Cristina de Guzman Strong, Ph.D.

Assistant Professor
Internal Medicine
Dermatology
Center for Pharmacogenomics

Human and Statistical Genetics Program
Molecular Genetics and Genomics Program
Computational and Systems Biology Program
Developmental, Regenerative and Stem Cell Biology Program

  • 314-362-7695

  • McDonnell Basic Sciences Building Room 770

  • cristinastrong@wustl.edu

  • http://csi.wustl.edu/faculty/de_guzman_strong_cristina

  • epigenetics, genetics, genomics, chromatin, enhancer, skin, transcriptional regulation, disease, translational research

  • Genomics of Skin Barrier: Development and Disease

Research Abstract:

Additional web site -- https://pharmacogenomics.wustl.edu/research/strong-lab/

The long-term goal of the Strong laboratory is to understand the morphogenesis and homeostasis of functional tissue barriers. Perturbations in this complex biological processes often lead to inflammation and opportunistic infections. We use the mammalian skin as a model system to explore the molecular mechanisms governing protective barrier formation informative for human disease studies. The Epidermal Differentiation Complex locus (EDC) encodes proteins that are cross-linked together to form the barrier in the skin epidermis. EDC genes are coordinately expressed in the developing epidermis and are upregulated during barrier disruption. Using genomics, bioinformatics, molecular and gene targeting approaches, we are investigating molecular control of coordinate EDC gene expression through epigenetic, chromosomal structure, transcription factor, and regulatory element studies.

Our lab is also interested in bringing the bench to the bedside. Our translational research component seeks to identify the genetic basis of inflammatory skin diseases. We are currently using “next-generation” sequencing to identify risk genetic variants in targeted genomic regions of affected patients.

Selected Publications:

Brettmann E.A., Oh I.Y., de Guzman Strong C. (2018) High-throughput identification of gene regulatory sequences using next-generation sequencing of circular chromosome conformation capture (4C-seq). J. Vis Exp. 2018 Oct 5;(140). doi: 10.3791.58030.

Mathyer M.E., Quiggle A.M., Wong X.F.C.C., Denil S.L.I.J., Kumar M.G., Ciliberto H.M., Bayliss S.J., Common J.E., de Guzman Strong C. (2018) Tiled array-based sequencing identifies enrichment of loss-of-function variants in the highly homologous filaggrin gene in African American children with severe atopic dermatitis. Exp Dermatol. 2018 Sep;27(9):989-992. doi: 10.1111/exd.13691.

Goodwin, Z.A. and de Guzman Strong, C. (2017) Recent Positive Selection in Genes of the Mammalian Epidermal Differentiation Complex Locus. Frontiers in Genetics, in press.

Quiggle, A.M., Goodwin, Z.A., Marfatia, T.R., Kumar, M.G., Ciliberto, H., Bayliss, S.J., de Guzman Strong, C. (2015) Low filaggrin monomer repeats in African American pediatric patients with moderate to severe atopic dermatitis. JAMA Dermatol. 151(5):557-9.PMID: 25564772.

Oh, I.Y., Albea, D.M., Goodwin, Z.A., Quiggle, A.M., Baker, B.P., Guggisberg, A.M., Geahlen, J.H., Kroner, G.M., de Guzman Strong, C. (2014) Regulation of the dynamic chromatin architecture of the epidermal differentiation complex is mediated by a c-Jun/AP-1-modulated enhancer. J. Invest. Dermatol. 134(9): 2371-80.PMID: 24468747.

de Guzman Strong CG, Conlan S, Deming CB, Cheng J, Sears KE, Segre JA. (2010). A milieu of regulatory elements in the epidermal differentiation complex syntenic block: implications for atopic dermatitis and psoriasis. Hum Mol Genet.19(8):1453-60. PMID: 20089530

de Guzman Strong CG, Wertz P, Wang C, Yang F, Meltzer PS, Andl T, Millar SE, Ho I-C, Pai SY, Segre JA. (2006). Lipid defect underlies selective skin barrier impairment of an epidermal-specific deletion of Gata-3. Journal of Cell Biology 175(4):661-70. PMID: 17116754.

Last Updated: 12/26/2018 12:10:08 PM

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