Bio

I'm an all-in-one biochemist, cell-culturist, and human-health enthusiast whose interests include therapeutics development, and tools for medical diagnostics.

I strive to maintain a healthy balance of breadth and depth in my areas of expertise, and have a strong affinity to interdisciplinary approaches. My background includes software development within the protein structure prediction module of the Rosetta software suite, design and initial development of cancer therapeutics, and basic research into understanding the mechanistic details of cell-cycle gene regulation.

My current research within the Tobias Lanz Lab aims to understand the role of certain targets of autoimmunity in Multiple Sclerosis and use this understanding to develop therapies and diagnostic aides.

Professional Education

  • Doctor of Philosophy, University of California Santa Cruz (2023)
  • PhD, University of California, Santa Cruz, Chemistry (Biochemistry) (2023)
  • BS, University of California, Santa Cruz, Biochemistry and Molecular Biology, Minor in Bioinformatics (2016)

Stanford Advisors

Contact

  • Academic
    University - Scholar Department: Institute for Immunity, Transplantation, and Infection Position: Postdoctoral Scholar

Additional Info

Links

All Publications

  • HDAC activity is dispensable for repression of cell-cycle genes by DREAM and E2F:RB complexes. Nature communications Barrett, A. K., Shingare, M. R., Rechtsteiner, A., Rodriguez, K. M., Le, Q. N., Wijeratne, T. U., Mitchell, C. E., Membreno, M. W., Rubin, S. M., Muller, G. A. 2024; 15 (1): 4450

    Abstract

    Histone deacetylases (HDACs) play a crucial role in transcriptional regulation and are implicated in various diseases, including cancer. They are involved in histone tail deacetylation and canonically linked to transcriptional repression. Previous studies suggested that HDAC recruitment to cell-cycle gene promoters via the retinoblastoma (RB) protein or the DREAM complex through SIN3B is essential for G1/S and G2/M gene repression during cell-cycle arrest and exit. Here we investigate the interplay among DREAM, RB, SIN3 proteins, and HDACs in the context of cell-cycle gene repression. Knockout of SIN3B does not globally derepress cell-cycle genes in non-proliferating HCT116 and C2C12 cells. Loss of SIN3A/B moderately upregulates several cell-cycle genes in HCT116 cells but does so independently of DREAM/RB. HDAC inhibition does not induce general upregulation of RB/DREAM target genes in arrested transformed or non-transformed cells. Our findings suggest that E2F:RB and DREAM complexes can repress cell-cycle genes without relying on HDAC activity.

    View details for DOI 10.1038/s41467-024-48724-0

    View details for PubMedID 38789411

https://orcid.org/0009-0007-4570-5265