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Targeting the HTLV-I-Regulated BATF3/IRF4 Transcriptional Network in Adult T Cell Leukemia/Lymphoma
Nakagawa, Masao,Shaffer, Arthur L.,Ceribelli, Michele,Zhang, Meili,Wright, George,Huang, Da Wei,Xiao, Wenming,Powell, John,Petrus, Michael N.,Yang, Yibin,Phelan, James D.,Kohlhammer, Holger,Dubois, Si Elsevier Science B.V., Amsterdam 2018 CANCER CELL Vol.34 No.2
Targeting Non-proteolytic Protein Ubiquitination for the Treatment of Diffuse Large B Cell Lymphoma
Yang, Y.,Kelly, P.,Shaffer, A.L.,Schmitz, R.,Yoo, H.M.,Liu, X.,Huang, D.W.,Webster, D.,Young, R.M.,Nakagawa, M.,Ceribelli, M.,Wright, G.W.,Yang, Y.,Zhao, H.,Yu, X.,Xu, W.,Chan, W.C.,Jaffe, E.S.,Gascoy Cell Press 2016 CANCER CELL Vol.29 No.4
Chronic active B cell receptor (BCR) signaling, a hallmark of the activated B cell-like (ABC) subtype of diffuse large B cell lymphoma (DLBCL), engages the CARD11-MALT1-BCL10 (CBM) adapter complex to activate IκB kinase (IKK) and the classical NF-κB pathway. Here we show that the CBM complex includes the E3 ubiquitin ligases cIAP1 and cIAP2, which are essential mediators of BCR-dependent NF-κB activity in ABC DLBCL. cIAP½ attach K63-linked polyubiquitin chains on themselves and on BCL10, resulting in the recruitment of IKK and the linear ubiquitin chain ligase LUBAC, which is essential for IKK activation. SMAC mimetics target cIAP½ for destruction, and consequently suppress NF-κB and selectively kill BCR-dependent ABC DLBCL lines, supporting their clinical evaluation in patients with ABC DLBCL.