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Amy Moran
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E-mail:
moran137@umn.edu
Thesis advisor: Kris
Hogquist
Year entered: 2006
Degree received:
B.S., Biology, Gonzaga University, Spokane, WA 2001
Honors and Awards:
- 3M Fellowship
- Immunology Training Grant 2008-2010
- Minnesota Medical Foundation’s Jan Lunden Award
- College of Biological Sciences Outstanding Performance
Award for a Teaching Assistant 2008
Thesis research:
The process of clonal deletion and the elimination
of self-reactive T cells highlight the importance of apoptosis
within the thymus. A few key molecules have been identified
as necessary in facilitating cell death after a high affinity
TCR signal and this includes the transcription factor Nur77.
Nur77 is an orphan nuclear steroid receptor that is up-regulated
after high affinity TCR engagement. This increased expression
is shown to sequester the pro-survival protein, Bcl-2 away
from the mitochondria and promote apoptosis. In addition,
functional studies performed on constitutively expressed Nur77
as well as dominant negative Nur77 mice have illustrated the
important role of this molecule in mediating apoptosis. Specifically,
over expression of a Nur77 dominant negative protein results
in the inhibition of apoptosis associated with negative selection
while constitutive expression of Nur77 in thymocytes results
in increased apoptosis. Although high affinity TCR engagement
gives rise to two possible outcomes, clonal deletion or agonist
selection, very little is known about that latter. The ability
of a thymocyte to become a regulatory T cell via a clonal
deletion type signal is poorly understood. Moreover, the idea
that a cell that is highly self-reactive could be selected
to survive and migrate into the periphery where it can regulate
other potentially self-reactive T cells is an intriguing idea
that warrants further investigation. Thus, I am interested
in studying the fate of thymocytes that have received a high
affinity signal via their TCR and survived.
Publications:
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