Department: Genetics

I refer you to my web page for detailed list of interests, projects and publications. In addition to pressing the link here, you can search "Russ Altman" on http://www.google.com/

Our research is aimed at defining the pathways of p53-mediated apoptosis and tumor suppression, using a combination of biochemical, cell biological, and mouse genetic approaches. Our strategy is to start by generating hypotheses about p53 mechanisms of action using primary mouse embryo fibroblasts (MEFs), and then to test them using gene targeting technology in the mouse.

Our laboratory is focused on identifying proteins based upon their ability to alter a variety of cell fate decisions - including mesodermal, endodermal, neural, endothelial, and somitic - within the vertebrate embryo.

Our laboratory investigates how complex, elaborately patterned tissues form during vertebrate embryonic development. In particular we aim to add a new dimension to our understanding of how cells “know” where to go, when to move, and differentiate. We combine classical embryology with state-of-the-art biochemistry, imaging, and genomics. Major research areas include delineating the translational regulatory code of the mammalian genome and cutting-edge imaging of tissue patterning.

Genetics of color variation

The lesions of Parkinson's disease (PD) spread within the central nervous system (CNS) with characteristics of prion diseases. The prion in this case is a misfolded form of alpha-synuclein. We are investigating the mechanism of spread on alpha-synuclein prions with a special attention to axonal transport and transfer of prions between neurons. Understanding these pathways could lead to using drugs to slow down or halt disease progression.

Our lab studies the molecular basis of longevity. We are interested in the mechanism of action of known longevity genes, including FOXO and SIRT, in the mammalian nervous system. We are particularly interested in the role of these longevity genes in neural stem cells. We are also discovering novel genes and processes involved in aging using two short-lived model systems, the invertebrate C. elegans and an extremely short-lived vertebrate, the African killifish N. furzeri.

Please visit my personal page at: https://sites.google.com/site/jdbuenrostro/

My research focuses on analyzing genome wide patterns of variation within and between species to address fundamental questions in biology, anthropology, and medicine. My group works on a variety of organisms and model systems ranging from humans and other primates to domesticated plant and animals. Much of our research is at the interface of computational biology, mathematical genetics, and evolutionary genomics.

The Butte Lab at Stanford builds and applies tools that convert more than 300 billion points of molecular, clinical, and epidemiological data -- measured by researchers and clinicians over the past decade -- into diagnostics, therapeutics, and new insights into disease.

My lab is developing innovative gene and cell therapies for genetic diseases, with a focus on stem cell therapies and regenerative medicine. We have created novel methods for inserting therapeutic genes into the chromosomes at specific places by using homologous recombination and recombinase enzymes. We are working on two forms of muscular dystrophy. We created induced pluripotent stem cells from patient fibroblasts, added therapeutic genes, differentiated, and engrafted the cells.

I am interested in how human genomes change over time and how population histories influence disease susceptibilities in different populations.

I spent most of my PH.D time on identifying and elucidating the functions of cis-regulatory modules (CRMs) through functional genomic, comparative genomics approaches. My current projects include: 1) Annotate the human functional sequences using human ENCODE and Mouse ENCODE data. 2) Improve the understanding of personal genomics by combing functional genomics, comparative genomics and population genomics approaches. 3) Relationship between immune system and micro biome.

My research involves identifying, validating and integrating scientific facts into encyclopedic databases essential for research and scientific education. Published results of scientific experimentation are a foundation of our understanding of the natural world and provide motivation for new experiments. The combination of in-depth understanding reported in the literature with computational analyses is an essential ingredient of modern biological research.

We study RNA decay and mechanisms that affect microbial antibiotic resistance, as well as the exploitation of host genes by pathogens. A small bioinformatics team within our lab has developed knowledge based systems to aid in investigations of gene expression on a genome-wide basis.

I am mainly interested in understanding the relative roles of recombination, mutation and selection in shaping genetic variation in and determining the genetic structure of populations of microorganism, especially those that are etiological agents of infectious diseases. I am also interested in disentangling the contribution of forces generating and maintaining variation genome wide and the use of new technologies for the assessment of variation in different organisms.

We are using Saccharomyces cerevisiae and Human to conduct whole genome analysis projects. The yeast genome sequence has approximately 6,000 genes. We have made a set of haploid and diploid strains (21,000) containing a complete deletion of each gene. In order to facilitate whole genome analysis each deletion is molecularly tagged with a unique 20-mer DNA sequence. This sequence acts as a molecular bar code and makes it easy to identify the presence of each deletion.

We study natural cellular mechanisms for adapting to genetic change. These include systems activated during normal development and those for detecting and responding to foreign or unwanted genetic activity. Underlying these studies are questions of how a cells can distinguish information as "self" versus "nonself" or "wanted" versus "unwanted".

Mammalian DNA repair and DNA damage inducible responses; p53 tumor suppressor gene; transcription in nucleotide excision repair and mutagenesis; genetic determinants of cancer cell sensitivity to DNAdamage; genetics of inherited cancer susceptibility syndromes and human GI malignancies; clinical cancer genetics of BRCA1 and BRCA2 breast cancer and mismatch repair deficient colon cancer.

Functional consequences and pathogenetic mechanisms of mutations and microdeletions in human neurogenetic syndromes and mouse models. Integration of genomic information into medical care.

Regulation of stem cell division and self-renewal Cell type specific transcription machinery and regulation of cell differentiation Developmental regulation of cell cycle progression during male meiosis Molecular dissection of the mechanism of cytokinesis.

We investigate the mechanisms of human neurodegenerative diseases, including Alzheimer disease, Parkinson disease, and ALS. We don't limit ourselves to one model system or experimental approach. We start with yeast, perform genetic and chemical screens, and then move to other model systems (e.g. mammalian tissue culture, mouse, fly) and even work with human patient samples (tissue sections, patient-derived cells, including iPS cells) and next generation sequencing approaches.

Since 1992 my work has concentrated on ethical, legal, and social issues in the biosciences. I am particularly active on issues arising from neuroscience, human genetics, and stem cell research, with cross-cutting interests in human research protections, human biological enhancement, and the future of human reproduction.

Our lab focuses on developing methods to probe the genome and epigenome at the single-cell and single-molecule levels. Our efforts are split between building new tools to leverage the power of high-throughput sequencing and cutting-edge microscopies, and bringing these new technologies to bear against basic biological questions of genomic and epigenomic variation.

The overarching goal of the Brunet lab is to understand the genetic mechanisms of aging and longevity. Aging is a highly plastic process regulated by a combination of genetic and environmental factors. I am interested in the basic molecular components that characterize “young” and “aged” cellular states. Aging is associated with an increased onset of cancer, and I seeks to define the set of factors that can rejuvenate an aged cell, without the risk of malignant transformation. Ultimately, w..

Population Genetics, Human Evolution

Gene Regulation; Molecular Immunology; Lymphocyte subsets; Fluorescence-Activated CellSorter (FACS) development; AIDS; Apoptosis; Redox Regulation; Gene Arrays; and the theraphy of AIDS using the anti-oxidant N'acetylcysteine(NAC).

B-cell development; Ig rearrangement and repertoire analysis; T cell regulation of antibodyresponses; T cell subsets; glutathione regulation of HIV disease progression; Fluorescence-Activated Cell Sorting (FACS) related software development and gene arrays.

Mark A. Kay, M.D., Ph.D. Director of the Program in Human Gene Therapy and Professor in the Departments of Pediatrics and Genetics. Respected worldwide for his work in gene therapy for hemophilia, Dr. Kay and his laboratory focus on establishing the scientific principles and developing the technologies needed for achieving persistent and therapeutic levels of gene expression in vivo. The major disease models are hemophilia, hepatitis C, and hepatitis B viral infections.

Mechanisms of Aging in C. elegans and humans.

Co-founder, Pacific Symposium on Biocomputing NIEHS, Site Visit Reviewer NIH, Study Section Reviewer

My primary research interests lie in host-microbe interactions and specifically how mutualistic or commensal microbiota influence the host’s response to various abiotic and biotic stressors.

Function and evolution of the Myb oncogene family; function and evolution of E2F transcriptional regulators and RB tumor suppressors; epigenetic regulation of chromatin and chromosomes; cancer genetics.

Transcriptome variation across the Human Genome Diversity Project (HGDP) The impact of genetic diversity on skin pigmentation variation within the ≠Khomani San population

My current computational research focuses on the integration of existing (and developing) omics technologies and their application in personalized medicine. This includes the study of dynamics of transcriptomic, proteomic, metabolomic, autoantibodyomic components, their emergent patterns and biological significance. In addition, my investigations include studies in dynamic biological network characterization, protein-protein interactions & biomarker determination using protein microarrays.

We focus on understanding the effects of genome variation on cellular phenotypes and cellular modeling of disease through genomic approaches such as next generation RNA sequencing in combination with developing and utilizing state-of-the-art bioinformatics and statistical genetics approaches. See our website at http://montgomerylab.stanford.edu/

My research area is the genetic epidemology of musculoskeletal and endocrine disease, with a special focus on osteoporosis and diabetes-related bone disease. I have been a representative researcher for the Rotterdam Study (the Netherlands) in several collaborative consortia, including: GEFOS: Genetic Factors for Osteoporosis; GENOMOS: Genetic Markers for Osteoporosis; CHARGE: Cohorts for Heart and Aging Research in Genomic Epidemiology; NCHA: Netherlands Consortium for Healthy Ageing.

While my primary role is to direct the MS in Human Genetics and Genetic Counseling program, my research focuses on the intersection between genetics and ethics, particularly around the translation of new genetic technologies (such as genome sequencing or non-invasive prenatal diagnosis) into clinical practice. I am especially interested in patient decision making, informed consent, and the interface between genetics and disability.

Acetaminophen – Tylenol™ - is an OTC drug used for its analgesic and antipyretic effects. APAP overdose has been reported to cause liver injury, acute liver failure and over 450 deaths yearly in the United State. Implicated its toxicity is N-acetyl-p-benzoquinone imine (NAPQI) one of its metabolites excreted by GSH. We propose that administration of formulated NAC-APAP drug may mitigate toxic effect seen in inadvertent APAP overdose via NAC mediated replenishment of intracellular GSH.

Much of our research exploits the power of yeast as an experimentally tractable model eukaryote to investigate fundamental problems in cell and developmental biology such as the mechanisms of cell polarization and cytokinesis. In another project, we are developing the small sea anemone Aiptasia as a model system for study of the molecular and cellular biology of dinoflagellate-cnidarian symbiosis, which is critical for the survival of most corals but still very poorly understood.

We are interested in the links between the basic cell cycle machinery and the factors controlling self-renewal, differentiation, and regeneration. In particular, we are intrigued by the differences and the similarities between "normal" cells, cancer cells, and stem cells. We investigate the mechanisms by which normal cells become tumor cells, and we aim to understand the differences between the proliferative response in response to injury and the hyperproliferative phenotype of cancer cells.

Population Genetics of Native Americans, Anthropology, Human Migrations Process, Ancient Populations.

Our research is focused on the genetic regulation of animal development and its relation to birth defects, cancer, and neurodegeneration. We study mechanisms and functions of Hedgehog (Hh) signaling, which controls cell fates and growth, in the context of normal development and brain cancer. We study a neurodegenerative disease, Niemann-Pick C syndrome, that affects intracellular organelle movements and sterol homeostasis.

Evolution and the adaptive landscape using yeast as a model; Defining yeast transcriptomes; chromosomal evolution in hybrid yeast species

We are interested in the systems biology of molecular phenotypes, and how genetic variation affects them. The lab combines experimental approaches in developing mouse embryos as well as human cancers with computational analyses. Our main data engine is high-throughput sequencing. Please refer to our web site for more information: http://mendel.stanford.edu/SidowLab/index.html

We are presently in an omics revolution in which genomes and other omes can be readily characterized. Our laboratory uses a variety of approaches to analyze genomes and regulatory networks. Our research focuses on yeast, an ideal model organism ideally suited to genetic analysis, and humans. 1) Transcriptomes To annotate genomes, we developed RNA sequencing for annotation the yeast and human transcriptomes. We discovered that the eukaryotic transcriptome is much more complex than previously..

We use the tools of genetics, microscopy, and biochemistry to understand fundamental questions of cell biology: How are cells organized by the cytoskeleton? How do the centrosome and cilium control cell control cell signaling? How is cell division coordinated with duplication of the centrosome, and what goes wrong in cancer cells defective in this coordination?

My lab focuses on understanding the molecular mechanism of transcription factors that govern the transformation of normal mammalian cells to a neoplastic state. We are especially interested in the action of the nuclear hormone receptors and the interactions between the receptors and other signaling pathways in related human disorders.

Develop statistical and computational methods for population genomics analyses; modeling human evolutionary history; genetic association studies in admixed populations.

The key to understanding mechanisms that mediate cnidarian-dinoflagellate symbioses is to do experiments that target functional questions. With my background and training in developmental and larval biology, along with the lab group’s success of inducing Aiptasia to spawn in the lab, I see great opportunities to look at larvae and their specificity with certain strains of Symbiodinium and how might that progress through settlement and metamorphosis. Analysis of the transcriptomic changes betwee..

Mechanisms underlying homologous chromosome pairing, DNA recombination and chromosome remodeling during meiosis, using the nematode Caenorhabditis elegans as an experimental system. High-resolution 3-D imaging of dynamic reorganization of chromosome architecture. Role of protease inhibitors in regulating sperm activation.

The Vollrath lab works to uncover molecular mechanisms relevant to the health and pathology of the outer retina. We study the retinal pigment epithelium (RPE), a cell monolayer adjacent to photoreceptors that performs a variety of tasks crucial for retinal homeostasis. Specific areas of interest include the circadian regulation of RPE phagocytosis of photoreceptor outer segment tips, and how RPE metabolic dysfunction contributes to retinal degenerative diseases.

Stem cell function requires both the establishment and maintenance of particular epigenetic states. Perturbation of the epigenetic status of stem cells may compromise both self-renewal and multipotency. Work from our lab has identified the Forkhead family transcription factor, FoxO3, as a regulator of adult neural stem cell (NSCs) quiescence, which prevents the depletion of this population of cells. Along with recent evidence that Forkhead family members act as ‘pioneer factors’ in the opening ..

Our laboratory uses genome-wide methods to uncover alterations that drive cancer progression and metastasis in genetically-engineered mouse models of human cancers. We combine cell-culture based mechanistic studies with our ability to alter pathways of interest during tumor progression in vivo to better understand each step of metastatic spread and to uncover the therapeutic vulnerabilities of advanced cancer cells.

My goal is to combine theoretical and experimental approaches to uncover the mystery of gene regulatory networks. My current research focuses on the fine-tuning function of RNA editing, a post-transcriptional-processing mechanism that contributes to the diversity of gene products.