Linked Life Data

11159844

Source:http://linkedlifedata.com/resource/pubmed/id/11159844

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2001-2-22
pubmed:abstractText
Cholecystokinin (CCK) is a potent intestinal hormone that regulates several digestive functions. Despite the physiological importance of CCK, the cellular and molecular mechanisms that govern its synthesis and secretion are not completely identified. Peptones, which are fair counterparts of the protein fraction in the intestinal lumen, are good stimulants of CCK secretion. We have previously shown that peptones activate CCK gene transcription in STC-1 enteroendocrine cells. The DNA element(s) necessary to induce the transcriptional stimulation was preliminary, localized in the first 800 bp of the CCK gene promoter. In the present study, we identify a DNA element [peptone-response element (PepRE)] essential to confer peptone-responsiveness to the CCK promoter, and we characterize the transcription factors implicated. Localization of the PepRE between -93 and -70 bp of the promoter was established using serial 5'-3'deletions. Systematic site-directed mutagenesis demonstrated that the core PepRE sequence, spanning from nucleotide -72 to -83, overlapped with the putative AP-1/CRE site. Mutations in the core sequence dramatically decreased peptone-responsiveness of CCK promoter fragments. The PepRE functioned as a low-affinity CRE consensus site, binding only transcription factors of the CREB family. Overexpression, in STC-1 cells, of a dominant-negative protein (A-CREB), that prevented the binding of CREB factors to DNA, completely abolished the peptone-induced transcriptional stimulation. Peptone treatment did not modify the nature and the abundance of proteins bound to the PepRE but led to increased phosphorylation of the CREB factors. In conclusion, the present study first demonstrates that CCK gene expression is under the control of protein-derived nutrients in the STC-1 enteroendocrine cell line.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0013-7227
pubmed:author
pubmed:issnType
Print
pubmed:volume
142
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
721-9
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:11159844-Animals, pubmed-meshheading:11159844-Base Sequence, pubmed-meshheading:11159844-Cells, Cultured, pubmed-meshheading:11159844-Cholecystokinin, pubmed-meshheading:11159844-Chromosome Mapping, pubmed-meshheading:11159844-Cyclic AMP Response Element-Binding Protein, pubmed-meshheading:11159844-Genes, Dominant, pubmed-meshheading:11159844-Intestines, pubmed-meshheading:11159844-Mice, pubmed-meshheading:11159844-Multigene Family, pubmed-meshheading:11159844-Mutagenesis, Site-Directed, pubmed-meshheading:11159844-Peptones, pubmed-meshheading:11159844-Promoter Regions, Genetic, pubmed-meshheading:11159844-Response Elements, pubmed-meshheading:11159844-Transcription, Genetic, pubmed-meshheading:11159844-Transcription Factor AP-1, pubmed-meshheading:11159844-Transcription Factors
pubmed:year
2001
pubmed:articleTitle
Peptones stimulate intestinal cholecystokinin gene transcription via cyclic adenosine monophosphate response element-binding factors.
pubmed:affiliation
Institut National de la Santé et de la Recherche Médicale U45, Hôpital Edouard Herriot, 69437 Lyon, France.
pubmed:publicationType
Journal Article