panepinto, J., Kurkchubasche, A., Thurman, G.,
Gonzalez-Aller, C., de Boer, M., Harbeck, R.J., Oyer, R., Johnson, G.L. & Roos, D. 2000. Human
neutrophil immunodeficiency syndrome associated with an inhibitory Rac2 mutation. Proc.
Natl. Acad. Sci. USA. 97:4654-4659.
McLeish, K.R., Knall, C., Ward, R.A., Gerwins, P., Coxon, P.Y., Klein, J.B. & Johnson, G.L.
1998. Activation of mitogen-activated protein kinase cascades during priming of human
neutrophils by Tumor Necrosis Factor-CSF. J. Leuk. Biol. 64:537-545.
Knall, C., Worthen, G.S. & Johnson, G.L. 1997. Interleukin 8 stimulated
phosphatidylinositol-3-kinase activity regulates the migration of human neutrophils
independent of extracellular signal-regulated kinase and p38 mitogen-activated protein
kinases. Proc. Natl. Acad. Sci. USA. 94:3052-3057.
Knall, C., Young, S., Nick, J., Buhl, A.M., Worthen, G.S. & Johnson, G.L. 1996. IL-8
regulation of the Ras/Raf/MAP kinase pathway in human neutrophils. J. Biol. Chem.
271:2832-2838.
Knall, C., Smith, P.A. & Potter, T.A. 1995. CD8 dependent CTL require coengagement of
CD8 and the TCR for phosphatidylinositol hydrolysis, but CD8 independent CTL do not and
can kill in the absence of phosphatidylinositol hydrolysis. Internatl. Immunol. 7:995-1004.
Knall, C., Ingold, A.L. & Potter, T.A. 1994. Analysis of co-receptor versus accessory
molecule function of CD8 as a correlate of exogenous peptide concentration. Mol. Immunol.
31:875-883.
Ingold, A.L., Landel, C., Knall, C., Evans, G.A. & Potter, T.A. 1991. Co-engagement of CD8
with the T cell receptor is required for negative selection. Nature 352:721-723.
Siliciano, R.F., Lawton, T., Knall, C., Karr, R.W., Berman, P., Gregory, T. & Reinherz, E.L.
1988. Analysis of host-virus interactions in AIDS with anti-gp120 T cell clones: Effect of HIV
sequence variation and a mechanism for CD4+ depletion. Cell 54:561-575.
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