contact sites) until 16-cells morulae stage (apical microvillous zones) during early embryogenesis; then maternal cingulin is degraded by endocytic turn-over from the 32-cells stage. Regarding the zygotic cingulin, it accumulates at the tight junctions from 16-cells stage, 10 hours after ZO-1 assembly. Furthermore, the synthesis of cingulin in early mouse embryos is tissue-specific and it occurs in blastocyst (up-regulated in trophectoderm and down-regulated in inner-cells). In Xenopus laevis embryos, maternal cingulin is recruited to apical cell-cell junctions from 2-cells stage. Homologs In 2004, a protein homologous to cingulin was discovered and named JACOP (also known as paracingulin, or cingulin-like 1 protein; CGNL1). Human diseases Although cingulin has been involved in regulation of RhoA signaling and gene expression in cultured cells and KO mice, nothing is known about the specific role of cingulin in human diseases. Cingulin expression has been studied in human carcinomas and shown to be expressed in adenocarcinomas and down-regulated in squamous carcinomas. Furthermore, histone deacetylase inhibitors, such as sodium butyrate, strongly upregulate its expression in some cultured cells. Cingulin, as other junctional proteins could be used as a marker of epithelial differentiation, and as a diagnostic marker to distinguish adenocarcinomas from squamous carcinomas. References Further reading