
Frederick Anokye-Danso, MSC, PhD
- Johns Hopkins School of Medicine Faculty
Languages
- English
Gender
MaleAbout Frederick Anokye-Danso
Primary Academic Title
Assistant Professor of Medicine
Background
Dr. Frederick Anokye-Danso is an Assistant Professor of Medicine at the Johns Hopkins University School of Medicine. His research focuses on developmental and molecular mechanisms by which precursor mesenchymal stem cells are programmed to become fat cells and their functions (and dysfunctions) in metabolic health and diseases such as insulin resistance, diabetes and obesity.
The long-term goal of Dr. Anokye-Danso is to investigate the early mechanisms by which genetic factors such as PPARG and C/EBPs orchestrate formation of fat cells and adipose tissues as a whole. He uses computer simulations and biological models in answering major questions in the field. Currently, he seeks to determine genetic factors that independently regulate PPARG isoforms. The overall aim is to develop a therapeutic strategy where the desirable effects of one isoform (in tackling insulin resistance) could be harvested in the absence of the other isoform.
Dr. Anokye-Danso received BSc from University of Ghana and PhD from Okayama University, Japan. He then trained as Postdoctoral Researcher at the University of Pennsylvania before joining the faculty at the Johns Hopkins University School of Medicine.
Centers and Institutes
Contact for Research Inquiries
5501 Hopkins Bayview Circle
Asthma & Allergy Building
Baltimore, MD 21224
Research Interests
Adipocytes and Pluripotent Stem Cells
Lab Website
Anokye-Danso Lab
- Our long-term goal is to investigate the mechanisms by which genetic factors such as PPARG and C/EBPs orchestrate formation of fat cells and adipose tissues as a whole. We use computer simulations and biological models in answering major questions in the field. Currently, we seek to determine genetic factors that independently regulate PPARG isoform 2 but not isoform 1 (and vice-versa). The overall aim is to develop a therapeutic strategy where the desirable effects of one isoform in tackling insulin resistance could be harvested in the absence of the other isoform.