Abstract

The major objective of the Transgenic / Gene-Disruption Mouse Core is to provide a centralized service oriented facility that will insure the capacity of each participating project lab to produce transgenic and gene-disrupted mice. Moreover, this will result in an economy of effort as well as expense by avoiding duplication of a highly technical skill requiring specialized equipment and animal facilities. The Transgenic / Gene-Disruption Core is a major avenue for collaborations. The ability to perform gain of function and loss of function experiments in vivo will enhance our understanding of the molecular mechanisms guiding airway inflammation and the pathogenesis of asthma. Moreover, the capacity to follow the tissue and cell type expression of a Promoter/Enhancer combination throughout normal embryonic and adult development is crucial to furthering our understanding of airway differentiation and regulation of inflammation.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Specialized Center (P50)
Project #
1P50HL056419-02
Application #
6242720
Study Section
Project Start
1997-09-01
Project End
1998-08-31
Budget Start
1996-10-01
Budget End
1997-09-30
Support Year
2
Fiscal Year
1997
Total Cost
Indirect Cost

  Institution

Name
Washington University
Department
Type
DUNS #
062761671
City
Saint Louis
State
MO
Country
United States
Zip Code
63130

  Publications

Liu, Michael; Subramanian, Vijay; Christie, Chandrika et al. (2012) Immune responses to self-antigens in asthma patients: clinical and immunopathological implications. Hum Immunol 73:511-6
Holtzman, Michael J; Patel, Dhara A; Zhang, Yong et al. (2011) Host epithelial-viral interactions as cause and cure for asthma. Curr Opin Immunol 23:487-94
Mikols, Cassandra L; Yan, Le; Norris, Jin Y et al. (2006) IL-12 p80 is an innate epithelial cell effector that mediates chronic allograft dysfunction. Am J Respir Crit Care Med 174:461-70
Jung, Yong Woo; Schoeb, Trenton R; Weaver, Casey T et al. (2006) Antigen and lipopolysaccharide play synergistic roles in the effector phase of airway inflammation in mice. Am J Pathol 168:1425-34
Atkinson, Jeffrey J; Holmbeck, Kenn; Yamada, Susan et al. (2005) Membrane-type 1 matrix metalloproteinase is required for normal alveolar development. Dev Dyn 232:1079-90
Nabe, Takeshi; Zindl, Carlene L; Jung, Yong Woo et al. (2005) Induction of a late asthmatic response associated with airway inflammation in mice. Eur J Pharmacol 521:144-55
Wikenheiser-Brokamp, Kathryn A (2004) Rb family proteins differentially regulate distinct cell lineages during epithelial development. Development 131:4299-310
Surendran, Kameswaran; Simon, Theodore C; Liapis, Helen et al. (2004) Matrilysin (MMP-7) expression in renal tubular damage: association with Wnt4. Kidney Int 65:2212-22
Lorenz, Robin G; Chaplin, David D; McDonald, Keely G et al. (2003) Isolated lymphoid follicle formation is inducible and dependent upon lymphotoxin-sufficient B lymphocytes, lymphotoxin beta receptor, and TNF receptor I function. J Immunol 170:5475-82
Fu, Xiaoyun; Kassim, Sean Y; Parks, William C et al. (2003) Hypochlorous acid generated by myeloperoxidase modifies adjacent tryptophan and glycine residues in the catalytic domain of matrix metalloproteinase-7 (matrilysin): an oxidative mechanism for restraining proteolytic activity during inflammation. J Biol Chem 278:28403-9

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