ER stress does not cause upregulation and activation of caspase-2 to initiate apoptosis

SandowJ.J.; DorstynL.; OReillyL.A.; TaillerM.; KumarS.; StrasserA.; EkertP.G.

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ER stress does not cause upregulation and activation of caspase-2 to initiate apoptosis

机译：内质网应激不会引起caspase-2的上调和激活以引发细胞凋亡

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A recent report claimed that endoplasmic reticulum (ER) stress activates the ER trans-membrane receptor IRE1α, leading to increased caspase-2 levels via degradation of microRNAs, and consequently induction of apoptosis. This observation casts caspase-2 into a central role in the apoptosis triggered by ER stress. We have used multiple cell types from caspase-2-deficient mice to test this hypothesis but failed to find significant impact of loss of caspase-2 on ER-stress-induced apoptosis. Moreover, we did not observe increased expression of caspase-2 protein in response to ER stress. Our data strongly argue against a critical role for caspase-2 in ER-stress-induced apoptosis.

机译：最近的一份报告声称，内质网（ER）应力激活了ER跨膜受体IRE1α，通过降解microRNA导致caspase-2水平升高，从而诱导了细胞凋亡。该观察结果表明，胱天蛋白酶2在内质网应激触发的细胞凋亡中起着核心作用。我们已经使用了来自caspase-2缺陷小鼠的多种细胞类型来检验这一假设，但未能发现caspase-2缺失对内质网应激诱导的凋亡的重大影响。此外，我们没有观察到响应内质网应激的caspase-2蛋白表达增加。我们的数据强烈反对caspase-2在内质网应激诱导的细胞凋亡中的关键作用。

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《Cell death and differentiation》 |2014年第3期|共6页
作者
SandowJ.J.; DorstynL.; OReillyL.A.; TaillerM.; KumarS.; StrasserA.; EkertP.G.;
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正文语种 eng
中图分类细胞生物学;
关键词
apoptosis; caspase-2; ER stress;

机译：凋亡;caspase-2;内质网应激;

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1. ER stress does not cause upregulation and activation of caspase-2 to initiate apoptosis [J] . SandowJ.J., DorstynL., OReillyL.A., Cell death and differentiation . 2014,第3期

机译：内质网应激不会引起caspase-2的上调和激活以引发细胞凋亡
2. Partial inactivation of cardiac 14-3-3 protein in vivo elicits endoplasmic reticulum stress (ERS) and activates ers-initiated apoptosis in ERS-induced mice [J] . Sari F.R., Watanabe K., Widyantoro B., Cellular Physiology and Biochemistry . 2010,第2期

机译：体内心脏14-3-3蛋白的部分失活会引起内质网应激（ERS）并激活ERS诱导的小鼠中ERS诱导的凋亡
3. Partial Inactivation of Cardiac 14-3-3 Protein in vivo Elicits Endoplasmic Reticulum Stress (ERS) and Activates ERS-initiated Apoptosis in ERS-induced Mice [J] . Flori R. Sari, Kenichi Watanabe, Bambang Widyantoro, Cellular Physiology and Biochemistry . 2010,第2期

机译：体内心脏14-3-3蛋白的部分失活引发内质网应激（ERS）并激活ERS诱导的小鼠中ERS诱导的细胞凋亡。
4. Measurement of caspase-2 activation during different anti-tumor drugs induced apoptosis by FRET technique [C] . Juqiang Lin, Shaoqun Zeng, Qingming Luo, Conference on Optics in Health Care and Biomedical Optics . 2008

机译：用焦点技术测量不同抗肿瘤药物诱导细胞凋亡的胱天蛋白酶-2活化
5. DLX4 homeoprotein promotes PI3K/Akt anti-apoptosis pathway in ER negative breast cancer cells through upregulation of VEGFA. [D] . Wu, Weiwei. 2010

机译：DLX4同源蛋白通过上调VEGFA促进ER阴性乳腺癌细胞中的PI3K / Akt抗凋亡途径。
6. ER stress does not cause upregulation and activation of caspase-2 to initiate apoptosis [O] . J J Sandow, L Dorstyn, L A OReilly, 2014

机译：内质网应激不会引起caspase-2的上调和激活以引发细胞凋亡
7. ER stress does not cause upregulation and activation of caspase-2 to initiate apoptosis [O] . Sandow, J., Dorstyn, L., O'Reilly, L., 2014

机译：ER应激不会引起caspase-2的上调和激活，从而引发细胞凋亡

ER stress does not cause upregulation and activation of caspase-2 to initiate apoptosis

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