Cleavage of 14-3-3 Protein by Caspase-3 Facilitates Bad Interaction with Bcl-x(L) during Apoptosis

Jung, Won Seok; Kim, Doo Yeon; La, Muhnho; Kim, Doyeun; Meadows, Gary G.; Joe, Cheol O.

doi:10.1074/jbc.m213098200

Cited by 70 publications

(65 citation statements)

References 34 publications

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“…In the apoptotic signaling cascade, the resultant release of Bad leads to its translocation to the mitochondrial outer membrane, where Bad heterodimerizes with Bcl-xL. In fact, one recent study reported that caspase-3 could cleave 14-3-3⑀ at Asp-238 in yeast EGY48 cells (38). However, it has yet to be investigated at which site caspase-3 cleaves the Bad⅐14-3-3 complex in cardiomyocytes.…”

Section: Discussionmentioning

confidence: 99%

Kallikrein/Kinin Protects against Myocardial Apoptosis after Ischemia/Reperfusion via Akt-Glycogen Synthase Kinase-3 and Akt-Bad·14-3-3 Signaling Pathways

Yin

Chao

2005

Journal of Biological Chemistry

109

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Our previous study has shown that human tissue kallikrein protected against ischemia/reperfusion-induced myocardial injury. In the present study, we investigated the protective role of local kallikrein gene delivery in ischemia/reperfusion-induced cardiomyocyte apoptosis and its signaling mechanisms in promoting cardiomyocyte survival. Adenovirus carrying the human tissue kallikrein gene was delivered locally into the heart using a catheter-based technique. Expression and localization of recombinant human kallikrein in rat myocardium after gene transfer were determined immunohistochemically. Kallikrein gene delivery markedly reduced reperfusion-induced cardiomyocyte apoptosis identified by both in situ nick end-labeling and DNA fragmentation. Delivery of the kallikrein gene increased phosphorylation of Src, Akt, glycogen synthase kinase (GSK)-3␤, and Bad(Ser-136) but reduced caspase-3 activation in rat myocardium after reperfusion. The protective effect of kallikrein on apoptosis and its signaling mediators was blocked by icatibant and dominant-negative Akt, indicating a kinin B2 receptor-Akt-mediated event. Similarly, kinin or transduction of kallikrein in cultured cardiomyocytes promoted cell viability and attenuated apoptosis induced by hypoxia/reoxygenation. The effect of kallikrein on cardiomyocyte survival was blocked by dominant-negative Akt and a constitutively active mutant of GSK-3␤, but it was facilitated by constitutively active Akt, catalytically inactive GSK-3␤, lithium, and caspase-3 inhibitor. Moreover, kallikrein promoted Bad⅐14-3-3 complex formation and inhibited Akt-GSK-3␤-dependent activation of caspase-3, whereas caspase-3 administration caused reduction of the Bad⅐14-3-3 complex, indicating an interaction between Akt-GSK-caspase-3 and Akt-Bad⅐14-3-3 signaling pathways. In conclusion, kallikrein/kinin protects against cardiomyocyte apoptosis in vivo and in vitro via Akt-Bad⅐14-3-3 and Akt-GSK-3␤-caspase-3 signaling pathways.

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Section: Discussionmentioning

confidence: 99%

Kallikrein/Kinin Protects against Myocardial Apoptosis after Ischemia/Reperfusion via Akt-Glycogen Synthase Kinase-3 and Akt-Bad·14-3-3 Signaling Pathways

Yin

Chao

2005

Journal of Biological Chemistry

109

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“…ESR1 might activate caspases-8, -9 and -3 and induce tumor cell apoptosis, it also showed the downregulation of β-catenin signaling implicating the suppression of proliferation and metastasis of tumor cells (31,32). The cleavage of YWHAE by caspase-3 during apoptosis might contribute to cell death by preventing the association of YWHAE with Bad (33). The key event during apoptosis that is common to all pathways is the activation of caspases.…”

Section: Discussionmentioning

confidence: 99%

The expression and functional characterization associated with cell apoptosis and proteomic analysis of the novel gene MLAA-34 in U937 cells

Zhang

et al. 2012

Oncology Reports

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Abstract. MLAA-34 is a novel acute monocytic leukemia (M5)-associated antigen (MLAA) that plays a role in the apoptosis of U937 cells. However, the expression and molecular mechanism of MLAA-34 in U937 cells remain largely unclear. Here, we utilized three strategies to gain insight into the expression and molecular functions of MLAA-34 and to identify its interacting proteins and pathways involved in the fine-tuning of the MLAA-34 response. Western blot analysis was performed to assess the expression of MLAA-34 in 41 cell lines and five mixed cell types, which revealed that MLAA-34 is most strongly expressed in U937 cells. Immunostaining indicated that MLAA-34 is localized in the cytoplasm and cell membrane. Furthermore, lentivirus-mediated overexpression of MLAA-34 in the U937 cell line led to significant suppression of apoptosis and increased the potential of tumorigenicity. Co-immunoprecipitation (Co-IP), shotgun and bioinformatic analysis identified 256 proteins and 225 of them were annotated by gene ontology categories. This analysis revealed 71 proteins involved in cell apoptosis or proliferation of biological processes and signaling pathways. Moreover, the effect of MLAA-34 apoptosis may be through interaction with the Ras, Wnt, calcium and chemokine signaling pathways and thirteen of the annotated proteins may interact with MLAA-34 and participate in carcinogenesis directly. This study provides a basis for a better understanding of the molecular mechanism and proteomics in the inhibition of apoptosis by MLAA-34 in U937 cells and indicates that MLAA-34 may be a potential candidate for the early diagnosis and therapeutic application of M5.

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“…Furthermore, BAD, a member of the BCL-2 family of proapoptotic genes, maps to 11q13.1, a region of frequent copy number loss. This protein is inhibited by the 14-3-3⑀ protein but promotes cell death on its release, which occurs via the cleavage of 14-3-3⑀ by caspase-3 (53). The tumor suppressor CDKN2A (P16-INK4A), an activator of caspase-3-mediated apoptosis (54), is located within the region of deletion on chromosome 9p21-p22.…”

Section: Discussionmentioning

confidence: 99%

Array Comparative Genomic Hybridization Analysis of Colorectal Cancer Cell Lines and Primary Carcinomas

et al. 2004

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Array comparative genomic hybridization, with a genome-wide resolution of ϳ1 Mb, has been used to investigate copy number changes in 48 colorectal cancer (CRC) cell lines and 37 primary CRCs. The samples were divided for analysis according to the type of genomic instability that they exhibit, microsatellite instability (MSI) or chromosomal instability (CIN). Consistent copy number changes were identified, including gain of chromosomes 20, 13, and 8q and smaller regions of amplification such as chromosome 17q11.2-q12. Loss of chromosome 18q was a recurrent finding along with deletion of discrete regions such as chromosome 4q34-q35. The overall pattern of copy number change was strikingly similar between cell lines and primary cancers with a few obvious exceptions such as loss of chromosome 6 and gain of chromosomes 15 and 12p in the former. A greater number of aberrations were detected in CIN؉ than MSI؉ samples as well as differences in the type and extent of change reported. For example, loss of chromosome 8p was a common event in CIN؉ cell lines and cancers but was often found to be gained in MSI؉ cancers. In addition, the target of amplification on chromosome 8q appeared to differ, with 8q24.21 amplified frequently in CIN؉ samples but 8q24.3 amplification a common finding in MSI؉ samples. A number of genes of interest are located within the frequently aberrated regions, which are likely to be of importance in the development and progression of CRC.

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Cleavage of 14-3-3 Protein by Caspase-3 Facilitates Bad Interaction with Bcl-x(L) during Apoptosis

Cited by 70 publications

References 34 publications

Kallikrein/Kinin Protects against Myocardial Apoptosis after Ischemia/Reperfusion via Akt-Glycogen Synthase Kinase-3 and Akt-Bad·14-3-3 Signaling Pathways

Kallikrein/Kinin Protects against Myocardial Apoptosis after Ischemia/Reperfusion via Akt-Glycogen Synthase Kinase-3 and Akt-Bad·14-3-3 Signaling Pathways

The expression and functional characterization associated with cell apoptosis and proteomic analysis of the novel gene MLAA-34 in U937 cells

Array Comparative Genomic Hybridization Analysis of Colorectal Cancer Cell Lines and Primary Carcinomas

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