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Research Project
As an NSF Summer Research Student in Tim’s lab, my role
was similar to those of graduate students doing their rotations.
I worked closely with Mark and Rob to study how 2,3,7,8-tetrachlorodibenzo-p-dioxin
(TCDD) modulates p120 gene expression. TCDD elicits a wide variety
of biochemical and toxic effects in a tissue-, sex-, and species-specific
manner, some of which include tumor promotion, immuno- hepato-
and dermal toxicity, lethality, teratogenicity, developmental
and reproductive toxicity, and induction of numerous detoxifying
enzymes. Modulation of target gene expression is dependent upon
the binding of the aryl hydrocarbon receptor (AhR)/aryl hydrocarbon
receptor nuclear translocator (ARNT) to upstream activating
sequences called dioxin response elements (DREs). According
to Mark’s database search, eight DREs were present in the
promoter region of the nucleolar antigen p120. This led us to
hypothesize that TCDD induces the p120 gene through the AhR
signaling pathway. My responsibilities were to create a p120
promoter construct containing the luciferase reporter gene,
to transfect wild type mouse hepatoma cells with p120CAT reporter
gene containing the ?2498/+132 p120 promoter region upstream
of the chloramphenicol acetyl transferase gene (CAT), and to
treat the cells with TCDD. I also helped Rob obtain IMAGE clone
IDs from NCBI's Unigene database.
The experience allowed me to refine my techniques in molecular
biology and provided me with an introduction to bioinformatics.
Not only was I able to see the amount of dedication, hard work,
and passion that was required to be a successful graduate student,
but also saw how intellectually rewarding research can be.
I am planning to take a year off following my graduation (May
2000) to apply to medical school. While awaiting my acceptance
to medical school, I will be working as a Post-Baccalaureate
IRTA research fellow in Dr. Judith Levin’s lab at the National
Institutes of Child Health and Development in Maryland. I will
assist her lab in elucidating the molecular mechanisms involved
in retrovirus replication, in particular, the process of reverse
transcription (a major target of anti-HIV therapy).
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