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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.
13 6 encodes a homologue of human mitochondrial endonuclease G, and its protein product similarly locali
19 and both apoptosis-inducing factor (AIF) and endonuclease G (Endo G) were released from the mitochond
20 ochrome c, Smac/Diablo and HtrA2/Omi but not endonuclease G (EndoG) and apoptosis-inducing factor (AI
22 f cisplatin and found that the expression of endonuclease G (EndoG) increased whereas the expression
27 ed with the mitochondrial endonuclease CPS-6/endonuclease G (EndoG) to promote DNA degradation and ap
30 factors, apoptosis-inducing factor (AIF) and endonuclease G (EndoG), through p53-dependent upregulati
32 oles for the conserved mitochondrial protein endonuclease G in budding yeast apoptosis and proliferat
33 ation of apoptosis-inducing factor (AIF) and endonuclease G in CNGA3(-/-)/Nrl(-/-) and CNGB3(-/-)/Nrl
34 Based on these findings, we propose that endonuclease G initiates the a sequence-mediated inversi
35 drion, such as apoptosis-inducing factor and endonuclease G, may induce caspase-9-independent apoptos
39 lso depends on apoptosis-inducing factor and endonuclease G, which are effectors of caspase-independe
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