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Our group has also developed genome-editing protocols for primary human chondrocytes to produce single-cell derived colonies with homozygous knockout of target genes. We are using engineered tissues from these cells to dissect the mechanism of genes implicated in OA development by genome-wide association studies, as well as coupling these technologies to high throughput screening approaches for OA drug discovery.

Sleep is an essential and evolutionarily conserved process that modifies synapses in the brain to support cognitive functions such as learning and memory. We are interested in understanding the molecular mechanisms of synaptic plasticity with a particular interest in sleep. Using mouse models of human disease as well as primary cultured neurons, we are applying this work to understanding and treating neurodevelopmental disorders including autism and intellectual disability.

The lab focuses on biochemistry, pharmacology, animal behavior and genetics.

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Our lab tries to understand viral pathogenesis. Basic and translational studies address mechanisms of host defense, including recruitment and function of leukocytes, vascular permeability leading to edema, bacterial clearance and resolution. Cell signaling pathways initiated by binding of leukocyte-endothelial cell adhesion molecules and molecular mechanisms underlying the functions of neutrophils are two particular areas. We use an integrated approach genomics, proteomics, computational biology to study the molecular mechanisms of hormone and drug desensitization.

Our current focus is on RGS proteins regulators of G protein signaling and post-translational modifications including ubiquitination and phosphorylation. The Dominguez lab studies how gene expression is controlled by proteins that bind RNA. RNA binding proteins control the way RNAs are transcribed, spliced, polyadenylated, exported, degraded, and translated. The overall focus of the laboratory is to develop immunotherapy strategies to treat human malignancies.

Specifically, one area of research is dedicated to the genetic engineering of immune cells to redirect their specificity to tumor-associated antigens. The most effective strategies developed in the laboratory are then translated into phase I clinical studies since we have access to the cellular therapeutic facility at UNC. The second area of research is dedicated to the tumor microenvironment and the development of engineering strategies aimed at countering its immunosuppressive properties.

My lab studies how genes function within the three-dimensional context of the nucleus to control development and prevent disease. Our current research efforts are divided into 3 areas: 1 Mapping the folding pattern of the genome 2 Dynamics of three-dimensional genome organization as cells differentiate and 3 Functional analysis of altered chromosome structure in cancer and other diseases. Appropriate allocation of cellular lipid stores is paramount to maintaining organismal energy homeostasis. Dysregulation of these pathways can manifest in human metabolic syndromes, including cardiovascular disease, obesity, diabetes, and cancer.

The goal of my lab is to elucidate the molecular mechanisms that govern the storage, metabolism, and intercellular transport of lipids; as well as understand how these circuits interface with other cellular homeostatic pathways e. We utilize C. The Drewry lab is focused on designing, synthesizing, evaluating, and sharing small molecule chemical probes for protein kinases. These tools are used to build a deeper understanding of disease pathways and facilitate identification of important targets for drug discovery. Through wide ranging partnerships with academic and industrial groups, the Drewry lab is building a Kinase Chemogenomic Set KCGS that is available to the community for screening.

Humans have a remarkable ability to learn from their environment after birth, but this plasticity also makes them susceptible to environmental insults. At the cellular level, learning is accomplished by changing the strength of the synaptic connections between neurons.

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Therefore, the Dudek lab is working to identify the underlying processes of synaptic plasticity. Using molecular techniques, patch clamp recordings and confocal microscopic imaging from neurons in brain slices and culture, we ask how neuronal activity controls gene transcription and brain circuitry and what determines why some brain regions are more plastic than others. These studies are likely to shed light on environmental causes of psychiatric diseases such as schizophrenia and autism. My lab studies a recently identified pathogen-sensing signaling complex known as the inflammasome.

The inflammasome is responsible for the proteolytic maturation of some cytokines and induces a novel necrotic cell death program. We have found that critical virulence factors from certain pathogens are able to activate NLRP3-mediated signaling, suggesting these pathogens may exploit this host signaling system in order to promote infections.

Our lab has active research projects in several areas relating to inflammasome signaling ranging from understanding basic molecular mechanisms of the pathway to studying the role of the system in animal models of infectious diseases. My lab studies how cell proliferation is controlled during animal development, with a focus on the genetic and epigenetic mechanisms that regulate DNA replication and gene expression throughout the cell cycle.

Many of the genes and signaling pathways that we study are frequently mutated in human cancers. The Elston lab is interested in understanding the dynamics of complex biological systems, and developing reliable mathematical models that capture the essential components of these systems. The projects in the lab encompass a wide variety of biological phenomena including signaling through MAPK pathways, noise in gene regulatory networks, airway surface volume regulation, and understanding energy transduction in motor proteins. A major focus of our research is understanding the role of molecular level noise in cellular and molecular processes.

We have developed the software tool BioNetS to accurately and efficiently simulate stochastic models of biochemical networks. Our lab applies cutting edge genetic and proteomic technologies to unravel dynamic signaling networks involved in cell proliferation, genome stability and cancer. These powerful technologies are used to systematically interrogate the ubiquitin proteasome system UPS , and allow us to gain a systems level understanding of the cell at unparalleled depth.

We are focused on UPS signaling in cell cycle progression and genome stability, since these pathways are universally perturbed in cancer.

Introduction

The research in my lab is divided into two main areas — 1 Atomic force microscopy and fluorescence studies of protein-protein and protein-nucleic acid interactions, and 2 Mechanistic studies of transcription elongation. My research spans the biochemical, biophysical, and analytical regimes. Falk is recognized world wide as a leader in research on kidney diseases related to autoimmune responses. Air pollution exposure is associated with increased hospital visits and mortality, and is a major area of research for the United States Environmental Protection Agency.

The primary research interest of my laboratory is the examination of the effects and mechanisms of air pollutants in the environment on normal cardiopulmonary function cardiac toxicology , particularly in models of cardiovascular disease, using state-of-the-art targeted and high throughput methods. Fenton, focuses on the role of environmental chemicals in breast developmental timing as it relates to puberty, increased susceptibility to form breast tumors, altered lactational ability, and the effects of chemicals on independent breast cancer risk factors such as obesity, breast density and pubertal timing.

The projects within the lab often take a systems biology approach to the problem and instead of delving into exact mechanisms of an insult, which is in line with the missions of the NTP. The group also provides expertise in the use of whole mount mammary gland preparations in evaluating early life development of both male and female rat offspring and lifelong effects in female mice. Fessler laboratory investigates mechanisms of the innate immune response, in particular Toll like Receptor TLR pathways and how they regulate inflammatory and host defense responses in the lung.

To this end, we use both in vitro macrophage cultures and in vivo mouse models of acute lung injury and pneumonia model systems, and also use translational approaches e. An area of particular interest within the laboratory is defining how cholesterol trafficking and dyslipidemia innate immunity. Our lab studies the underlying structural and functional substrates of behavior in disease using rodent models.

Specifically our goal is to develop a better understanding of how cellular function in the CNS is affected by drug-related substances opioids, cannabinoids in the context of HIV infection. That includes the study of how drugs of abuse exacerbate the pathogenesis of neuroAIDS but also the study of targets within the endocannabinoid system for the potential treatment of HIV.

We use various in vivo and in vitro techniques, including primary cell culture models, behavioral conditioning tasks, live cell imaging, and electrophysiology. Our laboratory studies the role of the blood coagulation system in inflammatory, infectious, and malignant disease.

Bacterial toxins : tools in cell biology and pharmacology

Current studies suggest that coagulation factors drive mechanisms of disease both dependent and independent of their traditional roles in hemostasis and thrombosis. Our overall goal is to translate this knowledge into novel approaches for treating these common yet deadly diseases. My lab has a long-standing interest in gene regulation, epigenetics, chromatin and RNA biology, especially as it pertains to cancer.

We are interested in studying the formation and function of transcriptional enhancers and the non-coding RNAs that are actively produced at enhancers, known as enhancer RNAs, which are involved in modulating several aspects of gene regulation. In addition, we aim to understand how transcriptional enhancers help orchestrate responses to external stimuli found in the tumor microenvironment.

We address these research aims by using an interdisciplinary approach that combines molecular and cellular techniques with powerful genomic and computational approaches. Our goal is to revolutionize the treatment of psychiatric and neurological illness by developing novel brain stimulation paradigms. We identify and target network dynamics of physiological and pathological brain function.

We combine computational modeling, optogenetics, in vitro and in vivo electrophysiology in animal models and humans, control engineering, and clinical trials. We strive to make our laboratory a productive, collaborative, and happy workplace. The lab focuses on understanding how environmental exposures are associated with human disease with a particular focus on genomic and epigenomic perturbations. Using environmental toxicogenomics and systems biology approaches, we aim to identify key molecular pathways that associate environmental exposure with diseases.

A current focus in the lab is to study prenatal exposure to various types of metals including arsenic, cadmium, and lead. We aim to understand molecular mechanisms by which such early exposures are associated with long-term health effects in humans. For example, we are examining DNA methylation epigenetic profiles in humans exposed to metals during the prenatal period.

This research will enable the identification of gene and epigenetic biomarkers of metal exposure. The identified genes can serve as targets for study to unravel potential molecular bases for metal-induced disease. Ultimately, we aim to identify mechanisms of metal -induced disease and the basis for inter-individual disease susceptibility. The Furey Lab is interested in understanding gene regulation processes in specific cell types, especially with respect to complex phenotypes, and the effect of genetic and environmental variation on gene regulation.

We have explored these computationally by concentrating on the analysis of genome-wide open chromatin data generated from high-throughput sequencing experiments; and the development of statistical methods and computational tools to investigate underlying genetic and biological mechanisms of complex phenotypes. Our current projects include determining the molecular effects of exposure to 1,3-butadiene, a known carcinogen, on chromatin, gene regulation, and gene expression in lung, liver, and kidney tissues of genetically diverse mouse strains.

We are also exploring chromatin, transcriptional, and microbial changes in inflammatory bowel diseases to identify biomarkers of disease onset, severity, and progression. Over millions of years of coexistence humans and pathogens have develop intricate and very intimate relationships.

These highly specialized interactions are the basic determinants of pathogenesis and disease progression. Our laboratory is interested in elucidating the molecular basis of disease. Our multidisciplinary approach to molecular medicine is based on our interest in the translation of basic research observations into clinical implementation.

Bacterial Toxins: Tools in Cell Biology and Pharmacology by Klaus Aktories - indotnale.tk

For this purpose we use a variety of in vitro and in vivo approaches to study AIDS, Cancer, immunological diseases, gene therapy, etc. In addition, we are interested in the development and implementation of novel approaches to prevent viral transmission using pre-expossure prophylaxis and vaccines. As a pediatric neurologist and brain tumor researcher, I seek to understand the link between brain growth and childhood brain tumors. During postnatal cerebellar development, neural progenitors divide rapidly.

Pharmacology – ANTIBIOTICS – DNA, RNA, FOLIC ACID, PROTEIN SYNTHESIS INHIBITORS (MADE EASY)

This wave of neurogenesis must be strictly controlled to prevent formation of medulloblastoma, a malignant neuroblastic tumor of the cerebellum. Using transgenic mice that express constitutively active Smoothened, we are able to recapitulate tumorigenesis in mice. These tumor-prone mice develop medulloblastomas that model the human tumor in pathology and gene expression. We use this primary brain tumor model to gain novel insight into medulloblastoma pathogenesis and treatment.

Approaches include structural, diffusion tensor, and resting state functional imaging, with a focus on cortical gray and white matter development and its relationship to cognitive development. Studies include normally developing children, twins, and children at high risk for schizophrenia and bipolar illness. We also study the contributions of genetic and environmental risk factors to early brain development in humans.

A developing collaborative project with Flavio Frohlich, PhD will use imaging to study white and gray matter development in ferrets and its relationship with cortical oscillatory network development. He received an Honors degree in microbiology from the University of Glasgow, and a doctorate in aerosol science and mucosal immunology from the University of Bristol in In he joined the EPA fellowship program and in became a permanent staff member.