Biochemical and Biophysical Research Communications
Regular ArticleAnalysis of Ras-Dependent Signals That Prevent Caspase-3 Activation and Apoptosis Induced by Cytokine Deprivation in Hematopoietic Cells☆,☆☆
References (35)
- et al.
J. Biol. Chem.
(1995) - et al.
J. Biol. Chem.
(1999) - et al.
J. Biol. Chem.
(1997) - et al.
J. Biol. Chem.
(1997) - et al.
Cell
(1997) - et al.
Methods Cell Biol.
(1991) - et al.
Biochem. Biophys. Res. Commun.
(1998) Curr. Opin. Cell Biol.
(1998)- et al.
Mol. Cell
(1999) - et al.
J. Biol. Chem.
(1999)
J. Biol. Chem.
Annu. Rev. Biochem.
Proc. Natl. Acad. Sci. USA
Proc. Natl. Acad. Sci. USA
EMBO J.
EMBO J.
FASEB J.
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Repeated low-dose 17β-estradiol treatment prevents activation of apoptotic signaling both in the synaptosomal and cellular fraction in rat prefrontal cortex following cerebral ischemia
2015, Neurochemistry InternationalCitation Excerpt :As ERK and Akt pathways can cross-talk and result in the prevention of apoptosis (Cardone et al., 1998), intrinsic apoptotic pathway may be affected at several different levels. Activation of these pathways inhibits Bax conformational change required for its translocation to the mitochondria (Tsuruta et al., 2002; Yamaguchi and Wang, 2001), Akt may inhibit opening of the mitochondrial permeability transition pore, thereby retaining cytochrome c within the mitochondrial inter membranous space (Hausenloy and Yellon, 2004), while ERK activation has been shown to inhibit apoptosis over inhibition of caspase 3 activation (Terada et al., 2000). In accordance with that, it should not be surprising that increased levels of phospho forms of both ERK (42 kDa pERK and 44 kDa pERK) and Akt (pAkt) were observed in the cytosolic and nuclear fraction of the prefrontal cortex.
The protective effect of hispidin against hydrogen peroxide-induced apoptosis in H9c2 cardiomyoblast cells through Akt/GSK-3β and ERK1/2 signaling pathway
2014, Experimental Cell ResearchCitation Excerpt :The activation of either the PI3K/Akt or the ERK1/2 pathway inhibits the conformational change in Bax required for its translocation to the mitochondria, therefore preventing apoptosis [40,41]. Furthermore the up-regulation of ERK1/2 and Akt inactivates the caspase cascade, a proposition which is supported by inhibiting caspase-3 and caspase-9 activation [42,43]. In the present study hispidin increased the phosphorylation of Akt/GSK-3β and ERK1/2 but not p38 MAPK and JNK, which are reduced by H2O2 (Fig. 4).
Apurinic/apyrimidinic endonuclease1/redox factor-1 (Ape1/Ref-1) is essential for IL-21-induced signal transduction through ERK1/2 pathway
2012, Biochemical and Biophysical Research CommunicationsCitation Excerpt :Further study is needed for this point. Previous reports that showed MEK-ERK activity prevented IL-3 deprivation-induced cell death in BaF3 cells are consistent with our results [35,36]. MEK-ERK pathway plays pivotal roles in the development of various organs and in cell proliferation and survival.
Anti-apoptotic pro-survival effect of clotrimazole in a normothermic ischemia reperfusion injury animal model
2011, Journal of Surgical ResearchCitation Excerpt :In an experimental model of reduced size liver transplantation, Liang et al. also found that activation of the ERK1/2 pathway is associated with significantly less apoptosis in the liver [28]. ERK1/2 activation inhibits apoptosis through a conformational change in Bax required for its translocation to the mitochondria [29] and caspase-3 activation [30]. JNK is known to be stimulated in vivo after rat liver transplantation or partial hepatectomy [15, 16].
The powerful cardioprotective effects of urocortin and the corticotropin releasing hormone (CRH) family
2009, Biochemical PharmacologyCitation Excerpt :This results in it binding to the 14-3-3 protein, thereby preventing it from interacting with mitochondria, and thus conferring resistance against apoptosis [62]. Both MEK1/2 and PI3K are responsible for preventing procaspases 9 and 3 from being cleaved into their active forms [63,64]. Furthermore, chemical inhibitors of the PI3K pathway, such as wortmannin and LY294002, have been reported to block Ucn 1-mediated cardioprotection in both neonatal and adult cardiomyocytes [61].
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This work was supported in part by CREST of the Japan Science and Technology Corporation. Our laboratory at Tokyo Institute of Technology is supported by Shering-Plough Corporation.
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Abbreviations used: DTT, dithiothreitol; ERK, extracellular signal-regulated kinase; GM-CSF, granulocyte/macrophage colony-stimulating factor; IL-3, interleukin-3; MEK, mitogen-activated protein kinase/ERK kinase; PI3-K, phosphatidylinositol 3-kinase; PMSF, phenylmethylsulfonyl fluoride
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