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Computational Analysis of Isoform‐Specific Signal Regulation by CEACAM1—A Cell Adhesion Molecule Expressed in PC12 Cells
Author(s) -
ÖBRINK BJÖRN,
SAWA HIROKI,
SCHEFFRAHN INKA,
SINGER BERNHARD B.,
SIGMUNDSSON KRISTMUNDUR,
SUNDBERG ULLA,
HEYMANN ROBERT,
BEAUCHEMIN NICOLE,
WENG GEHZI,
RAM PRAHLAD,
IYENGAR RAVI
Publication year - 2002
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2002.tb04536.x
Subject(s) - gene isoform , cell adhesion molecule , microbiology and biotechnology , chemistry , cell adhesion , signal (programming language) , cell , biology , biochemistry , computer science , gene , programming language
A bstract : CEACAM1 is a signal‐regulating, homophilic cell adhesion receptor system expressed in epithelia, vessel endothelia, and leukocytes. Here, we demonstrate that CEACAM1 is expressed also in PC12 cells, both as the common transmembrane isoforms, CEACAM1‐L and CEACAM1‐S, and as a novel, secreted, differentially spliced isoform. CEACAM1 can have both positive and negative effects on cell signaling. In an attempt to explain this dual behavior, we have initiated computational analysis of the signal‐regulating effects of CEACAM1. This suggests that CEACAM1 can exert its signal‐regulating activities by discriminating between binding of Src kinases and SHP phosphatases, respectively. Major factors that regulate this discrimination are the expression levels and expression ratios of transmembrane CEACAM1‐L and CEACAM1‐S, the concentration of secreted CEACAM1, and homophilic binding of CEACAM1 presented by neighboring cells.