Stem Cells and Human Diseases (SC&HD)
Pluripotent stem cells (PSCs), including embryo-derived ESCs and somatic cell-derived iPSCs, possess unlimited self-renewal potential in culture and the ability to differentiate into all cell types of the adult organism. Given these unique cellular properties, PSCs are not only considered a major promise for regenerative medicine but also a valuable tool to interrogate molecular underpinnings controlling cell fate determination, and a powerful platform to uncover altered molecular mechanisms linked to human disease.
Our global aim is focused on understanding how regulatory information encoded by the genome is integrated with the epigenetic and epitranscriptomic machineries to control cellular plasticity in the context of cellular reprogramming and pluripotency, and how perturbations of these mechanisms could be associated with defects in development and disease.
Some of the ongoing questions we are interested in studying are:
- Which molecular programs are in place to unleash the full potential of pluripotent cells for therapeutic purposes?
- How do dietary perturbations lead to aberrant epigenetic and metabolic regulation which compromise the generation of safe iPSCs from elderly donors?
- Can we modulate the impact of obesity and aging in induced reprogramming technology to achieve cellular rejuvenation without affecting cell identity?
For this purpose, we are employing a broad combination of methods of cell and molecular biology, genome interventions, high-throughput genomic and proteomic approaches, and bioinformatics.
For additional information on our group, please visit the website: http://www.fidalgostemlab.com
Detecting and Modulating ER Stress to Improve Generation of Induced Pluripotent Stem Cells.
An Optimized Immunoprecipitation Protocol for Assessing Protein-RNA Interactions In Vitro.
ADAR1-Dependent RNA Editing Promotes MET and iPSC Reprogramming by Alleviating ER Stress
BMAL1 coordinates energy metabolism and differentiation of pluripotent stem cells
Zfp281 Coordinates Opposing Functions of Tet1 and Tet2 in Pluripotent States.