Brain ischemia/reperfusion-induced expression of DP5 and its interaction with Bcl-2, thus freeing Bax from Bcl-2/Bax dimmers are mediated by c-Jun N-terminal kinase (JNK) pathway
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Acknowledgement
Project supported by the Key Item National Nature Science Foundation (No. 30330190).
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Functionalized graphene oxide against U251 glioma cells and its molecular mechanism
2020, Materials Science and Engineering CCitation Excerpt :Therefore, we concluded that the PGD complex activated the apoptosis pathway by acting on the MAPK signaling pathway, inducing U251 cell apoptosis. The JNK and ERK1/2 pathways were chosen as the entry point to study the mechanism of PGD-inducing apoptosis of U251 glioma cells, both can interact with the key molecular of the mitochondrial apoptosis pathway, including signaling molecular Bax and Bcl-2, which affects cell apoptosis [55–61], as shown in Fig. 8. After interaction with U251 cells, PGD promotes the phosphorylation of JNK.
Putative roles of mitochondrial Voltage-Dependent Anion Channel, Bcl-2 family proteins and c-Jun N-terminal Kinases in ischemic stroke associated apoptosis
2017, Biochimie OpenCitation Excerpt :Cellular ischemia causes Bax to translocate towards outer mitochondrial membrane [41,42]. There are reports which suggest that during cerebral ischemia cytosolic Bax gets phosphorylated by JNKs and phosphorylation activated Bax then translocates towards mitochondria and causes cytochrome c release [43,44]. JNK3 has been shown to phosphorylate Bax in vitro [45].
Suppression of mitochondrial fission in experimental cerebral ischemia: The potential neuroprotective target of p38 MAPK inhibition
2015, Neurochemistry InternationalCitation Excerpt :Mitochondrial morphology and their dynamic networks are highly relevant to many pathological processes, such as neural diseases including acute stroke (Bertoni-Freddari et al., 2006; Bolanos et al., 2009; Grohm et al., 2012), neurodegenerative diseases (Cho et al., 2010) and heart ischemic diseases (Marin-Garcia and Goldenthal, 2004). There is increasing evidence that p38/JNK MAPKs could be involved in the apoptosis process via the regulating of mitochondrial pro-apoptotic proteins, such as Bcl-2 family members (Guan et al., 2006; Lei et al., 2002; Okuno et al., 2004). The ERK pathway could also regulate mitochondrial morphology and functions with the modulation of mitochondrial fission and fusion balance (Gan et al., 2014).
Bex2 regulates cell proliferation and apoptosis in malignant glioma cells via the c-Jun NH2-terminal kinase pathway
2012, Biochemical and Biophysical Research CommunicationsCitation Excerpt :The phosphorylation can adjust the expression of the downstream genes, such as FasL and TNF, which are related to apoptosis [31], and then induce the death receptor pathway of apoptosis. It can also raise the expression of Bim and Bid, which can activate Bax, promoting apoptosis through the mitochondrial pathway [32]. Naderi reported that Bex2 down-regulation decreases the c-Jun phosphorylation in breast cancer cells [15].
Blocking Daxx trafficking attenuates neuronal cell death following ischemia/reperfusion in rat hippocampus CA1 region
2011, Archives of Biochemistry and BiophysicsCitation Excerpt :Taken together, our results suggest that SP600125, NAC and Daxx AS-ODS have a neuroprotective effect against ischemia–reperfusion-induced neuronal cell death in vivo, and furthermore blocking of Daxx trafficking is involved in the event. Recently lots of researches have focused on Daxx, as consequently, manifold functions of Daxx were found [5–9,25–29]. Among all the results there were contradictory opinions, death or survival, there was no coincidence.
The P38MAPK/ATF2 signaling pathway is involved in PND in mice
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