Journal
TRENDS IN IMMUNOLOGY
Volume 40, Issue 9, Pages 799-808Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.it.2019.07.001
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Funding
- Imperial College London
- Francis Crick Institute (London)
- British Heart Foundation Project grant [PG/15/57/31580]
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Mammalian TPL-2 kinase (MAP3K8) mediates Toll-like receptor activation of ERK1/2 and p38 alpha MAP kinases and is critical for regulating immune responses to pathogens. TPL-2 also has an important adaptor function, maintaining stability of associated ABIN-2 ubiquitin-binding protein. Consequently, phenotypes detected in Map3k8(-/-) mice can be caused by lack of TPL-2, ABIN-2, or both proteins. Recent studies show that increased inflammation of Map3k8(-/-) mice in allergic airway inflammation and colitis results from reduced ABIN-2 signaling, rather than blocked TPL-2 signaling. However, Map3k8(-/-) mice have been employed extensively to evaluate the potential of TPL-2 as an anti-inflammatory drug target. We posit that Map3k8(D2)(7)(0A)(/)(D2)(70A) mice, expressing catalytically inactive TPL-2 and physiologic ABIN-2, should be used to evaluate the potential effects of TPL-2 inhibitors in disease.
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