- Abstract:
-
In T lymphocytes, the mitogen-activated protein kinase (MAPK) p38 regulates pleiotropic functions and is activated by canonical MAPK signaling or the alternative activation pathway downstream of the T cell antigen receptor (TCR). Here we found that senescent human T cells lacked the canonical and alternative pathways for the activation of p38 but spontaneously engaged the metabolic master regulator AMPK to trigger recruitment of p38 to the scaffold protein TAB1, which caused autophosphorylati...
Expand abstract - Publication status:
- Published
- Peer review status:
- Peer reviewed
- Version:
- Accepted manuscript
- Files:
-
-
(pdf, 1.7MB)
-
- Publisher copy:
- 10.1038/ni.2981
-
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- Funding agency for:
- Henson, SM
- Funding agency for:
- Akbar, AN
- Publisher:
- Nature Publishing Group Publisher's website
- Journal:
- Nature Immunology Journal website
- Volume:
- 15
- Issue:
- 10
- Pages:
- 965-972
- Publication date:
- 2014-08-24
- DOI:
- EISSN:
-
1529-2916
- ISSN:
-
1529-2908
- URN:
-
uuid:b7b0a355-f100-45ef-a3e0-45dd72eb4bbe
- Source identifiers:
-
616425
- Local pid:
- pubs:616425
- Language:
- English
- Keywords:
- Copyright holder:
- Lanna et al.
- Copyright date:
- 2014
- Notes:
- Author(s) retain copyright; published by Nature Publishing Group under license. This is the accepted manuscript version of the article. The final version is available online from Nature at: [10.1038/ni.2981].
Journal article
The kinase p38 activated by the metabolic regulator AMPK and scaffold TAB1 drives the senescence of human T cells.
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+ Biotechnology and Biological Science Research Council
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