p53 increases MHC class I expression by upregulating the endoplasmic reticulum aminopeptidase ERAP1
Bei Wang,
Dandan Niu,
Liyun Lai and
Ee Chee Ren ()
Additional contact information
Bei Wang: Singapore Immunology Network, A*STAR
Dandan Niu: Singapore Immunology Network, A*STAR
Liyun Lai: Singapore Immunology Network, A*STAR
Ee Chee Ren: Singapore Immunology Network, A*STAR
Nature Communications, 2013, vol. 4, issue 1, 1-11
Abstract:
Abstract The p53 tumour suppressor has an important role in cancer cells. Here we show that p53 regulates expression of major histocompatibility complex I on the cell surface. We show that the tumour cell line HCT116, which lacks p53 exhibits significantly lower major histocompatibility complex I expression than its wild-type counterpart. Using a combination of chromatin immunoprecipitation sequencing and gene expression analysis, we demonstrate that p53 upregulates expression of endoplasmic reticulum aminopeptidase 1 by binding to its cognate response element in the ERAP1 gene. Silencing of p53 decreases endoplasmic reticulum aminopeptidase 1 protein levels and therefore major histocompatibility complex I expression. We further show that this mechanism operates in A549 cells infected with H1N1 influenza virus, in which H1N1 activates p53, leading to endoplasmic reticulum aminopeptidase 1 upregulation and a corresponding increase in major histocompatibility complex I expression. Our study suggests a previously unrecognized link between p53 function and the immunosurveillance of cancer and infection.
Date: 2013
References: Add references at CitEc
Citations: View citations in EconPapers (1)
Downloads: (external link)
https://www.nature.com/articles/ncomms3359 Abstract (text/html)
Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.
Export reference: BibTeX
RIS (EndNote, ProCite, RefMan)
HTML/Text
Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:4:y:2013:i:1:d:10.1038_ncomms3359
Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/
DOI: 10.1038/ncomms3359
Access Statistics for this article
Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie
More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().