[
    {
        "id": "authors:kpefn-0m097",
        "collection": "authors",
        "collection_id": "kpefn-0m097",
        "cite_using_url": "https://resolver.caltech.edu/CaltechAUTHORS:20120807-123207702",
        "type": "article",
        "title": "Mitotic exit kinase Dbf2 directly phosphorylates chitin synthase Chs2 to regulate cytokinesis in budding yeast",
        "author": [
            {
                "family_name": "Oh",
                "given_name": "Younghoon",
                "clpid": "Oh-Younghoon"
            },
            {
                "family_name": "Chang",
                "given_name": "Kuang-Jung",
                "clpid": "Chang-Kuang-Jung"
            },
            {
                "family_name": "Orlean",
                "given_name": "Peter",
                "clpid": "Orlean-P"
            },
            {
                "family_name": "Wloka",
                "given_name": "Carsten",
                "clpid": "Wloka-C"
            },
            {
                "family_name": "Deshaies",
                "given_name": "Raymond",
                "orcid": "0000-0002-3671-9354",
                "clpid": "Deshaies-R-J"
            },
            {
                "family_name": "Bi",
                "given_name": "Erfei",
                "clpid": "Bi-E"
            }
        ],
        "abstract": "How cell cycle machinery regulates extracellular matrix (ECM) remodeling during cytokinesis remains poorly understood. In the budding yeast Saccharomyces cerevisiae, the primary septum (PS), a functional equivalent of animal ECM, is synthesized during cytokinesis by the chitin synthase Chs2. Here, we report that Dbf2, a conserved mitotic exit kinase, localizes to the division site after Chs2 and directly phosphorylates Chs2 on several residues, including Ser-217. Both phosphodeficient (chs2\u2011S217A) and phosphomimic (chs2\u2011S217D) mutations cause defects in cytokinesis, suggesting that dynamic phosphorylation\u2013dephosphorylation of Ser-217 is critical for Chs2 function. It is striking that Chs2\u2011S217A constricts asymmetrically with the actomyosin ring (AMR), whereas Chs2-S217D displays little or no constriction and remains highly mobile at the division site. These data suggest that Chs2 phosphorylation by Dbf2 triggers its dissociation from the AMR during the late stage of cytokinesis. Of interest, both chs2\u2011S217A and chs2\u2011S217D mutants are robustly suppressed by increased dosage of Cyk3, a cytokinesis protein that displays Dbf2\u2011dependent localization and also stimulates Chs2\u2011mediated chitin synthesis. Thus Dbf2 regulates PS formation through at least two independent pathways: direct phosphorylation and Cyk3\u2011mediated activation of Chs2. Our study establishes a mechanism for direct cell cycle control of ECM remodeling during cytokinesis.",
        "doi": "10.1091/mbc.E12-01-0033",
        "pmcid": "PMC3386209",
        "issn": "1059-1524",
        "publisher": "American Society for Cell Biology",
        "publication": "Molecular Biology of the Cell",
        "publication_date": "2012-07-01",
        "series_number": "13",
        "volume": "23",
        "issue": "13",
        "pages": "2445-2456"
    },
    {
        "id": "authors:qphtd-ve766",
        "collection": "authors",
        "collection_id": "qphtd-ve766",
        "cite_using_url": "https://resolver.caltech.edu/CaltechAUTHORS:TAGpnas06",
        "type": "article",
        "title": "NF-{kappa}B-dependent induction of microRNA miR-146, an inhibitor targeted to signaling proteins of innate immune responses",
        "author": [
            {
                "family_name": "Taganov",
                "given_name": "Konstantin D.",
                "clpid": "Taganov-Konstantin-D"
            },
            {
                "family_name": "Boldin",
                "given_name": "Mark P.",
                "orcid": "0000-0003-4593-0669",
                "clpid": "Boldin-M-P"
            },
            {
                "family_name": "Chang",
                "given_name": "Kuang-Jung",
                "clpid": "Chang-Kuang-Jung"
            },
            {
                "family_name": "Baltimore",
                "given_name": "David",
                "orcid": "0000-0001-8723-8190",
                "clpid": "Baltimore-D"
            }
        ],
        "abstract": "Activation of mammalian innate and acquired immune responses must be tightly regulated by elaborate mechanisms to control their onset and termination. MicroRNAs have been implicated as negative regulators controlling diverse biological processes at the level of posttranscriptional repression. Expression profiling of 200 microRNAs in human monocytes revealed that several of them (miR-146a/b, miR-132, and miR-155) are endotoxin-responsive genes. Analysis of miR-146a and miR-146b gene expression unveiled a pattern of induction in response to a variety of microbial components and proinflammatory cytokines. By means of promoter analysis, miR-146a was found to be a NF-{kappa}B-dependent gene. Importantly, miR-146a/b were predicted to base-pair with sequences in the 3' UTRs of the TNF receptor-associated factor 6 and IL-1 receptor-associated kinase 1 genes, and we found that these UTRs inhibit expression of a linked reporter gene. These genes encode two key adapter molecules downstream of Toll-like and cytokine receptors. Thus, we propose a role for miR-146 in control of Toll-like receptor and cytokine signaling through a negative feedback regulation loop involving down-regulation of IL-1 receptor-associated kinase 1 and TNF receptor-associated factor 6 protein levels.",
        "doi": "10.1073/pnas.0605298103",
        "pmcid": "PMC1567904",
        "issn": "0027-8424",
        "publisher": "National Academy of Sciences",
        "publication": "Proceedings of the National Academy of Sciences of the United States of America",
        "publication_date": "2006-08-15",
        "series_number": "33",
        "volume": "103",
        "issue": "33",
        "pages": "12481-12486"
    }
]