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Salk Institute for Biological Studies

Salk Institute for Biological Studies

Life sciences research institute

The Salk Institute for Biological Studies is a private, not-for-profit research institute in La Jolla, San Diego, California, United States. Major Salk study areas are cancer biology, neuroscience and neurological disorders, immune system biology, aging and regenerative medicine, metabolism and diabetes, and plant biology.

The Salk Institute was founded by Jonas Salk, developer of the first safe polio vaccine, who had a vision to "create a collaborative environment where researchers could explore the basic principles of life and contemplate the wider implications of their discoveries for the future of humanity".

The institute was designed by Philadelphia architect Louis Kahn and opened its doors in 1963.

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Author
Date
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May 20, 2021
BioSpace
IconOVir Bio Announces Preclinical Proof-of-Concept Data for Proprietary Mutations Designed to Improve Selectivity of Novel Oncolytic Viruses, Including Lead Product Candidate ICVB-1042 - read this article along with other careers information, tips and advice on BioSpace
Reid, D. A., Reed, P. J., Schlachetzki, J. C. M., Nitulescu, I. I., Chou, G., Tsui, E. C., Jones, J. R., Chandran, S., Lu, A. T., McClain, C. A., Ooi, J. H., Wang, T.-W., Lana, A. J., Linker, S. B., Ricciardulli, A. S., Lau, S., Schafer, S. T., Horvath, S., Dixon, J. R., Hah, N., Glass, C. K., Gage, F. H.
April 2, 2021
Science
Humans have only a limited capacity to generate new neurons. These cells thus need to repair errors in the genome. To better understand this process, Reid et al. developed Repair-seq, a method to locate DNA repair within the genome of stem cell-derived neurons. DNA repair hotspots (DRHs) were more likely to occur within specific genomic features such as gene bodies as well as in genomic formations, open chromatin, and active regulatory regions. This method showed that repair was enriched at sites involved in neuronal function and identity. Furthermore, proteomic data indicated that genes in DRHs are enriched in Alzheimer's disease and that DRHs are more active in aging. These observations link neuronal DNA repair to aging and neurodegeneration. Science , this issue p. [91][1] Neurons are the longest-lived cells in our bodies and lack DNA replication, which makes them reliant on a limited repertoire of DNA repair mechanisms to maintain genome fidelity. These repair mechanisms decline with age, but we have limited knowledge of how genome instability emerges and what strategies neurons and other long-lived cells may have evolved to protect their genomes over the human life span. A targeted sequencing approach in human embryonic stem cell-induced neurons shows that, in neurons, DNA repair is enriched at well-defined hotspots that protect essential genes. These hotspots are enriched with histone H2A isoforms and RNA binding proteins and are associated with evolutionarily conserved elements of the human genome. These findings provide a basis for understanding genome integrity as it relates to aging and disease in the nervous system. [1]: /lookup/doi/10.1126/science.abb9032
Reid, D. A., Reed, P. J., Schlachetzki, J. C. M., Nitulescu, I. I., Chou, G., Tsui, E. C., Jones, J. R., Chandran, S., Lu, A. T., McClain, C. A., Ooi, J. H., Wang, T.-W., Lana, A. J., Linker, S. B., Ricciardulli, A. S., Lau, S., Schafer, S. T., Horvath, S., Dixon, J. R., Hah, N., Glass, C. K., Gage, F. H.
April 2, 2021
Science
Humans have only a limited capacity to generate new neurons. These cells thus need to repair errors in the genome. To better understand this process, Reid et al. developed Repair-seq, a method to locate DNA repair within the genome of stem cell-derived neurons. DNA repair hotspots (DRHs) were more likely to occur within specific genomic features such as gene bodies as well as in genomic formations, open chromatin, and active regulatory regions. This method showed that repair was enriched at sites involved in neuronal function and identity. Furthermore, proteomic data indicated that genes in DRHs are enriched in Alzheimer's disease and that DRHs are more active in aging. These observations link neuronal DNA repair to aging and neurodegeneration. Science , this issue p. [91][1] Neurons are the longest-lived cells in our bodies and lack DNA replication, which makes them reliant on a limited repertoire of DNA repair mechanisms to maintain genome fidelity. These repair mechanisms decline with age, but we have limited knowledge of how genome instability emerges and what strategies neurons and other long-lived cells may have evolved to protect their genomes over the human life span. A targeted sequencing approach in human embryonic stem cell-induced neurons shows that, in neurons, DNA repair is enriched at well-defined hotspots that protect essential genes. These hotspots are enriched with histone H2A isoforms and RNA binding proteins and are associated with evolutionarily conserved elements of the human genome. These findings provide a basis for understanding genome integrity as it relates to aging and disease in the nervous system. [1]: /lookup/doi/10.1126/science.abb9032
Adlai Nortye
March 8, 2021
www.prnewswire.com:443
/PRNewswire/ -- Adlai Nortye, a global clinical-stage biopharmaceutical company, today announced the formation of its new Scientific Advisory Board (SAB)...
David A. Raichlen
December 17, 2019
Scientific American
Scientific American is the essential guide to the most awe-inspiring advances in science and technology, explaining how they change our understanding of the world and shape our lives.
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