Header Logo

Hayla K Sluss PhD

TitleAssistant Professor
InstitutionUMass Chan Medical School
AddressUMass Chan Medical School
364 Plantation Street LRB
Worcester MA 01605
vCardDownload vCard
    Other Positions
    InstitutionT.H. Chan School of Medicine
    DivisionEndocrinology & Diabetes

    InstitutionMorningside Graduate School of Biomedical Sciences
    DepartmentInterdisciplinary Graduate Program

    Collapse Biography 
    Collapse education and training
    Wheaton College, Norton, MA, United StatesBABiology
    University of Massachusetts Medical School, Worcester, MA, United StatesPHDMolecular Medicine

    Collapse Overview 
    Collapse overview


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

    p53 Stress Pathways in Cancer and Chronic Illness

    The research goals of the Sluss lab are to have a better understanding of the pathophysiology of chronic illness to improve patient lives and ultimately reclaim health. Our lab’s research focus is to investigate chronic illnesses focusing on post-infection and chronic fatiguing illnesses. We propose these post-infection diseases share common pathway dysfunction that contributes to the disease. To this end, we are studying both pediatric and adult patients with diabetes and post-infectious associated/fatiguing chronic illness, including, but not limited to, Long-COVID, ME/CFS, FM, Gulf-War Syndrome and Hypermobility Syndrome.

    In our work on to understand diabetes and metabolic control, we demonstrated a novel role of the tumor suppressor p53 in glucose homeostasis. We have applied genetic engineering and biochemistry to address this and other roles of p53 in metabolism.  We also study the overall disruption of metabolism in other chronic illnesses. We are examining common disrupted pathways to explain the overlapping symptoms in chronic illness, and to find unique pathway pathology for each disease. We are particularly interested in the role of the p53 stress pathway in these diseases.

    The long term goal of the lab is to elucidate the pathology of chronic disease, to create mouse models to interrogate the pathology and provide a vehicle for therapeutic discovery.


    Collapse 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.

    Collapse Bibliographic 
    Collapse selected publications
    Publications listed below are automatically derived from MEDLINE/PubMed and other sources, which might result in incorrect or missing publications. Faculty can login to make corrections and additions.
    Newest   |   Oldest   |   Most Cited   |   Most Discussed   |   Timeline   |   Field Summary   |   Plain Text
    PMC Citations indicate the number of times the publication was cited by articles in PubMed Central, and the Altmetric score represents citations in news articles and social media. (Note that publications are often cited in additional ways that are not shown here.) Fields are based on how the National Library of Medicine (NLM) classifies the publication's journal and might not represent the specific topic of the publication. Translation tags are based on the publication type and the MeSH terms NLM assigns to the publication. Some publications (especially newer ones and publications not in PubMed) might not yet be assigned Field or Translation tags.) Click a Field or Translation tag to filter the publications.
    1. Armata HL, Chamberland S, Watts L, Ko HJ, Lee Y, Jung DY, Kim JK, Sluss HK. Deficiency of the tumor promoter gene wip1 induces insulin resistance. Mol Endocrinol. 2015 Jan; 29(1):28-39. PMID: 25379953.
      Citations: 4     Fields:    Translation:AnimalsCells
    2. Franck D, Tracy L, Armata HL, Delaney CL, Jung DY, Ko HJ, Ong H, Kim JK, Scrable H, Sluss HK. Glucose Tolerance in Mice is Linked to the Dose of the p53 Transactivation Domain. Endocr Res. 2013 Aug; 38(3):139-150. PMID: 23102272.
      Citations: 14     Fields:    
    3. 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. PMID: 21980358.
      Citations: 2     Fields:    Translation:HumansAnimalsCells
    4. 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. PMID: 21127973.
      Citations: 1     Fields:    Translation:AnimalsCells
    5. 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. PMID: 20956556.
      Citations: 65     Fields:    Translation:HumansAnimalsCells
    6. 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 Aug 30; 5(8):e12469. PMID: 20814571.
      Citations: 28     Fields:    Translation:Animals
    7. 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 01; 184(11):6177-87. PMID: 20483782.
      Citations: 13     Fields:    Translation:Animals
    8. 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. PMID: 20145032.
      Citations: 8     Fields:    Translation:AnimalsCells
    9. 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. PMID: 18089799.
      Citations: 44     Fields:    Translation:AnimalsCells
    10. 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 02; 104(40):15759-64. PMID: 17893331.
      Citations: 82     Fields:    Translation:AnimalsCells
    11. 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. PMID: 16857581.
      Citations: 24     Fields:    Translation:Cells
    12. 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. PMID: 14729946.
      Citations: 79     Fields:    Translation:AnimalsCells
    13. 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 08; 23(1):303-6. PMID: 14712235.
      Citations: 21     Fields:    Translation:AnimalsCells
    14. 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 01; 17(5):629-37. PMID: 12629045.
      Citations: 57     Fields:    Translation:AnimalsCells
    15. Sluss HK, Jones SN. Analysing p53 tumour suppressor functions in mice. Expert Opin Ther Targets. 2003 Feb; 7(1):89-99. PMID: 12556205.
      Citations: 2     Fields:    Translation:HumansAnimalsCells
    Sluss's Networks
    Click the
    buttons for more information and interactive visualizations!
    Concepts (120)
    Co-Authors (9)
    Similar People (60)
    Same Department Expand Description
    Physical Neighbors