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Non‐functional role of syntaxin 2 in insulin exocytosis by pancreatic β cells
Author(s) -
Nagamatsu Shinya,
Sawa Hiroki,
Nakamichi Yoko,
Kondo Yoshinori,
Matsushima Satsuki,
Watanabe Takashi
Publication year - 1997
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/(sici)1099-0844(199712)15:4<237::aid-cbf746>3.0.co;2-u
Subject(s) - syntaxin 3 , exocytosis , syntaxin , monoclonal antibody , western blot , microbiology and biotechnology , insulin , islet , snap23 , pancreatic islets , chemistry , munc 18 , pancreas , antibody , biology , secretion , endocrinology , membrane protein , immunology , gene , biochemistry , vesicle , synaptic vesicle , membrane , vesicle associated membrane protein 8
This study was designed in order to examine the expression and functional role of syntaxin 2/epimorphin in pancreatic β cells. Northern blot analysis revealed that syntaxin 2 mRNA was able to be detected in mouse βTC3 cells, but not in isolated mouse islets. In agreement with this result, immunoblot analysis detected an appreciable amount of syntaxin 2 protein in βTC3 cells, but not in mouse islets. Immunohistochemistry of the mouse pancreas demonstrated that syntaxin 2 was little evident in islet cells of Langerhans, and somewhat predominant in exocrine tissues. In order to examine whether syntaxin 2 is anchored to cell surfaces in βTC3 cells, living cells were incubated with a monoclonal antibody against syntaxin 2 (MC‐1). The antibody bound to their surfaces, indicating that syntaxin 2 was localized on cell surfaces. The addition of MC‐1 to the culture medium of βTC3 cells did not affect insulin release under the presence or absence of 11 m M glucose, indicating that syntaxin 2 is not associated with insulin exocytosis. Thus, the expression of syntaxin 2 in islets of Langerhans is very low and the function of this protein is probably unrelated to the insulin exocytosis pathway. © 1997 John Wiley & Sons, Ltd.