Department of Biochemistry & Molecular Biology

Michael Leffak, Ph.D., Interim Chair

Michael P. Markey, Ph.D.

Research Assistant Professor
Director, Center for Genomics Research

Lab: 035 Diggs lab
Office: 048 Diggs Lab
(937) 775-4536
Email: michael.markey@wright.edu

Education:

Doctoral: University of Cincinnati (Erik S. Knudsen)
Postdoctoral: Wood Hudson Cancer Research Laboratory (Taiping Chen)
Postdoctoral: Wright State University (Steven J. Berberich)

Research:

The specific aims of my current project are to determine the mechanism for MDM4 transcript repression following genotoxic stress, and to examine the expression and biological significance of alternative transcripts of MDM4. My preliminary data indicate that the MDM4 gene is repressed in response to DNA damage regardless of cellular p53 status or transformation, in contrast to constitutive expression described previously. Another project (recently funded) uses comparative genomic hybridization to characterize genomic changes in melanoma samples. An additional project (pending funding) aims to use microarrays to determine the changes in gene expression and splicing that occur in response to nanoparticle exposure, and to define a molecular signature nanoparticles toxicity.

Selected References:

Markey, MP. "Regulation of MDM4." In press at Frontiers in Bioscience, November 2010.

Schaeper JP, Chen T, Deddens JA, Colligan BM, Markey MP, Jackson CR, Wang KS, Shields RJ, Lucas D, Pemberton JO, Douglass LE, Graff JR, and Carter JH. "The Int7G24A germline variant of the TGFβR1 gene is associated with human ovarian cancer incidence, progression, and surviva.l" Submitted to Clinical Cancer Research, January 2010.

Heminger H, Markey M, Mpagi M and Berberich SJ. "Alterations in gene expression and sensitivity to genotoxic stress following HdmX knockdown in human tumor cells harboring wild-type p53." Aging. 2009 Jan 7;1(1):89-108.

Markey, M and Berberich, S. "HdmX Transcripts are Reduced Following Genotoxic Stress." Oncogene, 2008 Nov 27;27(52):6657-66.

Markey, MP, Bergseid J, Bosco EE, Stengel K, Xu H, Mayhew CN, Schwemberger SJ, Braden WA, Jiang Y, Babcock GF, Jegga AG, Aronow BJ, Reed MF, Wang JY, Knudsen ES. "Loss of the retinoblastoma tumor suppressor: differential action on transcriptional programs related to cell cycle control and immune function." Oncogene (2007) 26, 6307-6318.

Chen, T., Jackson, C., Link, A., Markey, M., et al. "Int7G24A variant of transforming growth factor-beta receptor type I is associated with invasive breast cancer." Clinical Cancer Research. 2006 Jan 15;12(2):392-7.

Markey, M., et al. "Loss of the Retinoblastoma Tumor Suppressor: Differential Action on Transcriptional Programs Related to Cell Cycle Control and Immune Function." Submitted to Oncogene, December 2005.

Markey, M., et al. "Geminin is Targeted for Repression by the RB Pathway Through Intragenic E2F Sites." J Biol Chem. 2004 Jul 9;279(28):29255-62.

Angus, S., Mayhew, C., Solomon, D., Braden, W., Markey, M. et. al. "RB Reversibly Inhibits DNA Replication by Two Temporally Distinct Mechanisms." Mol Cell Biol. 2004 Jun;24(12):5404-20.

Markey, M. et al. "Unbiased Analysis of RB-Mediated Transcriptional Repression Identifies Novel Targets and Distinctions from E2F Action." Cancer Research. 2002 Nov 15; 62(22):6587-97.

Angus, S., Wheeler, L., Zhang, X., Markey, M., et al. "The Retinoblastoma Tumor Suppressor Targets dNTP Metabolism To Regulate Cell Cycle Progression." J Biol Chem. 2002 Nov 15;277(46):44376-84.

Angus, S., Fribourg, A., Markey, M., et al. "Active Rb Elicits Late G1/S Inhibition." Exp Cell Res. 2002 Jun 10;276(2):201-13.