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Baker, Tracie
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Blanke, Kristina
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Brinkman, Ashley
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Booth, Clarissa
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Brody, Matthew
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Burns, Felipe
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Chesney, Alexandra
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Cholewa, Brian
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Clements, Justin
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Coriano, Carlos
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Ding, Lina
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Hutchinson, John
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Irving, Amy
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Irving, Roy
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Johnson, Brian
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Johnson, Delinda
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Johnson, Shaina
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Kim Tae Won
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Kumar, Kartik
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Lee, Sung-Kyoung
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Lorch, Jeff
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Olson, Jake
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Palenski, Tammy
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Park, Heesoo
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Pham, Ly
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Poenitzsch, Ashley
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Rodriguez, Carlos
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Rivera, Emmanuel
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Shanle, Erin
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Shea, Michael
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Velasco, Javier
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Wiecinski, Paige
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Wong, Letitia
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Yang, Sarah
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Yang, Zhao
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Yue, Monica
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Zhao, Yun
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Schmit, Travis
Travis Schmit - Email
PhD Candidate - Started 2005
Stoughton, WI
Lab of Nihal Ahmad, PhD
Undergraduate Work
University of Wisconsin-Madison
Bachelors of Science, Genetics (2005)
Memberships
Associate Member of American Association for Cancer Research
Interests/Hobbies
Photography, football, baseball, hunting, fishing, in other words, anything outdoors, and playing with my 2-year old son Mason.
Research as of May 2006
The focus of my research is to explore the involvement of the Polo-like kinases (Plks), a conserved serine/threonine family of kinases critical for mitosis regulation, in the development of cancer. Many environmental stresses (such as shifts in temperature, osmolarity, radiation and chemicals) may lead to problems with actin cytoskeleton and cytokinesis, and Plks have been shown to be critical regulators of these processes. Further, a major hallmark of cancer is the dysregulation of key cell cycle components arising from mutations produced by environmentally induced oxidative stress and the resulting DNA damage. These include tumor suppressor genes that, when mutated, are unable to control cell cycle checkpoints and allow the cell to proliferate unchecked, or oncogenes which become constitutively active and promote cellular growth. The Plk family of mitotic kinases contains both members that can act in an oncogenic manner and members that act as tumor suppressors.
I am studying the role of Plk1 and Plk3 in cancer development. Plk1, the most widely studied member of this kinase family, promotes Cdk1/CyclinB1 activity which is the main driving force into and through mitosis. Conversely, Plk3 acts in an inhibitory manner in the presence of DNA damage opposing the activity of Plk1 and halting cell cycle progression until repair is performed or the cell undergoes apoptosis. Thus, my focus is to determine the role of the Plks in cancer development and to establish if their dysregulation has a cause-and-effect association with disease progression. The outcome of this work may lead to development of novel strategies for the management of cancer.
Publications- Schmit TL, Setaluri V, Spiegelman VS, and Ahmad N. Human Numb regulates Polo-like kinase 1 stability and localization during mitosis. Presubmission
- Jung-Hynes B, Schmit TL, Reagan-Shaw SR, Siddiqui IA, Mukhtar H, and Ahmad N. Melatonin is a novel Sirt1 inhibitor and imparts anti-proliferative effects against PCa in vitro in cell culture and in vivo in transgenic adenocarcinoma of mouse prostate (TRAMP) model. Submitted
- Schmit TL, Ledesma MC, and Ahmad N. Modulating Polo-Like Kinase 1 as a Means for Cancer Chemoprevention. Pharm Res. 2010 Jan 27. Ahead of Press
- Schmit TL, Zhong W, Nihal M, and Ahmad N. Polo-like kinase 1 (Plk1) in non-melanoma skin cancers. Cell Cycle. 2009 Sep 1;8(17):2697-702.
- Schmit TL, Zhong W, Setaluri V, Spiegelman VS, and Ahmad N. Targeted depletion of Polo-like kinase (Plk) 1 through lentiviral shRNA or a small-molecule inhibitor causes mitotic catastrophe and induction of apoptosis in human melanoma cells. J Invest Dermatol. 2009 Dec;129(12):2843-53.
- Schmit TL and Ahmad N. Regulation of mitosis via mitotic kinases: new opportunities for cancer management. Mol Cancer Ther. 2007 Jul;6(7):1920-31.
Travis Schmit
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Graduate Seminars Given
04/15/10
FINAL DEFENSE
Dysregulation of the neuronal stem cell fate determinant Numb and Polo-like kinase 1 in the melanoma cell
02/14/08
The role of Plk1 expression in melanoma - Possible regulation of Notch signaling
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