Chemical biology suggests a role for calcium signaling in mediating sustained JNK activation during apoptosis

被引：29

作者：

Brnjic, Slavica ^{[1
]}

Olofsson, Maria Hagg ^{[1
]}

Havelka, Aleksandra Mandic ^{[2
]}

Linder, Stig ^{[1
]}

机构：

[1] Karolinska Inst, Dept Oncol Pathol, Canc Ctr Karolinska, S-17176 Stockholm, Sweden

[2] Karolinska Inst, Karolinska Univ Hosp, Dept Mol Med & Surg, S-17176 Stockholm, Sweden

来源：

MOLECULAR BIOSYSTEMS | 2010年 / 6卷 / 05期

关键词：

CISPLATIN-INDUCED APOPTOSIS; CELL-DEATH; ENDOPLASMIC-RETICULUM; MAP KINASES; MEMBRANE PERMEABILIZATION; INTRACELLULAR CA2+; ANTICANCER AGENTS; RELEASE CHANNEL; DNA-DAMAGE; CALPAIN;

D O I：

10.1039/b920805d

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Calcium (Ca2+) is used as a signaling molecule to regulate many cellular processes. Calcium signaling generally involves transient elevations of the concentration of free Ca2+ in the cytosol. More pronounced and sustained elevations of intracellular Ca2+ concentrations are observed during apoptosis (programmed cell death). These Ca2+ elevations have been shown to lead to the activation of proteases (calpains) and to changes in protein phosphorylation. Recent evidence, using chemical biology, has raised the possibility that calcium signaling is involved in sustained JNK activation during late phases of apoptosis. For at least some stimuli, calcium release leads to activation of calmodulin kinase II (CaMKII), apoptosis signaling kinase I (ASKI) and JNK. Calcium signaling may help to orchestrate the apoptotic response during the execution phase.

引用

页码：767 / 774

页数：8

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