BayGenomics has used gene-trap vectors to inactivate thousands of genes in mouse embryonic stem (ES) cells. More than 8000 cell lines with well-characterized insertional mutations have been generated and posted on our website (http:// baygenomics.ucsf.edu./). The ES cells have been made freely availble to the scientific community for the purpose of generating knockout mice. Thus far, we have responded to the requests for more than 930 different ES cell lines. The vast majority of our mutant ES cell lines yield germline-transmitting chimeras, and hundreds of knockout mice have been generated by our group and outside laboratories. Many of the knockout mice are highly relevant to cardiopulmonary disease and development. BayGenomics has also produced two widely used programs for analyzing microarray expression data according to biochemical pathways (GenMAPP and MAPPFinder). In addition, BayGenomics investigators have generated and characterized multiple lines of knockout mice for cardiopulmonary development and disease. BayGenomics has an active, high-quality education program. BayGenomics involves two leading San Francisco Bay Area research institutions: The J. David Gladstone Institutes and the University of California, San Francisco. BayGenomics is organized into seven Components: (1) Gene Trapping in Embryonic Stem Cells, (2) Computational Methods and Genomics Education, (3) In Situ Hybridization, (4) Mouse Resource for Lipid Metabolism, (5) Mouse Resoruce for Pulmonary Disease, (6) Mouse Resource for Cardiopulmonary Development and (7) Administration. A major objective of BayGenomics will be to use custom gene-trap vectors to generate 2,500 ES cell lines per year with well characterized insertional mutations (Component 1). Each """"""""trapped"""""""" ES cell line will be posted on our website and will be distributed freely to the research community. A second objective will be to improve the annotation of our website and to provide relevant genomics education programs to our users (Component 2). A third objective is to use in situ hybridization studies to define gene-expression patterns for a subset of the trapped genes, making it easier for our group and others to make informed choices about which genes are likely to be relevant to cardiopulmonary development (Component 3). A fourth objective is to generate a limited number of genetically modified mice, for the purpose of defining the relevance of specific genes to cardiopulmonary development and disease (Component 4-6).

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Project--Cooperative Agreements (U01)
Project #
5U01HL066600-08
Application #
7276004
Study Section
Special Emphasis Panel (ZHL1-CSR-K (M1))
Program Officer
Gan, Weiniu
Project Start
2000-09-30
Project End
2008-07-31
Budget Start
2007-08-01
Budget End
2008-07-31
Support Year
8
Fiscal Year
2007
Total Cost
$1,059,278
Indirect Cost
Name
University of California San Francisco
Department
Internal Medicine/Medicine
Type
Schools of Medicine
DUNS #
094878337
City
San Francisco
State
CA
Country
United States
Zip Code
94143
Maier, Viola; Jolicoeur, Christine; Rayburn, Helen et al. (2011) Semaphorin 4C and 4G are ligands of Plexin-B2 required in cerebellar development. Mol Cell Neurosci 46:419-31
Atabai, Kamran; Jame, Sina; Azhar, Nabil et al. (2009) Mfge8 diminishes the severity of tissue fibrosis in mice by binding and targeting collagen for uptake by macrophages. J Clin Invest 119:3713-22
Singh, Purva; Chen, Chun; Pal-Ghosh, Sonali et al. (2009) Loss of integrin alpha9beta1 results in defects in proliferation, causing poor re-epithelialization during cutaneous wound healing. J Invest Dermatol 129:217-28
Beigneux, Anne P; Gin, Peter; Davies, Brandon S J et al. (2008) Glycosylation of Asn-76 in mouse GPIHBP1 is critical for its appearance on the cell surface and the binding of chylomicrons and lipoprotein lipase. J Lipid Res 49:1312-21
Weinstein, Michael M; Yin, Liya; Beigneux, Anne P et al. (2008) Abnormal patterns of lipoprotein lipase release into the plasma in GPIHBP1-deficient mice. J Biol Chem 283:34511-8
Gin, Peter; Yin, Liya; Davies, Brandon S J et al. (2008) The acidic domain of GPIHBP1 is important for the binding of lipoprotein lipase and chylomicrons. J Biol Chem 283:29554-62
Davies, Brandon S J; Waki, Hironori; Beigneux, Anne P et al. (2008) The expression of GPIHBP1, an endothelial cell binding site for lipoprotein lipase and chylomicrons, is induced by peroxisome proliferator-activated receptor-gamma. Mol Endocrinol 22:2496-504
Mak, Kinglun Kingston; Bi, Yanming; Wan, Chao et al. (2008) Hedgehog signaling in mature osteoblasts regulates bone formation and resorption by controlling PTHrP and RANKL expression. Dev Cell 14:674-88
Mak, Kinglun Kingston; Kronenberg, Henry M; Chuang, Pao-Tien et al. (2008) Indian hedgehog signals independently of PTHrP to promote chondrocyte hypertrophy. Development 135:1947-56
Su, George; Hodnett, Maki; Wu, Nanyan et al. (2007) Integrin alphavbeta5 regulates lung vascular permeability and pulmonary endothelial barrier function. Am J Respir Cell Mol Biol 36:377-86

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