An increasing variety of technologies are now available to investigators to manipulate individual genes or to monitor biological processes with precision. These technologies are crucial to the study of the molecular bases of skin diseases because they allow us to establish a clear, causative relationship between a gene and an observed phenotype. However, such technologies are often complicated and not available to many investigators involved in cutaneous biology and skin diseases research. In the Cell and Gene Modification Core, we will provide the following services: 1) Generate keratinocytes, fibroblasts, or other skin cells with targeted reporter genes or gene knockdowns. 2) Generate genetically defined skin or induced pluripotent stem cells by use of state-of-the-art genome editing technologies. 3) Provide consultation and training to investigators interested in employing cell-based models for skin research. We envision that genetically modified cells are likely to be derived from tissues obtained in the Tissue Procurement and Analysis Core (Core D) and further incorporated into animal and tissue models generated in the Animal Models and Tissue Engineering Core (Core C) to create relevant skin disease models. As such, services to be provided by the Cell and Gene Modification Core will significantly enhance the ability of Duke research community to carry out mechanism-based skin research.

Public Health Relevance

Skin diseases affect a large percentage of the population. The Cell and Gene Modification Core will facilitate mechanism-based skin disease research by allowing investigators to precisely examine the functions of genes and cells that play a role in skin biology and disease. This ability, in turn, will accelerate discovery and basic understanding that can lead to new therapies

Agency
National Institute of Health (NIH)
Institute
National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS)
Type
Center Core Grants (P30)
Project #
1P30AR066527-01
Application #
8753399
Study Section
Special Emphasis Panel (ZAR1-KM (M1))
Project Start
Project End
Budget Start
2014-08-01
Budget End
2015-07-31
Support Year
1
Fiscal Year
2014
Total Cost
$140,563
Indirect Cost
$51,127
Name
Duke University
Department
Type
DUNS #
044387793
City
Durham
State
NC
Country
United States
Zip Code
27705
Jin, Yingai Jane; Wang, Sally; Cho, Joshua et al. (2016) Epidermal CYLD inactivation sensitizes mice to the development of sebaceous and basaloid skin tumors. JCI Insight 1:
Thakore, Pratiksha I; Gersbach, Charles A (2016) Design, Assembly, and Characterization of TALE-Based Transcriptional Activators and Repressors. Methods Mol Biol 1338:71-88
Liu, Xinjian; Zhou, Min; Mei, Ling et al. (2016) Key roles of necroptotic factors in promoting tumor growth. Oncotarget 7:22219-33
Thakore, Pratiksha I; Black, Joshua B; Hilton, Isaac B et al. (2016) Editing the epigenome: technologies for programmable transcription and epigenetic modulation. Nat Methods 13:127-37
Chen, Yong; Fang, Quan; Wang, Zilong et al. (2016) Transient Receptor Potential Vanilloid 4 Ion Channel Functions as a Pruriceptor in Epidermal Keratinocytes to Evoke Histaminergic Itch. J Biol Chem 291:10252-62
Ousterout, David G; Gersbach, Charles A (2016) The Development of TALE Nucleases for Biotechnology. Methods Mol Biol 1338:27-42
Black, Joshua B; Adler, Andrew F; Wang, Hong-Gang et al. (2016) Targeted Epigenetic Remodeling of Endogenous Loci by CRISPR/Cas9-Based Transcriptional Activators Directly Converts Fibroblasts to Neuronal Cells. Cell Stem Cell 19:406-14
Li, Fang; Liu, Xinjian; Sampson, John H et al. (2016) Rapid Reprogramming of Primary Human Astrocytes into Potent Tumor-Initiating Cells with Defined Genetic Factors. Cancer Res 76:5143-50
Hilton, Isaac B; D'Ippolito, Anthony M; Vockley, Christopher M et al. (2015) Epigenome editing by a CRISPR-Cas9-based acetyltransferase activates genes from promoters and enhancers. Nat Biotechnol 33:510-7
Polstein, Lauren R; Perez-Pinera, Pablo; Kocak, D Dewran et al. (2015) Genome-wide specificity of DNA binding, gene regulation, and chromatin remodeling by TALE- and CRISPR/Cas9-based transcriptional activators. Genome Res 25:1158-69

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