B.A., Computer Science, Gustavus Adolphus College Ph.D., Cancer
Biology, University of Wisconsin - Madison Postdoctoral fellowship,
Howard Hughes Medical Institute, University of Utah
After working as a computer scientist, Dr. Habig obtained his
Ph.D. at the University of Wisconsin research aimed at understanding
how cancer-causing hepatitis B virus (HBV) replicates its genome
through reverse transcription in the liver of infected individuals.
Since then, he has researched the mechanism of RNA interference in C.
elegans to better understand cellular defense against viral
Habig, J.W., P.J. Aruscavage, and B.L. Bass (2008). In C.
elegans, high levels of dsRNA allow RNAi in the absence of RDE-4.
PLoS ONE, 3(12):e4052.
Welker, N., J.W. Habig, and B.L. Bass (2007). Genes misregulated
in C. elegans deficient in Dicer, RDE-4 or RDE-1, are enriched
for innate immunity genes. RNA, 13:1-13.
Habig, J.W., T. Dale, and B.L. Bass (2007). miRNA Editing â€“
We Should Have Inosine This Coming. Molecular Cell, 25:792-793.
Habig, J.W. and D.D. Loeb (2006). Sequence identity of the direct
repeats, DR1 and DR2, contributes to the discrimination between
primer translocation and in situ priming during replication of duck
hepatitis B virus. Journal of Molecular Biology, 364(1):32-43.
Habig, J.W. and D.D. Loeb (2003). Template switches during
plus-strand DNA synthesis of duck hepatitis B virus are influenced by
the base composition of the minus-strand terminal redundancy. Journal
of Virology, 77:12412-20.
Habig, J.W. and D.D. Loeb (2003). The conformation of the 3â€™
end of the minus-strand DNA makes multiple contributions to template
switches during plus-strand DNA synthesis of duck hepatitis B virus.
Journal of Virology, 77:12401-11.
Habig, J.W. and D.D. Loeb (2002). Small DNA hairpin negatively
regulates in situ priming during duck hepatitis B virus reverse
transcription. Journal of Virology, 76:980-9.