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    Hayla K Sluss PhD

    TitleAssistant Professor
    InstitutionUniversity of Massachusetts Medical School
    DepartmentMedicine
    AddressUniversity of Massachusetts Medical School
    364 Plantation Street, LRB
    Worcester MA 01605
    Phone508-856-3372
      Other Positions
      InstitutionUMMS - Graduate School of Biomedical Sciences
      DepartmentInterdisciplinary Graduate Program

        Overview 
        Narrative

        Biography

        Dr. Sluss received her Ph.D. from the University of Massachusetts Medical School, Worcester in 1997.

        Tumor Suppressors and Metabolic Control

        Dr.H.Sluss

        The research goals of the Sluss lab are to have a better understanding of the tumor suppressor p53. We investigate classical roles of p53 in tumor suppression and novel roles of p53 in metabolic disease. p53 is a protein that is mutated in over 50% of human cancer. This observation underscores its importance in prevention of cancer. We are using mouse models and perform in vitro studies to investigate p53 function.

        We have generated mouse knock-in models in phosphorylation and acetylation of p53. We have determined that p53 phosphorylation is critical for tumor suppressor function of p53. One aim of the lab is to continue to generate more knock-in mutations to study the synergy of the various phosphorylation sites on p53. We have also generated a knock-in model in which an acetylation site has been mutated. This mutant has lead to studies on the effects of dominant negative mutations on p53 in cancer.

        Another aim of the laboratory is to better understand the role of p53 in metabolism. This is a very new area of research for the p53 signaling pathway. We have applied genetic engineering and biochemistry to address this novel role of p53.



        Rotation Projects

        Rotation Projects

        Laboratory rotations are available to study p53 signaling pathway. Several projects are available, including studies of gene expression, the cell cycle, apoptosis, and tumor suppression. Targeted gene disruption approaches in mice combined with biochemical and molecular biology studies will be examined. Examples of potential rotation projects include the following:

        1. Generate a triple mutant in p53 amino-terminal phosphorylation sites. The rotation would involve learning molecular biology techniques such as recombinant DNA purification, analysis, mutation, and subcloning.

        2. Create cells from various genetically modified mice and analyze p53 function. The rotation would involve learning protein expression and purification techniques such as Western Blotting, protein purification, and FACS analysis.



        Bibliographic 
        selected publications
        List All   |   Timeline
        1. Armata HL, Shroff P, Garlick DE, Penta K, Tapper AR, Sluss HK. Loss of p53 Ser18 and Atm Results in Embryonic Lethality without Cooperation in Tumorigenesis. PLoS One. 2011; 6(9):e24813.
          View in: PubMed
        2. Regeling A, Armata HL, Gallant J, Jones SN, Sluss HK. Mice defective in p53 nuclear localization signal 1 exhibit exencephaly. Transgenic Res. 2011 Aug; 20(4):899-912.
          View in: PubMed
        3. Armata HL, Golebiowski D, Jung DY, Ko HJ, Kim JK, Sluss HK. Requirement of the ATM/p53 tumor suppressor pathway for glucose homeostasis. Mol Cell Biol. 2010 Dec; 30(24):5787-94.
          View in: PubMed
        4. Cellurale C, Weston CR, Reilly J, Garlick DS, Jerry DJ, Sluss HK, Davis RJ. Role of JNK in a Trp53-dependent mouse model of breast cancer. PLoS One. 2010; 5(8):e12469.
          View in: PubMed
        5. Guikema JE, Schrader CE, Brodsky MH, Linehan EK, Richards A, El Falaky N, Li DH, Sluss HK, Szomolanyi-Tsuda E, Stavnezer J. p53 represses class switch recombination to IgG2a through its antioxidant function. J Immunol. 2010 Jun 1; 184(11):6177-87.
          View in: PubMed
        6. Sluss HK, Gannon H, Coles AH, Shen Q, Eischen CM, Jones SN. Phosphorylation of p53 serine 18 upregulates apoptosis to suppress Myc-induced tumorigenesis. Mol Cancer Res. 2010 Feb; 8(2):216-22.
          View in: PubMed
        7. Armata HL, Garlick DS, Sluss HK. The ataxia telangiectasia-mutated target site Ser18 is required for p53-mediated tumor suppression. Cancer Res. 2007 Dec 15; 67(24):11696-703.
          View in: PubMed
        8. Das M, Jiang F, Sluss HK, Zhang C, Shokat KM, Flavell RA, Davis RJ. Suppression of p53-dependent senescence by the JNK signal transduction pathway. Proc Natl Acad Sci U S A. 2007 Oct 2; 104(40):15759-64.
          View in: PubMed
        9. Sluss HK, Davis RJ. H2AX is a target of the JNK signaling pathway that is required for apoptotic DNA fragmentation. Mol Cell. 2006 Jul 21; 23(2):152-3.
          View in: PubMed
        10. Sluss HK, Armata H, Gallant J, Jones SN. Phosphorylation of serine 18 regulates distinct p53 functions in mice. Mol Cell Biol. 2004 Feb; 24(3):976-84.
          View in: PubMed
        11. Steinman HA, Sluss HK, Sands AT, Pihan G, Jones SN. Absence of p21 partially rescues Mdm4 loss and uncovers an antiproliferative effect of Mdm4 on cell growth. Oncogene. 2004 Jan 8; 23(1):303-6.
          View in: PubMed
        12. Kennedy NJ, Sluss HK, Jones SN, Bar-Sagi D, Flavell RA, Davis RJ. Suppression of Ras-stimulated transformation by the JNK signal transduction pathway. Genes Dev. 2003 Mar 1; 17(5):629-37.
          View in: PubMed
        13. Sluss HK, Jones SN. Analysing p53 tumour suppressor functions in mice. Expert Opin Ther Targets. 2003 Feb; 7(1):89-99.
          View in: PubMed
        14. Sluss HK, Davis RJ. Embryonic morphogenesis signaling pathway mediated by JNK targets the transcription factor JUN and the TGF-beta homologue decapentaplegic. J Cell Biochem. 1997 Oct 1; 67(1):1-12.
          View in: PubMed
        15. Sluss HK, Han Z, Barrett T, Goberdhan DC, Wilson C, Davis RJ, Ip YT. A JNK signal transduction pathway that mediates morphogenesis and an immune response in Drosophila. Genes Dev. 1996 Nov 1; 10(21):2745-58.
          View in: PubMed
        16. Gupta S, Barrett T, Whitmarsh AJ, Cavanagh J, Sluss HK, Dérijard B, Davis RJ. Selective interaction of JNK protein kinase isoforms with transcription factors. EMBO J. 1996 Jun 3; 15(11):2760-70.
          View in: PubMed
        17. Ewen ME, Oliver CJ, Sluss HK, Miller SJ, Peeper DS. p53-dependent repression of CDK4 translation in TGF-beta-induced G1 cell-cycle arrest. Genes Dev. 1995 Jan 15; 9(2):204-17.
          View in: PubMed
        18. Kallunki T, Su B, Tsigelny I, Sluss HK, Dérijard B, Moore G, Davis R, Karin M. JNK2 contains a specificity-determining region responsible for efficient c-Jun binding and phosphorylation. Genes Dev. 1994 Dec 15; 8(24):2996-3007.
          View in: PubMed
        19. Sluss HK, Barrett T, Dérijard B, Davis RJ. Signal transduction by tumor necrosis factor mediated by JNK protein kinases. Mol Cell Biol. 1994 Dec; 14(12):8376-84.
          View in: PubMed
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