Casey Wright

  • Associate Professor

    Phone: (409) 772-0461
    Fax: (409) 747-1938

  • 1992-1996 Kansas State University, Manhattan, Kansas
    Bachelor of Science in Biology, December 14, 1996 

    1998-2003 Kansas State University,Manhattan, Kansas
    Doctor of Philosophy in Molecular, Cellular, and Developmental Biology, December 12, 2003  

    2003-2008 University of Michigan Medical School, Ann Arbor, Michigan
    Postdoctoral Fellow, Department of Pathology and Internal Medicine, August 14, 2008
  • My research program is focused on studying the contribution of inflammatory signaling to the development and progression of autoimmune diseases, including hematological malignancies. Specifically, we focus on the regulatory mechanisms of two transcription factors that play a role in promoting cancer and autoimmunity, nuclear factor-kappaB (NF-kB) and the aryl hydrocarbon receptor (AHR). We have found a common link between these two pathways and, given that the AHR is a major sensor of xenobiotics, we are committed to understanding how the environment influences the development of autoimmune disorders. Our long-term goal is to better understand how the NF-kB and AHR signaling pathways are regulated on a molecular level in order to identify possible therapeutic targets for the myriad immunological disorders that arise from deregulated signaling.  To achieve our goal we mostly employ molecular, biochemical, and immunological techniques in order to test our hypotheses. I encourage enthusiastic postdoctoral candidates and prospective students with similar backgrounds/interests to contact me regarding available positions in the laboratory.
    1. Gardella, K.A., Tiwary, R., Wright, C.W. Lymphoid malignancies ARNT unstoppable. Aging, 2016, 8, 1292-1293, PMID: 27466280.
    2. Gardella*, K.A., Muro*, I., Fang, G., Sarkar, K., Mendez, O., and Wright, C.W. Aryl hydrocarbon receptor nuclear translocator (ARNT) isoforms control lymphoid cancer cell proliferation through differentially regulating tumor suppressor p53 activity. Oncotarget, Priority Report, 2016, 7, 10710-10722, PMID: 26909609. *Equal Contributors.
    3. Nowinski, S.M., Solmonson, A., Rundhaug, J.E., Rho, O., Cho, J., Lago, C.U., Riley, C.L., Lee, S., Kohno, S., Dao, C.K., Nikawa, T., Bratton, S.B., Wright, C.W., Fischer, S.M., DiGiovanni, J., and Mills, E.M. Mitochondrial uncoupling links lipid catabolism to Akt inhibition and resistance to tumorigenesis. Nature Communications, 2015, 6:8137. doi: 10.1038/ncomms9137, PMID: 26310111.
    4. Lee, S., Challa-Malladi, M., Bratton, S.B., and Wright, C.W. Nuclear Factor-κB-inducing kinase (NIK) contains an amino terminal inhibitor of apoptosis (IAP)-binding motif (IBM) that potentiates NIK degradation by cellular IAP1 (c-IAP1). Journal of Biological Chemistry, 2014, 289, 30680-30689, PMID: 25246529.
    5. Muro, I., Fang, G., Gardella, K.A., Mahajan, I.M., and Wright, C.W. The TRAF3 adaptor protein drives proliferation of anaplastic large cell lymphoma cells by regulating multiple signaling pathways. Cell Cycle, 2014, 13, 1918-1926, PMCID: PMC4111755.  
    6. Mahajan, I.M., Chen, M., Muro, I., Robertson, J.D., Wright, C.W., and Bratton, S.B. BH3-only protein BIM mediates heat shock-induced apoptosis. Plos One, 2014, 9(1): e84388, 1-10, PMCID: PMC3888412.
    7. Wright, C.W. and Duckett, C.S. The aryl hydrocarbon nuclear translocator alters CD30- mediated NF-κB-dependent transcription. Science, 2009, 323, 251-255, PMCID: PMC2682336.  
    8. Csomos, R.A., Wright, C.W., Galbán, S., Oetjen, K.A., and Duckett, C.S. Two distinct signaling cascades target the NF-κB regulatory factor c-IAP1 for degradation. Biochemical Journal, 2009, 420, 83-91, PMCID: PMC2677214.

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