Faculty Speakers
Johnson V. John
Assistant Professor and Principal Investigator at Terasaki Institute for Biomedical Innovation (TIBI)
Dr. Johnson V. John is an Assistant Professor and Principal Investigator at the Terasaki Institute for Biomedical Innovation (TIBI). His research focuses on the design and development of advanced biomaterials and nanotechnology-based platforms for applications in regenerative medicine, drug delivery, and tissue engineering. Dr. John’s work integrates materials science, bioengineering, and translational approaches to develop innovative therapeutic solutions aimed at improving patient outcomes. He leads a multidisciplinary research group dedicated to advancing next-generation biomedical technologies from bench to clinical application.
Title of the Talk
Building Healing from the Bottom Up: Modular Biomaterials in Regenerative Medicine
Affiliation
Terasaki Institute for Biomedical Innovation, 21100 Erwin St, Woodland Hills, CA 91367
Abstract
Traditional scaffold technologies in regenerative medicine have largely relied on bulk materials such as nanofibrous membranes and hydrogels. While effective in certain contexts, these static and homogeneous systems often fail to adapt to the dynamic and heterogeneous microenvironments of injured tissues. Over the past decade, growing efforts have focused on the development of modular biomaterials, which introduce a fundamentally different design philosophy for tissue repair. Rather than forming uniform bulk matrices, modular scaffolds assemble healing environments from microscale building blocks that are injectable, customizable, and inherently microporous. This modularity enables enhanced nutrient and oxygen transport, dynamic cell–material interactions, and the integration of multifunctional therapeutic elements, including growth-factor sequestration, immunomodulatory cues, and mechanically responsive features. Importantly, properties such as porosity, shape, mechanics, and bioactivity can be independently programmed to match specific wound microenvironments. Early successes with microgel-based fillers and microporous matrices highlight a clear shift away from static, one-size-fits-all dressings toward dynamic, adaptive, and modular therapeutics. This talk will place modular biomaterials within the broader trajectory of scaffold evolution and discuss how they are poised not only to accelerate healing outcomes but also to redefine regenerative strategies across diverse tissue types.
Khaja Shameem Mohammed Abdul
Postdoctoral Fellow in the Cardiovascular Signaling Laboratory at Huntington Medical Research Institutes (HMRI)
Dr. Khaja Shameem Mohammed Abdul is a Postdoctoral Fellow in the Cardiovascular Signaling Laboratory at the Huntington Medical Research Institutes (HMRI) in Pasadena, California. He earned his PhD from the University of Ruhuna, Sri Lanka, where he was recognized with two prestigious awards: the Vice Chancellor’s Fellowship from University of Ruhuna and the President’s Research Scholarship from the Ministry of Higher Education.
During 2018-2020, he was a post-doctoral fellow at Guangdong University of Technology, China. Where he discovered cardioprotective effects of a novel drug molecule JC105 which was later patented by the lab. Since 2021, Dr. Khaja Shameem joined HMRI as a post-doctoral fellow, where he investigates the role of protein phosphatases PHLPP1 and PHLPP2 in myocardial aging and injury. His work has been published in multiple peer-reviewed journals, including Journal of Molecular and Cellular Cardiology, International Journal of Cardiology, Journal of Cellular and Molecular Medicine and Biochimica et Biophysica Acta-Molecular Cell Research.
Dr. Mohammed Abdul’s long‑term career goal is to become an independent scientist advancing the field of cardiovascular research. Dr. Mohammed Abdul also contributes to the scientific community as an Editorial Board Fellow for Current Opinion in Physiology and as an Editorial Board Member for The Open Cardiovascular Medicine Journal. Beyond his laboratory work, he has served as a Social Media Ambassador for the American Heart Association and as a communications Committee member for the Society for South Asian Heart Research.
Title of the Talk
PHLPP1: The Missing Link in Nicotine Induced Cardiac Damage
Abstract
Nicotine exposure is known to cause oxidative stress and mitochondrial dysfunction in the heart, yet the molecular mechanisms linking nicotine to cardiomyocyte injury remain unclear. Our work identifies Pleckstrin Homology Domain Leucine-Rich Repeat Protein Phosphatase 1 (PHLPP1) as a key mediator of nicotine induced cardiac damage. We found that nicotine significantly elevates PHLPP1 expression in the adolescent rodent heart and in cardiomyocytes, coinciding with increased NOX4 levels, reactive oxygen species production, and apoptosis. Mechanistic studies revealed that nicotine activates the ERK–4E BP1 signaling axis to promote PHLPP1 protein synthesis, and inhibiting ERK or translation effectively blocks this response. Importantly, PHLPP1 was necessary and sufficient for nicotine induced mitochondrial dysfunction. Together, these findings uncover a novel pathway through which nicotine drives cardiomyocyte injury and highlight PHLPP1 as a potential therapeutic target in tobacco and e cigarette related cardiac injury.
Student Presentations
Title of the Talk
B Cells vs. the Furin-Loop Region: Can Antibodies Target Flexible Viral Epitopes
Program
Doctor of Philosophy in Applied Life Sciences (PhD)
Abstract
B-cell immunity depends on the ability to recognize pathogen-derived antigenic structures. Although antibody responses to well-folded viral epitopes have been extensively studied, many viral proteins also contain conformationally dynamic and intrinsically disordered regions that play important roles in host interaction, proteolytic activation, and immune evasion. Because these regions do not present a single stable structure, it’s unclear how they are recognized as epitopes for effective antibody binding. Here, we investigated B-cell responses to flexible Spike-derived peptide epitopes after full-length Spike immunization. We designed a panel spanning the receptor binding motif (RBM), the S1/S2 cleavage loop, representing dynamic and intrinsically disordered regions, with full-length RBD as a structured reference. Using a single-cell approach linking antigen binding, gene expression, and B-cell receptor (BCR) sequences, we identified over 120 antigen-specific B cells and recovered paired heavy–light BCR sequences, including 23 selected for structural analysis. These cells spanned activated and plasma-like states; structural modeling supports sustained, structurally consistent interactions. These findings suggest that flexible viral protein regions can serve as effective immune targets, with implications for vaccine design.
Title of the Talk
Synthesis of Positive Allosteric Modulators of NMDA Receptors
Program
Doctor of Philosophy in Applied Life Sciences (PhD)
Abstract
Glutamate-mediated neuronal hyperexcitation plays a role in causing seizures in epilepsy via the N-methyl-D-aspartate (NMDA) receptor. Prior research has shown that the positive allosteric modulator (PAM) EU1622-14 increases NMDAR function in the presence of glutamate while preventing excessive calcium influx. Although this compound has a profile of activity at the NMDAR to prevent unprovoked seizures, it has poor drug properties. We have optimized the synthesis of organic analogs of EU1622-14 and synthesized them to serve as the positive controls for an NMDAR PAM. Additionally, we are using a scaffold-hopping approach to replace the core heterocycle of the structure, which itself limits improvements in the candidates' drug properties. Thus, we have synthesized two EU1622-14 analogs in which the central heterocycle has been replaced with alternative scaffolds to display the critical functional portions of the molecule.
Title of the Talk
All by All Browser Analysis: Comparative Assessment of Colorectal Cancer Variant Distributions in African and European Ancestry Populations in the All of Us Research
Program
Doctor of Philosophy in Applied Life Sciences (PhD)
Abstract
The genetic architecture of colorectal cancer (CRC), encompassing rare coding variants, ancestry-specific loci, and functional classes, remains incompletely characterized. Whole-genome and exome sequencing data from the All of Us Research Program enabled ancestry-stratified analyses of African-ancestry (AFR) and European-ancestry (EUR) participants within a framework. Three analytical layers were assessed: common-variant genome-wide association studies (GWAS), exome-wide single-variant tests, and gene-based rare-variant association studies (RVAS) using burden and SKAT models. Variants were annotated by consequence, allele frequency, and type, and both variant density and effect distributions were evaluated. AFR participants exhibited higher variant density than EUR (1.20 - 1.75-fold). GWAS identified significant associations at POT1 and FGFR2 in AFR, and at RBFOX1, DCC, and DMD in EUR, in addition to ancestry-specific loci. Exonic GWAS identified a coding association at FGFR2 in AFR. Although most GWAS signals were non-coding, exome data was ~ 52 to 53 percent coding. RVAS highlighted MLH1 in AFR and MSH2, and APC in EUR. These results demonstrate shared and ancestry-specific CRC loci and underscore the importance of longitudinal studies to refine risk estimates.
Title of the Talk
Matched Adjusted Indirect Comparison Analyses among Clinical Trial Patients within Oncology: ROS-1 Positive Advanced or Metastatic Non-Small Cell Lung Cancer
Program
Doctor of Philosophy in Applied Life Sciences (PhD)
Abstract
Among the current landscape within oncology, direct head-to-head randomized controlled trials comparing novel therapies are often unavailable. This alone can create challenges for evidence-based decision making, especially in the United States payor audience. A recent methodology called: Matched Adjusted Indirect Comparison [MAIC] has been used to complete analyses to compare the treatment effects across clinical trials. Data needed to complete MAIC include individual patient data (IPD) and aggregate data for the interventions of interest which are reported for comparators. MAICs adjust for cross trial differences in baseline patient characteristics by re weighting IPD to match the published summary statistics of comparator trials, thereby reducing bias attributable to population heterogeneity. This oral presentation will review the application of MAIC analyses among clinical trial patients within oncology, focusing on application of MAIC in real-case scenarios of patients with ROS-1 Positive Advanced or Metastatic Non-Small Cell Lung Cancer. The presentation will also provide overview on the methodological principles, strengths, and limitations with MAIC. Among the oncology settings, where trials frequently enroll distinct patient populations based on tumor type, disease stage, biomarker status, and prior treatments, the use of MAIC enable more credible comparative effectiveness and safety assessments in the real-world settings. Outcomes will be discussed and include overall survival, progression free survival, response rates, and treatment related adverse events.
Title of the Talk
Development of a Genome-Wide CRIPSR based Target Identification Platform
Program
Doctor of Philosophy in Applied Life Sciences (PhD)
Abstract
TBD
Title of the Talk
Design, Delivery, and Mechanism of Action of Small Activating RNA (saRNA) as a Therapeutic Strategy for TBK1 Regulation in the CNS
Program
Doctor of Philosophy in Applied Life Sciences (PhD)
Abstract
TBD
Title of the Talk
CRISPR-Cas9-Mediated Knockout of GPR65 in Jurkat T cells Impacts Tcell and Metabolic Function
Program
Master of Science in Applied Life Sciences
Abstract
In recent decades, autoimmune diseases have become a significant and increasing health burden with a crucial need for the development of targeted therapies. An example of this is Multiple Sclerosis (MS), a chronic autoimmune disorder of the central nervous system (CNS) characterized by demyelination, neurodegeneration, and progressive decline in neurological function. In MS pathogenesis, dysregulated T-helper 17 (Th17) cell activation primarily drives the amplification of inflammatory responses by producing interleukin-17A (IL-17A) and other proinflammatory cytokines. Recent studies in mice have implicated G-protein-coupled receptor 65 (GPR65), an acid-sensing GPCR, as a promoter of Th17 cell pathogenesis, therefore making it a promising therapeutic target. To translate these findings into human systems, we performed a GPR65 knockout in a human T cell line using a CRISPR-Cas9 gene-editing approach. In our study, generating a GPR65 knockout line resulted in decreased T-cell activity as well as reduced cellular metabolism. Collectively, these findings support GPR65 inhibition as a promising therapeutic strategy for the treatment of MS and other Th17-mediated autoimmune diseases.
Title of the Talk
Identifying Direct Regulatory Targets of PHLPP2 through Multi-omic Analyses
Program
Master of Science in Human Genetics and Genomic Data Analytics
Abstract
Cardiovascular disease remains a leading cause of death worldwide, with cardiac hypertrophy being a compensatory response of the heart to increased workload that eventually leads to heart failure. This project investigates the isoform-specific role of the serine/threonine phosphatase PHLPP2, in regulating maladaptive cardiac hypertrophy. Using RNA-sequencing and ATAC-sequencing datasets from the hearts of wild-type and PHLPP2 knockout mouse models, this study evaluates how the loss of PHLPP2 alters gene expression and chromatin accessibility throughout the cardiac genome, specifically focusing on those associated with hypertrophic signaling pathways. Previous studies have shown that deletion of the PHLPP1 isoform enhances Akt signaling and provides protection from pathological hypertrophy and ischemic injury, while loss of PHLPP2 leads to pathological cardiac growth and heart failure. The analyses are expected to reveal differential expressions of hypertrophic gene programs and epigenetic remodeling in the PHLPP2 knockout model. By defining the specific contribution of PHLPP2 to cardiac growth and stress response, this work aims to clarify isoform-dependent signaling mechanisms. Future studies will further dissect these molecular mechanisms through functional assays and determine their impact on cardiomyocyte growth and survival.