Disease relevance of Endog

• Early nuclear translocation of endonuclease G and subsequent DNA fragmentation after transient focal cerebral ischemia in mice [1].
• PPAR-alpha ligand ameliorates acute renal failure by reducing cisplatin-induced increased expression of renal endonuclease G [2].

High impact information on Endog

• Endonuclease G is required for early embryogenesis and normal apoptosis in mice [3].
• Endonuclease G (EndoG) is a nuclear-encoded mitochondrial protein reported to be important for both nuclear DNA fragmentation during apoptosis and mitochondrial DNA replication [3].
• Endonuclease G (endo G) is one of the most abundant nucleases in eukaryotic cells [4].
• The mitochondrial protein, endonuclease G (EndoG), is one of the endonucleases implicated in DNA fragmentation during apoptosis [5].
• Endonuclease G: a mitochondrial protein released in apoptosis and involved in caspase-independent DNA degradation [6].

Biological context of Endog

• These data indicate that endonuclease G may be involved in CAD-independent DNA fragmentation during cell death pathways in which truncated Bid is generated [6].
• Withdrawal of IL-3 caused down-regulation of Bcl-xL, resulting in a drop in mitochondrial membrane transition potential followed by the release of cytochrome c and endonuclease G from mitochondria [7].
• We previously found that endonuclease G (EndoG) plays an important role in both normal apoptosis in vivo and in pre-implantation embryogenesis [8].

Anatomical context of Endog

• We investigated whether the endonuclease G (endoG) translocated from mitochondria to nucleus after transient focal cerebral ischemia (tFCI), thereby contributed to subsequent DNA fragmentation [1].
• The translocation of AIF and endonuclease G correlated with mitochondrial dysfunction as indicated by the progressive loss of the mitochondrial membrane potential (measured with the JC-1 assay) and the appearance of nuclear DNA fragments in the cytosol (determined by an anti-histone ELISA) [9].
• Using immunofluorescence microscopy, it was shown that in primary cultured mouse hepatocytes, endonuclease G and AIF translocated to the nucleus between 3 and 6 h after exposure to 5 mM AAP [9].

Associations of Endog with chemical compounds

• Pretreatment with 20mM N-acetylcysteine prevented mitochondrial dysfunction, the nuclear translocation of endonuclease G and AIF, and the nuclear DNA fragmentation [9].
• At day 4 after cisplatin injection mRNA, protein levels and enzyme activity of proapoptotic renal endonuclease G (Endo G) were increased compared with saline-treated mice [2].

Other interactions of Endog

• The caspase-independent apoptosis is mediated by the translocation of endonuclease G from mitochondria into nuclei [7].
• The in vivo occurrence of endonuclease G release from mitochondria during apoptosis was confirmed in the liver from mice injected with agonistic anti-Fas antibody and is completely prevented in Bcl-2 transgenic mice [6].
• This DNAse activity was identified by mass spectrometry as endonuclease G, an abundant 30 kDa protein released from mitochondria under apoptotic conditions [6].
• Uracil DNA glycosylase and endonuclease G activities did not change with age in nucleus or mitochondria [10].
• In contrast, in PPAR-alpha-null mice treated with the ligand and cisplatin, Endo G protein expression was not reduced and this was accompanied by lack of protection of kidney function [2].

Analytical, diagnostic and therapeutic context of Endog

• In situ hybridization and immunohistochemical studies localized the increased expression of Endo G mRNA to the cytosolic compartment and Endo G protein to the nuclear compartment of proximal tubules in cisplatin-treated mice [2].

References