K27-linked ubiquitination of BRAF by ITCH engages cytokine response to maintain MEK-ERK signaling

K27-linked ubiquitination of BRAF by ITCH engages cytokine response to maintain MEK-ERK signaling

BRAF drives MEK/ERK activation to facilitate tumorigenesis. Here, the authors show that in response to pro-inflammatory cytokines, ITCH mediates a non-proteolytic ubiquitination and activation of BRAF, which in turn sustains MEK/ERK signaling to facilitate melanoma cell growth.

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Auteurs principaux: Qing Yin, Tao Han, Bin Fang, Guolin Zhang, Chao Zhang, Evan R. Roberts, Victoria Izumi, Mengmeng Zheng, Shulong Jiang, Xiu Yin, Minjung Kim, Jianfeng Cai, Eric B. Haura, John M. Koomen, Keiran S. M. Smalley, Lixin Wan
Format: article
Langue:EN
Publié: Nature Portfolio 2019
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Science
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Accès en ligne:https://doaj.org/article/93c520999b9f45c68aaee7bea2c8f9cf
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Résumé:BRAF drives MEK/ERK activation to facilitate tumorigenesis. Here, the authors show that in response to pro-inflammatory cytokines, ITCH mediates a non-proteolytic ubiquitination and activation of BRAF, which in turn sustains MEK/ERK signaling to facilitate melanoma cell growth.

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