Browse our anti-Endonuclease G (ENDOG) Antibodies

Human Endonuclease G (ENDOG) interaction partners

1. EndoG is an endonuclease with the unique ability to inactivate another endonuclease, DNase I, and to modulate the development of apoptosis.

2. 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.

3. 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.

4. 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.

5. Overexpression of EndoG in CD4+ T cells downregulated the expression of the active full-length hTERT variant and upregulated the inactive alternatively spliced variant.

6. 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.

7. EndoG is not a mediator of exogenous DNA clearance, but in non-physiological circumstances, it may nonspecifically cleave intracellular DNA regardless of its origin.

8. These findings suggest that non-viral DNA vectors are also substrates for EndoG in its role in homologous recombination

9. our study established a link between Endo G and mitochondrial function during cardiac hypertrophy

10. Results show that BNIP3 interacts with the voltage-dependent anion channel (VDAC) to directly induce mitochondrial release and nuclear translocation of EndoG.

11. Endonuclease G (EndoG), an apoptotic nuclease, as an essential factor for MLLbcr-specific DNA recombination after induction of replication stress.

12. Ethyl gallate induces apoptosis of HL-60 cells by promoting the expression of caspases-8, -9, -3, apoptosis-inducing factor and endonuclease G.

13. 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.

14. 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

15. 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.

16. Data indicate that older muscles showed a 3-fold greater fraction of endonuclease G (a mitochondrial proapoptotic factor)-positive myonuclei.

17. CHIP overexpression reduces EndoG levels, and results in reduced or no oxidative stress-induced cell death in cultured cancer cells.

18. Endonuclease G mediates alpha-synuclein cytotoxicity during Parkinson's disease.

19. 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.

20. Conclude that EndoG and TOPO2a may actively participate in apoptotic chromatin degradation.

Mouse (Murine) Endonuclease G (ENDOG) interaction partners

1. These results support the involvement of redox signaling in the control of cardiomyocyte growth by ENDOG and suggest a pathway relating mtDNA content to the regulation of cell growth probably involving humanin, which prevents reactive oxygen radicals accumulation and hypertrophy induced by Endog deficiency.

2. Deficiency of AKT2 in myocardium results in diminished MEF2A abundance, which induced decreased size of cardiomyocytes. We additionally confirmed that EndoG, which is also regulated by AKT2, is a suppressor of MEF2A in myocardium.

3. increased browning of white adipose tissue elicited by the lack of EndoG was associated with a better glucose tolerance and reduced fat mass

4. This study demonistated that Endonuclease G knockout mice reveals a new putative molecular player in the regulation of anxiety.

5. These findings determine a role for EndoG in the generation of Switch region double-strand DNA breaks and class switch DNA recombination.

6. EndoG is essential during early embryogenesis and plays a critical role in normal apoptosis and nuclear DNA fragmentation

7. endonuclease G is essential for embryonic survival, but not through a mitochondrial or apoptosis function

8. These data suggest that the early nuclear translocation of endoG occurs and could induce DNA fragmentation in the ischemic brain after cerebral ischemia.

9. EndoG null mice are viable and develop to adulthood with no obvious abnormalities, suggesing that EndoG is not essential for early embryogenesis and apoptosis.

10. Overexpression of DNase I in cultured mouse tubular epithelial cells also induced EndoG. Both DNase I and EndoG mediate cisplatin injury to tubular epithelial cells.

11. high levels of EndoG were found in adult liver, heart, muscle & to a lesser extent, brain & kidney; EndoG had little or no expression in adult spleen & in embryonic organs at E13.5 stage

12. The translocation of EndoG to the nucleus of neurons in the infarct implicates EndoG in ischemic neuronal degeneration after permanent MCA occlusion in mice.

13. Mouse EndoG without the mitochondrial localization signal (amino-acid residues 1-43) was successfully overexpressed, purified and crystallized using a microbatch method under oil

14. Data demonstrate the importance of DNase I and EndoG in host cell defense against gene and RNA delivery to renal tubular epithelial cells in vitro.

15. Endo G has a role in neuronal cell death as a result of oxidative stress.

Cow (Bovine) Endonuclease G (ENDOG) interaction partners

1. Results describe the mechanism of catalysis and substrate binding by the apoptotic mitochondrial nuclease EndoG, which belongs to the large family of DNA/RNA non-specific betabetaalpha-Me-finger nucleases.