Cellular Inhibitor of Apoptosis Protein 1 ubiquitinates endonuclease G but does not affect endonuclease G-mediated cell death

Seo, Tae Woong; Lee, Ji Sun; Yoo, Soon Ji

doi:10.1016/j.bbrc.2014.08.047

Cited by 4 publications

(4 citation statements)

References 33 publications

(51 reference statements)

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“…We previously reported that cIAP1, an E3 ligase, binds and ubiquitinates EndoG without affecting intracellular levels of EndoG and EndoG‐mediated cell death [ 22 , 23 ]. Thus, we hypothesized that cIAP1 might be involved in the nuclear localization of EndoG through its Ring activity.…”

Section: Resultsmentioning

confidence: 99%

“…Moreover, cIAP1, a member of the Inhibitor of Apoptotic Proteins family, shares baculoviral IAP repeat (BIR) domains [ 22 ] and binds and ubiquitinates EndoG P199E and WT EndoG, and cIAP1 depletion decreases nuclear EndoG localization (Figs 3H–J and 4H,G ). Considering that EndoG binds to the BIR domains of cIAP1 [ 23 ], EndoG might interact with Survivin, a component of the CPC and a member of the IAP family with a single BIR domain. Therefore, we postulate that nuclear EndoG might augment the formation of CPC through its binding to AurB and potentially to Survivin.…”

Section: Discussionmentioning

confidence: 99%

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Nuclear endonuclease G controls cell proliferation in ovarian cancer

et al. 2023

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Ovarian cancer is characterized by a high degree of genetic heterogeneity. Platinum‐based chemotherapy and some gene‐targeted therapies have shown limited treatment efficacy due to toxicity and recurrence, and thus, it is essential to identify additional therapeutic targets based on an understanding of the pathological mechanism. Here, we report that endonuclease G, which exhibits altered expression in ovarian cancer, does not function as a cell death effector that digests chromosomal DNA in ovarian cancer. Endonuclease G is modulated by intracellular reactive oxygen species dynamics and plays a role in cell proliferation in ovarian cancer, suggesting that targeting endonuclease G alone or in combination with other antitumor agents may have the potential for development into a treatment for endonuclease G‐overexpressing cancers, including ovarian cancer.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Nuclear endonuclease G controls cell proliferation in ovarian cancer

et al. 2023

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“…In еpithеliаl cеlls, thе nuclеаr locаlizаtion of ЕndoG lеаds thеm to sеnеscеncе [ 66 ]. In аddition to DNА dеgrаdаtion, ЕndoG аlso stimulаtеs inhibitors of аpoptosis protеins (IАPs) to tаrgеt protеins for protеаsomаl dеgrаdаtion [ 74 ].…”

Section: Regulatory Mechanisms For Htert Pre-mrna Asmentioning

confidence: 99%

Alternative Splicing of Human Telomerase Reverse Transcriptase (hTERT) and Its Implications in Physiological and Pathological Processes

Plyasova

Zhdanov

2021

Biomedicines

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Alternative splicing (AS) of human telomerase catalytic subunit (hTERT, human telomerase reverse transcriptase) pre-mRNA strongly regulates telomerase activity. Several proteins can regulate AS in a cell type-specific manner and determine the functions of cells. In addition to being involved in telomerase activity regulation, AS provides cells with different splice variants that may have alternative biological activities. The modulation of telomerase activity through the induction of hTERT AS is involved in the development of different cancer types and embryos, and the differentiation of stem cells. Regulatory T cells may suppress the proliferation of target human and murine T and B lymphocytes and NK cells in a contact-independent manner involving activation of TERT AS. This review focuses on the mechanism of regulation of hTERT pre-mRNA AS and the involvement of splice variants in physiological and pathological processes.

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“…The extrinsic and intrinsic pathways are initiated by specific ligands or various intracellular stimuli that activate effector caspases, ultimately fragmenting DNA and inducing cell death ( 14 ). Each pathway is involved in radiation-induced apoptosis ( 15 ). Inhibitor of apoptosis proteins (IAPs) are a family of endogenous anti-apoptotic proteins characterized by one or several baculoviral IAP repeat (BIR) domains.…”

Section: Introductionmentioning

confidence: 99%

Novel recombinant protein FlaA N/C increases tumor radiosensitivity via NF-κB signaling in murine breast cancer cells

Fan

et al. 2016

Oncology Letters

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The recombinant protein flagellin A (FlaA) N/C, derived from the flagellin protein of Legionella pneumophila, has been shown to increase the expression of cytoprotective cytokines, activate the nuclear factor-κB (NF-κB) signaling pathway, and increase the survival of mice following total body irradiation. Determi ning whether FlaA N/C has a sensitizing effect on tumor radiation or a direct tumoricidal effect is critical for its application as an effective radiation protection agent. The present study investigated the molecular mechanism underlying the tumor radiosensitivity of FlaA N/C. FlaA N/C was found to increase tumor apoptosis and autophagy, regulate the cell cycle and increase radiosensitivity in 4T1 tumor cells. Furthermore, FlaA N/C was found to promote radiosensitivity by activating NF-κB signaling. Finally, the present study analyzed FlaA N/C-enhanced radiosensitivity in animal models, and FlaA N/C was found to significantly prolong the survival period of mice after total body radiation. This indicates that FlaA N/C might be a novel radiation sensitizer in tumor radiation therapy.

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Cellular Inhibitor of Apoptosis Protein 1 ubiquitinates endonuclease G but does not affect endonuclease G-mediated cell death

Cited by 4 publications

References 33 publications

Nuclear endonuclease G controls cell proliferation in ovarian cancer

Nuclear endonuclease G controls cell proliferation in ovarian cancer

Alternative Splicing of Human Telomerase Reverse Transcriptase (hTERT) and Its Implications in Physiological and Pathological Processes

Novel recombinant protein FlaA N/C increases tumor radiosensitivity via NF-κB signaling in murine breast cancer cells

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