
Genetically engineered mice with mutations in the 3 TGFß ligands and in FGF2 are being used to determine the function of these genes. The research has resulted in mouse models for the following human diseases: i) autoimmune disease, ii) colon cancer, iii) congenital heart defects, and iv) cardiac hypertrophy. These mouse models are providing a better understanding of these diseases and the roles that TGFß and FGF2 play in the development and/or prevention of these diseases.
Bommireddy R, Bueno OF, Martin J, Ormsby I, Chen H, Gard C, Molkentin JD, Boivin GP, Babcock GF, Doetschman T. Aug 2009. Calcineurin deficiency decreases inflammatory lesions in transforming growth factor beta1-deficient mice. Clin Exp Immunol,2009 Aug 18;
Azhar M, Yin M, Bommireddy R, Duffy JJ, Yang J, Pawlowski SA, Boivin GP, Engle SJ, Sanford LP, Grisham C, Singh RR, Babcock GF, Doetschman T. Jun 2009. Generation of mice with a conditional allele for transforming growth factor beta 1 gene. Genesis, 47:423-31
Doetschman T. Dec 2008. Influence of genetic background on genetically engineered mouse phenotypes. Methods Mol Biol, 530:423-33
Azhar M, Runyan RB, Gard C, Sanford LP, Miller ML, Andringa A, Pawlowski S, Rajan S, Doetschman T. Feb 2009. Ligand-specific function of transforming growth factor beta in epithelial-mesenchymal transition in heart development. Dev Dyn, 238:431-42