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1 kb of the lactase‐phlorizin hydrolase promoter directs post‐weaning decline and small intestinal‐specific expression in transgenic mice
Author(s) -
Troelsen Jesper T.,
Mehlum Anja,
Olsen Jørgen,
Spodsberg Nikolaj,
Hansen Gert H.,
Prydz Hans,
Norén Ove,
Sjöström Hans
Publication year - 1994
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(94)80519-9
Subject(s) - lactase , weaning , biology , lactose , phlorizin , small intestine , hydrolase , transgene , population , genetically modified mouse , endocrinology , gene , medicine , enzyme , andrology , genetics , biochemistry , glucose transporter , environmental health , insulin
Adult‐type hypolactasia is a genetic condition making approximately one half of the human population intolerant to milk because of abdominal symptoms. The cause is a post‐weaning down‐regulation of the intestinal‐specific enzyme lactase‐phlorizin hydrolase (LPH) reducing the intestinal capacity to hydrolyze lactose. We here demonstrate that the stretch −17 to −994 in the pig LPH‐promoter carries cis‐elements which direct a small intestinal‐specific expression and a post‐weaning decline of a linked rabbit β‐globin gene. These data demonstrate that the post‐weaning decline of LPH is mainly due to a transcriptional down‐regulation.