Search

Your search keyword '"Negative cis element"' showing total 2 results
Start Over Descriptor "Negative cis element"
2 results on '"Negative cis element"'

1. An upstream negative regulatory element in human granulocyte-macrophage colony-stimulating factor promoter is recognised by AP1 family members

Author

Cecilia Garrè, Roberto Ravazzolo, Giovanna Bianchi-Scarrà, Claudia Gramigni, and Silvana Penco

Subjects
Proto-Oncogene Proteins c-jun, medicine.medical_treatment, Response element, Negative regulatory element, Biophysics, DNA Footprinting, Oligonucleotides, Biology, Transfection, Biochemistry, Binding, Competitive, Antibodies, Transcriptional regulation, Structural Biology, Genes, Reporter, Consensus Sequence, Genetics, medicine, Tumor Cells, Cultured, Humans, Point Mutation, Promoter Regions, Genetic, AP1, Molecular Biology, Transcription factor, Sequence Deletion, Reverse Transcriptase Polymerase Chain Reaction, Negative cis element, Granulocyte-Macrophage Colony-Stimulating Factor, Cell Biology, Molecular biology, Gene Expression Regulation, Neoplastic, Transcription Factor AP-1, Haematopoiesis, AP-1 transcription factor, Cytokine, Granulocyte macrophage colony-stimulating factor, U87MG, Proto-Oncogene Proteins c-fos, medicine.drug
Abstract

Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a cytokine involved in haematopoiesis and host defence. Production of GM-CSF has been detected in tumour cells including the U87MG astrocytoma cell line. Previous studies have been focused on the regulatory role of the proximal region of the GM-CSF promoter. Our studies on the distal region of the promoter in U87MG cells identify a negative cis element (−1377/−1298) which contains a AP1-like site able to bind c-jun and c-fos transcription factors, according to the results of DNA/protein binding assays. Mutagenesis of the AP1-like site eliminates AP1 binding and the negative effect on promoter activity.

Published
1998

2. PKC-dependent phosphorylation of the p97 repressor regulates the transcription of aldolase A L-type promoter

Author

Paola Costanzo, Paola D'Agostino, Paola Izzo, Chiara Zevino, Angelo Lupo, L. Medugno, Costanzo, Paola, Lupo, A., Medugno, L., D'Agostino, P., Zevino, C., Izzo, P., Costanzo, P, Lupo, A, Medugno, L, D'Agostino, P, Zevino, C, and Izzo, Paola

Subjects
Time Factors, Transcription, Genetic, Recombinant Fusion Proteins, Biophysics, Repressor, Biology, Cell cycle, Biochemistry, Models, Biological, Dephosphorylation, Mice, Transcriptional regulation, Structural Biology, Transcription (biology), Protein kinase C, Fructose-Bisphosphate Aldolase, Genetics, Animals, Humans, Phosphorylation, Promoter Regions, Genetic, Molecular Biology, Messenger RNA, Dose-Response Relationship, Drug, Negative cis element, Aldolase A, Nuclear Proteins, Cell Biology, 3T3 Cells, Molecular biology, Repressor Proteins, biology.protein, Caco-2 Cells
Abstract

Expression of mouse aldolase A L-type mRNA is negatively modulated by a cis element (AldA-NRE), located within the aldolase A distal promoter (pL). AldA-NRE interacts with a 97-kDa repressor protein (p97), which binds DNA in a cell cycle-dependent manner. We demonstrate that the binding between AldA-NRE and p97 decreases during differentiation of human Caco-2 cells and is inversely correlated with L-type mRNA expression. Phosphorylation of the p97 repressor weakened its DNA binding activity in differentiated Caco-2 cells, while dephosphorylation enhanced the binding in proliferating cells. Stimulation of protein kinase C (PKC) in vivo decreased the binding of p97 to AldA-NRE and stimulated transcription, while inhibition of PKC stimulated p97 binding and downregulated transcription. These findings suggest that PKC is a mediator of the binding and silencing function of the p97/AldA-NRE repressor complex. Copyright (C) 1999 Federation of European Biochemical Societies.

Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results