The development of sophisticated animal models for human diseases often requires additional human keratinocyte-based cell culture models to reach valid conclusions regarding human disease mechanisms. The tissue culture models are increasingly relying on iPS technology to provide a potentially unlimited source of genetically -defined patient cells which can be turned into keratinocytes. These cells can then be used to establish skin equivalent in vitro as a model of human genodermatoses. Both animal design and the design of iPS-derived disease models increasingly require the ability to manipulate mammalian genes using new genome editing tools, such as zinc finger nucleases (ZFN), TALEN or the CRISPR/Cas system. Designing, generating, preserving and distributing sophisticated animal models that carry three or four different genetic elements or alleles often exceed the technical abilities of individual laboratories. Core facilities with an established track record of expert and reliable services are thus increasingly mission critical for the research program of our customer base. The proposed Bioengineering Core will enable researcher without prior experience in genetic engineering of mice to establish sophisticated animal models to study skin diseases. Further, using iPS cell technology, the proposed Bioengineering Core will support researchers in generating an unlimited resource of patient material, a prerequisite for establishing tissue culture-based models for human skin diseases. As in the past, we will continue to introduce new experimental tools to our research base to broaden and facilitate our research capabilities. Support from the SDRC will sustain this Core and enable SDRC researchers to receive continued discounted access to our services.

Public Health Relevance

The proposed services of the Bioengineering Core will enable our research base to continue with the design and generation of sophisticated animal models and human cell-based disease models. Access to the latest transgenic technology and consultations with respect to the latest genome editing tools will enable our customers to pursue new research avenues without delays caused by a lack resources and of expertise in Core-provided technologies

Agency
National Institute of Health (NIH)
Institute
National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS)
Type
Center Core Grants (P30)
Project #
2P30AR057212-06
Application #
8753459
Study Section
Special Emphasis Panel (ZAR1-KM (M1))
Project Start
Project End
Budget Start
2014-07-01
Budget End
2015-06-30
Support Year
6
Fiscal Year
2014
Total Cost
$124,223
Indirect Cost
$44,101
Name
University of Colorado Denver
Department
Type
DUNS #
041096314
City
Aurora
State
CO
Country
United States
Zip Code
80045
Riching, Andrew S; Zhao, Yuanbiao; Cao, Yingqiong et al. (2018) Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes. J Vis Exp :
Ravindran Menon, Dinoop; Luo, Yuchun; Arcaroli, John J et al. (2018) CDK1 Interacts with Sox2 and Promotes Tumor Initiation in Human Melanoma. Cancer Res 78:6561-6574
Cao, Yu; Liu, Han; Gao, Liwei et al. (2018) Cooperation Between Pten and Smad4 in Murine Salivary Gland Tumor Formation and Progression. Neoplasia 20:764-774
Mukherjee, Nabanita; Strosnider, Andrew; Vagher, Bay et al. (2018) BH3 mimetics induce apoptosis independent of DRP-1 in melanoma. Cell Death Dis 9:907
Kogut, Igor; McCarthy, Sandra M; Pavlova, Maryna et al. (2018) High-efficiency RNA-based reprogramming of human primary fibroblasts. Nat Commun 9:745
Gaskill, Christa F; Carrier, Erica J; Kropski, Jonathan A et al. (2017) Disruption of lineage specification in adult pulmonary mesenchymal progenitor cells promotes microvascular dysfunction. J Clin Invest 127:2262-2276
Mukherjee, Nabanita; Lu, Yan; Almeida, Adam et al. (2017) Use of a MCL-1 inhibitor alone to de-bulk melanoma and in combination to kill melanoma initiating cells. Oncotarget 8:46801-46817
Miller, Shannon M; Miles, Brodie; Guo, Kejun et al. (2017) Follicular Regulatory T Cells Are Highly Permissive to R5-Tropic HIV-1. J Virol 91:
Yang, N; Leung, E L-H; Liu, C et al. (2017) INTU is essential for oncogenic Hh signaling through regulating primary cilia formation in basal cell carcinoma. Oncogene 36:4997-5005
Shah, Khadim; Mehmood, Sabba; Jan, Abid et al. (2017) Sequence variants in nine different genes underlying rare skin disorders in 10 consanguineous families. Int J Dermatol 56:1406-1413

Showing the most recent 10 out of 61 publications