Positions

Professor
Baylor College of Medicine
Gordon Cain Professorship
Baylor College of Medicine
Houston, Texas, United States
Member
Dan L Duncan Comprehensive Cancer Center
Baylor College of Medicine
Houston, Texas, United States

Education

BS from University Of Wisconsin, Madison
MS from University Of Wisconsin, Madison
PhD from University Of California, Davis
Post-Doctoral Fellowship at Cornell University

Professional Interests

  • Physiological role of nuclear receptors during development

Professional Statement

Our research focuses on two main areas: the first is to examine the physiological role of nuclear orphan receptor COUP-TFII in mouse development. COUP-TFs are members of the nuclear receptor superfamily. We have previously demonstrated that COUP-TFs, I and II, function as negative or positive regulators to regulate their target gene expression. COUP-TFI is highly expressed in the CNS and PNS, and COUP-TFII is highly expressed in the mesenchyme of the developing organs. Although the expression of COUP-TFI and II overlaps, ablation of either COUP-TF I or II in mice results in lethality, indicating that each has its distinct function and both are vital for animal survival. COUP-TFI null mutants exhibit defects in axon guidance, myelination, forebrain regionalization, bone and inner ear morphogenesis while COUP-TFII null mutants exhibit defects in angiogenesis and heart development. Currently, we concentrate our effort in studying the underlying mechanism by which COUP-TFII regulates angiogenesis and heart development using floxed COUP-TFII mice. We are also examining its role in the development and function of stomach, liver, limb and brain by crossing them to various Cre mice to generate tissue specific COUP-TFII null mice. Finally, we use chimera analysis and demonstrate that COUP-TFII plays cell autonomous function in limb outgrowth and umbilical vessel development.

The second area of our research is to study the interaction of oncogenes and hormones in mammary gland tumorigenesis. We generated a ligand inducible system to express oncogenes in mammary gland and demonstrated ectopic inducible expression of int-2 in mammary gland results in mammary gland hyperplasia. The induced hyperplasia is reversible, and the extent of hyperplasia depends on the levels and the length of expression of int-2. Currently, we are using three transgenic models, to induce expression of either int-2, AIB-1 or Cdc25B, to investigate the interaction of oncogenes and hormones in the transformation of the mammary gland epithelium.

Selected Publications