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Endonuclease G

endonuclease G, EndoG
The protein encoded by this gene is a nuclear encoded endonuclease that is localized in the mitochondrion. The encoded protein is widely distributed among animals and cleaves DNA at GC tracts. This protein is capable of generating the RNA primers required by DNA polymerase gamma to initiate replication of mitochondrial DNA. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: PrP, bcl-2, Bax, caspase-3, Endo
Papers on endonuclease G
Effect of Superoxide Anion Scavenger on Rat Hearts with Chronic Intermittent Hypoxia.
Lee et al., Taiwan. In J Appl Physiol, Feb 2016
Superoxide anion scavenger decreased HYPOXIA-induced Fas ligand, Fas death receptors, Fas-associated death domain (FADD), activated caspase-8, and activated caspase-3 (Fas-dependent apoptotic pathway) as well as Bad, activated caspase-9 and activated caspase-3 (mitochondria-dependent apoptotic pathway), endonuclease G (EndoG), apoptosis-inducing factor (AIF) and TUNEL-positive apoptosis.
MGL Induces Nuclear Translocation of Endog and AIF in Caspase-Independent T Cell Death.
Wei et al., In Cell Mol Biol Lett, Dec 2015
Furthermore, MGL treatment triggers the translocation of endonuclease G (EndoG) and apoptosis-inducing factor (AIF) from the mitochondria to the nucleus.
Improved cellular thermotolerance in cloned Holstein cattle derived with cytoplasts from a thermotolerant breed.
Shen et al., Taiwan. In Theriogenology, Nov 2015
At the protein level, the relative abundances of apoptosis-inducing factor, B cell lymphoma 2-associated X protein, endonuclease G, cytochrome c, cysteinyl aspartate-specific proteinases 3, 8 and 9 in ear fibroblasts derived from SCNT-Yo-Hd cattle were significantly (P < 0.05) lower than those of cells derived from SCNT-Ho-Hd cattle after heat shock.
The p53 tumor suppressor protein protects against chemotherapeutic stress and apoptosis in human medulloblastoma cells.
Albanese et al., Washington, D.C., United States. In Aging (albany Ny), Oct 2015
The inhibition of p53 in the presence of VMY revealed increased late stage apoptosis, increased DNA fragmentation and increased expression of genes involved in apoptosis, including CAPN12 and TRPM8, p63, p73, BIK, EndoG, CIDEB, P27Kip1 and P21cip1.
Killing of cancer cells through the use of eukaryotic expression vectors harbouring genes encoding nucleases and ribonuclease inhibitor.
Glinka, Moscow, Russia. In Tumour Biol, May 2015
This review is focused on vectors bearing genes for nucleases such as deoxyribonucleases (caspase-activated DNase, deoxyribonuclease I-like 3, endonuclease G) and ribonucleases (human polynucleotide phosphorylase, ribonuclease L, α-sarcin, barnase), as well as vectors harbouring gene encoding ribonuclease inhibitor.
The role of excitotoxic programmed necrosis in acute brain injury.
Fujikawa, Los Angeles, United States. In Comput Struct Biotechnol J, 2014
Calpain I activation produces mitochondrial release of cytochrome c (cyt c), truncated apoptosis-inducing factor (tAIF) and endonuclease G (endoG), the lysosomal release of cathepsins B and D and DNase II, and inactivation of the plasma membrane Na(+)-Ca(2 +) exchanger, which add to the buildup of intracellular Ca(2 +).
Endonuclease G depletion may improve efficiency of first generation adenovirus vector DNA replication in HeLa cells.
Haj-Ahmad et al., Canada. In Cell Mol Biol (noisy-le-grand), 2014
In this study, we tried to increase the efficiency of Ad5 ΔE1,E3 DNA replication in the cervical carcinoma HeLa cells by using RNA interference (RNAi) to target endonuclease G (EndoG) whose depletion leads to an accumulation of cells in the G2/M transition.
Central roles of apoptotic proteins in mitochondrial function.
Prehn et al., Dublin, Ireland. In Oncogene, 2013
Cell stress stimuli can result in outer membrane permeabilization, after which mitochondria release numerous proteins involved in apoptotic signaling, including cytochrome c, apoptosis-inducing factor, endonuclease G, Smac/DIABLO and Omi/HtrA2.
[A pathophysiological role of cytochrome p450 involved in production of reactive oxygen species].
Shimamoto, Japan. In Yakugaku Zasshi, 2012
These results in the accumulation of mitochondrial BimEL, which then induces the release of cytochrome c and endonuclease G (EndoG).
Endonuclease G interacts with histone H2B and DNA topoisomerase II alpha during apoptosis.
Kozubek et al., Brno, Czech Republic. In Mol Cell Biochem, 2012
Conclude that EndoG and TOPO2a may actively participate in apoptotic chromatin degradation.
Oxidant stress, mitochondria, and cell death mechanisms in drug-induced liver injury: lessons learned from acetaminophen hepatotoxicity.
Ramachandran et al., Kansas City, United States. In Drug Metab Rev, 2012
In addition, the release of intermembrane proteins, such as apoptosis-inducing factor and endonuclease G, and their translocation to the nucleus, leads to nuclear DNA fragmentation.
Nonsynonymous single-nucleotide polymorphisms of the human apoptosis-related endonuclease--DNA fragmentation factor beta polypeptide, endonuclease G, and Flap endonuclease-1--genes show a low degree of genetic heterogeneity.
Yasuda et al., Izumo, Japan. In Dna Cell Biol, 2012
Data show that among the 13 SNPs in the 3 genes, only 3 were found to be polymorphic: R196K and K277R in the DFFB gene, and S12L in the EndoG gene, and all 6 SNPs in the FEN-1 gene were entirely monoallelic.
Endonuclease G is a novel determinant of cardiac hypertrophy and mitochondrial function.
Cook et al., London, United Kingdom. In Nature, 2011
present study has further established the link between mitochondrial dysfunction, reactive oxygen species and heart disease and has uncovered a role for Endog in maladaptive cardiac hypertrophy
The roles of AIF and Endo G in the apoptotic effects of benzyl isothiocyanate on DU 145 human prostate cancer cells via the mitochondrial signaling pathway.
Chung et al., Japan. In Int J Oncol, 2011
Benzyl isothiocyanate induces apoptosis in DU 145 cells through the release of AIF and Endo G from the mitochondria and also promotes caspase-3 activation.
EndoG links Bnip3-induced mitochondrial damage and caspase-independent DNA fragmentation in ischemic cardiomyocytes.
Sanchis et al., Lleida, Spain. In Plos One, 2010
These data establish a link between Bnip3 and EndoG-dependent, TUNEL-positive, DNA fragmentation in ischemic cardiomyocytes in the absence of caspases, defining an alternative cell death pathway in postmitotic cells.
Mechanisms of AIF-mediated apoptotic DNA degradation in Caenorhabditis elegans.
Xue et al., Boulder, United States. In Science, 2002
In addition, WAH-1 associated and cooperated with the mitochondrial endonuclease CPS-6/endonuclease G (EndoG) to promote DNA degradation and apoptosis.
Endonuclease G is an apoptotic DNase when released from mitochondria.
Wang et al., Dallas, United States. In Nature, 2001
This nuclease is endonuclease G (endoG), a mitochondrion-specific nuclease that translocates to the nucleus during apoptosis.
Mitochondrial endonuclease G is important for apoptosis in C. elegans.
Xue et al., Boulder, United States. In Nature, 2001
cps-6 encodes a homologue of human mitochondrial endonuclease G, and its protein product similarly localizes to mitochondria in C. elegans.
Primers for mitochondrial DNA replication generated by endonuclease G.
Ruiz-Carrillo et al., Québec, Canada. In Science, 1993
Endonuclease G (Endo G) is widely distributed among animals and cleaves DNA at double-stranded (dG)n.(dC)n
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