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. bioRxiv : the preprint server for biology Barrett, A., Shingare, M. R., Rechtsteiner, A., Wijeratne, T. U., Rodriguez, K. M., Rubin, S. M., Muller, G. A. 2023

    Abstract

    Histone deacetylases (HDACs) are pivotal in transcriptional regulation, and their dysregulation has been associated with various diseases including cancer. One of the critical roles of HDAC-containing complexes is the deacetylation of histone tails, which is canonically linked to transcriptional repression. Previous research has indicated that HDACs are recruited to cell-cycle gene promoters through the RB protein or the DREAM complex via SIN3B and that HDAC activity is essential for repressing G1/S and G2/M cell-cycle genes during cell-cycle arrest and exit. In this study, we sought to explore the interdependence of DREAM, RB, SIN3 proteins, and HDACs in the context of cell-cycle gene repression. We found that genetic knockout of SIN3B did not lead to derepression of cell-cycle genes in non-proliferating HCT116 and C2C12 cells. A combined loss of SIN3A and SIN3B resulted in a moderate upregulation in mRNA expression of several cell-cycle genes in arrested HCT116 cells, however, these effects appeared to be independent of DREAM or RB. Furthermore, HDAC inhibition did not induce a general upregulation of RB and DREAM target gene expression in arrested transformed or non-transformed cells. Our findings provide evidence that E2F:RB and DREAM complexes can repress cell-cycle genes without reliance on HDAC activity.

    View details for DOI 10.1101/2023.10.28.564489

    View details for PubMedID 37961464

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