M. Isabel Dominguez, PhD
Title: Assistant Professor
Research interests: Wnt signaling in development and cancer
Department of Medicine
Boston University School of Medicine
650 Albany Street, 4th floor (X438)
Boston MA 02118
Office (X438): +1-617-414-1829
Laboratory (X430): +1-617-638-7560
Wnt signaling is essential for organ development and maintenance and its deregulation is the cause of several human diseases. My research interest is to understand the cascade of intracellular events that leads to the activation of Wnt signaling and the biological role of the Wnt pathway during organ development and maintenance. We have two areas of interest:
1) Our first area of interest is to characterize the molecular mechanism leading to activation of β-catenin, the key intracellular Wnt component that is upregulated in many human tumors. Using Xenopus embryos and mammalian cell lines, we have been collaborating with Dr. David Seldin’s group to determine the molecular mechanism utilized by a kinase upregulated in human tumors, CK2, to activate β-catenin. We found that CK2 is important for the stabilization of β-catenin by decreasing β-catenin interaction with its negative regulator, axin. Our ongoing studies focus on further characterizing the role of CK2 in the regulation of β-catenin activation in vivo and in vitro. As we acquire a better understanding of the molecular events leading to β-catenin activation, we will be able to develop novel and specific inhibitors for the treatment of cancers with upregulated nuclear β-catenin levels.
2) Our second area of interest is to characterize the cellular and molecular mechanisms regulated by Wnt/β-catenin signaling during morphogenesis. Wnt/β-catenin signaling is essential for proper morphogenesis and thus, embryonic survival. Our recent data show that CK2 regulates morphogenesis in mice and Xenopus embryos. Ongoing experiments will determine the cellular, molecular and signaling processes that CK2 regulates during morphogenesis in mice. In addition, since CK2 activity can be regulated by environmental factors that are postulated to contribute to congenital diseases, we are studying the possible role of transient CK2 modulation in mediating embryonic malformations in Xenopus embryos. Our long-term goal is to identify means of preventing or correcting defects in morphogenetic processes that lead to congenital defects.
This work has been supported by the NIH, the American Heart Association, the American Cancer Society, the Karin Grunebaum Cancer Research Foundation and the Avon Foundation.
For more information about Dr. Dominguez’s research work please see below laboratory website