[
    {
        "id": "authors:k8rx1-bcs92",
        "collection": "authors",
        "collection_id": "k8rx1-bcs92",
        "cite_using_url": "https://resolver.caltech.edu/CaltechAUTHORS:20120620-143827080",
        "type": "book_section",
        "title": "Molecular Insights into Parkinson's Disease",
        "book_title": "Molecular Biology of Neurodegenerative Diseases",
        "author": [
            {
                "family_name": "Rochet",
                "given_name": "Jean-Christophe",
                "clpid": "Rochet-J-C"
            },
            {
                "family_name": "Hay",
                "given_name": "Bruce A.",
                "clpid": "Hay-B-A"
            },
            {
                "family_name": "Guo",
                "given_name": "Ming",
                "clpid": "Guo-Ming"
            }
        ],
        "contributor": [
            {
                "family_name": "Teplow",
                "given_name": "David B.",
                "clpid": "Teplow-D-B"
            }
        ],
        "abstract": "Mutations in SNCA, PINK1, parkin, and DJ-1 are associated with autosomal-dominant or autosomal-recessive forms of Parkinson's disease (PD), the second most common neurodegenerative disorder. Studies on the structural and functional properties of the corresponding gene products have provided significant insights into the molecular underpinnings of familial PD and the much more common sporadic forms of the disease. Here, we review recent advances in our understanding of four PD-related gene products: \u03b1-synuclein, parkin, PINK1, and DJ-1. In Part 1, we review new insights into the role of \u03b1-synuclein in PD. In Part 2, we summarize the latest developments in understanding the role of mitochondrial dysfunction in PD, emphasizing the role of the PINK1/parkin pathway in regulating mitochondrial dynamics and mitophagy. The role of DJ-1 is also discussed. In Part 3, we point out converging pathways and future directions.",
        "doi": "10.1016/B978-0-12-385883-2.00011-4",
        "isbn": "9780123858832",
        "publisher": "Academic Press",
        "place_of_publication": "Amsterdam",
        "publication_date": "2012",
        "pages": "125-188"
    },
    {
        "id": "authors:kdwgx-yww42",
        "collection": "authors",
        "collection_id": "kdwgx-yww42",
        "cite_using_url": "https://resolver.caltech.edu/CaltechAUTHORS:20200421-075723029",
        "type": "book_section",
        "title": "Identifying MicroRNA Regulators of Cell Death in Drosophila",
        "book_title": "MicroRNA Protocols",
        "author": [
            {
                "family_name": "Chen",
                "given_name": "Chun-Hong",
                "clpid": "Chen-Chun-Hong"
            },
            {
                "family_name": "Guo",
                "given_name": "Ming",
                "clpid": "Guo-Ming"
            },
            {
                "family_name": "Hay",
                "given_name": "Bruce A.",
                "clpid": "Hay-B-A"
            }
        ],
        "contributor": [
            {
                "family_name": "Ying",
                "given_name": "Shao-Yao",
                "clpid": "Ying-Shao-Yao"
            }
        ],
        "abstract": "Animal genomes contain on the order of at least hundreds of microRNAs (miRNAs). Although most remain uncharacterized, it is already clear that miRNAs regulate many bio-logical processes. A number of Drosophila miRNAs have been identified as likely cell death regulators, but functions for most have simply not been explored. Here we describe a protocol for identifying miRNAs that can act as cell death regulators. We also describe a simple protocol for testing roles for mRNAs identified as candidate miRNA targets using computational or other approaches.",
        "doi": "10.1385/1-59745-123-1:229",
        "isbn": "978-1-58829-581-1",
        "publisher": "Humana Press",
        "place_of_publication": "Totowa, NJ",
        "publication_date": "2006-09-06",
        "pages": "229-240"
    },
    {
        "id": "authors:nxdkr-r3014",
        "collection": "authors",
        "collection_id": "nxdkr-r3014",
        "cite_using_url": "https://resolver.caltech.edu/CaltechAUTHORS:20200428-142551477",
        "type": "book_section",
        "title": "Monitoring Activity of Caspases and Their Regulators in Yeast Saccharomyces cerevisiae",
        "book_title": "Apoptosis",
        "author": [
            {
                "family_name": "Hawkins",
                "given_name": "Christine J.",
                "clpid": "Hawkins-C-J"
            },
            {
                "family_name": "Wang",
                "given_name": "Susan L.",
                "clpid": "Wang-Susan-L"
            },
            {
                "family_name": "Hay",
                "given_name": "Bruce A.",
                "clpid": "Hay-B-A"
            }
        ],
        "contributor": [
            {
                "family_name": "Reed",
                "given_name": "John C.",
                "clpid": "Reed-J-C"
            }
        ],
        "abstract": "Caspases are a family of site-specific proteases that play important signaling and effector roles in most apoptotic death pathways. Caspases are made as zymogens and become activated after cleavage. Caspase activity is regulated by both activators and inhibitors. Yeast provide a useful system in which to characterize the function of caspases and their regulators because yeast appear to lack endogenous caspases as well as other components of the apoptotic machinery. Also, yeast are genetically the most tractable eukaryote with which to work. Finally, transformation occurs at a high frequency, making them suitable for library screening or large-scale mutagenesis. In addition to caspases, yeast systems have also been used to analyze other cell death pathway components.2, 3, 4, 5, 6, 7, 8, 9, 10, 11 These approaches are discussed in [27] and [28].",
        "doi": "10.1016/s0076-6879(00)22016-8",
        "isbn": "9780121822231",
        "publisher": "Academic Press",
        "place_of_publication": "London",
        "publication_date": "2000",
        "pages": "162-174"
    }
]