The Salk Institute for Biological Studies is an independent, non-profit, scientific research institute located in La Jolla, California. It was founded in 1960 by Jonas Salk, the developer of the polio vaccine; among the founding consultants were Jacob Bronowski and Francis Crick. Building did not start until spring of 1962. The institute consistently ranks among the top institutions in the US in terms of research output and quality in the life science. In 2004, the Times Higher Education Supplement ranked Salk as the world's top biomedicine research institute, and in 2009 it was ranked number one globally by ScienceWatch in the neuroscience and behavior areas.The institute employs 850 researchers in 60 research groups and focuses its research in three areas: Molecular Biology and Genetics; Neuroscience; and Plant Biology. Research topics include cancer, diabetes, birth defects, Alzheimer's disease, Parkinson's disease, AIDS, and the neurobiology of American Sign Language. The March of Dimes provided the initial funding and continues to support the institute. Current research is funded by a variety of organizations, such as the NIH, the HHMI and private organizations such as Paris-based Ipsen and the Waitt Family Foundation. In addition, the internally administered Innovation Grants Program encourages cutting-edge high-risk research. The institute appointed genome biologist Eric Lander and stem cell biologist Irving Weissman as non-resident fellows in November 2009.The campus was designed by Louis Kahn. Salk had sought to make a beautiful campus in order to draw the best researchers in the world. Salk and Kahn having both descended from Russian Jewish parents that had immigrated to the United States had a deeper connection than just mere partners on an architectural project. The results of their connection is seen in the design that resulted from their collaboration. The original buildings of the Salk Institute were designated as a historical landmark in 1991. The entire 27-acre site was deemed eligible by the California Historical Resources Commission in 2006 for listing on the National Register of Historic Places. Wikipedia.
Salk Institute for Biological Studies | Date: 2016-11-22
The invention features compositions comprising in vitro generated beta cells capable of glucose-stimulated insulin secretion, methods of inducing beta cell maturation from embryonic or induced pluripotent stem cell-derived beta-like cells, and methods of using in vitro generated beta cells for the treatment of type 1 diabetes, type 2 diabetes, or a related disorder.
Salk Institute for Biological Studies | Date: 2016-11-14
The method provides methods and compositions for treating metabolic disorders such as impaired glucose tolerance, elevated blood glucose, insulin resistance, dyslipidemia, obesity, and fatty liver.
Salk Institute for Biological Studies and University of Sydney | Date: 2016-09-12
Novel compounds having a formula embodiments of a method of making the same, and of a composition comprising them are disclosed herein. Also disclosed are embodiments of a method of treating or preventing a metabolic disorder in a subject, comprising administering to a subject (e.g., via the gastrointestinal tract) a therapeutically effective amount of one or more of the disclosed compounds, thereby activating FXR receptors in the intestines, and treating or preventing a metabolic disorder in the subject. Additionally disclosed are embodiments of a method of treating or preventing inflammation in an intestinal region of a subject, comprising administering to the subject (e.g., via the gastrointestinal tract) a therapeutically effective amount of one or more of the disclosed compounds, thereby activating FXR receptors in the intestines, and thereby treating or preventing inflammation in the intestinal region of the subject.
Salk Institute for Biological Studies and The Regents Of The University Of California | Date: 2015-03-05
The present invention relates to methods for producing polyketide synthase variants, and for altering the activity and/or substrate specificity of putative native and variant polyketide synthases. The present invention further relates to compositions comprising said polyketide synthase variants, compounds prepared using said polyketide synthase variants, and uses of said polyketide synthase variants. In one embodiment, said polyketide synthase variant is 2-pyrone synthase.
Salk Institute for Biological Studies, The Regents Of The University Of California and Labrys Biologics | Date: 2016-10-11
The disclosure features compositions and methods for treating a metabolic disorder, including diabetes, conditions associated with inhibition of insulin secretion, or for increasing longevity. In some embodiments, the methods comprise administering an anti-CGRP antagonist antibody.
Osakada F.,Salk Institute for Biological Studies
Nature protocols | Year: 2013
Rabies viruses, negative-strand RNA viruses, infect neurons through axon terminals and spread trans-synaptically in a retrograde direction between neurons. Rabies viruses whose glycoprotein (G) gene is deleted from the genome cannot spread across synapses. Complementation of G in trans, however, enables trans-synaptic spreading of G-deleted rabies viruses to directly connected, presynaptic neurons. Recombinant rabies viruses can encode genes of interest for labeling cells, controlling gene expression and monitoring or manipulating neural activity. Cre-dependent or bridge protein-mediated transduction and single-cell electroporation via the EnvA-TVA or EnvB-TVB (envelope glycoprotein and its specific receptor for avian sarcoma leukosis virus subgroup A or B) system allow cell type-specific or single cell-specific targeting. These rabies virus-based approaches permit the linking of connectivity to cell morphology and circuit function for particular cell types or single cells. Here we describe methods for construction of rabies viral vectors, recovery of G-deleted rabies viruses from cDNA, amplification of the viruses, pseudotyping them with EnvA or EnvB and concentration and titration of the viruses. The entire protocol takes 6-8 weeks.
Allen N.J.,Salk Institute for Biological Studies
Annual review of cell and developmental biology | Year: 2014
Astrocytes regulate multiple aspects of neuronal and synaptic function from development through to adulthood. Instead of addressing each function independently, this review provides a comprehensive overview of the different ways astrocytes modulate neuronal synaptic function throughout life, with a particular focus on recent findings in each area. It includes the emerging functions of astrocytes, such as a role in synapse formation, as well as more established roles, including the uptake and recycling of neurotransmitters. This broad approach covers the many ways astrocytes and neurons constantly interact to maintain the correct functioning of the brain. It is important to consider all of these diverse functions of astrocytes when investigating how astrocyte-neuron interactions regulate synaptic behavior to appreciate the complexity of these ongoing interactions.
Taylor R.C.,Salk Institute for Biological Studies
Cold Spring Harbor perspectives in biology | Year: 2011
Aging cells accumulate damaged and misfolded proteins through a functional decline in their protein homeostasis (proteostasis) machinery, leading to reduced cellular viability and the development of protein misfolding diseases such as Alzheimer's and Huntington's. Metabolic signaling pathways that regulate the aging process, mediated by insulin/IGF-1 signaling, dietary restriction, and reduced mitochondrial function, can modulate the proteostasis machinery in many ways to maintain a youthful proteome for longer and prevent the onset of age-associated diseases. These mechanisms therefore represent potential therapeutic targets in the prevention and treatment of such pathologies.
Mihaylova M.M.,Salk Institute for Biological Studies |
Shaw R.J.,Salk Institute for Biological Studies
Nature Cell Biology | Year: 2011
One of the central regulators of cellular and organismal metabolism in eukaryotes is AMP-activated protein kinase (AMPK), which is activated when intracellular ATP production decreases. AMPK has critical roles in regulating growth and reprogramming metabolism, and has recently been connected to cellular processes such as autophagy and cell polarity. Here we review a number of recent breakthroughs in the mechanistic understanding of AMPK function, focusing on a number of newly identified downstream effectors of AMPK. © 2011 Macmillan Publishers Limited. All rights reserved.
Hunter T.,Salk Institute for Biological Studies
Philosophical Transactions of the Royal Society B: Biological Sciences | Year: 2012
The advantageous chemical properties of the phosphate ester linkage were exploited early in evolution to generate the phosphate diester linkages that join neighbouring bases in RNA and DNA (Westheimer 1987 Science 235, 1173-1178). Following the fixation of the genetic code, another use for phosphate ester modification was found, namely reversible phosphorylation of the three hydroxyamino acids, serine, threonine and tyrosine, in proteins. During the course of evolution, phosphorylation emerged as one of the most prominent types of post-translational modification, because of its versatility and ready reversibility. Phosphoamino acids generated by protein phosphorylation act as new chemical entities that do not resemble any natural amino acid, and thereby provide a means of diversifying the chemical nature of protein surfaces. A protein-linked phosphate group can form hydrogen bonds or salt bridges either intra- or intermolecularly, creating stronger hydrogen bonds with arginine than either aspartate or glutamate. The unique size of the ionic shell and charge properties of covalently attached phosphate allow specific and inducible recognition of phosphoproteins by phosphospecific-binding domains in other proteins, thus promoting inducible protein-protein interaction. In this manner, phosphorylation serves as a switch that allows signal transduction networks to transmit signals in response to extracellular stimuli. © 2012 The Royal Society.