解开 发表于 2025-3-25 06:01:31
http://reply.papertrans.cn/31/3099/309851/309851_21.pngcatagen 发表于 2025-3-25 09:53:56
http://reply.papertrans.cn/31/3099/309851/309851_22.png竖琴 发表于 2025-3-25 14:29:40
http://reply.papertrans.cn/31/3099/309851/309851_23.pngObituary 发表于 2025-3-25 19:05:27
http://reply.papertrans.cn/31/3099/309851/309851_24.pnglibertine 发表于 2025-3-25 21:41:06
http://reply.papertrans.cn/31/3099/309851/309851_25.pngBRIEF 发表于 2025-3-26 03:15:55
http://reply.papertrans.cn/31/3099/309851/309851_26.pngTerminal 发表于 2025-3-26 05:46:08
also developed strategies to get around UPR-induced death signals. In the present chapter, we describe how cancer cells use the UPR or have altered the UPR signaling machinery to gain selective advantage over surrounding cells. We also discuss how UPR signaling is connected to classical carcinogenic案发地点 发表于 2025-3-26 12:21:36
http://reply.papertrans.cn/31/3099/309851/309851_28.png清洗 发表于 2025-3-26 14:38:48
http://reply.papertrans.cn/31/3099/309851/309851_29.pngAirtight 发表于 2025-3-26 20:51:48
ER Stress and UPR Through Dysregulated ER Ca2+ Homeostasis and Signaling and –release mechanisms by ER chaperones and the main controller of the ER-stress sensors, GRP78/BiP. Furthermore, recently identified Ca.-transport systems also seem to target ER-stress proteins. Overall, it is clear that altered Ca. signaling and UPR during ER stress are closely related through d