PubMed:31981797 JSONTXT

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    sonoma2

    {"project":"sonoma2","denotations":[{"id":"T0","span":{"begin":0,"end":34},"obj":"GENE"},{"id":"T1","span":{"begin":54,"end":61},"obj":"GENE"},{"id":"T2","span":{"begin":54,"end":71},"obj":"GENE"},{"id":"T3","span":{"begin":81,"end":109},"obj":"CPA"},{"id":"T4","span":{"begin":114,"end":123},"obj":"CPA"},{"id":"T5","span":{"begin":125,"end":132},"obj":"GENE"},{"id":"T6","span":{"begin":125,"end":142},"obj":"GENE"},{"id":"T7","span":{"begin":144,"end":148},"obj":"GENE"},{"id":"T8","span":{"begin":199,"end":210},"obj":"VAR"},{"id":"T9","span":{"begin":214,"end":218},"obj":"GENE"},{"id":"T10","span":{"begin":239,"end":247},"obj":"REG"},{"id":"T11","span":{"begin":299,"end":305},"obj":"DISEASE"},{"id":"T12","span":{"begin":321,"end":324},"obj":"GENE"},{"id":"T13","span":{"begin":342,"end":350},"obj":"GENE"},{"id":"T14","span":{"begin":441,"end":466},"obj":"GENE"},{"id":"T15","span":{"begin":468,"end":472},"obj":"GENE"},{"id":"T16","span":{"begin":506,"end":509},"obj":"GENE"},{"id":"T17","span":{"begin":535,"end":539},"obj":"GENE"},{"id":"T18","span":{"begin":555,"end":559},"obj":"GENE"},{"id":"T19","span":{"begin":699,"end":703},"obj":"GENE"},{"id":"T20","span":{"begin":699,"end":703},"obj":"GENE"},{"id":"T21","span":{"begin":754,"end":768},"obj":"GENE"},{"id":"T22","span":{"begin":777,"end":786},"obj":"VAR"},{"id":"T23","span":{"begin":790,"end":794},"obj":"GENE"},{"id":"T24","span":{"begin":809,"end":818},"obj":"NEGREG"},{"id":"T25","span":{"begin":819,"end":847},"obj":"CPA"},{"id":"T26","span":{"begin":852,"end":861},"obj":"CPA"},{"id":"T27","span":{"begin":880,"end":893},"obj":"CPA"},{"id":"T28","span":{"begin":906,"end":912},"obj":"DISEASE"},{"id":"T29","span":{"begin":989,"end":993},"obj":"GENE"},{"id":"T30","span":{"begin":1023,"end":1043},"obj":"MPA"},{"id":"T31","span":{"begin":1051,"end":1055},"obj":"GENE"},{"id":"T32","span":{"begin":1055,"end":1058},"obj":"VAR"},{"id":"T33","span":{"begin":1059,"end":1065},"obj":"NEGREG"},{"id":"T34","span":{"begin":1076,"end":1104},"obj":"CPA"},{"id":"T35","span":{"begin":1109,"end":1118},"obj":"CPA"},{"id":"T36","span":{"begin":1122,"end":1136},"obj":"GENE"},{"id":"T37","span":{"begin":1203,"end":1207},"obj":"GENE"}],"relations":[{"id":"R0","pred":"CauseOf","subj":"T8","obj":"T10"},{"id":"R1","pred":"ThemeOf","subj":"T11","obj":"T10"},{"id":"R2","pred":"CauseOf","subj":"T22","obj":"T24"},{"id":"R3","pred":"ThemeOf","subj":"T23","obj":"T22"},{"id":"R4","pred":"ThemeOf","subj":"T25","obj":"T24"},{"id":"R5","pred":"ThemeOf","subj":"T26","obj":"T24"},{"id":"R6","pred":"ThemeOf","subj":"T31","obj":"T32"},{"id":"R7","pred":"CauseOf","subj":"T32","obj":"T33"}],"text":"Cyclin-dependent kinase 1-mediated phosphorylation of protein kinase N1 promotes anchorage-independent growth and migration.\nProtein kinase N1 (PKN1) is a member of the protein kinase C superfamily. Aberrations of PKN1 kinase activity are involved in several human pathological processes, including cancer. We found that PKN family proteins (PKN1/2/3) are phosphorylated in response to antitubulin drug-induced mitotic arrest. We identified cyclin-dependent kinase 1 (CDK1) as the corresponding kinase for PKN protein phosphorylation. CDK1 phosphorylates PKN1 at S533, S537, S562, and S916 in vitro and in cells during drug-induced mitotic arrest. Immunofluorescence staining further confirmed that PKN1 phosphorylation occurs during normal mitosis in a CDK1-dependent manner. Knockdown of PKN1 significantly inhibited anchorage-independent growth and migration without affecting proliferation in multiple cancer cell lines. We further showed that mitotic phosphorylation is essential for PKN1's oncogenic function, as the non-phosphorylatable mutant PKN1-4A failed to rescue anchorage-independent growth and migration in PKN1-knockdown cells. Thus, our findings reveal a novel regulatory mechanism for PKN1 in mitosis and its role in tumorigenesis."}