Janet Mertz
Professor of Oncology
Ph.D., Stanford University, 1975
Postdoctoral Research: MRC Laboratory of Molecular Biology, Cambridge, England
Address: 713A McArdle
Telephone: 262-2383
E-mail: mertz@oncology.wisc.edu
Research Interests:
Transcriptional regulation in DNA tumor viruses and breast cancer
Research Fields:
Cancer Genetics
Gene Expression
Microbial Genetics
Research Description: One of our
group's long-term interests involves regulation of gene
expression and mechanisms of oncogenesis by DNA tumor
viruses implicated in a variety of human cancers. Recently,
we have identified the cellular transcription factor ZEB-1
as a key player in establishment and maintenance of latency
following primary infection, reactivation out of latency
and, possibly, malignant transformation of cells by the
human herpes virus Epstein-Barr virus. These studies could
lead to the development of new ZEB-based therapies for the
treatment of EBV-associated diseases such as infectious
mononucleosis, nasopharyngeal carcinoma, and some
lymphomas.
Our group's second area of research concerns the roles of
the human estrogen-related receptor a (ERRalpha) in
regulation of estrogen responsiveness and breast
carcinogenesis. We have found that ERRalpha can function as either a down-modulator or
a constitutive activator of estrogen response
element-directed transcription, with its activity regulated
in part by post-translational phosphorylations occurring via
EGFR/ErbB2 (HER2) signaling pathways. ERRalpha-positivity has been shown to be associated
with poor prognosis and tamoxifen resistance in breast
cancer. This finding is likely due to the active form of
ERRalpha substituting for estrogen
receptor to activate genes regardless of the presence of
ligands. We are currently working to develop reagents that
specifically detect the activator form of ERRalpha in primary breast tumors for use in
prognosis and determination of best currently available
therapeutic options for treatment of individual breast
cancers. We also hope to identify drugs that can interfere
with ERRalpha's functional activities
for use as a novel therapy, especially for the treatment of
ER-negative and tamoxifen-resistant breast cancers for which
there are currently a paucity of good therapeutic options.
Representative Publications:
Iempridee, T., Das, S., Xu, I.,and Mertz J.E.
Transforming Growth Factor
{beta}-Induced Reactivation of Epstein-Barr Virus Involves Multiple
Smad-Binding Elements Cooperatively Activating Expression of the Latent-Lytic
Switch BZLF1 Gene.
J Virol. Aug;85(15):7836-48, 2011.
Yu, X., McCarthy, P.J., Lim, H.J., Iempridee, T., Kraus ,R.J.,
Gorlen, D.A., and Mertz J.E. (2011)
The
ZIIR element of the Epstein-Barr virus BZLF1 promoter plays a central role in
establishment and maintenance of viral latency
. J Virol. May;85(10):5081-90, 2011.
Ellis, A. L., Iempridee, T., Xu, I., and Mertz, J. E. Cellular MicroRNAs 200b and 429 Regulate the Epstein-Barr Virus Switch
Between Latency and Lytic Replication. J Virol. Oct;84(19):10329-43, 2010.
Berg, P., and Mertz, J. E. Personal Reflections on the Origins and Emergence of Recombinant DNA Technology. Genetics, 184: 9-17, 2010.
Ellis, A. L., Wang, Z., Yu, X., and Mertz, J. E.
Either ZEB1 or ZEB2/SIP1 Can Play a Central Role in Regulating the
Epstein-Barr Virus Latent-Lytic Switch in a Cell-Type-Specific Manner.
J. Virol., 84: 6139-6152, 2010.
Ellis-Connell, A. L., Iempridee, T., Xu, I., and Mertz, J. E.
Cellular MicroRNAs 200b and 429 Regulate the Epstein-Barr Virus Switch
Between Latency and Lytic Replication. J. Virol., in press, 2010 [Epub
ahead of print Jul 28, 2010].
Hagemeier, S. R., Dickerson, S. J., Meng, Q., Yu, X., Mertz, J. E., and Kenney, S. C.
Sumoylation of the Epstein-Barr Virus BZLF1 Protein Inhibits Its
Transcriptional Activity and Is Regulated by the Virus-Encoded Protein
Kinase. J. Virol., 84: 4383-4394, 2010.
Das, S., Becker, B. N., Hoffmann, F. M., and Mertz, J. E.
Complete Reversal of Epithelial to Mesenchymal Transition Requires
Inhibition of Both ZEB Expression and the Rho Pathway. BMC Cell Biol.,
10:94, 2009.
Hyde, J. S., and Mertz, J. E. Gender, Culture, and Mathematics Performance. Proc. Natl. Acad. Sci. USA, 106: 8801-8807, 2009.
Mertz, J. E.
Why Females Remain Underrepresented in Mathematics at the Highest
Level. Am. Soc. Cell Biol. Newsletter, pp. 7-9, August 2009.
Andreescu, T., Gallian, J. A., and Mertz, J. E. Identifying and Cultivating Extraordinary Mathematical Talent. Teachers College Record, November 26, 2008.
Andreescu, T., Gallian, J. A., Kane, J. M., and Mertz, J. E. Cross-Cultural Analysis of Students with Exceptional Talent in Mathematical Problem Solving. Notices of the AMS, 55: 1248-1260, 2008.
Ariazi, E. A., Kraus, R. J., Farrell, M. L.,
Jordan, V. C., and Mertz, J. E.
Estrogen-Related Receptor a1
Transcriptional Activities Are Regulated in Part via the
ErbB2/HER2 Signaling Pathway. Mol. Cancer Res., 5: 71-85, 2007.
Feng, W.-h., Kraus, R. J., Dickerson, S. J., Lim,
H. J., Jones, R. J., Yu, X., Mertz, J. E., and Kenney, S.
C. ZEB1 and c-Jun Levels Contribute to the
Establishment of Highly Lytic Epstein-Barr Virus Infection
in Gastric AGS Cells. J. Virol., 81:
10113-10122, 2007.
Vu, E. H., Kraus, R. J., and Mertz, J.
E. Phosphorylation-Dependent Sumoylation of
Estrogen-Related Receptor a1. Biochemistry, 46:
9795-9804, 2007.
Yu, X., Wang, Z., and Mertz, J. E.
ZEB1 Regulates the Latent-Lytic Switch in Infection by
Epstein-Barr Virus. PLoS Pathog., 3:e194,
2007.
Professor of Oncology
Ph.D., Stanford University, 1975
Postdoctoral Research: MRC Laboratory of Molecular Biology, Cambridge, England
Address: 713A McArdle
Telephone: 262-2383
E-mail: mertz@oncology.wisc.edu
Research Interests:
Transcriptional regulation in DNA tumor viruses and breast cancer
Research Fields:
Cancer Genetics
Gene Expression
Microbial Genetics
One of our
group's long-term interests involves regulation of gene
expression and mechanisms of oncogenesis by DNA tumor
viruses implicated in a variety of human cancers. Recently,
we have identified the cellular transcription factor ZEB-1
as a key player in establishment and maintenance of latency
following primary infection, reactivation out of latency
and, possibly, malignant transformation of cells by the
human herpes virus Epstein-Barr virus. These studies could
lead to the development of new ZEB-based therapies for the
treatment of EBV-associated diseases such as infectious
mononucleosis, nasopharyngeal carcinoma, and some
lymphomas.
Our group's second area of research concerns the roles of
the human estrogen-related receptor a (ERRalpha) in
regulation of estrogen responsiveness and breast
carcinogenesis. We have found that ERRalpha can function as either a down-modulator or
a constitutive activator of estrogen response
element-directed transcription, with its activity regulated
in part by post-translational phosphorylations occurring via
EGFR/ErbB2 (HER2) signaling pathways. ERRalpha-positivity has been shown to be associated
with poor prognosis and tamoxifen resistance in breast
cancer. This finding is likely due to the active form of
ERRalpha substituting for estrogen
receptor to activate genes regardless of the presence of
ligands. We are currently working to develop reagents that
specifically detect the activator form of ERRalpha in primary breast tumors for use in
prognosis and determination of best currently available
therapeutic options for treatment of individual breast
cancers. We also hope to identify drugs that can interfere
with ERRalpha's functional activities
for use as a novel therapy, especially for the treatment of
ER-negative and tamoxifen-resistant breast cancers for which
there are currently a paucity of good therapeutic options.
Iempridee, T., Das, S., Xu, I.,and Mertz J.E.
Transforming Growth Factor
{beta}-Induced Reactivation of Epstein-Barr Virus Involves Multiple
Smad-Binding Elements Cooperatively Activating Expression of the Latent-Lytic
Switch BZLF1 Gene.
J Virol. Aug;85(15):7836-48, 2011.
Yu, X., McCarthy, P.J., Lim, H.J., Iempridee, T., Kraus ,R.J., Gorlen, D.A., and Mertz J.E. (2011) The ZIIR element of the Epstein-Barr virus BZLF1 promoter plays a central role in establishment and maintenance of viral latency . J Virol. May;85(10):5081-90, 2011.
Ellis, A. L., Iempridee, T., Xu, I., and Mertz, J. E. Cellular MicroRNAs 200b and 429 Regulate the Epstein-Barr Virus Switch Between Latency and Lytic Replication. J Virol. Oct;84(19):10329-43, 2010.
Berg, P., and Mertz, J. E. Personal Reflections on the Origins and Emergence of Recombinant DNA Technology. Genetics, 184: 9-17, 2010.
Ellis, A. L., Wang, Z., Yu, X., and Mertz, J. E. Either ZEB1 or ZEB2/SIP1 Can Play a Central Role in Regulating the Epstein-Barr Virus Latent-Lytic Switch in a Cell-Type-Specific Manner. J. Virol., 84: 6139-6152, 2010.
Ellis-Connell, A. L., Iempridee, T., Xu, I., and Mertz, J. E. Cellular MicroRNAs 200b and 429 Regulate the Epstein-Barr Virus Switch Between Latency and Lytic Replication. J. Virol., in press, 2010 [Epub ahead of print Jul 28, 2010].
Hagemeier, S. R., Dickerson, S. J., Meng, Q., Yu, X., Mertz, J. E., and Kenney, S. C. Sumoylation of the Epstein-Barr Virus BZLF1 Protein Inhibits Its Transcriptional Activity and Is Regulated by the Virus-Encoded Protein Kinase. J. Virol., 84: 4383-4394, 2010.
Das, S., Becker, B. N., Hoffmann, F. M., and Mertz, J. E. Complete Reversal of Epithelial to Mesenchymal Transition Requires Inhibition of Both ZEB Expression and the Rho Pathway. BMC Cell Biol., 10:94, 2009.
Hyde, J. S., and Mertz, J. E. Gender, Culture, and Mathematics Performance. Proc. Natl. Acad. Sci. USA, 106: 8801-8807, 2009.
Mertz, J. E. Why Females Remain Underrepresented in Mathematics at the Highest Level. Am. Soc. Cell Biol. Newsletter, pp. 7-9, August 2009.
Andreescu, T., Gallian, J. A., and Mertz, J. E. Identifying and Cultivating Extraordinary Mathematical Talent. Teachers College Record, November 26, 2008.
Andreescu, T., Gallian, J. A., Kane, J. M., and Mertz, J. E. Cross-Cultural Analysis of Students with Exceptional Talent in Mathematical Problem Solving. Notices of the AMS, 55: 1248-1260, 2008.
Ariazi, E. A., Kraus, R. J., Farrell, M. L., Jordan, V. C., and Mertz, J. E. Estrogen-Related Receptor a1 Transcriptional Activities Are Regulated in Part via the ErbB2/HER2 Signaling Pathway. Mol. Cancer Res., 5: 71-85, 2007.
Feng, W.-h., Kraus, R. J., Dickerson, S. J., Lim, H. J., Jones, R. J., Yu, X., Mertz, J. E., and Kenney, S. C. ZEB1 and c-Jun Levels Contribute to the Establishment of Highly Lytic Epstein-Barr Virus Infection in Gastric AGS Cells. J. Virol., 81: 10113-10122, 2007.
Vu, E. H., Kraus, R. J., and Mertz, J. E. Phosphorylation-Dependent Sumoylation of Estrogen-Related Receptor a1. Biochemistry, 46: 9795-9804, 2007.
Yu, X., Wang, Z., and Mertz, J. E. ZEB1 Regulates the Latent-Lytic Switch in Infection by Epstein-Barr Virus. PLoS Pathog., 3:e194, 2007.
