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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
3                                          The irreversible cell cycle arrest and apoptosis induced by
4 nce mechanisms, which ultimately induces the irreversible cell cycle arrest and apoptosis.
5 n of S- or G2-phase checkpoints resulting in irreversible cell cycle arrest and cell death.
6            Generally senescent cells undergo irreversible cell cycle arrest and produce inflammatory
7                      Senescent cells undergo irreversible cell cycle arrest and release an inflammato
8 hanism of cell death seemed to be due to the irreversible cell cycle arrest at the G2-M checkpoint, r
9           p21Waf1/Cip1/Sdi1 induction caused irreversible cell cycle arrest in both G1 and G2/M, and
10 nsformation, it can paradoxically promote an irreversible cell cycle arrest known as oncogene-induced
11 fe span, at the end of which they undergo an irreversible cell cycle arrest known as replicative sene
12  that observed for p53 alone and produced an irreversible cell cycle arrest that displayed features o
13            Cellular senescence is a state of irreversible cell cycle arrest that has been documented
14            Cellular senescence is a state of irreversible cell cycle arrest that has been involved in
15        Cellular senescence is a programme of irreversible cell cycle arrest that normal cells undergo
16 xpression of VentX in cancer cells caused an irreversible cell cycle arrest with a typical senescence
17 tion is the initiation and maintenance of an irreversible cell cycle arrest with the complex involvem
18 re of centriole duplication that produced an irreversible cell cycle arrest within a few divisions.
19 mic and mitochondrial DNA damage, leading to irreversible cell cycle arrest, and secretion of proinfl
20              Cellular senescence, a state of irreversible cell cycle arrest, is thought to help prote
21 ve senescence, an end stage characterized by irreversible cell cycle arrest, multiple genetic and fun
22 wed these cells to evade differentiation and irreversible cell cycle arrest.
23  is a signal transduction program leading to irreversible cell cycle arrest.
24  undergo senescence, which is typified by an irreversible cell cycle arrest.
25 ere each cell in the culture is driven to an irreversible cell cycle arrest.
26 tal muscle, Rb has been reported to regulate irreversible cell cycle exit and muscle-specific transcr
27  Differentiation is a coordinated process of irreversible cell cycle exit and tissue-specific gene ex
28     We conclude that HES1 safeguards against irreversible cell cycle exit both during normal cellular
29 mal cells in culture leads to senescence, an irreversible cell cycle exit characterized by biochemica
30 oci (SAHF), are thought to contribute to the irreversible cell cycle exit in many senescent cells by
31 umor-suppressive process characterized by an irreversible cell cycle exit, a unique morphology, and e
32 ordered proteolytic events are essential for irreversible cell cycle progression and the robustness o
33                                              Irreversible cell cycle withdrawal occurs as normal kera
34 sults in terminal cell divisions followed by irreversible cell cycle withdrawal of hemoglobinized cel
35 cle regeneration after injury is limited by "irreversible" cell cycle exit.
36     Cellular senescence refers to a state of irreversible cell-cycle arrest combined with the secreti
37 enescence has historically been viewed as an irreversible cell-cycle arrest mechanism that acts to pr
38                             Senescence is an irreversible cell-cycle arrest that has a crucial role b
39  led to extensive replication fork collapse, irreversible cell-cycle arrest, and synergistic vulnerab
40 c changes in gene expression that trigger an irreversible cell-cycle arrest.
41 kly defined and is frequently referred to as irreversible cell-cycle arrest.
42      Cellular senescence is characterized by irreversible cell-cycle exit, a pro-inflammatory secreto
43                       Senescence, a state of irreversible cell-cycle withdrawal, is difficult to dist
44            Lack of blood perfusion can cause irreversible cell damage.
45 teins encompasses key regulators proximal to irreversible cell damage.
46 ) is a critical determinant of the extent of irreversible cell damage.
47 e cells did not co-localise with a marker of irreversible cell death (TUNEL).
48 production of PAP I led to slower growth and irreversible cell death.
49 non-selective cation channel, which leads to irreversible cell depolarization and unregulated Ca2+ en
50 (the reversibly immortalized IDH4 cells), or irreversible cell differentiation (HL60 promyelocytic le
51 ukaryotes can thus control low rates of near irreversible cell fate decisions through a balancing act
52  dynamics are integrated to yield long-term, irreversible cell fate decisions.
53 omoting agents to induce maladaptive CIN and irreversible cell fates.
54               Cellular senescence defines an irreversible cell growth arrest state linked to loss of
55                                              Irreversible cell growth arrest, a process termed cellul
56 in PrECs contribute to senescence-associated irreversible cell growth arrest.
57 t, indicating that inhibition was not due to irreversible cell injury and suggesting that other signa
58 ory response that can result in necrosis and irreversible cell injury to both local vascular endothel
59 the MPT is causally linked to the genesis of irreversible cell injury with TNF.
60 eability for intracellular cargo delivery or irreversible cell membrane disruption using electric fie
61                   Electric fields can induce irreversible cell membrane pores in direct relation to c
62                                  As death is irreversible, cells must continually integrate developme
63 armacological effects of a single dose of an irreversible cell permeant general (nonselective) caspas
64            Senescence is characterized by an irreversible cell proliferation arrest.
65 n has ceased, indicating that this is a true irreversible cell reprogramming event.
66 influences the transition from reversible to irreversible cell shape change, which defines the onset