title: Depletion of IK causes mitotic arrest through aberrant regulation of mitotic kinases and phosphatases.
abstract: IK is known to inhibit the expression of major histocompatibility complex (MHC) class II antigen, but other cellular functions of IK remain to be uncovered. In this study, IK depletion caused misalignment of chromosomes through an increase in Aurora A and PLK1 phosphorylation, which was mediated by a decrease in PP1 and PP2A activities. On the other hand, the treatment of a dual inhibitor against CDK and Aurora kinases overrode IK depletion-induced mitotic arrest through the activation of phosphatase activity. These findings imply that IK is an essential protein for achieving correct mitotic progress through the regulation of mitotic kinases and phosphatases.
authors.affiliation: Research Center for Women's Disease, Department of Life Systems, Sookmyung Women's University, Seoul 140-742, Republic of Korea.
authors.forename: Sunyi
authors.initials: S
authors.lastname: Lee
authors.affiliation: Research Center for Women's Disease, Department of Life Systems, Sookmyung Women's University, Seoul 140-742, Republic of Korea.
authors.forename: Sora
authors.initials: S
authors.lastname: Han
authors.affiliation: Research Center for Women's Disease, Department of Life Systems, Sookmyung Women's University, Seoul 140-742, Republic of Korea.
authors.forename: Ae Lee
authors.initials: AL
authors.lastname: Jeong
authors.affiliation: Research Center for Women's Disease, Department of Life Systems, Sookmyung Women's University, Seoul 140-742, Republic of Korea.
authors.forename: Jeong Su
authors.initials: JS
authors.lastname: Park
authors.affiliation: Research Center for Women's Disease, Department of Life Systems, Sookmyung Women's University, Seoul 140-742, Republic of Korea. Electronic address: yyang@sookmyung.ac.kr.
authors.forename: Young
authors.initials: Y
authors.lastname: Yang
mesh_terms: D000818:Animals; D017209:Apoptosis; D064096:Aurora Kinase A / Q000378:metabolism*; D001483:Base Sequence; D016203:CDC2 Protein Kinase / Q000378:metabolism; D059447:Cell Cycle Checkpoints; D018797:Cell Cycle Proteins / Q000378:metabolism; D002460:Cell Line; D016207:Cytokines / Q000172:deficiency* / Q000235:genetics / Q000378:metabolism; D020868:Gene Silencing; D006801:Humans; D051379:Mice; D008938:Mitosis; D010749:Phosphoprotein Phosphatases / Q000037:antagonists & inhibitors / Q000378:metabolism*; D010766:Phosphorylation; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism; D011518:Proto-Oncogene Proteins / Q000378:metabolism; D034741:RNA, Small Interfering / Q000235:genetics; D000097869:Polo-Like Kinase 1
chemical_list: D064096:Aurora Kinase A; D016203:CDC2 Protein Kinase; D018797:Cell Cycle Proteins; D016207:Cytokines; D010749:Phosphoprotein Phosphatases; D017346:Protein Serine-Threonine Kinases; D011518:Proto-Oncogene Proteins; D034741:RNA, Small Interfering; D000097869:Polo-Like Kinase 1; C090444:IK protein, human; C484250:Ik protein, mouse
keywords: Aurora A; CDK1; IK; Mitotic arrest; Protein phosphatase