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Review article: transcriptional events controlling the terminal differentiation of intestinal endocrine cells
Author(s) -
Mutoh H.,
Ratineau C.,
Ray S.,
Leiter A. B.
Publication year - 2000
Publication title -
alimentary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.308
H-Index - 177
eISSN - 1365-2036
pISSN - 0269-2813
DOI - 10.1046/j.1365-2036.2000.014s1170.x
Subject(s) - secretin , enteroendocrine cell , microbiology and biotechnology , enhancer , transcription factor , coactivator , cellular differentiation , biology , progenitor cell , transcription (linguistics) , gene , endocrine system , genetics , stem cell , endocrinology , hormone , pancreas , linguistics , philosophy
Summary Secretin‐producing enteroendocrine cells arise from a multipotential endocrine progenitor in the crypts of the small intestine. As these cells migrate up the crypt‐villus axis, they produce secretin and stop dividing as they terminally differentiate and die. Transcription of the secretin gene is controlled by a complex enhancer binding to multiple transcription factors. The basic helix‐loop‐helix protein, BETA2, binds to an E box sequence and associates with the p300 coactivator to activate transcription of the secretin gene. Basic helix‐loop‐helix proteins appear to play a pivotal role in the control of cellular differentiation. BETA2 induces cell cycle arrest and apoptosis in addition to activating secretin gene expression. Thus BETA2 may function as a master regulatory gene to coordinate terminal differentiation of secretin cells.