{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,4]],"date-time":"2026-06-04T23:19:53Z","timestamp":1780615193076,"version":"3.54.1"},"reference-count":63,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2006,5,4]],"date-time":"2006-05-04T00:00:00Z","timestamp":1146700800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Cellular Biochemistry"],"published-print":{"date-parts":[[2006,10,15]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The promyelocytic leukemia zinc finger (PLZF) protein has been described as a transcriptional repressor of the BTB\u2010domain\/zinc\u2010finger family, and shown to regulate the expression of Hox genes during embryogenesis and the expression of cyclin A in the cell cycle progression. Here, a 45\u2010kDa isoform of PLZF without a BTB domain was identified via yeast two\u2010hybrid screening using the C\u2010terminal region of ATP7B as bait in our determination of the biological roles of the Wilson disease protein outside of its copper\u2010binding domain. Our immunoprecipitation experiments showed that the hepatocytic isoform of PLZF could specifically interact with the C\u2010terminal region of ATP7B. The immunostaining of HepG2 cells revealed that the ATP7B and PLZF proteins were apparently colocalized into the trans\u2010Golgi complexes. It was also determined that disruption of PLZF expression in the HepG2 cells affected an attenuation of ERK activity in a dose\u2010dependent manner. The hepatocytic activities of ERK kinase were found to be enhanced as the result of PLZF or ATP7B expression, but this enhancement was abrogated by the deletion of the C\u2010terminal region of ATP7B. Furthermore, a transgenic Drosophila strain that ectopically expressed the hepatocytic \u0394BTB\u2010PLZF exhibited phenotypic changes in eye and wing development, and these alterations were fully recovered as the result of ATP7B expression, indicating the obvious in vivo interaction between the two proteins. Those PLZF\u2010induced abnormalities were attributed to the enhancement of ERK signaling, as was shown by phenotypic reversions with loss\u2010of\u2010function mutations in ERK signal transduction in Drosophila. These data suggest the existence of a mechanism that regulates ERK signaling via the C\u2010terminus of ATP7B and the ATP7B\u2010interacting hepatocytic PLZF. J. Cell. Biochem. 99: 719\u2013734, 2006. \u00a9 2006 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jcb.20980","type":"journal-article","created":{"date-parts":[[2006,5,4]],"date-time":"2006-05-04T22:00:45Z","timestamp":1146780045000},"page":"719-734","source":"Crossref","is-referenced-by-count":17,"title":["A new hepatocytic isoform of PLZF lacking the BTB domain interacts with ATP7B, the Wilson disease protein, and positively regulates ERK signal transduction"],"prefix":"10.1002","volume":"99","author":[{"given":"Jung Ho","family":"Ko","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wonseok","family":"Son","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gab Yong","family":"Bae","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joo 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