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/

The Ashley lab is focused on the application of genomics to medicine. We develop methods for the interpretation of whole genome sequencing data to improve diagnosis of genetic disease and to personalize the practice of medicine. We also use RNA sequencing data to generate gene networks and link communities. Half of the lab is wet benches where we take advantage of cell systems, transgenic models and microsurgical models of disease to prove causality of our favorite targets.

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.

Familial adenomatous polyposis (FAP), a heritable colon cancer syndrome, causes colorectal adenocarcinoma (CRC) in children as young as 9 years, and confers 100% lifetime risk of CRC. FAP patient CRCs have accumulation of alterations in multiple tumor suppressors (i.e. Kras, p53), which accumulate due to the initial APC mutation. We hypothesize that there is a reproducible cascade of molecular changes in FAP that lead to CRC and will test this using genomic and transcriptomic technologies.

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.