Honors & Awards

  • Postdoctoral Research Fellow, Institutional Research and Academic Career Development Award (2012 - Present)
  • Graduate Teaching Fellow, Howard Hughes Medical Institute (2010 - 2011)
  • Predoctoral Fellow - Grant number: T32 HD060555-01, Eunice Kennedy Shriver National Institute of Child Health and Human Development (2009 - 2010)
  • Stem Cell Research Fellowship, Paul H. Silverman Memorial Fellowship (2009)

Professional Education

  • Doctor of Philosophy, University of California Irvine (2011)
  • Bachelor of Science, San Jose State University (2004)
  • Diploma, Capuchino High School (1999)

Stanford Advisors


Journal Articles

  • Follistatin modulates a BMP autoregulatory loop to control the size and patterning of sensory domains in the developing tongue DEVELOPMENT Beites, C. L., Hollenbeck, P. L., Kim, J., Lovell-Badge, R., Lander, A. D., Calof, A. L. 2009; 136 (13): 2187-2197


    The regenerative capacity of many placode-derived epithelial structures makes them of interest for understanding the molecular control of epithelial stem cells and their niches. Here, we investigate the interaction between the developing epithelium and its surrounding mesenchyme in one such system, the taste papillae and sensory taste buds of the mouse tongue. We identify follistatin (FST) as a mesenchymal factor that controls size, patterning and gustatory cell differentiation in developing taste papillae. FST limits expansion and differentiation of Sox2-expressing taste progenitor cells and negatively regulates the development of taste papillae in the lingual epithelium: in Fst(-/-) tongue, there is both ectopic development of Sox2-expressing taste progenitors and accelerated differentiation of gustatory cells. Loss of Fst leads to elevated activity and increased expression of epithelial Bmp7; the latter effect is consistent with BMP7 positive autoregulation, a phenomenon we demonstrate directly. We show that FST and BMP7 influence the activity and expression of other signaling systems that play important roles in the development of taste papillae and taste buds. In addition, using computational modeling, we show how aberrations in taste papillae patterning in Fst(-/-) mice could result from disruption of an FST-BMP7 regulatory circuit that normally suppresses noise in a process based on diffusion-driven instability. Because inactivation of Bmp7 rescues many of the defects observed in Fst(-/-) tongue, we conclude that interactions between mesenchyme-derived FST and epithelial BMP7 play a central role in the morphogenesis, innervation and maintenance of taste buds and their stem/progenitor cells.

    View details for DOI 10.1242/dev.030544

    View details for Web of Science ID 000266731800006

    View details for PubMedID 19474151

  • The Role of Foxg1 in the Development of Neural Stem Cells of the Olfactory Epithelium INTERNATIONAL SYMPOSIUM ON OLFACTION AND TASTE Kawauchi, S., Santos, R., Kim, J., Hollenbeck, P. L., Murray, R. C., Calof, A. L. 2009; 1170: 21-27


    The olfactory epithelium (OE) of the mouse is an excellent model system for studying principles of neural stem cell biology because of its well-defined neuronal lineage and its ability to regenerate throughout life. To approach the molecular mechanisms of stem cell regulation in the OE, we have focused on Foxg1, also known as brain factor 1, which is a member of the Forkhead transcription factor family. Foxg1(-/-) mice show major defects in the OE at birth, suggesting that Foxg1 plays an important role in OE development. We find that Foxg1 is expressed in cells within the basal compartment of the OE, the location where OE stem and progenitor cells are known to reside. Since FoxG1 is known to regulate proliferation of neuronal progenitor cells during telencephalon development, we performed bromodeoxyuridine pulse-chase labeling of Sox2-expressing neural stem cells during primary OE neurogenesis. We found the percentage of Sox2-expressing cells that retained bromodeoxyuridine was twice as high in Foxg1(-/-) OE cells as in the wild type, suggesting that these cells are delayed and/or halted in their development in the absence of Foxg1. Our findings suggest that the proliferation and/or subsequent differentiation of Sox2-expressing neural stem cells in the OE is regulated by Foxg1.

    View details for DOI 10.1111/j.1749-6632.2009.04372.x

    View details for Web of Science ID 000270495700006

    View details for PubMedID 19686101

  • Clinical review: A critical evaluation of the role of soy protein and isoflavone supplementation in the control of plasma cholesterol concentrations JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM Dewell, A., Hollenbeck, P. L., Hollenbeck, C. B. 2006; 91 (3): 772-780


    The purpose of this review was to critically evaluate current research on the effect of soy protein and isoflavone supplements on plasma lipoproteins and place the potential role of soy in the prevention of coronary artery disease (CAD) into a clinical perspective.An extensive literature search was performed using a variety of medical and scientific databases including Medline, PubMed, Science Direct, Ovid, NIST, and Infotrac to identify relevant articles. Journal articles were cross-referenced for additional sources of information. Articles were evaluated based on level of experimental control as well as statistical, quantitative, and clinical analysis.Soy and soy isoflavones have been the object of extensive research investigating their potential hypocholesterolemic effects and possible role in the prevention of CAD. It has been suggested that soy, especially the isoflavones contained in soy, improves lipoprotein levels, thus reducing the risk for CAD. This belief, however, is not uniformly accepted. Moreover, the experimental evidence in support of this notion is not as overwhelming as generally perceived, and the current available data reveal that the discrepancies observed are primarily statistical in nature rather than reflecting actual quantitative differences in the hypocholesterolemic effects detected.A critical analysis of the investigations to date indicates the data are not quantitatively impressive and raises substantial questions about the clinical importance of the hypocholesterolemic effects observed.

    View details for DOI 10.1210/jc.2004-2350

    View details for Web of Science ID 000235889700007

    View details for PubMedID 16384855

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