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Oct-2 regulates CD36 gene expression via a consensus octamer, which excludes the co-activator OBF-1.
- Source :
-
Nucleic acids research [Nucleic Acids Res] 2002 Apr 15; Vol. 30 (8), pp. 1767-73. - Publication Year :
- 2002
-
Abstract
- The POU domain transcription factor, Oct-2, is essential for the B cell-specific expression of CD36 in mouse B cells. In order to determine how Oct-2 mediates expression of CD36 in B cells, we cloned and analysed the mouse CD36 promoter. In contrast to the human CD36 promoter, the mouse promoter contains a consensus octamer element of the type ATGCTAAT. This octamer element can be bound by either Oct-1 or Oct-2 but requires the expression of Oct-2 to activate transcription in B cells. Mutation of the octamer element renders the CD36 promoter refractory to activation by Oct-2. Furthermore, we demonstrate that the CD36 octamer element does not support recruitment of the B cell-specific co-activator OBF-1 and that CD36 expression is unaffected in primary B cells derived from obf-1(-/-) mice. We conclude that Oct-2 activates CD36 gene expression in mouse B cells via the octamer element in the promoter. Our data also demonstrate that CD36 is the first example of an Oct-2-dependent gene whose expression in B cells is independent of OBF-1. These findings support the notion that Oct-2 regulates gene transcription by both OBF-1-dependent and -independent mechanisms.
- Subjects :
- Animals
Base Sequence
CD36 Antigens biosynthesis
Cell Line
Cells, Cultured
Cloning, Molecular
Consensus Sequence
Genes, Reporter
Host Cell Factor C1
Humans
Mice
Octamer Transcription Factor-1
Octamer Transcription Factor-2
RNA, Messenger biosynthesis
Sequence Alignment
B-Lymphocytes metabolism
CD36 Antigens genetics
DNA-Binding Proteins metabolism
Trans-Activators metabolism
Transcription Factors metabolism
Transcriptional Activation
Subjects
Details
- Language :
- English
- ISSN :
- 1362-4962
- Volume :
- 30
- Issue :
- 8
- Database :
- MEDLINE
- Journal :
- Nucleic acids research
- Publication Type :
- Academic Journal
- Accession number :
- 11937630
- Full Text :
- https://doi.org/10.1093/nar/30.8.1767