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快照:细胞坏死性凋亡

SnapShot: Necroptosis.

机构信息

Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.

出版信息

Cell. 2014 Jul 17;158(2):464-464.e1. doi: 10.1016/j.cell.2014.06.041.

DOI:10.1016/j.cell.2014.06.041
PMID:25036639
Abstract

Regulated necrosis, termed necroptosis, is mediated by the kinase activity of RIPK1 and RIPK3. It has distinct cellular features that are different than apoptosis. Necroptosis can be triggered by extracellular stimuli known to activate inflammation and cell death and its intracellular signaling pathway involves necrosome formation and MLKL activation. Inhibition of necroptosis has been shown to mitigate pathology in numerous mouse models, providing potential strategies to treat human diseases.

摘要

受调控的细胞坏死,也被称为程序性坏死,由 RIPK1 和 RIPK3 的激酶活性所介导。程序性坏死具有不同于细胞凋亡的独特细胞特征。细胞外刺激可以引发程序性坏死,已知这些刺激会激活炎症和细胞死亡,其细胞内信号通路涉及坏死小体的形成和 MLKL 的激活。抑制程序性坏死已被证明可以减轻许多小鼠模型中的病理学,为治疗人类疾病提供了潜在策略。

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SnapShot: Necroptosis.快照:细胞坏死性凋亡
Cell. 2014 Jul 17;158(2):464-464.e1. doi: 10.1016/j.cell.2014.06.041.
2
RIPK3 deficiency or catalytically inactive RIPK1 provides greater benefit than MLKL deficiency in mouse models of inflammation and tissue injury.在炎症和组织损伤的小鼠模型中,RIPK3缺陷或催化失活的RIPK1比MLKL缺陷带来更大的益处。
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Necroptosis in development and diseases.细胞坏死性凋亡在发育和疾病中的作用。
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Complex Pathologic Roles of RIPK1 and RIPK3: Moving Beyond Necroptosis.RIPK1和RIPK3的复杂病理作用:超越坏死性凋亡
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CK1α, CK1δ, and CK1ε are necrosome components which phosphorylate serine 227 of human RIPK3 to activate necroptosis.CK1α、CK1δ 和 CK1ε 是坏死小体的组成部分,可将人 RIPK3 的丝氨酸 227 磷酸化以激活坏死性凋亡。
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RIPK1/RIPK3 promotes vascular permeability to allow tumor cell extravasation independent of its necroptotic function.RIPK1/RIPK3促进血管通透性,以使肿瘤细胞外渗,这一过程独立于其坏死性凋亡功能。
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Characterization of RIPK3-mediated phosphorylation of the activation loop of MLKL during necroptosis.坏死性凋亡过程中RIPK3介导的MLKL激活环磷酸化的特征分析。
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