Bio

Professional Education


  • Fellowship, Stanford University, Gastroenterology and Hepatology (2014)
  • Residency, Stanford University, Internal Medicine (2010)
  • Doctor of Medicine, University of Chicago (2008)
  • Doctor of Philosophy, The Rockefeller University (2007)
  • Bachelor of Science, Northwestern University (1999)

Stanford Advisors


Publications

Journal Articles


  • Adult Intestinal Malrotation: When Things Turn the Wrong Way DIGESTIVE DISEASES AND SCIENCES Palmer, O. P., Rhee, H. H., Park, W. G., Visser, B. C. 2012; 57 (2): 284-287

    View details for DOI 10.1007/s10620-011-1818-4

    View details for Web of Science ID 000299487500005

    View details for PubMedID 21805171

  • Lhx2 maintains stem cell character in hair follicles SCIENCE Rhee, H., Polak, L., Fuchs, E. 2006; 312 (5782): 1946-1949

    Abstract

    During embryogenesis, stem cells are set aside to fuel the postnatal hair cycle and repair the epidermis after injury. To define how hair follicle stem cells are specified and maintained in an undifferentiated state, we developed a strategy to isolate and transcriptionally profile embryonic hair progenitors in mice. We identified Lhx2 as a transcription factor positioned downstream of signals necessary to specify hair follicle stem cells, but upstream from signals required to drive activated stem cells to terminally differentiate. Using gain- and loss-of-function studies, we uncovered a role for Lhx2 in maintaining the growth and undifferentiated properties of hair follicle progenitors.

    View details for DOI 10.1126/science.1128004

    View details for Web of Science ID 000238848100058

    View details for PubMedID 16809539

  • A developmental conundrum: a stabilized form of beta-catenin lacking the transcriptional activation domain triggers features of hair cell fate in epidermal cells and epidermal cell fate in hair follicle cells JOURNAL OF CELL BIOLOGY Dasgupta, R., Rhee, H., Fuchs, E. 2002; 158 (2): 331-344

    Abstract

    Wnt signaling orchestrates morphogenetic processes in which changes in gene expression are associated with dramatic changes in cell organization within developing tissue/organs. Upon signaling, excess beta-catenin not utilized at cell-cell junctions becomes stabilized, where it can provide the transcriptional activating domain for Lef/Tcf DNA binding proteins. In skin epithelium, forced stabilization of beta-catenin in epidermis promotes hair follicle morphogenesis, whereas conditional removal of beta-catenin in hair progenitor cells specifies an epidermal fate. We now report that a single protein, a stabilized version of beta-catenin lacking the COOH-terminal transactivation domain, acts in epidermis to promote hair fates and in hair cells to promote epidermal fate. This reveals fundamental differences in ways that epidermal and hair cells naturally respond to beta-catenin signaling. In exploring the phenotype, we uncovered mechanistic insights into the complexities of Lef1/Tcf/beta-catenin signaling. Importantly, how a cell will respond to the transgene product, where it will be localized, and whether it can lead to activation of endogenous beta-catenin/Tcf/Lef complexes is specifically tailored to skin stem cells, their particular lineage and their relative stage of differentiation. Finally, by varying the level of beta-catenin signaling during a cell fate program, the skin cell appears to be pliable, switching fates multiple times.

    View details for DOI 10.1083/jcb.200204134

    View details for Web of Science ID 000177106200015

    View details for PubMedID 12135986

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