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1 otic factors, apoptosis inducing factor, and endonuclease G.
2 and apoptosis-inducing factor (AIF), but not endonuclease G.
3 e c, Smac/DIABLO, Omi/HtrA2, and AIF but not endonuclease G.
4 lacking the mitochondrial endonuclease CPS-6/endonuclease G.
5 rocess requiring the mitochondrial nuclease, Endonuclease G.
6           In the current study, we show that Endonuclease G, a mitochondrial nuclease responsible for
7                                              Endonuclease G, a protein historically thought to be inv
8       Data is presented localizing rat liver endonuclease G activity exclusively to the mitochondrial
9                                              Endonuclease G activity, measured by a plasmid relaxatio
10                                              Endonuclease G also showed the predicted recombination p
11                    Furthermore, we show that endonuclease G, an apoptotic nuclease downstream of Casp
12        Microsequencing showed it to be human endonuclease G, an enzyme with a strong preference for G
13  related factors (apoptosis-inducing factor, endonuclease G, and HtrA2/Omi).
14 6 encodes a homologue of human mitochondrial endonuclease G, and its protein product similarly locali
15 anslocation of apoptosis-inducing factor and endonuclease G, and supra-nucleosomal DNA fragmentation,
16                                              Endonuclease G appears to be the only cellular enzyme th
17  In summary, we identify a novel property of Endonuclease G, besides its role in apoptosis and the re
18 itro and intracellular studies, we show that Endonuclease G binds to G-quadruplex structures formed a
19  and distinct in its properties from that of endonuclease G can be detected.
20               Additionally, it is shown that endonuclease G can be selectively released from the mito
21 enerated by cleavage of viral a sequences by endonuclease G during genome isomerization.
22                                              Endonuclease G (endo G) is one of the most abundant nucl
23 and both apoptosis-inducing factor (AIF) and endonuclease G (Endo G) were released from the mitochond
24 ochrome c, Smac/Diablo and HtrA2/Omi but not endonuclease G (EndoG) and apoptosis-inducing factor (AI
25                                        Using endonuclease G (endoG) as a model IMS protein, we found
26 f cisplatin and found that the expression of endonuclease G (EndoG) increased whereas the expression
27                                              Endonuclease G (EndoG) is a mitochondrial protein that t
28                                              Endonuclease G (EndoG) is a nuclear-encoded mitochondria
29                                              Endonuclease G (endoG) is released from mitochondria dur
30 rome c, apoptosis-inducing factor (AIF), and endonuclease G (EndoG) release.
31 ed with the mitochondrial endonuclease CPS-6/endonuclease G (EndoG) to promote DNA degradation and ap
32  In mammals, one such apoptogenic protein is Endonuclease G (EndoG), a conserved mitochondrial nuclea
33       Our earlier studies had suggested that endonuclease G (EndoG), a member of the evolutionarily c
34                                              Endonuclease G (ENDOG), a mitochondrial nuclease, is kno
35                             This nuclease is endonuclease G (endoG), a mitochondrion-specific nucleas
36 factors, apoptosis-inducing factor (AIF) and endonuclease G (EndoG), through p53-dependent upregulati
37                           Here we identified endonuclease G (Endog), which previously was implicated
38 oles for the conserved mitochondrial protein endonuclease G in budding yeast apoptosis and proliferat
39 ation of apoptosis-inducing factor (AIF) and endonuclease G in CNGA3(-/-)/Nrl(-/-) and CNGB3(-/-)/Nrl
40         Therefore, we uncover a new role for Endonuclease G in generating mtDNA deletions, which depe
41     Based on these findings, we propose that endonuclease G initiates the a sequence-mediated inversi
42 drion, such as apoptosis-inducing factor and endonuclease G, may induce caspase-9-independent apoptos
43               We demonstrate here that mouse endonuclease G (mEndoG) shows specificity for both 5hmC
44 ace the magnesium (Mg(2+)) cofactor in mouse endonuclease G (mEndoG).
45                                           In Endonuclease G mutants, persisting nucleoids are swept o
46                       CPS-6, a mitochondrial endonuclease G, serves as a paternal mitochondrial facto
47 but release of apoptosis-inducing factor and endonuclease G was detected only in TK6 cells.
48 lso depends on apoptosis-inducing factor and endonuclease G, which are effectors of caspase-independe