2023年10月11日 · Using the antibody BAX6A7, which detects an active form of BAX 15, we found using 3D-SIM microscopy that, in senescent cells, peripheral globular mitochondria dissociated from the main network...

2021年8月13日 · BAX is a pro-apoptotic member of the BCL-2 family, which regulates the balance between cellular life and death. During homeostasis, BAX predominantly resides in the cytosol as a latent monomer...

ER stress-induced apoptosis was shown to require the pro-apoptotic members BAX and BAK of the BCL2 family to initiate mitochondrial dysfunction and cell death. Afterwards, a study reported for the first time that BAX and BAK can colocalize to the IRE1α sensor on the ER membrane, uncovering a direct link between an essential gateway for cell ...

2020年9月18日 · We show here that the apoptotic stimuli cisplatin and staurosporine induce a Bax/Bak-dependent degradation and subcellular redistribution of nesprin-1 and nesprin-2 but not nesprin-3, of the...

Cancer therapies induce differential cell responses, ranging from efficient cell death to complete stress resistance. The BCL-2 proteins BAX and BAK govern the cellular decision between survival and mitochondrial apoptosis. Therefore, the status of BAX/BAK regulation can predict the cellular apoptosis predisposition.

Conclusively, TDZ induced Bax-Bak dependent and independent apoptosis by enhancing ROS production followed by ER stress. Keywords: Apoptosis; Autophagy; Bcl-2; ER stress; Reactive oxygen species; Thioridazine.

2018年10月1日 · Thioridazine (TDZ) induces ROS generation leading to ER stress mediated apoptosis. ROS inhibitor NAC and overexpression of Bcl-2 inhibit TDZ induced apoptosis. Autophagy acts as a survival factor in TDZ mediated apoptosis. TDZ effectively induces Bax-Bak independent apoptosis by ROS generation.

4 天之前 · Different Flag-TRAF3IP3 plasmids or empty plasmids were transfected into A549 cells, and the results revealed that wild-type and transmembrane domain of TRAF3IP3 overexpression markedly upregulated STRN3, as well as ER stress proteins GRP78 and ATF, and apoptosis-related protein Bax (Figure 7H). These findings suggest that transmembrane domains ...

当ER stress发生时，Bip/GRp78与内质网跨膜蛋白PERK、ATF6等的解离均能激活CHOP[1]。 CHOP诱导凋亡蛋白（如：GADD34、ERO1、DR5）的表达，可直接激活GADD34，促进ER下游蛋白的生物合成。

We reveal that chronic, but not acute, stress increases cortical levels of Bax oligomer 270, a complex revealed in previous studies to be associated with apoptosis. Several recent studies have revealed that physical exercise can protect rodents from neurochemical and/or behavioral changes occurring with stress.