Sam68 modulates the promoter specificity of NF-κB and mediates expression of CD25 in activated T cells

Kai Fu, Xin Sun, Wenxin Zheng, Eric M. Wier, Andrea Hodgson, Dat Q. Tran, Stéphane Richard and Fengyi Wan ()
Additional contact information
Kai Fu: Bloomberg School of Public Health, Johns Hopkins University
Xin Sun: Bloomberg School of Public Health, Johns Hopkins University
Wenxin Zheng: Bloomberg School of Public Health, Johns Hopkins University
Eric M. Wier: Bloomberg School of Public Health, Johns Hopkins University
Andrea Hodgson: Bloomberg School of Public Health, Johns Hopkins University
Dat Q. Tran: University of Texas-Houston Medical School
Stéphane Richard: Terry Fox Molecular Oncology Group and the Bloomfield Center for Research on Aging, Lady Davis Institute for Medical Research, Sir Mortimer B. Davis Jewish General Hospital
Fengyi Wan: Bloomberg School of Public Health, Johns Hopkins University

Nature Communications, 2013, vol. 4, issue 1, 1-11

Abstract: Abstract CD25, the alpha chain of the interleukin-2 receptor, is expressed in activated T cells and has a significant role in autoimmune disease and tumorigenesis; however, the mechanisms regulating transcription of CD25 remain elusive. Here we identify the Src-associated substrate during mitosis of 68 kDa (Sam68) as a novel non-Rel component in the nuclear factor-kappaB (NF-κB) complex that confers CD25 transcription. Our results demonstrate that Sam68 has an essential role in the induction and maintenance of CD25 in T cells. T-cell receptor engagement triggers translocation of the inhibitor of NF-κB kinase alpha (IKKα) from the cytoplasm to the nucleus, where it phosphorylates Sam68, causing complex formation with NF-κB in the nucleus. These findings reveal the important roles of KH domain-containing components and their spatial interactions with IKKs in determining the binding targets of NF-κB complexes, thus shedding novel insights into the regulatory specificity of NF-κB.

Date: 2013
References: Add references at CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/ncomms2916 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_ncomms2916

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/ncomms2916

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 ().