NIH Training Program

Stem Cell Engineering represents the convergence of the biological and physical sciences, engineering, and ethics and law. Our interdisciplinary Stem Cell Biological Engineering program funded by the National Institutes of Health was established in 2011 to formally organize new training opportunities in stem cell biological engineering, while dissolving traditional academic barriers to interdisciplinary graduate science education. Fellows are supported for 24 months, in the 2nd and 3rd years of their doctoral studies.

This program provides pre-doctoral training opportunities in the biology of stem cells and its application to the enhancement of human health. Program participants work at the interface of biology and engineering, preparing them to be leaders in academia and industry. A three-month industrial internship experience is a key facet of this program.

Program Leadership

Dr. David Schaffer
Program Director
Chemical and Biomolecular Engineering, and
Helen Wills Neuroscience Institute
Director, Berkeley Stem Cell Center
  Dr. Kevin Healy
Program Director
Bioengineering, and
Materials Science and Engineering


2017-18 Stem Cell Biological Engineering Fellows

Tiama Hamkins-Indik

Dysfunction and leakiness in vasculature due to breakdown in tight junctions are associated with many known diseases, including cancer and Alzheimer’s. The tight junction protein ZO-1 is implicated in transducing force at cell junctions in endothelial cells, and its absence leads to embryonic lethality in mouse models. However, its function during differentiation is unknown. I am using induced pluripotent stem (iPS) cells to test the hypothesis that ZO-1 serves as a mechanosensor to direct endothelial cell differentiation.

Alec Heckert

Type II nuclear receptors are vertebrate transcription factors that directly transduce small molecule inputs - such as retinoic acid, vitamin D3, and thyroid hormone - into changes in gene expression. Understanding how cells "read out" the concentration of these inputs is complicated by interactions between individual receptors, most of which compete for heterodimerization with special partners called retinoid X receptors in order to bind DNA. My project uses live cell single-molecule microscopy to determine how the DNA binding and transcriptional activation of individual receptor species are affected by the expression levels and oligomeric states of other receptors, with the goal of understanding how competition for the shared retinoid X receptors places limits on signaling.

Marcela Preininger

Cellular senescence is an irreversible stress response that arrests proliferation, decreases a cells functional capacity, and elicits a pathological secretory phenotype. In the brain, an emerging paradigm suggests that the accumulation of senescent astrocytes during aging is a driving force for neurodegenerative diseases. Since we know that disruption of the blood-brain-barrier during aging also contributes to neuropathology via astrocyte dysfunction, my project hopes to reconcile the mechanistic underpinnings of these two processes with hopes to identify novel therapeutic targets for preventing and mitigating age-onset neurodegenerative diseases.

Andrew Widjaja

Neurodegenerative diseases become more prevalent with age and are affected by mitochondrial dysfunction resulting from mitochondrial DNA mutations and oxidative stress. Studies suggest that the accumulation of reactive oxygen species produced by mitochondria of mature cell populations results in cognitive decline that accompanies aging. I am using neural stem cells to investigate how certain stress response mechanisms may worsen with age, and whether such declines may be reversed.


Program Information