cDNA Cloning, Genomic Structure, and Chromosome Mapping of the Human Epithelial Membrane Protein CL-20 Gene (EMP1), a Member of the PMP22 Family

Abstract

tissues. Early in this terminal pathway of differentia-CL-20 is a novel gene encoding a protein that is struc-tion, cells undergo irreversible growth arrest that is turally related to but distinct from the peripheral myelin accompanied by a down-regulation of several cell cycle protein PMP22. Like PMP22, CL-20 is likely to play im-control genes, including RB and cdc2 (Jetten et al., portant roles in the regulation of cell proliferation, dif-1992; Saunders and Jetten, 1994). This is followed by ferentiation, and cell death. In this study, we describe the induction of differentiation-specific genes such as the cloning and sequencing of a cDNA encoding the hu-expression of several keratins and proteins involved man homologue of CL-20 and characterize the genomic in the formation of the cross-linked envelope such as structure of this gene. The hCL-20 gene (HGMW-ap-transglutaminase type I and cornifins (Eckert and proved symbol EMP1) encodes a protein of 157 amino Rorke, 1989;Jetten et al., 1992;Marvin et al., 1992). et al., 1995), which in several human tissues by Northern analysis. Retinoic might be the rat homologue of CL-20. The rabbit CLacid, which inhibits squamous differentiation, represses 20 exhibits moderate (43%) homology to the human CL-20 expression in normal human bronchial epithelial peripheral myelin protein, PMP22 protein (also known cells. The genomic structure of the hCL-20 gene was ana-as gas3) (Manfioletti et al., 1990; Welcher et al., 1991; lyzed using a P1 vector containing this gene. The hCL- Suter et al., 1992). CL-20, EMP-1, 20 gene contains five exons about 0.2, 0.12, 0.1, 0.14, and and PMP22 exhibit a great structural similarity, sug-2.2 kb and four introns about 15, 1.9, 0

Up-Regulation of Epithelial Membrane Protein-1 in the Temporal Neocortex of Patients with Intractable Epilepsy

“…They were the same as the earlier research; the earlier research found EMP1 was seen in the immature mouse brain, but lost in the adult [18]. In human tissues, EMP1 mRNA was not detected in brain [11]. We suggest that epilepsy maybe cause the expression of EMP1.…”

“…EMP1 transcript was detected in most of the adult tissues examined, but not in brain, liver, pancreas, or peripheral blood leukocytes [11]. In the study of drug-resistant tumors, Jain et al [12] suggested that EMP-1 may be the marker of a drug-resistant tumor and further suggested a probable cross-talk between this molecule and the epidermal growth factor receptor (EGFR) signaling pathway.…”

The epigenetic reprogramming of poorly aggressive melanoma cells by a metastatic microenvironment

“…EMP1, alternatively referred to as tumor-associated membrane protein, has been detected in embryonic kidney, brain, gut and is linked to cell-cell interactions and the regulation of cell proliferation, in addition to neuronal differentiation and neurite outgrowth [48][49][50]. Similarly, the induced expression of keratin 7, indicative of a simple epithelial cell type, in the mesenchymally-derived poorly aggressive melanoma cells, strongly suggests their transition to a dedifferentiated, interconverted phenotype, previously shown by our laboratory and others to be closely associated with aggressive behavior and metastatic disease [26,[51][52][53].…”

cDNA microarray analysis of genes associated with ERBB2 (HER2/neu) overexpression in human mammary luminal epithelial cells

“…Other MYCassociated genes, epithelial membrane proteins 1 (EMP1, TMP, CL20) and 3 (EMP3, YMP) were also significantly upregulated in our model system. EMP1 and EMP3 are members of the PMP22/EMP/MP20 family of membrane glycoproteins, involved in squamous cell differentiation (Chen et al, 1997;Ben-Porath et al, 1998Liehr et al, 1999). Their precise functions in the breast are unknown but associations with cell proliferation and tumorigenesis have been proposed, and differential expression of EMP1 has been reported in gastric cancer (Hippo et al, 2001) and in estrogen-resistant MCF7ADR breast cancer cells (Schiemann et al, 1997).…”