ENDOG (Endonuclease G) is a 28kDa mitochondria-localized protein mapped to human chromosome 9q34.1. However, in presence of certain conditions it can translocate to the nucleus through the BNIP3 (Bcl-2/adenovirus E1B 19kDa protein-interacting protein 3) cell death pathway.
Immunogen
EndoG antibody was raised with a synthetic peptide corresponding to 15 amino acids near the amino terminus of human EndoG.
Application
Anti-EndoG antibody produced in rabbit is suitable for immunohistochemistry, indirect ELISA and western blot analysis.
Biochem/physiol Actions
ENDOG (Endonuclease G) is a mitochondrial apoptotic DNase involved in the BNIP3 (Bcl-2/adenovirus E1B 19kDa protein-interacting protein 3) cell death pathway. During mitochondrial release and nuclear translocation of EndoG, BNIP3 interacts with the voltage-dependent anion channel (VDAC) to facilitate the process in the nucleus, it cleaves chromatin apoptotic DNA without the need of caspase activity. ENDOG causes DNA fragmentation during and after apoptosis. It is linked with cardiac hypertrophy and Parkinson′s disease.
Features and Benefits
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Linkage
The action of this antibody can be blocked using blocking peptide SBP3500213.
BNIP3 is a proapoptotic protein that induces cell death through a mitochondria-mediated pathway. We reported previously that mitochondrial localization of BNIP3 and translocation of EndoG from mitochondria to the nucleus are critical steps of the BNIP3 pathway. It is not
Apoptotic endonuclease G (EndoG) is responsible for DNA fragmentation both during and after cell death. Previous studies demonstrated that genetic inactivation of EndoG is cytoprotective against various pro-apoptotic stimuli; however, specific inhibitors for EndoG are not available. In this study
By using a PCR-based screening of a somatic cell hybrid panel and FISH, we have assigned the loci of mitochondrial single-stranded DNA-binding protein (SSBP), mitochondrial transcription factor A (TCF6), and mitochondrial endonuclease G (ENDOG) genes to human chromosomes 7q34, 10q21
Genotoxic insult causes nuclear and mitochondrial DNA damages with macroautophagy/autophagy induction. The role of mitochondrial DNA (mtDNA) damage in the requirement of autophagy for nuclear DNA (nDNA) stability is unclear. Using site-specific DNA damage approaches, we show that specific nDNA
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