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Depletion of endonuclease G selectively kills polyploid cells. Paper-13213945.
Endonuclease G is an apoptotic DNase when released from mitochondria. Paper-9017714.
Mitochondrial endonuclease G is important for apoptosis in C. elegans. Paper-9017713.
Increased expression of endonuclease G in gastric and colorectal carcinomas. Paper-12910306.
Endonuclease G: a role for the enzyme in recombination and cellular proliferation. Paper-12038152.
Endonuclease G expression in thalamic reticular nucleus after global cerebral ischemia. Paper-12965972.
Mitochondrial Endonuclease G function in apoptosis and mtDNA metabolism: a historical perspective. Paper-10957159.
Purification, crystallization and data collection of the apoptotic nuclease endonuclease G. Paper-13744593.
Decreased expression of endonuclease G (EndoG), a pro-apoptotic protein, in hepatocellular carcinomas. Paper-12921895.
We conclude that endonuclease G is important for the viability of polyploid mammalian and yeast cells. Paper-13213945.
Endonuclease G, a candidate human enzyme for the initiation of genomic inversion in herpes simplex type 1 virus. Paper-9163654.
AIMS: Endonuclease G (EndoG) is a mitochondrial protein that plays a role in DNA fragmentation during apoptosis. Paper-12910306.
However, endonuclease-G released from mitochondria with the decreased mitochondrial membrane potential was shown. Paper-13315370.
In addition, a caspase-independent pathway indicated by endonuclease G also contributed to apoptosis caused by 5-OH-HxMF. Paper-13309005.
This nuclease is endonuclease G (endoG), a mitochondrion-specific nuclease that translocates to the nucleus during apoptosis. Paper-9017714.
Endonuclease G (endoG), which predominantly resides in mitochondria, accounts for a large part of this nuclease activity. Paper-9271449.
Basal rates of release of cytochrome c and endonuclease G in SS mitochondria were 3.5- to 7-fold higher from senescent animals. Paper-12702083.
Endonuclease G (endoG) is released from mitochondria during apoptosis and is in part responsible for internucleosomal DNA cleavage. Paper-8891880.
Besides its role in apoptosis execution, we have recently shown that depletion of endonuclease G leads to necrotic cell death in yeast. Paper-13213945.
Endonuclease G (EndoG) is located in mitochondria yet translocates into the nucleus of apoptotic cells during human degenerative diseases. Paper-12437075.
These results suggest that PKC alpha inhibitor safingol induces an endonuclease G- mediated apoptosis in a caspase-independent manner. Paper-11348738.
Endonuclease G is a mitochondrial protein implicated in DNA fragmentation during apoptosis in cell types ranging from fungi to mammals. Paper-12666629.
Up-regulation of Bax and endonuclease G, and down-modulation of Bcl-XL involved in cardiotoxin III-induced apoptosis in K562 cells. Paper-12210554.
Induction of endonuclease G- mediated apopotosis in human oral squamous cell carcinoma cells by protein kinase C inhibitor safingol. Paper-11348738.
Here we provide evidence for AIF and Endo G mitochondrio-nuclear relocation in both cases, as a component of caspase-independent apoptosis pathways. Paper-13698404.
High extracellular KCl also attenuated translocation of apoptosis-inducing factor ( AIF) and endonuclease G (EndoG) from mitochondria to nuclei. Paper-12296753.
Bioinformatic and image analyses of the cellular localization of the apoptotic proteins endonuclease G, AIF, and AMID during apoptosis in human cells. Paper-13282978.
Induction of apoptosis of detached oral squamous cell carcinoma cells by safingol. Possible role of Bim, focal adhesion kinase and endonuclease G. Paper-13622535.
Endonuclease G immunoreactivity increased in the cytoplasm 12 h after ischemia and was translocated to the nucleus of parvalbumin(+) neurons after 24 h. Paper-12965972.
These results suggest that Bim, Bcl-xL, FAK and endonuclease G are involved in safingol- induced apoptosis of detached oral SCC cells. Paper-13622535.
For the first time we elucidate that, caspase-independent activation of a novel effector molecule, endonuclease G (LdEndoG), mediates BLN-induced cell death. Paper-12948128.
Psychomotor disturbance was assessed by the CORE measure and by seven classical endogeneity symptoms of melancholia which, when summed, created a ENDOG score. Paper-8928785.
Endonuclease G is a mitochondrial enzyme, known to be translocated to the nucleus after transient focal cerebral ischemia and contribute to DNA degradation. Paper-12965972.
Another apoptogenic factor endonuclease G, but not apoptosis-inducing factor ( AIF), was also released from mitochondria and translocated to the nucleus. Paper-11348738.
Based on these findings, we propose that endonuclease G initiates the a sequence-mediated inversion of the L and S components during HSV-1 DNA replication. Paper-9163654.
We have found that galectin-1 binding to human T cell lines triggered rapid translocation of endonuclease G from mitochondria to nuclei. Paper-10605424.
A novel analysis of time-lapse fluorescence image data during staurosporine-induced apoptosis revealed nuclear translocation only for endonuclease G and AIF. Paper-13282978.
Mutagenesis identifies the critical amino acid residues of human endonuclease G involved in catalysis, magnesium coordination, and substrate specificity. Paper-13656692.
Consistently, conditional knockdown of mammalian endonuclease G selectively kills tetraploid but not diploid clones of the human HCT116 colon carcinoma cell line. Paper-13213945.
Smac release from mitochondria was induced in both cell types, but release of apoptosis-inducing factor and endonuclease G was detected only in TK6 cells. Paper-10264419.
We have demonstrated that endonuclease G activities are not detectable among the proteins released from isolated mitochondria by hNoxa but are detectable in that by tBid. Paper-11988438.
Endonuclease G expression and enhanced production of reactive oxygen species were detected in 7beta-hydroxycholesterol treated cells, but not with 7beta-hydroxysitosterol. Paper-13097660.
ABSTRACT: BACKGROUND: Endonuclease G (EndoG), a member of DNA/RNA nonspecific betabetaalpha-Me-finger nucleases, is involved in apoptosis and normal cellular proliferation. Paper-13656692.
Subsequent studies however, established that this Endonuclease G activity was identical to the well known, major endonuclease activity isolated from mitochondria of several species. Paper-10957159.
Caspase-independent death of human osteosarcoma cells by flavonoids is driven by p53- mediated mitochondrial stress and nuclear translocation of AIF and endonuclease G. Paper-13282980.
Cisplatin treatment induced reactive oxygen species (ROS) generation, loss of the mitochondrial membrane potential (MMP) and nuclear translocation of endonuclease G (EndoG). Paper-12658619.
Caspase-independent apoptosis in Friend's erythroleukemia cells: role of mitochondrial ATP synthesis impairment in relocation of apoptosis-inducing factor and endonuclease G. Paper-13698404.
We have developed a hypoxia-inducible gene therapy approach for the expression of the mature form of human endonuclease G to facilitate cell death in hypoxic regions of the tumor. Paper-12992492.
More recently, it has been discovered that in response to apoptotic stimuli, mitochondria can also release caspase-independent cell death effectors such as AIF and Endonuclease G. Paper-10404671.
EST and genome sequencing provides evidence for the presence of endonuclease G, AIF, HtrA/ Omi and Smac/ DIABLO in Xenopus laevis and tropicalis. Paper-13162358.
Other released mitochondrial proteins include apoptosis-inducing factor ( AIF) and endonuclease G, both of which contribute to apoptotic nuclear DNA damage in a caspase-independent way. Paper-10404676.
Evidence of apoptosis was associated with overexpression of the heart mitochondrial voltage-dependent anion channel-2 protein and endonuclease G in tissue specimens from dogs with induced DCM. Paper-12116661.
A mechanistic analysis demonstrated that CTX III-induced apoptotic cell death was accompanied by up-regulation of both Bax and endonuclease G ( Endo G), and downregulation of Bcl-X(L). Paper-12210554.
Inhibition of K(+) efflux prevents mitochondrial dysfunction, and suppresses caspase-3-, apoptosis-inducing factor-, and endonuclease G-mediated constitutive apoptosis in human neutrophils. Paper-12296753.
We excluded the participation of several mitochondrial factors possibly involved in caspase-independent cell death such as apoptosis-inducing factor, endonuclease G, and reactive oxygen species. Paper-10208609.
The introduction of siRNA against PKCalpha into SAS cells resulted in an increase of Bim, a decrease of Bcl-xL, the translocation of endonuclease G, and a decrease in the phosphorylation of FAK. Paper-13622535.
Release of cytochrome c and SMAC, but not AIF or endonuclease G, occurred in the absence of caspase activity and correlated with the onset of apoptosis and loss of clonogenic potential. Paper-11349088.
Endonuclease G ( Endo G) is a nuclease of prokaryotic lineage found in the mitochondria of vertebrates that has been suggested to play a role in mitochondrial DNA (mtDNA) replication. Paper-1187298.
However, 7beta-hydroxycholesterol exhibited a specific enhancement of oxidative stress and of endonuclease G expression despite its closely related chemical structure with 7beta-hydroxysitosterol. Paper-13097660.
4-OOH-CY treatment induced reactive oxygen species production, upregulation of Bax, and nuclear relocation of the mitochondrial factors apoptosis-inducing factor ( AIF) and endonuclease G (EndoG). Paper-12687929.
Reduction of crn-1 activity by RNA interference resulted in cell death phenotypes similar to those displayed by a mutant lacking the mitochondrial endonuclease CPS-6/ endonuclease G. Paper-9770814.
HD-COS is produced from NCC by the action of Endo-G, whereas LD-COS is produced by exo-glucanase (Exo-G). beta-Glucosidase (beta-G) hydrolyzes LD-COS to produce cellobiose, but it does not hydrolyze HD-COS. Paper-13523712.
DNA degradation is also induced by AIF and endonuclease G, which are both released from mitochondria upon death stimuli but do not require prior processing by caspases for their DNase activity. Paper-9187439.
In the nucleus of astroglia, Endonuclease G was expressed after 2 days with an apoptotic-like morphology and the number of Endonuclease G-expressing astroglia increased during the later time points. Paper-12965972.
Stable MDA-MB-435 cells expressing the chimeric therapeutic gene under 1% O2 showed an increase in stable HIF-1alpha protein levels and synthesis of the endonuclease G protein in a time-dependent manner. Paper-12992492.
Modulation of Bax, Bcl-XL, and the Endo G proteins, release of mitochondrial cytochome c, and activation of caspase-3 and -9 all are involved in the CTX III-triggered apoptotic process in human leukemia K562 cells. Paper-12210554.
DIM-C-pPhtBu decreased mitochondrial membrane potential (MMP) and promoted the release of cytochrome c and caspase activation and nuclear uptake of endonuclease G leading to apoptosis of HEC1A cells. Paper-12825954.
DHE induces up-regulation of Bax and Bak, down-regulation of Bcl-2 and Bcl-XL, and nuclear relocation of the mitochondrial factors apoptosis-inducing factor ( AIF) and endonuclease G ( Endo G). Paper-13733132.
During apoptosis, the mitochondria also release AIF and endonuclease G, both of which are translocated to the nucleus and are implicated in apoptotic nuclear changes that occur in a caspase-independent manner. Paper-9676129.
The coding sequence of the single copy gene is interrupted by two introns and analysis of the transcripts does not support a model by which more than one Endo G isoform could be produced by alternative splicing. Paper-1187298.
The occurrence of apoptosis was proved by the increased expressions of Fas, Bax, caspase-3, -8, and -9, apoptosis-inducing factor ( AIF), and endonuclease G (EndoG), and the declined expressions of Bcl-2 and Bcl-xL. Paper-13750574.
The name Endonuclease G had originally been assigned to an endonuclease activity identified in nuclear extracts of chicken erythrocytes that was found to specifically nick within guanine ( G) tracts in DNA in vitro. Paper-10957159.
Cadmium induces caspase-independent apoptosis in liver Hep3B cells: role for calcium in signaling oxidative stress-related impairment of mitochondria and relocation of endonuclease G and apoptosis-inducing factor. Paper-10448789.
The purpose of this study was to identify if Endonuclease G was expressed in the cell nucleus of parvalbumin(+) GABA'ergic neurons in relation to cell death after global cerebral ischemia in the thalamic reticular nucleus. Paper-12965972.
The chimeric therapeutic gene is placed under the control of a hypoxia response element based promoter and contains a translocation motif linked in frame to an oxygen-dependent degradation domain and the endonuclease G gene. Paper-12992492.
Characterized mechanism of alpha-mangostin-induced cell death: caspase-independent apoptosis with release of endonuclease-G from mitochondria and increased miR-143 expression in human colorectal cancer DLD-1 cells. Paper-13315370.
In fact, endonuclease G and apoptosis-inducing factor were released into cytosol after the treatment of TCNAs, which indicated that caspase-independent apoptotic pathway is also one of the key mechanisms for the treatment of TCNAs. Paper-10837589.
Increase in apoptosis-inducing factor and endonuclease G expressions in nuclei, and increase in Bax and Bak expressions and decrease in Bcl-X(L) expression on mitochondria were also observed in formosanin C-treated HT-29 cells. Paper-13639847.
Both cations lead to Bax oligomerization and caused apoptosis inducing factor ( AIF), endonuclease G ( Endo G), and cytochrome c release from mitochondria, but they did not activate caspase dependent DNAse ( CAD). Paper-13724772.
Since then, other mitochondrial proteins, such as AIF, Smac/ DIABLO, endonuclease G and Omi/ HtrA2, were found to undergo release during apoptosis and have been implicated in various aspects of the cell death process. Paper-9333796.
Several caspase-independent death effectors including apoptosis-inducing factor, endonuclease G and a serine protease (Omi/ HtrA2) are released from the mitochondrial intermembrane space upon permeabilization of the outer membrane. Paper-10637127.
Taken together, our results show that cadmium induces Hep3B cells apoptosis mainly by calcium- and oxidative stress-related impairment of mitochondria, which probably favors release of apoptosis-inducing factor and endonuclease G. Paper-10448789.
However, endonuclease G nuclear translocation occurred without cytochrome c release from mitochondria, without nuclear translocation of apoptosis-inducing factor, and prior to loss of mitochondrial membrane potential. Paper-10605424.
One (designated ENGL) of the novel sequences was found to encode an amino-acid sequence homologous to the family of DNA/RNA endonucleases, especially endonuclease G. The other gene F56 revealed no significant homology to any known genes. Paper-1904490.
Chromosomal localization of mitochondrial transcription factor A ( TCF6), single-stranded DNA-binding protein ( SSBP), and endonuclease G ( ENDOG), three human housekeeping genes involved in mitochondrial biogenesis. Paper-263537.
Recently, genetic and biochemical evidence has emerged that Endonuclease G is released from the inter membrane space during early stages of programmed cell death, and translocates to the nucleus where it presumably facilitates degradation of chromatin. Paper-10957159.
In conclusion, this study has identified that Endonuclease G is translocated from the cytoplasm to the nucleus of neurons and expressed with apoptotic-like morphology in the nucleus of astroglia in the thalamic reticular nucleus after global cerebral ischemia. Paper-12965972.
Analysis of promoter sequences of all known human cytotoxic endonucleases showed that endonuclease G (EndoG) is the only endonuclease that contains a CpG island, a segment of DNA with high G+C content and a site for methylation, in the promoter region. Paper-12929417.
Our earlier studies had suggested that endonuclease G (EndoG), a member of the evolutionarily conserved DNA/RNA nonspecific betabetaalpha-Me-finger nuclease family, functioned in the a sequence-mediated segment inversion observed during herpes simplex virus 1 replication. Paper-12038152.
In the present study, we show that, on cadmium exposure, the human hepatocarcinoma Hep3B cells undergo caspase-independent apoptosis associated with nuclear translocation of endonuclease G and apoptosis-inducing factor, two mitochondrial apoptogenic proteins. Paper-10448789.
During the induction of apoptosis in cell suspensions by safingol, there was an increase of the pro-apoptotic BH-3 only protein Bim and decrease of pro-survival Bcl-2 family proteins Bcl-xL and mitochondrial pro-apoptogenic factor endonuclease G translocated to the nucleus. Paper-13622535.
TNF did not cause the mitochondrial release of apoptosis inducing factor ( AIF) and Endonuclease G ( Endo-G) but provoked the release of cytochrome c, Smac/ Diablo, and Omi/ HtrA2 at similar levels in both L929 and in L929-DeltaTM-BNIP3 cells. Paper-13683811.
Bcl-2 family members Bax and Bid then form pores in the outer mitochondrial membrane and release intermembrane proteins, e.g., apoptosis-inducing factor ( AIF) and endonuclease G, which then translocate to the nucleus and initiate chromatin condensation and DNA fragmentation, respectively. Paper-11335597.
MMP consists in a sudden increase in the permeability of mitochondrial membrane that results in the release of critical proapoptotic intermembrane space effectors into the cytosol such as cytochrome c, apoptosis-inducing factor ( AIF), Smac/ Diablo, Endo G, and pro-caspases. Paper-12044940.
This acidification not only promoted executive caspase activation, but also activated leucocyte elastase inhibitor/leucocyte-derived DNase II ( LEI/L-DNase II) pathway. p53 appeared to regulate mitochondria homeostasis, by initiating F0F1-ATPase reversal and endonuclease G ( Endo G) release. Paper-12219957.
The premature death of MDS MK was accompanied by the mitochondrial release of cytochrome c, Smac/ DIABLO and endonuclease G, a caspase-independent death effector, as well loss of the mitochondrial membrane potential and plasma membrane phosphatidylserine exposure before definitive loss of viability. Paper-13220467.
RCMF was shown to be capable of inducing apoptosis in HOS cells by inducing p53 in the cells resulting in the decrease in Bcl-2 level, activation of Bax, and cytoplasmic release of cytochrome c, which led to the translocation of apoptosis-inducing factor ( AIF) and endonuclease G (EndoG) into the nucleus. Paper-13282980.
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, and 9q34.1, respectively. Paper-263537.
To investigate the possibility that tumor cells undergoing linearly patterned programmed cell necrosis (LPPCN) establish a spatial foundation for vasculogenic mimicry (VM) and to reveal that hypoxia influences LPPCN formation as well as Endo G and DNase 1 expression, 78 C57 mice were divided evenly into two groups and engrafted with B16 melanoma. Paper-13739885.
Membrane permeabilization leads to the release of apoptogenic proteins: cytochrome c, apoptosis-inducing factor, Smac/ Diablo, HtrA2/Omi, and endonuclease G. Cytochrome c initiates the proteolytic activation of caspases, which in turn cleave hundreds of proteins to produce the morphological and biochemical changes of apoptosis. Paper-13362146.
These synonyms are used for gene ENDOG (endonuclease G): Endonuclease G, mitochondrial, Endo G.
These accession numbers are used for gene ENDOG: Q9BSP2 (UNIPROT__AC), Q5T281 (UNIPROT__AC), CAI15412 (NCBI_GENBANK__AC), AAH04922 (NCBI_GENBANK__AC).
ENDOG is a homologue of zgc:110020 (zgc:110020) from Danio rerio.
ENDOG is a homologue of NUC1 (Major mitochondrial nuclease, has RNAse and DNA endo- and exonucleolytic...) from Saccharomyces cerevisiae.
ENDOG is a homologue of nuc1 (endodeoxyribonuclease Pnu1) from Schizosaccharomyces pombe.
ENDOG is a homologue of NCU00030 (mitochondrial nuclease) from Neurospora crassa OR74A.
ENDOG is a homologue of MGG_05324 (hypothetical protein) from Magnaporthe grisea 70-15.
ENDOG is a homologue of KLLA0D00440g (hypothetical protein) from Kluyveromyces lactis NRRL Y-1140.
ENDOG is a homologue of ENDOG (endonuclease G) from Bos taurus.
ENDOG is a homologue of ENDOG (endonuclease G) from Gallus gallus.
ENDOG is a homologue of ENDOG (endonuclease G) from Canis lupus familiaris.
ENDOG is a homologue of Endog (endonuclease G) from Mus musculus.
ENDOG is a homologue of Endog (endonuclease G) from Rattus norvegicus.
ENDOG is a homologue of cps-6 (CED-3 Protease Suppressor) from Caenorhabditis elegans.
ENDOG is a homologue of CG8862 (CG8862 gene product from transcript CG8862-RA) from Drosophila melanogaster.
ENDOG is a homologue of AGOS_ADR144C (ADR144Cp) from Ashbya gossypii ATCC 10895.
ENDOG is a homologue of AgaP_AGAP007845 (AGAP007845-PA) from Anopheles gambiae str. PEST.
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