{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,31]],"date-time":"2026-08-31T11:20:53Z","timestamp":1788175253768,"version":"build-2803163510"},"reference-count":47,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"25","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[2012,12,18]]},"abstract":"<jats:sec>\n            <jats:title>Background\u2014<\/jats:title>\n            <jats:p>Sustained cardiac pressure overload\u2013induced hypertrophy and pathological remodeling frequently leads to heart failure. Casein kinase-2 interacting protein-1 (CKIP-1) has been identified to be an important regulator of cell proliferation, differentiation, and apoptosis. However, the physiological role of CKIP-1 in the heart is unknown.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Methods and Results\u2014<\/jats:title>\n            <jats:p>The results of echocardiography and histology demonstrate that CKIP-1\u2013deficient mice exhibit spontaneous cardiac hypertrophy with aging and hypersensitivity to pressure overload\u2013induced pathological cardiac hypertrophy, as well. Transgenic mice with cardiac-specific overexpression of CKIP-1 showed resistance to cardiac hypertrophy in response to pressure overload. The results of GST pull-down and coimmunoprecipitation assays showed the interaction between CKIP-1 and histone deacetylase 4 (HDAC4), through which they synergistically inhibited transcriptional activity of myocyte-specific enhancer factor 2C. By directly interacting with the catalytic subunit of phosphatase 2A, CKIP-1 overexpression enhanced the binding of catalytic subunit of phosphatase-2A to HDAC4 and promoted HDAC4 dephosphorylation.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions\u2014<\/jats:title>\n            <jats:p>CKIP-1 was found to be an inhibitor of cardiac hypertrophy by upregulating the dephosphorylation of HDAC4 through the recruitment of protein phosphatase 2A. These results demonstrated a unique function of CKIP-1, by which it suppresses cardiac hypertrophy through its capacity to regulate HDAC4 dephosphorylation and fetal cardiac genes expression.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/circulationaha.112.102780","type":"journal-article","created":{"date-parts":[[2012,11,15]],"date-time":"2012-11-15T02:01:58Z","timestamp":1352944918000},"page":"3028-3040","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":75,"title":["CKIP-1 Inhibits Cardiac Hypertrophy by Regulating Class II Histone Deacetylase Phosphorylation Through Recruiting PP2A"],"prefix":"10.1161","volume":"126","author":[{"given":"Shukuan","family":"Ling","sequence":"first","affiliation":[{"name":"From the State Key Laboratory of Space Medicine Fundamentals and Application, China Astronaut Research and Training Center, Beijing, China (S.L., Q.S., Yuheng Li, P.Z., X.W., O.L., J.S., H.L., G.K., H.C., Z.H., J.N., Y.B., S.C., Yinghui Li, Yingxian Li); State Key Laboratory of Proteomics, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing, China (Luo Zhang, C.T., F.H., Lingqiang Zhang); and Institute of Cancer Stem Cell, Dalian Medical University, Dalian, Liaoning..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qiao","family":"Sun","sequence":"additional","affiliation":[{"name":"From the State Key Laboratory of Space Medicine Fundamentals and Application, China Astronaut Research and Training Center, Beijing, China (S.L., Q.S., Yuheng Li, P.Z., X.W., O.L., J.S., H.L., G.K., H.C., Z.H., J.N., Y.B., S.C., Yinghui Li, Yingxian Li); State Key Laboratory of Proteomics, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing, China (Luo Zhang, C.T., F.H., Lingqiang Zhang); and Institute of Cancer Stem Cell, Dalian Medical University, Dalian, Liaoning..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuheng","family":"Li","sequence":"additional","affiliation":[{"name":"From the State Key Laboratory of Space Medicine Fundamentals and Application, China Astronaut Research and Training Center, Beijing, China (S.L., Q.S., Yuheng Li, P.Z., X.W., O.L., J.S., H.L., G.K., H.C., Z.H., J.N., Y.B., S.C., Yinghui Li, Yingxian Li); State Key Laboratory of Proteomics, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing, China (Luo Zhang, C.T., F.H., Lingqiang Zhang); and Institute of Cancer Stem Cell, Dalian Medical University, Dalian, Liaoning..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Luo","family":"Zhang","sequence":"additional","affiliation":[{"name":"From the State Key Laboratory of Space Medicine Fundamentals and Application, China Astronaut Research and Training Center, Beijing, China (S.L., Q.S., Yuheng Li, P.Z., X.W., O.L., J.S., H.L., G.K., H.C., Z.H., J.N., Y.B., S.C., Yinghui Li, Yingxian Li); State Key Laboratory of Proteomics, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing, China (Luo Zhang, C.T., F.H., Lingqiang Zhang); and Institute of Cancer Stem Cell, Dalian Medical University, Dalian, Liaoning..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pengfei","family":"Zhang","sequence":"additional","affiliation":[{"name":"From the State Key Laboratory of Space Medicine Fundamentals and Application, China Astronaut Research and Training Center, Beijing, China (S.L., Q.S., Yuheng Li, P.Z., X.W., O.L., J.S., H.L., G.K., H.C., Z.H., J.N., Y.B., S.C., Yinghui Li, Yingxian Li); State Key Laboratory of Proteomics, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing, China (Luo Zhang, C.T., F.H., Lingqiang Zhang); and Institute of Cancer Stem Cell, Dalian Medical University, Dalian, 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