Latest papers

Gata4 and Hnf1alpha are partially required for the expression of specific intestinal genes during development.

HNF-1α participates in glucose regulation of sucrase–isomaltase gene expression in epithelial intestinal cells

Methotrexate-induced mucositis in mucin 2-deficient mice.

Rapid expansion of intestinal secretory lineages following a massive small bowel resection in mice.

[Structure and evolution of mammalian maltase-glucoamylase and sucrase-isomaltase genes].

Mucosal function in rat jejunum and ileum is altered by induction of colitis.

The effect of cytostatic drug treatment on intestine-specific transcription factors Cdx2, GATA-4 and HNF-1alpha in mice.

Altered folding, turnover, and polarized sorting act in concert to define a novel pathomechanism of congenital sucrase-isomaltase deficiency.

Hepatocyte nuclear factor-1alpha is required for expression but dispensable for histone acetylation of the lactase-phlorizin hydrolase gene in vivo.

Sucrase-isomaltase gene expression is inhibited by mutant hepatocyte nuclear factor (HNF)-1alpha and mutant HNF-1beta in Caco-2 cells.

Haplotype insufficiency for suppressor of cytokine signaling-2 enhances intestinal growth and promotes polyp formation in growth hormone-transgenic mice.

Requirement for galectin-3 in apical protein sorting.

Novel mutations in the human sucrase-isomaltase gene (SI) that cause congenital carbohydrate malabsorption.

Concomitant cell growth and differentiation are dependent on erbB1 and integrin activation in an autonomously surviving colon adenocarcinoma: involvement of autocrine amphiregulin secretion.

Decreased sucrase and lactase activity in iron deficiency is accompanied by reduced gene expression and upregulation of the transcriptional repressor PDX-1.

Expression of small intestinal and colonic phenotypes in complete intestinal metaplasia of the human stomach.

Intestinal effects of long-lasting spermine ingestion by suckling rats.

A phenylalanine-based folding determinant in intestinal sucrase-isomaltase that functions in the context of a quality control mechanism beyond the endoplasmic reticulum.

Cholera toxin entry into pig enterocytes occurs via a lipid raft- and clathrin-dependent mechanism.

The Caco-2 cell line as a model of the intestinal barrier: influence of cell and culture-related factors on Caco-2 cell functional characteristics.