Our laboratory utilizes pharmacologic approaches and genetic models to examine how the changes in the neuronal microenvironment e.g. inflammation, oxidative stress affects cognitive function.
My research focuses on Melanocortin-4 receptor, a G-protein coupled receptor involved in appetite control.
My lab is focused on Alzheimer’s disease. Current research is examining the role of diabetes-related disruptions in glucose metabolism and the impact this has on brain function. Evidence indicates that both Alzheimer’s and diabetes involve processes connected to inflammation, which has been another of my longstanding areas of research.
The lab studies the role of DNases in tissue injury and cell death.
Dr. Michael Birrer will be focused on developing new types of drug models and molecular approaches to help create alternative forms of treatment for multiple types of ovarian cancers. While his primary focus will be on of ovarian cancer, he hopes his research, and ongoing clinical trials will also help in the development of new treatments for multiple types of cancers studied here at the Winthrop P. Rockefeller Cancer Institute. Dr. Birrer has also been chosen to lead the UAMS goal of achieving the National Cancer Institute designation, and he has assembled a top-notch team of doctors, oncologists, surgeons, and researchers to help him on this journey.
My research focuses on how environmental and occupational exposure, nutrition, and genetic diversity influence cancer initiation, promotion, and progress.
The major focus of my research is to characterize the molecular mechanisms of helicases involved in regulation of the DNA damage response using biochemical, biophysical, and systems biology approaches with the overall goal of designing better cancer treatments.
My research focuses on developing technologies for the high-resolution analysis of chromatin and histone post-translational modifications at specific genomic loci. Therefore, I analyze both the genomic, epigenomic, and proteomic data associated with the chromatin biology. I have formal training in bioinformatics and mass spectrometry. I recently successfully developed the ChAP-MS technology in yeast for proteomic study of a specific single genomic locus. I am also involved in many projects involving the analysis of next generation sequencing data, such as RNA-seq and ChIP-seq, as well as proteomic data.
Our research focus is aimed at investigating the epigenetic regulatory mechanisms at the enhancers and promoters of the critical oncogenes and tumor suppressors that drive malignant proliferation and invasion during leukemogenesis in the Acute Myeloid Leukemia (AML) patients, characterized with BET (BRD4), SET (KMT2A, EZH2, and NSD1) or runt (CBFA2T3) over-expressed domains. Using the multi-omics platform, we intend to identify the alterations in DNA methylation, histone modifications and transcription factor assemblies in and outside the topologically assorted domains (TAD) in AML. We also aim to study the recurrent epigenetic mutations in AML patients in relation to their effect on the cancer cell metabolism. Suitable cells or animals will be induced with the mutant proteins to study the deleterious effects on the chromatin spread, transcriptional dysfunctions and metabolic turnover in the course hematopoiesis. CRISPR-multiplex or small molecule based drugs would be screened for their efficacy against the vulnerable targets of the mutant phenotypes
The lab studies chromosome dynamics in meiosis.
The lab studies the structure and function of carbohydrate-binding proteins in prostate cancer and reproduction.
Dr. Enemark’s research focuses on DNA replication, a fundamental event that is required in all life forms, and its disruption can lead to several forms of the disease, including cancer.
Our lab studies DNA replication and DNA damage tolerance: mechanisms and roles in cancer.
Our lab studies central nervous system (CNS) injury mainly in the retina and brain. The lab employs different molecular/cell culture techniques, human tissue samples, and animal studies to model critical disease conditions in these two organs. Among the diseases under study are diabetic retinopathy, retinopathy of prematurity, traumatic optic neuropathy, traumatic brain injury, and stroke. Our studies aim to elucidate the underlying pathological mechanisms in these conditions and identify new therapies that can be translated from bench to bedside to help patients affected by these disease conditions.
Radiation and Cancer biology, exosomes and cell to cell crosstalk in stem cell differentiation and activity, nanomedicine applications. Dr. Griffin’s research interests include: molecular and physiological mechanisms of radiation and thermal sensitization; modulation of tumor blood flow, angiogenesis and oxygenation; biology and physiology of thermal therapy; and oxygen partial pressure as predictor of cancer treatment response.
My lab is interested in tumor biology. Our work has focused on extracellular matrix degrading proteases and their roles in facilitating tumor growth and metatstasis.
Our overall research goal is to identify the molecular mechanisms behind the genomic instability at critical oncogenes in lymphoma and the role DNA secondary structures may play in facilitating these genomic alterations. We are also interested in the impact of HIV infection on the molecular oncogenesis of lymphoma. To address these important questions we integrate basic and translational science using in silico, ex vivo, cell-based and tissue-based genomic and proteomic approaches.
My laboratory is interested in understanding the molecular mechanisms responsible for the generation and maintenance of intra-cellular membrane-bounded compartments. In all eukaryotic cells intracellular membrane trafficking is critical for a range of important cellular functions including protein secretion, post-translational modifications, cell signalling, cell polarization, and cell maintenance. Defects in membrane trafficking can underline, or even exacerbate, a number of human diseases including cancer, diabetes mellitus, Alzheimer’s, cystic fibrosis, Hermansky-Pudlak syndrome and Congenital Disorders of Glycosylation.
My research focuses on cell cycle control, stem cells, cancer stem cells, drug discovery, mRNA translation, and vertebrate development.
We are interested in studying primary effusion lymphoma (PEL), an aggressive B cell cancer caused by the Kaposi’s sarcoma-associated herpesvirus or human herpesvirus 8 (KSHV/HHV8). PEL tumor cells rely on the constitutive expression of virally encoded genes that globally reprogram host gene expression to create a conducive environment optimal for tumor cell proliferation and survival.
My research vision is to understand how cells perceive signals that vary in healthy and cancer cells and how this perception regulates tumorigenesis and metastasis.
My research group investigates the role of enzymes, especially cytochromes P450 (CYP), in the activation and processing of xenobiotic chemicals, such as drugs, pollutants, and dietary compounds, from a chemist’s perspective. We specialize in the identification and validation of biochemical mechanisms through experimental approaches and often develop analytical tools along the way. Nevertheless, our projects are often multi-disciplinary and collaborative to effectively tackle complex challenges by recruiting experts in computational, analytical, and clinical research.
I specialize in epigenetics, with a focus on how environmental factors linked to cancer affect DNA and histone methylation. I investigate how the supply and metabolism of the methyl donor methionine modulates these responses and alters cancer development. My current project studies how to modulate dietary methionine to alter autophagy and improve the response rate to immunotherapy in patients with metastatic melanoma.
We utilize genetically modified mouse models to understand the function of poorly characterized genes that have a function in skeletal development, homeostasis or disease. A special interest is in proteins that post-translationally modify collagens and in osteogenesis imperfecta.
My research focuses on the area of applied bioinformatics/computational biology and systems biology for biomedical research. I have developed novel advanced algorithms and frameworks to accelerate the utilization and mining for biological interpretation of omics data (genome, transcriptome, proteome and metabolome) for biomedical research translation (cancer, obesity, diabetes, autoimmune disease, metabolic dysfunction, etc.). In addition, I also focus on the impact of human gut microbiome on diseases progression and development.
Our laboratory is interested in autophagy in osteoblast lineage cells in efforts to understand the role of autophagy in bone remodeling and age-related bone loss.
The long-term interest of my laboratory is to understand molecular mechanisms responsible for cold storage (CS)-induced renal damage. My research focuses on exploring novel mechanisms by which CS alters protein quality and renal function after transplantation, and importantly, to identify a possible therapeutic target that could lead to improved renal outcome after transplantation. Specifically, I plan to investigate the roles of proteasome, heat shock proteins and complement pathway during CS plus transplantation. We have established a rat kidney transplantation model, which will be fundamental in studying my independent research project on CS mediated renal damage. In addition, I’m also collaborating with Dr. MacMillan-Crow to study the molecular mechanisms that disrupt mitochondrial dynamics during renal CS and transplantation using our rat kidney transplant model.
The overall goal of our research program is to better understand the role of the mitochondrion in health and disease. Areas of focus include studying the role of mitochondrial proton leaks in the regulation of metabolic rate, as well as studying the impact of lifestyle (i.e. diet/exercise) and pharmacological interventions on bioenergetics in several settings including developmental programming, obesity and trauma.
I am a cellular/molecular pharmacologist whose research interests involve understanding the neurobiological mechanisms underlying the addictive states produced by drugs of abuse. Specifically, for over 20 years I have been investigating the cellular and molecular mechanisms of signal transduction mediated by G-protein coupled receptors (GPCRs) with which drugs of abuse interact, specifically opioids and cannabinoids.
My research focuses on protein-nucleic acid interactions.
My research focuses on the molecular genetics of longevity and age-associated diseases. I was trained in genetics, and turned to C. elegans as a model system in which to define and characterize genes that govern longevity. Using novel gene-mapping methods we developed, we discovered over 27 highly-significant loci for lifespan, resistance to stresses, and Darwinian fitness.
My main research interests include the use of laser thermal ablation for brain tumors and understanding the immune microenvironment.
Primary areas of investigation are aimed at enhancing our understanding of cancer biology to discover and develop improved methods for cancer treatment. Our major future objective is to significantly and positively contribute to translational research and clinical practice.
Our laboratory is interested in the physiological drivers of colon and breast cancers. Current work in the laboratory and via our collaborations includes: 1) elucidating the role of Krüppel-like factor 9 (KLF9) in cancer suppression; 2) understanding how the hormonal milieu (focus on insulin and the obesogenic environment) affects tumor cell growth; and 3) characterizing the role of Malic Enzyme 1 (ME1) in oncogenesis. Projects use a combination of novel mouse models, human cell lines and tissues, and OMICs technologies and are translational and highly collaborative.
My research focuses on organelles of the secretory pathway using HeLa cells as an easy cell for molecular manipulations of the Golgi apparatus and platelets as structure/function example of a stored secretory granules.
My laboratory focuses on histone epigenetic mechanisms that regulate gene transcription and that are coupled to melanoma progression. We utilize a suite of techniques in our studies including proteomics of human biopsies, immunohistochemistry, cell culture, tumorigenicity assays, ChIPseq, biochemical and proteomic approaches for analyses of protein complexes, and cutting-edge mass spectrometry for the analysis of histone post-translational modifications.
We are using ‘third generation sequencing technology’ (such as Oxford Nanopore flow cells) to do metagenomics of clinical isolates and environmental samples.
My research focuses on chromosome dynamics, epigenetics, cellular growth controls.
My research focuses on the role of circulating blood platelets, in thrombosis, inflammation, and cancer
The focus of research in my laboratory is centered on CNS development, particularly with regard to the formation and maintenance of myelin.
In my lab, I conduct federally funded research that focuses on the Replication stress response and DNA damage repair mechanisms in normal and tumor cells after radiation therapy or chemotherapy. Understanding the interplay between defective DNA repair and cancer cell growth, as well as normal cell injury could lead to new avenues for both cancer prevention and personalized cancer treatment. My research team and I are motivated by an unyielding desire to find answers.
Our lab focus on two aspects 1. Role of Chlamydia variants in host pathogenesis. 2. Role of infant diet in gastrointestinal tract development and immune function.
We are interested in the pathophysiology of multiple myeloma (MM), a B cell cancer characterized by proliferation of malignant plasma cells in the bone marrow, presence of a monoclonal serum immunoglobulin, and osteolytic lesions. We are investigating roles/mechanisms of PTH axis (PTH signal transduction) in MM development and therapeutic agents that target this axis. Additionally we are exploring the roles of Hypoxia (low oxygen tension) and microRNA (miRNA) in MM.
Dr. Zhan is interested in understanding how the genetic alterations in cancer cells contribute to tumor progression, alter treatment response and create vulnerabilities that may be targeted therapeutically.
I am interested in the role of non-canonical DNA structures and long non-coding RNAs in human disease. I am also interested in clinical applications of microbiome-derived protein biomarkers