Identification of distal KIR promoters and transcripts

M. J. Stulberg, P. W. Wright, H. Dang, R. J. Hanson, Jeffrey S Miller, S. K. Anderson

Research output: Contribution to journalArticlepeer-review

25 Scopus citations

Abstract

A more complete understanding of the transcriptional control of the human and murine class I MHC receptors will help to shed light on the mechanism of selective, stochastic, gene activation that operates in these gene families. Studies of the murine Ly49 class I MHC receptor genes have revealed an important role for distal transcripts originating upstream of the proximal promoter. To date, there have been no reports of distal promoters within the functionally analogous human KIR family of class I MHC receptors. In the current study, reverse transcriptase-polymerase chain reaction (RT-PCR) and RNase protection assays were used to reveal the presence of distal KIR transcripts initiating upstream of the previously characterized proximal KIR promoter. The intergenic promoter elements detected were associated with repetitive elements of the Alu and L1 families. Unlike the proximal KIR promoter, the distal promoter regions were not NK cell-specific. KIR genes expressed in a variegated manner produced a low level of distal transcripts containing a large 5′ untranslated region. In contrast, the highly expressed KIR2DL4 gene possessed a higher level of spliced distal transcripts that were capable of producing KIR2DL4 protein. The identification of distal KIR promoter elements suggests that intergenic transcripts may influence the expression of KIR genes.

Original languageEnglish (US)
Pages (from-to)124-130
Number of pages7
JournalGenes and Immunity
Volume8
Issue number2
DOIs
StatePublished - Mar 2007

Bibliographical note

Funding Information:
Cancer Institute, Center for Cancer Research. This work was supported in part by NIH Grant R01 HL55417 (JSM).

Funding Information:
This project has been funded in whole or in part with federal funds from the National Cancer Institute and the National Institutes of Health, under contract no. DHHS N01-C0-12400. This research was supported in part by the Intramural Research Program of the NIH, National

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