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            "title": "Common variation near CDKN1A, POLD3 and SHROOM2 influences colorectal   cancer risk",
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                    "creatorType": "author",
                    "firstName": "Malcolm G.",
                    "lastName": "Dunlop"
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                    "firstName": "Paul",
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                    "creatorType": "author",
                    "firstName": "Annika",
                    "lastName": "Lindblom"
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                {
                    "creatorType": "author",
                    "firstName": "Tao",
                    "lastName": "Liu"
                },
                {
                    "creatorType": "author",
                    "firstName": "Christopher G.",
                    "lastName": "Smith"
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                {
                    "creatorType": "author",
                    "firstName": "Hannah",
                    "lastName": "West"
                },
                {
                    "creatorType": "author",
                    "firstName": "Jeremy P.",
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                {
                    "creatorType": "author",
                    "firstName": "Rachel",
                    "lastName": "Midgley"
                },
                {
                    "creatorType": "author",
                    "firstName": "David J.",
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                {
                    "creatorType": "author",
                    "firstName": "Harry",
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                    "creatorType": "author",
                    "firstName": "S. J.",
                    "lastName": "Lubbe"
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                {
                    "creatorType": "author",
                    "firstName": "A. M.",
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                    "firstName": "B.",
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                {
                    "creatorType": "author",
                    "firstName": "A.",
                    "lastName": "Lloyd"
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                {
                    "creatorType": "author",
                    "firstName": "J.",
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                },
                {
                    "creatorType": "author",
                    "firstName": "S.",
                    "lastName": "Naranjo"
                },
                {
                    "creatorType": "author",
                    "firstName": "S.",
                    "lastName": "Dobbins"
                },
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                    "creatorType": "author",
                    "firstName": "P.",
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                    "creatorType": "author",
                    "firstName": "J. L.",
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            "date": "AUG 2012",
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            "creatorSummary": "Gabdoulline et al.",
            "parsedDate": "2012-07",
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            "key": "J978BCU4",
            "version": 7693,
            "itemType": "journalArticle",
            "title": "3DTF: a web server for predicting transcription factor PWMs using 3D   structure-based energy calculations",
            "creators": [
                {
                    "creatorType": "author",
                    "firstName": "R.",
                    "lastName": "Gabdoulline"
                },
                {
                    "creatorType": "author",
                    "firstName": "D.",
                    "lastName": "Eckweiler"
                },
                {
                    "creatorType": "author",
                    "firstName": "A.",
                    "lastName": "Kel"
                },
                {
                    "creatorType": "author",
                    "firstName": "P.",
                    "lastName": "Stegmaier"
                }
            ],
            "abstractNote": "We present the webserver 3D transcription factor (3DTF) to compute position-specific weight matrices (PWMs) of transcription factors using a knowledge-based statistical potential derived from crystallographic data on protein-DNA complexes. Analysis of available structures that can be used to construct PWMs shows that there are hundreds of 3D structures from which PWMs could be derived, as well as thousands of proteins homologous to these. Therefore, we created 3DTF, which delivers binding matrices given the experimental or modeled protein-DNA complex. The webserver can be used by biologists to derive novel PWMs for transcription factors lacking known binding sites and is freely accessible at http://www.gene-regulation.com/pub/programs/3dtf/.",
            "publicationTitle": "Nucleic Acids Research",
            "publisher": "",
            "place": "",
            "date": "JUL 2012",
            "volume": "40",
            "issue": "W1",
            "section": "",
            "partNumber": "",
            "partTitle": "",
            "pages": "W180-W185",
            "series": "",
            "seriesTitle": "",
            "seriesText": "",
            "journalAbbreviation": "Nucleic Acids Res.",
            "DOI": "10.1093/nar/gks551",
            "citationKey": "",
            "url": "",
            "accessDate": "",
            "PMID": "",
            "PMCID": "",
            "ISSN": "0305-1048",
            "archive": "",
            "archiveLocation": "",
            "shortTitle": "3DTF",
            "language": "English",
            "libraryCatalog": "ISI Web of Knowledge",
            "callNumber": "",
            "rights": "",
            "extra": "WOS:000306670900029",
            "tags": [
                {
                    "tag": "factor-binding sites",
                    "type": 1
                },
                {
                    "tag": "protein-dna interactions",
                    "type": 1
                },
                {
                    "tag": "recognition",
                    "type": 1
                }
            ],
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            "dateAdded": "2013-03-12T10:48:22Z",
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            "creatorSummary": "Dallosso et al.",
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            "version": 7693,
            "itemType": "journalArticle",
            "title": "Long-range epigenetic silencing of chromosome 5q31 protocadherins is   involved in early and late stages of colorectal tumorigenesis through   modulation of oncogenic pathways",
            "creators": [
                {
                    "creatorType": "author",
                    "firstName": "A. R.",
                    "lastName": "Dallosso"
                },
                {
                    "creatorType": "author",
                    "firstName": "B.",
                    "lastName": "Oster"
                },
                {
                    "creatorType": "author",
                    "firstName": "A.",
                    "lastName": "Greenhough"
                },
                {
                    "creatorType": "author",
                    "firstName": "K.",
                    "lastName": "Thorsen"
                },
                {
                    "creatorType": "author",
                    "firstName": "T. J.",
                    "lastName": "Curry"
                },
                {
                    "creatorType": "author",
                    "firstName": "C.",
                    "lastName": "Owen"
                },
                {
                    "creatorType": "author",
                    "firstName": "A. L.",
                    "lastName": "Hancock"
                },
                {
                    "creatorType": "author",
                    "firstName": "M.",
                    "lastName": "Szemes"
                },
                {
                    "creatorType": "author",
                    "firstName": "C.",
                    "lastName": "Paraskeva"
                },
                {
                    "creatorType": "author",
                    "firstName": "M.",
                    "lastName": "Frank"
                },
                {
                    "creatorType": "author",
                    "firstName": "C. L.",
                    "lastName": "Andersen"
                },
                {
                    "creatorType": "author",
                    "firstName": "K.",
                    "lastName": "Malik"
                }
            ],
            "abstractNote": "Loss of tumour suppressor gene function can occur as a result of epigenetic silencing of large chromosomal regions, referred to as long-range epigenetic silencing (LRES), and genome-wide analyses have revealed that LRES is present in many cancer types. Here we utilize Illumina Beadchip methylation array analysis to identify LRES across 800 kb of chromosome 5q31 in colorectal adenomas and carcinomas (n = 34) relative to normal colonic epithelial DNA (n = 6). This region encompasses 53 individual protocadherin (PCDH) genes divided among three gene clusters. Hypermethylation within these gene clusters is asynchronous; while most PCDH hypermethylation occurs early, and is apparent in adenomas, PCDHGC3 promoter methylation occurs later in the adenoma-carcinoma transition. PCDHGC3 was hypermethylated in 17/28 carcinomas (60.7%) according to methylation array analysis. Quantitative real-time reverse transcription-polymerase chain reaction showed that PCDHGC3 is the highest expressed PCDH in normal colonic epithelium, and that there was a strong reciprocal relationship between PCDHGC3 methylation and expression in carcinomas (R = -0.84). PCDH LRES patterns are reflected in colorectal tumour cell lines; adenoma cell lines are not methylated at PCDHGC3 and show abundant expression at the mRNA and protein level, while the expression is suppressed in hypermethylated carcinoma cell lines (R = -0.73). Short-interfering RNA-mediated reduction of PCDHGC3 led to a decrease of apoptosis in RG/C2 adenoma cells, and overexpression of PCDHGC3 in HCT116 cells resulted in the reduction of colony formation, consistent with tumour suppressor capabilities for PCDHGC3. Further functional analysis showed that PCDHGC3 can suppress Wnt and mammalian target of rapamycin signalling in colorectal cancer cell lines. Taken together, our data suggest that the PCDH LRES is an important tumour suppressor locus in colorectal cancer, and that PCDHGC3 may be a strong marker and driver for the adenoma-carcinoma transition. Oncogene (2012) 31, 4409-4419; doi: 10.1038/onc.2011.609; published online 16 January 2012",
            "publicationTitle": "Oncogene",
            "publisher": "",
            "place": "",
            "date": "OCT 2012",
            "volume": "31",
            "issue": "40",
            "section": "",
            "partNumber": "",
            "partTitle": "",
            "pages": "4409-4419",
            "series": "",
            "seriesTitle": "",
            "seriesText": "",
            "journalAbbreviation": "Oncogene",
            "DOI": "10.1038/onc.2011.609",
            "citationKey": "",
            "url": "",
            "accessDate": "",
            "PMID": "",
            "PMCID": "",
            "ISSN": "0950-9232",
            "archive": "",
            "archiveLocation": "",
            "shortTitle": "",
            "language": "English",
            "libraryCatalog": "ISI Web of Knowledge",
            "callNumber": "",
            "rights": "",
            "extra": "WOS:000309591300007",
            "tags": [
                {
                    "tag": "Wnt",
                    "type": 1
                },
                {
                    "tag": "adenoma-carcinoma sequence",
                    "type": 1
                },
                {
                    "tag": "cancer-cells",
                    "type": 1
                },
                {
                    "tag": "cell-lines",
                    "type": 1
                },
                {
                    "tag": "colorectal cancer",
                    "type": 1
                },
                {
                    "tag": "cytoplasmic domain",
                    "type": 1
                },
                {
                    "tag": "dna methylation",
                    "type": 1
                },
                {
                    "tag": "epigenetic silencing",
                    "type": 1
                },
                {
                    "tag": "gamma-protocadherins",
                    "type": 1
                },
                {
                    "tag": "homophilic interaction",
                    "type": 1
                },
                {
                    "tag": "human breast",
                    "type": 1
                },
                {
                    "tag": "mTOR",
                    "type": 1
                },
                {
                    "tag": "microsatellite instability",
                    "type": 1
                },
                {
                    "tag": "protocadherin",
                    "type": 1
                },
                {
                    "tag": "tumor-suppressor",
                    "type": 1
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            ],
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            "relations": {},
            "dateAdded": "2013-03-12T10:48:22Z",
            "dateModified": "2013-03-12T10:48:22Z"
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            "title": "Germline mutations affecting the proofreading domains of POLE and POLD1   predispose to colorectal adenomas and carcinomas",
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                    "creatorType": "author",
                    "firstName": "Claire",
                    "lastName": "Palles"
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                    "firstName": "Jean-Baptiste",
                    "lastName": "Cazier"
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                    "firstName": "Kimberley M.",
                    "lastName": "Howarth"
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                    "creatorType": "author",
                    "firstName": "Enric",
                    "lastName": "Domingo"
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                {
                    "creatorType": "author",
                    "firstName": "Angela M.",
                    "lastName": "Jones"
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                    "creatorType": "author",
                    "firstName": "Peter",
                    "lastName": "Broderick"
                },
                {
                    "creatorType": "author",
                    "firstName": "Zoe",
                    "lastName": "Kemp"
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                {
                    "creatorType": "author",
                    "firstName": "Sarah L.",
                    "lastName": "Spain"
                },
                {
                    "creatorType": "author",
                    "firstName": "Estrella Guarino",
                    "lastName": "Almeida"
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                {
                    "creatorType": "author",
                    "firstName": "Israel",
                    "lastName": "Salguero"
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                {
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                    "firstName": "Amy",
                    "lastName": "Sherborne"
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                {
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                    "firstName": "Daniel",
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                {
                    "creatorType": "author",
                    "firstName": "Luis G.",
                    "lastName": "Carvajal-Carmona"
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                    "firstName": "Yusanne",
                    "lastName": "Ma"
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                    "lastName": "Kaur"
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                {
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                    "firstName": "Sara",
                    "lastName": "Dobbins"
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                {
                    "creatorType": "author",
                    "firstName": "Ella",
                    "lastName": "Barclay"
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                {
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                    "lastName": "Gorman"
                },
                {
                    "creatorType": "author",
                    "firstName": "Lynn",
                    "lastName": "Martin"
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                {
                    "creatorType": "author",
                    "firstName": "Michal B.",
                    "lastName": "Kovac"
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                {
                    "creatorType": "author",
                    "firstName": "Sean",
                    "lastName": "Humphray"
                },
                {
                    "creatorType": "author",
                    "firstName": "Anneke",
                    "lastName": "Lucassen"
                },
                {
                    "creatorType": "author",
                    "firstName": "Christopher C.",
                    "lastName": "Holmes"
                },
                {
                    "creatorType": "author",
                    "firstName": "David",
                    "lastName": "Bentley"
                },
                {
                    "creatorType": "author",
                    "firstName": "Peter",
                    "lastName": "Donnelly"
                },
                {
                    "creatorType": "author",
                    "firstName": "Jenny",
                    "lastName": "Taylor"
                },
                {
                    "creatorType": "author",
                    "firstName": "Christos",
                    "lastName": "Petridis"
                },
                {
                    "creatorType": "author",
                    "firstName": "Rebecca",
                    "lastName": "Roylance"
                },
                {
                    "creatorType": "author",
                    "firstName": "Elinor J.",
                    "lastName": "Sawyer"
                },
                {
                    "creatorType": "author",
                    "firstName": "David J.",
                    "lastName": "Kerr"
                },
                {
                    "creatorType": "author",
                    "firstName": "Susan",
                    "lastName": "Clark"
                },
                {
                    "creatorType": "author",
                    "firstName": "Jonathan",
                    "lastName": "Grimes"
                },
                {
                    "creatorType": "author",
                    "firstName": "Stephen E.",
                    "lastName": "Kearsey"
                },
                {
                    "creatorType": "author",
                    "firstName": "Huw J. W.",
                    "lastName": "Thomas"
                },
                {
                    "creatorType": "author",
                    "firstName": "Gilean",
                    "lastName": "McVean"
                },
                {
                    "creatorType": "author",
                    "firstName": "Richard S.",
                    "lastName": "Houlston"
                },
                {
                    "creatorType": "author",
                    "firstName": "Ian",
                    "lastName": "Tomlinson"
                }
            ],
            "abstractNote": "Many individuals with multiple or large colorectal adenomas or early-onset colorectal cancer (CRC) have no detectable germline mutations in the known cancer predisposition genes. Using whole-genome sequencing, supplemented by linkage and association analysis, we identified specific heterozygous POLE or POLD1 germline variants in several multiple-adenoma and/or CRC cases but in no controls. The variants associated with susceptibility, POLE p.Leu424Val and POLD1 p.Ser478Asn, have high penetrance, and POLD1 mutation was also associated with endometrial cancer predisposition. The mutations map to equivalent sites in the proofreading (exonuclease) domain of DNA polymerases E and 8 and are predicted to cause a defect in the correction of mispaired bases inserted during DNA replication. In agreement with this prediction, the tumors from mutation carriers were microsatellite stable but tended to acquire base substitution mutations, as confirmed by yeast functional assays. Further analysis of published data showed that the recently described group of hypermutant, microsatellite-stable CRCs is likely to be caused by somatic POLE mutations affecting the exonuclease domain.",
            "publicationTitle": "Nature Genetics",
            "publisher": "",
            "place": "",
            "date": "FEB 2013",
            "volume": "45",
            "issue": "2",
            "section": "",
            "partNumber": "",
            "partTitle": "",
            "pages": "136-144",
            "series": "",
            "seriesTitle": "",
            "seriesText": "",
            "journalAbbreviation": "Nature Genet.",
            "DOI": "10.1038/ng.2503",
            "citationKey": "",
            "url": "",
            "accessDate": "",
            "PMID": "",
            "PMCID": "",
            "ISSN": "1061-4036",
            "archive": "",
            "archiveLocation": "",
            "shortTitle": "",
            "language": "English",
            "libraryCatalog": "ISI Web of Knowledge",
            "callNumber": "",
            "rights": "",
            "extra": "WOS:000314333000008",
            "tags": [
                {
                    "tag": "cancer susceptibility",
                    "type": 1
                },
                {
                    "tag": "cell-lines",
                    "type": 1
                },
                {
                    "tag": "colon-cancer",
                    "type": 1
                },
                {
                    "tag": "dna-polymerase-delta",
                    "type": 1
                },
                {
                    "tag": "excision-repair",
                    "type": 1
                },
                {
                    "tag": "mice",
                    "type": 1
                },
                {
                    "tag": "mismatch repair",
                    "type": 1
                },
                {
                    "tag": "mutator",
                    "type": 1
                },
                {
                    "tag": "replication",
                    "type": 1
                },
                {
                    "tag": "yeast",
                    "type": 1
                }
            ],
            "collections": [
                "P5BTA2PX"
            ],
            "relations": {},
            "dateAdded": "2013-03-12T10:48:22Z",
            "dateModified": "2013-03-12T10:48:22Z"
        }
    },
    {
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        "version": 7693,
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            "creatorSummary": "Farkash-Amar et al.",
            "parsedDate": "2012-11-07",
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        "data": {
            "key": "GVM2AW4H",
            "version": 7693,
            "itemType": "journalArticle",
            "title": "Dynamic Proteomics of Human Protein Level and Localization across the   Cell Cycle",
            "creators": [
                {
                    "creatorType": "author",
                    "firstName": "Shlomit",
                    "lastName": "Farkash-Amar"
                },
                {
                    "creatorType": "author",
                    "firstName": "Eran",
                    "lastName": "Eden"
                },
                {
                    "creatorType": "author",
                    "firstName": "Ariel",
                    "lastName": "Cohen"
                },
                {
                    "creatorType": "author",
                    "firstName": "Naama",
                    "lastName": "Geva-Zatorsky"
                },
                {
                    "creatorType": "author",
                    "firstName": "Lydia",
                    "lastName": "Cohen"
                },
                {
                    "creatorType": "author",
                    "firstName": "Ron",
                    "lastName": "Milo"
                },
                {
                    "creatorType": "author",
                    "firstName": "Alex",
                    "lastName": "Sigal"
                },
                {
                    "creatorType": "author",
                    "firstName": "Tamar",
                    "lastName": "Danon"
                },
                {
                    "creatorType": "author",
                    "firstName": "Uri",
                    "lastName": "Alon"
                }
            ],
            "abstractNote": "Regulation of proteins across the cell cycle is a basic process in cell biology. It has been difficult to study this globally in human cells due to lack of methods to accurately follow protein levels and localizations over time. Estimates based on global mRNA measurements suggest that only a few percent of human genes have cell-cycle dependent mRNA levels. Here, we used dynamic proteomics to study the cell-cycle dependence of proteins. We used 495 clones of a human cell line, each with a different protein tagged fluorescently at its endogenous locus. Protein level and localization was quantified in individual cells over 24h of growth using time-lapse microscopy. Instead of standard chemical or mechanical methods for cell synchronization, we employed in-silico synchronization to place protein levels and localization on a time axis between two cell divisions. This non-perturbative synchronization approach, together with the high accuracy of the measurements, allowed a sensitive assay of cell-cycle dependence. We further developed a computational approach that uses texture features to evaluate changes in protein localizations. We find that 40% of the proteins showed cell cycle dependence, of which 11% showed changes in protein level and 35% in localization. This suggests that a broader range of cell-cycle dependent proteins exists in human cells than was previously appreciated. Most of the cell-cycle dependent proteins exhibit changes in cellular localization. Such changes can be a useful tool in the regulation of the cell-cycle being fast and efficient.",
            "publicationTitle": "Plos One",
            "publisher": "",
            "place": "",
            "date": "NOV 7 2012",
            "volume": "7",
            "issue": "11",
            "section": "",
            "partNumber": "",
            "partTitle": "",
            "pages": "",
            "series": "",
            "seriesTitle": "",
            "seriesText": "",
            "journalAbbreviation": "PLoS One",
            "DOI": "10.1371/journal.pone.0048722",
            "citationKey": "",
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            "PMID": "",
            "PMCID": "",
            "ISSN": "1932-6203",
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            "archiveLocation": "",
            "shortTitle": "",
            "language": "English",
            "libraryCatalog": "ISI Web of Knowledge",
            "callNumber": "",
            "rights": "",
            "extra": "WOS:000311935800110",
            "tags": [
                {
                    "tag": "cancer-cells",
                    "type": 1
                },
                {
                    "tag": "classification",
                    "type": 1
                },
                {
                    "tag": "cytokinesis",
                    "type": 1
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            "abstractNote": "Aurora B localization to mitotic centromeres, which is required for proper chromosome alignment during mitosis, relies on Haspin-dependent histone H3 phosphorylation and on Bub1-dependent histone H2A phosphorylation-which interacts with Borealin through a Shugoshin (Sgo) intermediate. We demonstrate that Mps1 stimulates the latter recruitment axis. Mps1 activity enhances H2A-T120ph and is critical for Sgo1 recruitment to centromeres, thereby promoting Aurora B centromere recruitment in early mitosis. Importantly, chromosome biorientation defects caused by Mps1 inhibition are improved by restoring Aurora B centromere recruitment. As Mps1 kinetochore localization reciprocally depends on Aurora B, we propose that this Aurora B-Mps1 recruitment circuitry cooperates with the Aurora B-Haspin feedback loop to ensure rapid centromere accumulation of Aurora B at the onset of mitosis.",
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                    "firstName": "Carolina",
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                    "creatorType": "author",
                    "firstName": "Alberto J.",
                    "lastName": "Schuhmacher"
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                    "creatorType": "author",
                    "firstName": "Maria",
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                    "creatorType": "author",
                    "firstName": "Janneke E.",
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                    "firstName": "Ariena",
                    "lastName": "Kersbergen"
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                    "creatorType": "author",
                    "firstName": "Serge A.",
                    "lastName": "Zander"
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                    "firstName": "Amal",
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                    "firstName": "Niall M. B.",
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                    "firstName": "Alan",
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                {
                    "creatorType": "author",
                    "firstName": "Mark J.",
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                    "creatorType": "author",
                    "firstName": "Shridar",
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                    "firstName": "Piet",
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                    "firstName": "Sven",
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