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In algae and invertebrates,\n                    <jats:italic>ICK<\/jats:italic>\n                    homologs are known to be associated with ciliary formation. However, it is unclear whether this role of ICK is conserved in mammals and whether clinical symptoms of ECO syndrome are caused by ciliary defects. In this study, using in vivo and in vitro approaches, we found that abnormal ICK function indeed resulted in defective cilia, leading to abnormal Hedgehog signaling. Our results suggest that the role of ICK in ciliogenesis may be highly conserved throughout evolution and that ECO syndrome may be categorized as a ciliopathy, an increasingly recognized class of human genetic disorders.\n                  <\/jats:p>","DOI":"10.1073\/pnas.1323161111","type":"journal-article","created":{"date-parts":[[2014,5,23]],"date-time":"2014-05-23T04:03:51Z","timestamp":1400817831000},"page":"8541-8546","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":88,"title":["Intestinal cell kinase, a protein associated with endocrine-cerebro-osteodysplasia syndrome, is a key regulator of cilia length and Hedgehog signaling"],"prefix":"10.1073","volume":"111","author":[{"given":"Heejung","family":"Moon","sequence":"first","affiliation":[{"name":"College of Pharmacy, Dongguk University-Seoul, Goyang, 410-820, 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