Effect of chemical modification on the ability of pyrrolidinium fullerene to induce apoptosis of cells transformed by JAK2 V617F mutant
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- 作者：Megumi Funakoshi-Tagoa ; tago-mg@pha.keio.ac.jp" class="auth_mail ; Masaki Tsukadaa ; Toshiro Watanabea ; Yuka Mamedaa ; Kenji Tagob ; Tomoyuki Ohec ; Shigeo Nakamurad ; Tadahiko Mashinoc ; Tadashi Kasaharaa
- 关键词：ASK1 ; apoptosis signal-regulating kinase 1 ; c-IAP1 ; cellular inhibitor of apoptosis protein 1 ; DCFH ; dichlorodihydrofluorescein ; DMSO ; dimethyl sulfoxide ; Epo ; erythropoietin ; ERK ; extracellular signal-regulated kinase ; EpoR ; erythropoietin receptor ; ET ; essential thrombocytosis ; JAK2 ; Janus kinase 2 ; JNK ; c-Jun N-terminal kinase ; MKK4/7 ; mitogen-activated protein kinase kinase 4/7 ; MPNs ; myeloproliferative neoplasms ; PMF ; primary myelofibrosis ; PV ; polycythemia vera ; STAT ; signal transducers an
- 刊名：International Immunopharmacology
- 出版年：May 2014
- 年：2014
- 卷：20
- 期：1
- 页码：258-263
- 全文大小：688 K
文摘
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Pyrrolidinium fullerene induces apoptosis of cells transformed by the JAK2 mutant.
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Pyrrolidinium fullerene inhibits the ASK1-MKK4/7-JNK pathway.
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Introduction of butyl group improves the ability of fullerene to induce apoptosis.
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Introduction of butyl group to fullerene potently inhibits the ASK1-MKK4/7-JNK pathway.