The Animal Core is essential for best serving the animal testing needs of the different projects. The cost effectiveness of this type of core service is readily realized by having well-equipped facilities and property trained personnel that are dedicated solely to performing the specific functions of the core. These include generating multiple lines of transgenic and knockout mice, essential for the experiments described here, as well as the performance of a variety of experimental colitis models. We will use our extensive experience in caring for large animal colonies to provide the investigators the animals they need. Centralization of these functions will allow for tight control over the genetic resources. The minimization of variability between animals and various endpoint assays will result in fewer animals being needed to generate statistically valid results that can be compared across different studies within the PPG. The existence of this Core will also eliminate the need for each investigator to spend their time working with the animals.
Aim 1 : To generate multiple lines of transgenic and knockout mice Aim 2: To backcross and intercross genetically engineered mice.
Aim 3 : To assist with the execution of the different models of experimental colitis.
Aim 4 : To sacrifice the mice at the end of each study and perform necropsies to collect the appropriate tissues and organs to be analyzed by the Pathology Core.

Agency
National Institute of Health (NIH)
Institute
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Type
Research Program Projects (P01)
Project #
5P01DK072201-09
Application #
8730611
Study Section
Special Emphasis Panel (ZDK1-GRB-8)
Project Start
Project End
Budget Start
2014-09-01
Budget End
2015-08-31
Support Year
9
Fiscal Year
2014
Total Cost
$406,956
Indirect Cost
$166,864
Name
Icahn School of Medicine at Mount Sinai
Department
Type
DUNS #
078861598
City
New York
State
NY
Country
United States
Zip Code
10029
Tang, Mei San; Bowcutt, Rowann; Leung, Jacqueline M et al. (2017) Integrated Analysis of Biopsies from Inflammatory Bowel Disease Patients Identifies SAA1 as a Link Between Mucosal Microbes with TH17 and TH22 Cells. Inflamm Bowel Dis 23:1544-1554
Blander, J Magarian (2017) The many ways tissue phagocytes respond to dying cells. Immunol Rev 277:158-173
Moretti, Julien; Blander, J Magarian (2017) Cell-autonomous stress responses in innate immunity. J Leukoc Biol 101:77-86
Blander, J Magarian; Longman, Randy S; Iliev, Iliyan D et al. (2017) Regulation of inflammation by microbiota interactions with the host. Nat Immunol 18:851-860
Moretti, Julien; Roy, Soumit; Bozec, Dominique et al. (2017) STING Senses Microbial Viability to Orchestrate Stress-Mediated Autophagy of the Endoplasmic Reticulum. Cell 171:809-823.e13
Campisi, Laura; Barbet, Gaetan; Ding, Yi et al. (2016) Apoptosis in response to microbial infection induces autoreactive TH17 cells. Nat Immunol 17:1084-92
Parkunan, Salai Madhumathi; Randall, C Blake; Astley, Roger A et al. (2016) CXCL1, but not IL-6, significantly impacts intraocular inflammation during infection. J Leukoc Biol 100:1125-1134
Blander, J Magarian (2016) Death in the intestinal epithelium-basic biology and implications for inflammatory bowel disease. FEBS J 283:2720-30
Wang, Juan; Peng, Liang; Zhang, Ruihua et al. (2016) 5-Fluorouracil targets thymidylate synthase in the selective suppression of TH17 cell differentiation. Oncotarget 7:19312-26
Ting, Adrian T; Bertrand, Mathieu J M (2016) More to Life than NF-?B in TNFR1 Signaling. Trends Immunol 37:535-45

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