eIF4E phosphorylation regulates ongoing pain, independently of inflammation, and hyperalgesic priming in the mouse CFA model

eIF4E phosphorylation regulates ongoing pain, independently of inflammation, and hyperalgesic priming in the mouse CFA model

Highlights • CFA-induced inflammation resolves more rapidly in mice lacking MNK-eIF4E signaling. • Ongoing pain responses are reduced in mice lacking MNK-eIF4E signaling while inflammatory responses are unchanged. • Hyperalgesic priming in CFA is absent in mice lacking MNK-eIF4E signaling.

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Bibliographische Detailangaben
Veröffentlicht in:Neurobiology of pain 2018-08, Vol.4, p.45-50
Hauptverfasser: Moy, Jamie K, Kuhn, Jasper L, Szabo-Pardi, Thomas A, Pradhan, Grishma, Price, Theodore J
Format: Artikel
Sprache:eng
Schlagworte:
CFA
eIF4E phosphorylation
Guarding
Inflammation
MNK
Original Research
Pain Medicine
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Zusammenfassung:Highlights • CFA-induced inflammation resolves more rapidly in mice lacking MNK-eIF4E signaling. • Ongoing pain responses are reduced in mice lacking MNK-eIF4E signaling while inflammatory responses are unchanged. • Hyperalgesic priming in CFA is absent in mice lacking MNK-eIF4E signaling.
ISSN:2452-073X
2452-073X
DOI:10.1016/j.ynpai.2018.03.001