There are four PhD programs and one dual MD/PhD program associated with the Department of Biochemistry and Molecular Genetics.

Two students wearing masks work together at a laboratory chalk board.

The over-arching goal of the graduate program in the Department of Biochemistry and Molecular Genetics is to train and mentor our PhD students so that our alumni are prepared to become critical thinkers, creative innovators and leaders in science, and succeed in their subsequent career paths in academia as well as industry. Our department offers a diverse array of research opportunities in the following areas so that potential PhD students can choose mentors and projects which best align with their scientific interests and career goals. Some of our focus areas include:

We also use a wide variety of state-of-the art molecular and cellular approaches as well as organisms in our department to address fundamental questions in molecular biology, cell biology, biochemistry and molecular genetics – during healthy biological processes as well as during disease states. The extraordinary diversity of research areas in our department is quite unique and offers our PhD students broad exposure to basic and translational biomedical research.

Our student seminars, departmental seminars and student activities, allow for frequent social and intellectual interactions among our students, resulting in a community of peers with different areas of expertise and who help each other grow. If you are passionate about biomedical research and interested in foundational cutting-edge questions in the life sciences, then our department could be ideally suited for you.

PhD programs associated with the department

It is important to us that the training of PhD students is individualized to suit each student’s needs which is why PhD students can join our departmental via several PhD graduate programs at our institution. Currently, PhD students in our department belong to the following programs.

Potential PhD applicants who are interested in joining our department but have not yet decided which formal PhD program is the best fit for them, can reach out to our Directors of graduate Studies (Dr. Nava Segev or Dr. Gaponenko) our Department Head (Dr. Jalees Rehman) or any individual faculty mentor in our department. Each of these PhD programs has their own admissions and coursework requirements, which can be reviewed by visiting their respective webpages.

Faculty engagement in the training of Graduate, Undergraduate, Medical Students, and Postdoctoral Fellows

Our faculty members are actively engaged in the following activities:

  • Providing summer research projects for Medical Students. See below for potential 2026 summer projects. Please reach out to individual faculty if interested.

    • Faculty NameProject Description
    Ackerman, StevenThe project would involve working on aspects of our current ADDF/HDI funded project on the "Development of novel CCR3 chemokine receptor peptide and small molecule functionally selective biased antagonists to treat neuroinflammation in Alzheimer’s disease. The student would conduct in vitro studies to demonstrate target engagement of the chemokine receptor CCR3, as expressed on microglial cells, by our R321 biased CCR3 antagonist peptide, this to demonstrate R321 peptide binding to CCR3 using various approaches, and the impact of binding on down-stream signaling pathways such as Galphai and ERK1,2 activation, and beta-arrestin recruitment to CCR3, in the neuroinflammatory activation of microglia.
    Benevolenskaya, ElizavetaThe Benevolenskaya laboratory focuses on elucidation how epigenetic mechanisms regulate cell growth and influence response to therapeutic interventions. We integrate molecular and cellular biology approaches with high-throughput genomic technologies, including bulk and single-cell RNA sequencing to profile gene expression, as well as ChIP-seq, ATAC-seq and single-cell ATAC-seq to map transcription factor location and chromatin accessibility, and CITE-seq and scRNA-seq-scATAC-seq for multiome analysis.

    1. Mechanisms of drug resistance at single-cell resolution.
    A central challenge in cancer therapy is that complete and durable responses are rare; instead, partial responses and relapse are common. This clinical reality is driven in part by cell-to-cell heterogeneity in drug sensitivity. We aim to identify genes and regulatory programs that play a causal role in drug resistance through genome-wide analyses of individual drug-resistant cells. Our primary focus is on lung and pancreatic cancers (PNAS, 2022, BioRxiv 2025).
    2. Prediction of effective combination therapies using single-cell data.
    We use single-cell transcriptomic data to predict responses to small-molecule combination therapies (Nature Communications, 2021). We are developing and rigorously validating a computational pipeline that leverages the LINCS database to identify candidate drug combinations, followed by functional validation in cell culture–based assays.
    3. KDM5A in differentiation and transcriptional regulation.
    We investigate the role of the histone demethylase KDM5A in regulating RB-dependent differentiation. Our work identifies genes and transcription factors controlled by KDM5A during cardiac and skeletal myogenesis, providing insight into how epigenetic regulators shape lineage commitment (Molecular Cell 2005, 2008; Genes & Dev. 2015).
    4. H3K4me3 dynamics and chromatin regulation in disease.
    We seek to advance understanding of chromatin regulation by dissecting how different levels of H3K4me3 and its associated “reader” proteins control transcriptional programs. Extending these studies to disease contexts, we investigate conditions in which failure to appropriately regulate H3K4me3 contributes to pathology (J. Immunology, 2025; The FASEB Journal, 2026).
    Frolov, MaximThe focus of the research in the Frolov laboratory is to uncover universal mechanisms that control cell proliferation and differentiation, using Drosophila as a model system. Our emphasis is on two major tumor suppressor pathways: Retinoblastoma and Hippo. By integrating cutting-edge single cell genomics and computational analysis with molecular, genetic and cellular biology approaches, we study how mutating these pathways affects different cell types throughout the entire animal. Our overarching goal is to generate the foundational knowledge regarding the control of cell proliferation and differentiation during development, thereby offering insights into why inactivation of Retinoblastoma and Hippo pathways are such key events in human cancers.

    Projects:
    1. To analyze single-cell genomics data from Retinoblastoma and Hippo mutant tissues generated in the lab with the Seurat computational pipeline.
    2. To explore cell proliferation and differentiation in Retinoblastoma and Hippo mutant tissues using immunofluorescence and confocal microscopy.
    3. To explore and refine a single cell atlas of developing muscle precursor cells built in the lab and determine the impact of the Retinoblastoma pathway inactivation.
    4. To determine systemic effects of the Retinoblastoma pathway inactivation in the adipose tissues on other organs using single cell genomics.

    Representative publications:
    1. E.V. Benevolenskaya and M.V. Frolov. 2015. Emerging links between E2F control and mitochondrial function. Cancer Research. 75: 619-623.
    2. Ariss, M., A.B. Islam, M. Critcher, M.P. Zappia and M.V. Frolov. 2018. Single cell RNA-sequencing identifies a metabolic aspect of apoptosis in Rbf mutant. Nature Communications. 9: 5024. doi: 10.
    3. Chen, X., M.M. Ariss, G. Ramakrishnan, V. Nogueira, C. Blaha, W. Putzbach, A.B. Islam, M.V. Frolov and N. Hay. 2020. Cell autonomous versus systemic Akt isoform deletions uncovered new roles for Akt1 and Akt2 in breast cancer. Molecular Cell. 80: 81-101.e5.
    4. Zappia, M.P., A. Guarner, N. Kellie-Smith, A. Rogers, R. Morris, B.N. Nicolay, M. Boukhali, W. Haas, N.J. Dyson and M.V. Frolov. 2021. E2F/Dp inactivation in fat body cells triggers systemic metabolic changes. eLife 10: e67753.
    5. Rader, A.E., B. Bayarmagnai and M.V. Frolov. 2023. Combined inactivation of RB and Hippo converts differentiating Drosophila photoreceptors into eye progenitor cells through derepression of homothorax. Developmental Cell. 58: 2261-2274.e6.
    Jun, Joon-IlProject: Resolution of injury-induced cell plasticity in intestinal regeneration
    Description: This work will define fundamental mechanisms that ensure regenerative plasticity is properly terminated, a process essential for maintaining tissue integrity. By identifying how metabolic and epigenetic programs are reset after injury, these studies will provide insight into how dysregulated regeneration contributes to disease and may reveal new strategies to prevent pathological tissue remodeling and tumor initiation.
    Kuchay, ShafiEliminating Pathogenic Proteins – The Next Frontier in Drug Discovery:

    Our focus is to build a next-generation drug discovery platform based on targeted protein degradation, using PROTACs and molecular glues to wholly eliminate disease-driving proteins rather than just inhibit them. Unlike traditional small molecules, which depend on continuous binding and are limited to druggable active sites, our approach harnesses the cell’s own degradation machinery to remove proteins entirely, unlocking previously undruggable targets. We are interested in targeting membrane-associated proteins, where many of the most critical and historically intractable disease drivers reside, including cancer drivers RAS and EGFR. What sets us apart is our ability to recruit the cells’ internal protein degradation machinery in specific compartments. This increases efficiency while minimizing off-target effects and toxicity. Together, this represents a shift from inhibition to precise, localized protein elimination for a wide ranges of diseases such as cancer, diabetes and autoimmune diseases.
    Markiewicz-Potoczny, MartaTelomere biology disorders (TBDs), such as dyskeratosis congenita, are caused by impaired telomere maintenance and lead to bone marrow failure, pulmonary fibrosis, and cancer. Many TBDs arise from mutations in telomerase components or associated factors, including members of the H/ACA complex such as DKC1 and NOP10. While coding mutations are well characterized, the functional consequences of many variants of unknown significance (VUS), including intronic variants that may affect RNA splicing, remain unclear.

    This project will focus on analyzing the functional impact of candidate DKC1 and NOP10 variants using established human cell models, including induced pluripotent stem cells and cancer cell lines. The student will work with existing cell lines and expression constructs available in the laboratory, without the need for genome editing.

    The student will:
    • Analyze expression of wild-type and variant forms of DKC1 or NOP10 at the RNA level using RT-qPCR, with a focus on detecting potential splicing alterations
    • Assess protein expression using Western blot
    • Quantify telomere-associated DNA damage by measuring γH2AX and 53BP1 foci colocalization (TIFs assay)
    • Evaluate effects of selected variants on cell growth and viability
    • Participate in basic data analysis and interpretation
    Merrill, BradAlthough genetic medicines have already reached the clinic with meaningful impact on human health, they are still in their early days as a new therapeutic modality. My group works to invent new synthetic biology tools that can be used to develop genetic medicines. Projects available over the summer involve nitty gritty molecular biology techniques for evaluating functionality of new synthetic biology tool. These all involve RNA-guided nucleases from CRISPR systems and will test variations of the RNA for conditionally activating the nuclease in human cells. Completion of a project will result in a new tool that could contribute to sophisticated synthetic genetic medicines.
    Segev, Nava Exploring the role of ESCRT complexes in a micro-autophagy pathway selective for aberrant proteins.
    Reference:
    First responder to starvation: microreticulophagy clears aberrant membrane proteins in quick bites.Alvarado Cartagena YM, Gyurkovska V, Segev N. Autophagy. 2025 Aug;21(8):1853-1855. doi: 10.1080/15548627.2025.2487675
  • Training Graduate students and Postdoctoral Fellows through various training grants at UIC, including:
  • Training Undergraduate students through Undergraduate Research Experience (URE) program.

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