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1 droxyurea, aphidicolin, or etoposide induced irreversible cell cycle arrest after several population
2 e interferon (IFN)-mediated and p53-mediated irreversible cell cycle arrest and apoptosis as part of
6 hanism of cell death seemed to be due to the irreversible cell cycle arrest at the G2-M checkpoint, r
8 nsformation, it can paradoxically promote an irreversible cell cycle arrest known as oncogene-induced
9 fe span, at the end of which they undergo an irreversible cell cycle arrest known as replicative sene
10 that observed for p53 alone and produced an irreversible cell cycle arrest that displayed features o
14 xpression of VentX in cancer cells caused an irreversible cell cycle arrest with a typical senescence
15 tion is the initiation and maintenance of an irreversible cell cycle arrest with the complex involvem
16 re of centriole duplication that produced an irreversible cell cycle arrest within a few divisions.
18 ve senescence, an end stage characterized by irreversible cell cycle arrest, multiple genetic and fun
21 tal muscle, Rb has been reported to regulate irreversible cell cycle exit and muscle-specific transcr
22 Differentiation is a coordinated process of irreversible cell cycle exit and tissue-specific gene ex
23 We conclude that HES1 safeguards against irreversible cell cycle exit both during normal cellular
24 mal cells in culture leads to senescence, an irreversible cell cycle exit characterized by biochemica
25 oci (SAHF), are thought to contribute to the irreversible cell cycle exit in many senescent cells by
26 umor-suppressive process characterized by an irreversible cell cycle exit, a unique morphology, and e
27 ordered proteolytic events are essential for irreversible cell cycle progression and the robustness o
29 sults in terminal cell divisions followed by irreversible cell cycle withdrawal of hemoglobinized cel
31 Cellular senescence refers to a state of irreversible cell-cycle arrest combined with the secreti
32 enescence has historically been viewed as an irreversible cell-cycle arrest mechanism that acts to pr
39 non-selective cation channel, which leads to irreversible cell depolarization and unregulated Ca2+ en
40 (the reversibly immortalized IDH4 cells), or irreversible cell differentiation (HL60 promyelocytic le
41 ukaryotes can thus control low rates of near irreversible cell fate decisions through a balancing act
44 t, indicating that inhibition was not due to irreversible cell injury and suggesting that other signa
45 ory response that can result in necrosis and irreversible cell injury to both local vascular endothel
49 armacological effects of a single dose of an irreversible cell permeant general (nonselective) caspas
52 influences the transition from reversible to irreversible cell shape change, which defines the onset
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