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EndoG is an endonuclease with the unique ability to inactivate another endonuclease, DNase I, and to modulate the development of apoptosis.
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These data indicated the participation of EndoG in alternative mRNA splicing of the telomerase catalytic subunit hTERT, regulation of telomerase activity and determination of cell fate.
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Galectin-3-induced cell death in HIV-1-infected macrophages is most likely related to the translocation of Endo G from the cytoplasm to the nucleus.
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ndoG digests long non-coding RNA and produces 47-mer RNA oligonucleotide complementary to hTERT pre-mRNA exon 8 and intron 8 junction place. Interaction of 47-mer RNA oligonucleotide and hTERT pre-mRNA causes alternative splicing.
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Overexpression of EndoG in CD4+ T cells downregulated the expression of the active full-length hTERT variant and upregulated the inactive alternatively spliced variant.
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Overexpression of EndoG in capital ES, Cyrillicsmall a, Cyrilliccapital ES, Cyrillicsmall o, Cyrillic-2 cells downregulated the expression of active full-length hTERT variant and upregulated non-active spliced variant.
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EndoG is not a mediator of exogenous DNA clearance, but in non-physiological circumstances, it may nonspecifically cleave intracellular DNA regardless of its origin.
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These findings suggest that non-viral DNA vectors are also substrates for EndoG in its role in homologous recombination
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our study established a link between Endo G and mitochondrial function during cardiac hypertrophy
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Results show that BNIP3 interacts with the voltage-dependent anion channel (VDAC) to directly induce mitochondrial release and nuclear translocation of EndoG.
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Endonuclease G (EndoG), an apoptotic nuclease, as an essential factor for MLLbcr-specific DNA recombination after induction of replication stress.
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Ethyl gallate induces apoptosis of HL-60 cells by promoting the expression of caspases-8, -9, -3, apoptosis-inducing factor and endonuclease G.
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Data suggest that endonuclease G (EndoG) inhibitors have the potential to be utilized for amelioration of cell injuries in which participation of EndoG is essential.
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study demonstrate EndoG interacts with cellular Inhibitor of Apoptosis Protein 1 (cIAP1); results indicate IAPs interact and ubiquitinate EndoG via K63-mediated isopeptide linkages without affecting EndoG levels and EndoG-mediated cell death, suggesting EndoG ubiquitination by IAPs may serve as a regulatory signal independent of proteasomal degradation
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Using gene reporter assays, we show that promoter variations in 11 intrinsic apoptosis genes, including ADPRT, APAF1, BCL2, BAD, BID, MCL1, BIRC4, BCL2L1, ENDOG, YWHAB, and YWHAQ, influence promoter activity in an allele-specific manner.
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Data indicate that older muscles showed a 3-fold greater fraction of endonuclease G (a mitochondrial proapoptotic factor)-positive myonuclei.
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CHIP overexpression reduces EndoG levels, and results in reduced or no oxidative stress-induced cell death in cultured cancer cells.
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Endonuclease G mediates alpha-synuclein cytotoxicity during Parkinson's disease.
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These data indicate that HSV-1 UL12.5 deploys cellular proteins, including ENDOG and EXOG, to destroy mtDNA and contribute to a growing body of literature highlighting roles for ENDOG and EXOG in mtDNA maintenance.
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Conclude that EndoG and TOPO2a may actively participate in apoptotic chromatin degradation.
