 |
Assistant Professor
B.A. University of California at Berkeley (1986) Ph.D. Brown University (1996) Post-doctoral Fellow, National Cancer Institute (1996-2000) |
Research:
The retrovirus
HTLV-I (human T lymphotrophic virus type I) was identified in 1980 and
causes adult T cell leukemia (ATL), a rapidly aggressive and lethal cancer
with no known cure. The cancer is highly resistant to standard cancer treatmentsÑchemotherapy
and radiationÑso that patients diagnosed with ATL have an average survival
time of six months. An estimated 10-20 million people in the world
are infected by HTLV-I, and transmission of the virus occurs primarily
human breast milk; therefore, most infected individuals were infected as
infants. To a lesser extent, the virus is also transmitted via blood
transfusions, IV drug use, and sexual contact. People who test positive
for HTLV-I are found predominantly in specific regions of the world: the
Carribean, southwestern Japan, northern and equatorial Africa, and southeastern
Italy. Other regions, including the United States, especially in
the Gulf coastal states, have small groups of infected individuals.
Infected individuals have a 3-5% chance of developing ATL.
The virus belongs to the Oncovirinae
subfamily of the Retroviridae family. The viral genome is approximately
9 kb in length and share similarity to other retroviruses in that HTLV-I
also encodes the gag, pol, env genes. The virus also encodes several
other HTLV-I-specific genes, including a 353 amino acid, 40 kDa protein
known as Tax. Tax is responsible for the transforming phenotype of
HTLV-I; however, the exact biochemical mechanism of transformation by Tax
is not known. Several Tax functions have been identified and the
commonality between all the studies is that Tax activates transcription.
Tax has been shown to modulate the activity of three transcriptional pathways:
NF-kB, CREB, SRF.
The research in our laboratory
is focused on Tax regulation of the SRF pathway. We have shown that
Tax interacts directly with the ternary complex factor (TCF) to activate
transcription via the serum response element (SRE). We are continuing
our studies in the regulation of TCFs by Tax, including kinase activation
pathways and inhibitory pathways.
Selected Publications:
Maureen Shuh and David Derse (2000). Ternary complex factors
and cofactors are essential for HTLV-I Tax transactivation of the serum
response element. Journal of Virology. 74(23):11394-11397.
David Derse, Maureen Shuh, Shawn Hill (1999). Examining HTLV-I gene function and expression with molecularly cloned proviruses. In Molecular Pathogenesis of HTLV-I: A Current Perspective. Edited by O. John Semmes and Marie-Louise Hamarskjold; ABI Professional Publications: Arlington, Virginia. Pages.123-130.
Shawn A. Hill, Maureen Shuh, and David Derse (1999). Comparisons of defective HTLV-I proviruses predict the mode of origin and coding potential of internally deleted genomes. Virology. 263:273-281.
Maureen Shuh, Shawn A. Hill, and David Derse (1999). Defective
and wild-type HTLV-I proviruses: Characterization of
gene products and potential trans- interactions between proviruses.
Virology.
262:442-451.
Laboratory:
 |
Frederick "Chuck" Streich, Jr.
B.S. Tulane University (2001)
|
| Past and present research undergraduate students: | Project: |
| Jessica E. Landry,
B.S., Loyola University New Orleans (2002): |
Tax regulation of signal transduction pathways. |
| Erin C. Cunningham,
Loyola University New Orleans (Class of 2003): |
Tax regulation of transcriptional inhibitors. |
Courses taught at Loyola:
Dr. Maureen Shuh
Loyola University New Orleans
Box 25
6363 St. Charles Avenue
New Orleans, LA 70118Office telephone: 504-865-3285
Lab telephone: 504-865-2502
Dept. office: 504-865-2288 (secretary)
FAX number: 504-865-2920e-mail: mshuh@loyno.edu