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Cell Mol Immunol. 2016 Jan;13(1):119-31. doi: 10.1038/cmi.2014.138. Epub 2015 Feb 2.

Focused transcription from the human CR2/CD21 core promoter is regulated by synergistic activity of TATA and Initiator elements in mature B cells.

Author information

1
School of Pathology and Laboratory Medicine, Centre for Genetic Origins of Health and Disease, The University of Western Australia, Crawley, WA, Australia.
2
Biochemistry and Molecular Biology, School of Chemistry and Biochemistry, The University of Western Australia, Crawley, WA, Australia.
3
Telethon Kids Institute, The University of Western Australia, Crawley, WA, Australia.
4
Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
5
US Department of Veterans Affairs Medical Center, Cincinnati, OH, USA.
6
Division of Rheumatology, Department of Medicine, University of California at Los Angeles, Los Angeles, CA, USA.
7
Division of Rheumatology, University of Colorado School of Medicine, Aurora, CO, USA.

Abstract

Complement receptor 2 (CR2/CD21) is predominantly expressed on the surface of mature B cells where it forms part of a coreceptor complex that functions, in part, to modulate B-cell receptor signal strength. CR2/CD21 expression is tightly regulated throughout B-cell development such that CR2/CD21 cannot be detected on pre-B or terminally differentiated plasma cells. CR2/CD21 expression is upregulated at B-cell maturation and can be induced by IL-4 and CD40 signaling pathways. We have previously characterized elements in the proximal promoter and first intron of CR2/CD21 that are involved in regulating basal and tissue-specific expression. We now extend these analyses to the CR2/CD21 core promoter. We show that in mature B cells, CR2/CD21 transcription proceeds from a focused TSS regulated by a non-consensus TATA box, an initiator element and a downstream promoter element. Furthermore, occupancy of the general transcriptional machinery in pre-B versus mature B-cell lines correlate with CR2/CD21 expression level and indicate that promoter accessibility must switch from inactive to active during the transitional B-cell window.

PMID:
25640655
PMCID:
PMC4711682
DOI:
10.1038/cmi.2014.138
[Indexed for MEDLINE]
Free PMC Article

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