ENDOG Antibodies

ENDOG (Endonuclease G) is a Protein Coding gene. Diseases associated with ENDOG include Drug-Induced Hearing Loss. Among its related pathways are Apoptotic Pathways in Synovial Fibroblasts and Apoptosis Modulation and Signaling. Gene Ontology (GO) annotations related to this gene include nucleic acid binding and endonuclease activity. An important paralog of this gene is EXOG.

Based on more than 13 years of development, CUSABIO has established a mature and efficient system for antibody preparation. The following ENDOG antibodies are manufactured under the system.
These ENDOG antibodies are featured with high specificity & sensitivity and wide species reactivity. In order to meet different requirements, CUSABIO is trying to include more antibody types (Monoclonal, Polyclonal, Recombinant, etc) and do more validations so that the researchers can break limits and discover more. In addition, CUSABIO also provides ENDOG antibody custom service in case you have specific needs for your research.

ENDOG Antibodies Catalog

ENDOG Antibodies for Homo sapiens (Human)

ENDOG Background

Endonuclease G (ENDOG) is one of the nucleases involved in nucleosomal fragmentation of DNA during apoptosis [1]. Genetically engineered mice lacking DFF45 or site-directed mutants of DFF45 lacking the caspase-cleavage site, still retain residual DNA fragmentation and are normal inphenotype [1][2]. These discoveries contributed to the identification and characterization of ENDOG. The ENDOG is resided within mitochondria and translocate to the nucleus upon apoptotic stimuli such as truncated Bid (tBid), tumor-necrosis factor-alpha (TNF-α), and UV irradiation [1][3]. Once released from mitochondria, ENDOG cleaves chromatin DNA into nucleosomal fragments independently of caspases. ENDOG null mice are viable and develop to adulthood with no obvious aberrations [4]. Fibroblasts generated from the EndoG null mice show no difference in susceptibility when induced to cell death by various intrinsic and extrinsic apoptotic stimuli [4]. Additionally, EndoG null mice are equally sensitive to excitotoxic stress [4]. David KK et al. therefore concluded that ENDOG is not essential for embryogenesis and apoptosis [4]. In addition to its dispensable role in apoptosis, EndoG acts as a homodimer that is thought to be implicated in mitochondrial DNA replication [5] with important roles in recombination and repair [6][7].

[1] Li LY, Luo X and Wang X. Endonuclease G is an apoptotic DNase when released from mitochondria [J]. Nature 2003, 12: 95–99.
[2] Zhang J, Liu X, et al. Resistance to DNA fragmentation and chromatin condensation in mice lacking the DNA fragmentation factor 45 [J]. Proc. Natl. Acad. Sci. 1998, USA 95: 12480–12485.
[3] van Loo G, Schotte P, et al. Endonuclease G: a mitochondrial protein released in apoptosis and involved in caspase-independent DNA degradation [J]. Cell Death Differ. 2001, 8: 1136–1142.
[4] David KK, Sasaki M, et al. EndoG is dispensable in embryogenesis and apoptosis [J]. Cell Death Differ. 2006 Jul;13(7):1147-55.
[5] Cote J and Ruiz-Carrillo A. Primers for mitochondrial DNA replication generated by endonuclease G [J]. Science 1993, 261: 765–769.
[6] Zassenhaus HP and Denniger G. Analysis of the role of the NUC1 endo/exonuclease in yeast mitochondrial DNA recombination [J]. Curr. Genet. 1994, 25: 142–149.
[7] Ikeda S and Ozaki K. Action of mitochondrial endonuclease G on DNA damaged by L-ascorbic acid, peplomycin, and cis-diamminedichloroplatinum (II) [J]. Biochem. Biophys. Res. Commun. 1997, 235: 291–294.

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