TY - JOUR
T1 - Cloning of the Human α-Catenin cDNA and Its Aberrant mRNA in a Human Cancer Cell Line
AU - Oda, Tatsuya
AU - Kanai, Yae
AU - Shimoyama, Yutaka
AU - Nagafuchi, Akira
AU - Tsukita, Shoichiro
AU - Hirohashi, Setsuo
PY - 1993/6/30
Y1 - 1993/6/30
N2 - Cadherin and catenin compose cell adhesion complex and are indispensable for tight cell-cell adhesion. Dysfunction of this adhesion complex causes dissociation of cancer cells from primary tumor nodules, thus possibly contributing to cancer invasion and metastasis. In this report, we present the human α-caienin sequence. Human α-catenin showed extensive homology with that of mouse, i.e., 91.8% and 99.3% at the nucleic acid and amino acid levels, respectively, indicating that this molecule has been evolutionarily conserved in mammals. Characterization of the mRNA sequence of α-catenin in PC9 was also carried out, and two distinct abnormal sequences, i.e., one of 957 bp deletion resulting in a 319-amino-acid deletion and another of 761 bp deletion resulting in a frameshift, were identified. These deletions were probably produced by an error of RNA splicing, presenting one possible mechanism for the loss of intact α-catenin expression.
AB - Cadherin and catenin compose cell adhesion complex and are indispensable for tight cell-cell adhesion. Dysfunction of this adhesion complex causes dissociation of cancer cells from primary tumor nodules, thus possibly contributing to cancer invasion and metastasis. In this report, we present the human α-caienin sequence. Human α-catenin showed extensive homology with that of mouse, i.e., 91.8% and 99.3% at the nucleic acid and amino acid levels, respectively, indicating that this molecule has been evolutionarily conserved in mammals. Characterization of the mRNA sequence of α-catenin in PC9 was also carried out, and two distinct abnormal sequences, i.e., one of 957 bp deletion resulting in a 319-amino-acid deletion and another of 761 bp deletion resulting in a frameshift, were identified. These deletions were probably produced by an error of RNA splicing, presenting one possible mechanism for the loss of intact α-catenin expression.
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U2 - 10.1006/bbrc.1993.1710
DO - 10.1006/bbrc.1993.1710
M3 - Article
C2 - 8323564
AN - SCOPUS:0027183788
SN - 0006-291X
VL - 193
SP - 897
EP - 904
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 3
ER -