Paraptosis and Photodynamic Therapy: A Progress Report
Paraptosis and Photodynamic Therapy: A Progress Report
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DOI：
10.1111/php.13242
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发表时间：
2020-04-23
影响因子：
3.3
通讯作者：
Kessel, David
中科院分区：
文献类型：
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作者：
Kessel, David
对内质网(ER)的光损伤可启动一种称为细胞凋亡的死亡途径。由某些药物和其他刺激启动的“规范”突触模型，需要蛋白质合成的短暂间隔，涉及MAP激酶的作用，并可由生化标记物遵循。后者包括AIP-1/Alix和IGF-1R蛋白表达的变化以及HMGB-1从核到质膜的移位。也有一份报告表明，自噬水平的增强可以通过细胞融合来削弱死亡。当内质网光损伤很小时，通向突触的途径遵循典型途径(
Photodamage to the endoplasmic reticulum (ER) can initiate a death pathway termed paraptosis. The "canonical" model of paraptosis, initiated by certain drugs and other stimuli, requires a brief interval of protein synthesis, involves the action of MAP kinases and can be followed by biochemical markers. The latter include changes in expression of AIP-1/Alix and IGF-1R proteins and translocation of HMGB-1 from nucleus to plasma membrane. There is also a report indicating that an enhanced level of autophagy can impair death by paraptosis. The pathway to paraptosis follows the canonical pathway when ER photodamage is minor (