Website:William Stanford's Lab
Stem cells and progenitors play indispensable roles in embryonic development and homeostasis in many adult tissues. Disruption of the transcriptional networks controlling stem cell function and fate determination results in developmental abnormalities and disease. The Stanford lab utilizes interdisciplinary approaches to identify and analyze key regulators of stem cell function and draft transcriptional networks that control stem cell fate. In this process, we have identified disease genes and pathways and generated animal models of human disease. This in turn has led to a new project to identify drug targets and to screen for small molecule drugs to treat a variety of diseases. Primarily, our lab studies embryonic stem cells, hematopoietic stem cells, and mesenchymal stem/ progenitor cells. We use gene trap, gene targeting, transgenesis, viral transduction, and ENU mutagenesis to genetically manipulate stem cells and generate mouse models of human disease. Various genomics, proteomics, and imaging modalities are used to study stem cell behavior. The knowledge gained by our transcriptional networks, cell fate analysis and models of disease projects drive our stem cell based-tissue engineering projects which also utilize microfabrication techniques to create microenvironments to guide stem cell differentiation and tissue development.
Recent Stem Cell Publications:
Walker E, M Ohishi, RE Davey, W Zhang, PA Cassar, TS Tanaka, SD Der, Q Morris, TR Hughes, PW Zandstra, and WL Stanford. Predicting and Testing Novel Transcriptional Networks Regulating Embryonic Stem Cell Self-Renewal and Commitment. Cell Stem Cell 1: 71-86, 2007
Wang C-H, N Anderson, RD Weisel, S-H Li, PE Szmitko, PWM Fedak, R-K Li, DAG Mickle, TM Yau, WL Stanford, and S Verma. Stem Cell Factor Deficiency is Vasculoprotective. Unraveling a New Therapeutic Potential of Imatinib Mesylate. Circulation Research 99: 617-625, 2006
Bonyadi, M, SD Waldman, D Liu, JE Aubin, MD Grynpas, and WL Stanford. Mesenchymal Precursor Self-Renewal Deficiency Leads to Age-Dependent Osteoporosis in Sca?1/Ly?6A Null Mice. Proc. Natl. Acad. Sci. USA, 100:5840-5845, 2003