ライフサイエンスコーパス: cell cycle arrest

1 ing cell proliferation through initiation of cell cycle arrest.

2 ing tubulin polymerization and inducing G2/M cell cycle arrest.

3 3, contributing to p53's enforcement of a G2 cell cycle arrest.

4 f the de novo synthesis of PA resulted in G1 cell cycle arrest.

5 of renalase caused tumor cell apoptosis and cell cycle arrest.

6 on in differentiated tissues did not prevent cell cycle arrest.

7 , HKL decreased CDK2 activity, leading to G1 cell cycle arrest.

8 umulation of DNA damage and an ATR-dependent cell cycle arrest.

9 clease subunit (SLX4) complex and to promote cell cycle arrest.

10 lting in either chromosomal instabilities or cell cycle arrest.

11 tion fork, causing replicative stress and/or cell cycle arrest.

12 by promoting mitochondrial apoptosis and G2 cell cycle arrest.

13 of tubulin polymerization, and induction of cell cycle arrest.

14 g to aROS-mediated activation of the DDR and cell cycle arrest.

15 n were mediated by Src through inducing G2/M cell cycle arrest.

16 enhances the G0/G1 cell cycle transition and cell cycle arrest.

17 ppaB activity, Bcl-xL downregulation, and G1 cell cycle arrest.

18 low cells accumulated DNA damage and entered cell cycle arrest.

19 pithelial cells cause p21- and Numb-mediated cell cycle arrest.

20 attributed to induction of apoptosis and G2 cell cycle arrest.

21 IP also leads to p21/p27 upregulation and G1 cell cycle arrest.

22 d ability to rescue Ecd-deficient cells from cell cycle arrest.

23 nificantly inhibits proliferation and causes cell cycle arrest.

24 the signal that activates the DDR leading to cell cycle arrest.

25 nhibition of Cdc2 kinase and subsequent G2/M cell cycle arrest.

26 s of hUPF1 induces a DNA damage response and cell cycle arrest.

27 LF4 accumulation, which, in turn, attenuates cell cycle arrest.

28 Cs increased p21 expression, thus triggering cell cycle arrest.

29 eads to suppression of protein synthesis and cell cycle arrest.

30 imary MDS/AML samples via induction of G0/G1 cell cycle arrest.

31 se, elements of which include cell death and cell cycle arrest.

32 by which p53 can enforce and maintain a G2/M cell cycle arrest.

33 impeded actin dynamics, cell spreading, and cell cycle arrest.

34 -mediated HLTF degradation or Vpr-induced G2 cell cycle arrest.

35 proliferation by promoting apoptosis not by cell cycle arrest.

36 curs in dividing cells and is independent of cell cycle arrest.

37 ion to repair functions for this protein and cell cycle arrest.

38 GDS depletion characteristically causes a G1 cell cycle arrest.

39 r genomic instability that ultimately causes cell-cycle arrest.

40 and cell proliferation is inhibited by G1-S cell-cycle arrest.

41 protein synthesis, but also for FGF-induced cell-cycle arrest.

42 ion of CDK2 and cyclin A expression and G2-M cell-cycle arrest.

43 creased proliferation and induced a G1 phase cell-cycle arrest.

44 tical physiological signal for cardiomyocyte cell-cycle arrest.

45 m activation of ERK1/2 and AKT, resulting in cell-cycle arrest.

46 cyclin dependent kinase 4) locus leading to cell-cycle arrest.

47 enuated melanoma growth by inducing G1 phase cell-cycle arrest.

48 FN-gamma and IL-2 production and inducing G1 cell-cycle arrest.

49 on promoted epithelial dedifferentiation and cell-cycle arrest.

50 iability through caspase activation and G2/M cell-cycle arrest.

51 ional target genes that induce apoptosis and cell-cycle arrest.

52 erial chemoembolization (TACE) in a state of cell cycle arrest-a function that may serve as a defensi

53 liferation and colony formation, and induced cell cycle arrest accompanied by increased expression of

54 nction as a crucial signal for cardiomyocyte cell-cycle arrest after birth and suggest interventions

55 ivation of cell cycle checkpoints results in cell cycle arrest, allowing time for DNA repair before c

56 nt activity, showed that compound 3c induced cell cycle arrest and 3g induced apoptosis through caspa

57 ether the mechanisms controlling endothelial cell cycle arrest and acquisition of specialized phenoty

58 -deficient SKOV-3 cells, citral induces G1/S cell cycle arrest and apoptosis as determined by Annexin

59 e emphasized the importance of p53-dependent cell cycle arrest and apoptosis for tumor suppression, r

60 required for p53-dependent gene expression, cell cycle arrest and apoptosis in response to DNA damag

61 We found that Neat1 is dispensable for cell cycle arrest and apoptosis in response to genotoxic

62 tively decreased the viability, promoted the cell cycle arrest and apoptosis of human EVI1-positive c

63 In addition to cell cycle arrest and apoptosis of NPCs, ZIKV infection

64 t induces non-small cell lung cancer (NSCLC) cell cycle arrest and apoptosis via restoring p53 expres

65 of cell death mechanism showed a mixture of cell cycle arrest and apoptosis was responsible for the

66 Moreover, we observed cell cycle arrest and apoptosis, associated with increas

67 constitutively active FOXO1 mutant triggered cell cycle arrest and apoptosis, indicating that increas

68 ype cells, both drugs induced significant G2 cell cycle arrest and apoptosis.

69 ubordinated bistable modules responsible for cell cycle arrest and apoptosis.

70 city for cancer cells by inducing G2/M phase cell cycle arrest and apoptosis.

71 of rapamycin signaling pathways, leading to cell cycle arrest and apoptosis.

72 suppresses microtubule dynamics and leads to cell cycle arrest and apoptosis.

73 sociated with proliferation, thus preventing cell cycle arrest and apoptosis.

74 esistant EOC cells through induction of G2/M cell cycle arrest and apoptotic cell death.

75 PSMB6, which together induces autophagy and cell cycle arrest and benefits virus replication.

76 show that toxin-induced DNA damage precedes cell cycle arrest and causes apoptosis when DNA-dependen

77 tral role for the miR-34 family in promoting cell cycle arrest and cell death following stress in hum

78 oma cell growth and migration, and increases cell cycle arrest and cell death, potentially through mo

79 D drug induces DNA damage, resulting in G2/M cell cycle arrest and cell death.

80 lator of tumor suppressor gene TP53-mediated cell cycle arrest and cell death.

81 er with defects in p53-mediated induction of cell cycle arrest and cell senescence) does not recapitu

82 erevisiae, a 13-residue peptide that elicits cell cycle arrest and chemotropic growth, has served as

83 etion of RNF31 in breast cancer cells caused cell cycle arrest and cisplatin-induced apoptosis in a p

84 pigmentation, ultraviolet-B-induced G1-like cell cycle arrest and control of senescence and melanoma

85 reatment with this enzyme selectively causes cell cycle arrest and death in cancer cells due to deple

86 ular proliferation was associated with G0/G1 cell cycle arrest and decrease expression of cell cycle

87 leads to a lack of responsiveness to IGF-1, cell cycle arrest and decreased viability of cancer cell

88 UV-induced PAF also activates cell cycle arrest and disrupts DNA repair, in part by in

89 more, we provide molecular evidence that the cell cycle arrest and DNA binding activities of IE2 appe

90 s that express the wild-type p53, leading to cell cycle arrest and growth inhibition.

91 MUTATED kinases, which cause postreplicative cell cycle arrest and increased endoreplication.

92 Independent cell cycle arrest and increased induction of apoptosis u

93 the bacterial algicide, IRI-160AA results in cell cycle arrest and induces biochemical changes consis

94 e microtubule fragmentation, leading to G2/M cell cycle arrest and intrinsic apoptosis.

95 iggered enhanced apoptosis, and induced G2/M cell cycle arrest and more overall cytotoxicity than its

96 its substrate adaptor Cdh1, is critical for cell cycle arrest and neuronal architecture.

97 upon glutamine deprivation, thus triggering cell cycle arrest and promoting cell survival.

98 amage response, a signaling cascade allowing cell cycle arrest and repair of lesions.

99 NA damage in IGF-1R-negative cells caused G1 cell cycle arrest and S phase fork stalling.

100 4 protein levels by RNA interference induces cell cycle arrest and senescence in a p53-dependent mann

101 verexpressing RCC1 evaded DNA damage-induced cell cycle arrest and senescence, mimicking colorectal c

102 Silencing MDMX induces RB accumulation, cell cycle arrest and senescence-like phenotypes, which

103 kdown of FEN1 resulted in G1/S or G2/M phase cell cycle arrest and suppressed in vitro cellular proli

104 ion (motif 3) is critical to 4E-BP1-mediated cell cycle arrest and that it partially overlaps with th

105 lts demonstrate that Notch signaling induces cell cycle arrest and thereby initiates chondrocyte hype

106 eration was strongly reduced by induction of cell cycle arrest and, to some extent, cell death.

107 tress responses that are capable of inducing cell cycle arrest and/or apoptosis, and they are propose

108 r senescence is characterized by a permanent cell-cycle arrest and a pro-inflammatory secretory pheno

109 * blocked cell growth leading to G0-G1 phase cell-cycle arrest and apoptosis in colorectal cancer cel

110 erence and small molecule inhibition induced cell-cycle arrest and apoptosis in DLBCL cell lines and

111 ssive transcriptional changes, and triggered cell-cycle arrest and apoptosis in Myc-induced B-cell ly

112 Specifically, it has been shown to cause cell-cycle arrest and apoptosis in response to DNA damag

113 ell proliferation/viability and by promoting cell-cycle arrest and apoptosis.

114 vated by a variety of stimuli, p53 regulates cell-cycle arrest and apoptosis.

115 rinapant alone also induced significant G2-M cell-cycle arrest and cell death in UM-SCC-46 cells.

116 l proliferation and that their loss leads to cell-cycle arrest and cellular senescence.

117 ion, as counteracting MYC repression reduced cell-cycle arrest and elevated apoptosis.

118 ion in vitro and in tumors in mice caused G1 cell-cycle arrest and eliminated Ki-67 mRNA in RB1-posit

119 cultures, Mif deletion led to enhanced G2/M cell-cycle arrest and increased expression of the CDK in

120 se-dependent cytotoxicity, caused a G1 phase cell-cycle arrest and induced apoptosis.

121 expression of activated ALK(F1174L) leads to cell-cycle arrest and promotes differentiation and survi

122 e latter mechanism involves p38-dependent G1 cell-cycle arrest and subsequent intrinsic mitochondrial

123 Our data show that p53-driven apoptosis and cell cycle arrest - and, in the absence of p53, non-apop

124 6OTD caused DNA damage, G1 cell cycle arrest, and apoptosis in GSCs but not in NSGC

125 tion caused catastrophic DNA damage, mitotic cell cycle arrest, and apoptosis specifically in PTEN-de

126 key cellular processes including DNA repair, cell cycle arrest, and apoptosis.

127 p53 and cyclin-dependent kinase inhibitors, cell cycle arrest, and apoptosis.

128 hindered cellular proliferation, induced G1 cell cycle arrest, and attenuated migration and colony f

129 in abrogation of adhesion and self-renewal, cell cycle arrest, and attenuation of proliferation with

130 s DNA damage, checkpoint activation, S-phase cell cycle arrest, and cell death in sensitive breast ca

131 (mTORC1), reduction of protein translation, cell cycle arrest, and conservation of energy.

132 sis, abolished cytarabine-induced S and G2/M cell cycle arrest, and cooperated with cytarabine in ind

133 nhances EGFR inhibitor-induced apoptosis and cell cycle arrest, and delays resistance to EGFR monothe

134 se, whose substrates induce gene expression, cell cycle arrest, and formation of the mating projectio

135 2780/WT and A2780/PTX(R), induced G2/M phase cell cycle arrest, and improved chemo-resistance.

136 cancer cells by inducing both apoptosis and cell cycle arrest, and that reducing DHX33 levels throug

137 e downregualtion of CTNNB1 led to apoptosis, cell cycle arrest, and the inhibition of migration, inva

138 y activating genes involved in apoptosis and cell cycle arrest, and these anticancer functions are in

139 ortant for mating, including gene induction, cell-cycle arrest, and polarized cell growth.

140 T to CAF induced DNA damage, p53 activation, cell-cycle arrest, and secretion of paracrine mediators,

141 on of proliferation, induction of apoptosis, cell-cycle arrest, and terminal differentiation in DNMT3

142 bility through critical roles in DNA repair, cell-cycle arrest, and transcriptional control.

143 nhibition significantly increased apoptosis, cell-cycle arrest, and tumor immunogenicity and generate

144 ional and physiological responses, including cell cycle arrest, apoptosis and epithelial-to-mesenchym

145 ficantly reduced cellular growth and induced cell cycle arrest, apoptosis of ATC cells by altering th

146 o genotoxic stress p53 activates DNA repair, cell cycle arrest, apoptosis or senescence, which are in

147 antiproliferative cellular outcomes, such as cell cycle arrest, apoptosis, and senescence, by activat

148 signal to the tumor suppressor p53 to induce cell cycle arrest, apoptosis, or senescence.

149 and inactivates CRLs and, in turn, triggers cell-cycle arrest, apoptosis, senescence and autophagy i

150 Phycocyanin induces G2/M cell cycle arrest, apoptotic and autophagic cell death i

151 TGM2-mediated autophagy and CDKN1A-mediated cell cycle arrest are two important barriers in the TP53

152 in cellular cyclin D1 degradation and caused cell cycle arrest as shown in Western blottings and flow

153 in Caenorhabditis elegans, we identified G1 cell-cycle arrest as a precisely regulated requirement o

154 Moreover, TTP augmented mitotic cell-cycle arrest as demonstrated by flow cytometry and

155 s showed that ailanthone induced G0/G1-phase cell cycle arrest, as indicated by decreased expression

156 ploit the cross-talk of signals activated by cell-cycle arrest, as well as pediatric-focused drug dev

157 cells during senescence, a form of terminal cell-cycle arrest associated with pro-inflammatory respo

158 More importantly, we found that the cell cycle arrest at G0/G1 phase and the alterations of

159 analysis indicated that simvastatin induced cell cycle arrest at G0/G1 phase, suggested by downregul

160 that suppression of p53, in conjunction with cell cycle arrest at G1 and appropriate extracellular en

161 ive than curcumin in apoptosis induction and cell cycle arrest at G1 phase.

162 ladder cancer cell proliferation and induced cell cycle arrest at G1/G0 phase via PPARgamma signallin

163 In addition, P-SMART treatment led to cell cycle arrest at G2/M phase and cell accumulation in

164 n and invasion as well as in vitro growth by cell cycle arrest at S phase with increased cell size an

165 ited osteosarcoma cell proliferation, led to cell cycle arrest at S phase, and decreased colony forma

166 iR-506 inhibited cell proliferation, induced cell cycle arrest at the G1/S transition and enhanced ap

167 SFN treatment induced apoptosis and cell cycle arrest at the G2/M phase.

168 t kinase (CDK) inhibitor p21, which promotes cell-cycle arrest at DNA damage checkpoints, and Gadd45

169 n addition, Nutlin-3 increased apoptosis and cell cycle arrest based on flow cytometry assays.

170 Interestingly, SpPrp18 depletion caused cell cycle arrest before S phase.

171 ive CDK4/6 inhibitors not only induce tumour cell cycle arrest, but also promote anti-tumour immunity

172 Berberine induces more apoptosis, cell cycle arrest, but less ROS production in CAR overex

173 The induction of cell cycle arrest by a pheromone, chemically distinct fr

174 appears to be a principal mechanism for G2/M cell cycle arrest by p53.

175 iR-200a in metastatic melanoma cells induces cell cycle arrest by targeting CDK6 and decreases the le

176 family, and repression of those involved in cell cycle arrest by the miR-17 family, but also suggest

177 ion plasmids could rescue the cells from the cell cycle arrest caused by ClC-3 siRNA treatments.

178 ltidimensional data from cell line models of cell-cycle arrest caused by inhibition of MEK1/2.

179 3 prevents cancer development via initiating cell-cycle arrest, cell death, repair, or antiangiogenes

180 senescence refers to a state of irreversible cell-cycle arrest combined with the secretion of proinfl

181 ed ATR-dependent phosphorylation of Chk1 and cell-cycle arrest, consistent with replication checkpoin

182 Correspondingly, here cell cycle arrest correlated with interaction with the g

183 ty of a panel of SIV Vpr proteins to mediate cell cycle arrest correlates with species-specific inter

184 Downregulation of METTL3 results in cell cycle arrest, differentiation of leukaemic cells an

185 ed in multiple cellular responses, including cell cycle arrest, DNA repair, apoptosis, metabolism, au

186 ells from proliferating through induction of cell cycle arrest, DNA repair, senescence or apoptosis.

187 (0.1-0.5 muM), pevonedistat induced G1-phase cell cycle arrest, downregulation of Bcl-xL levels, decr

188 3300 in vitro resulted in rapid induction of cell-cycle arrest followed by apoptosis.

189 primary endothelial cells from apoptosis and cell cycle arrest following Nutlin-3 treatment.

190 gesting that the evolutionarily conserved G2 cell cycle arrest function of Vpr is essential for HIV-1

191 SETD8 ablation rescued the pro-apoptotic and cell-cycle arrest functions of p53 by decreasing p53(K38

192 skin hyperpigmentation, whereas deletion of cell cycle arrest gene p21 does not rescue either phenot

193 Meanwhile, EVO induced cell cycle arrest in a dose- and time-dependent manner.

194 In this study, IRI-160AA induced cell cycle arrest in all dinoflagellates examined.

195 enitor (GMP) cells, accompanied by increased cell cycle arrest in CMPs.

196 stone deacetylase (HDAC) inhibition leads to cell cycle arrest in G1 and G2, suggesting HDACs as ther

197 p53, activation of a DNA-damage response and cell cycle arrest in G1 phase, followed by apoptosis.

198 pting a senescence-like state with permanent cell cycle arrest in G1 phase.

199 ibitor blocks cell proliferation by inducing cell cycle arrest in G2 phase, as well as apoptosis in C

200 esume growth; instead, they mostly underwent cell cycle arrest in G2.

201 ession can decrease proliferation and induce cell cycle arrest in hepatocellular carcinoma (HCC) cell

202 ed the cell growth and induced apoptosis and cell cycle arrest in HepG2 cells by significantly upregu

203 In all cases, SIV Vpr-mediated cell cycle arrest in human cells correlated with interac

204 proteins differ in their ability to promote cell cycle arrest in human cells.

205 Although Q deprivation causes G1 cell cycle arrest in non-transformed cells, its impact o

206 Regulation of cell cycle arrest in premeiotic G2 phase coordinates ger

207 cting upstream of p53, evoking p21-dependent cell cycle arrest in response not only to centrosome los

208 y, MageB2 plays a critical role in impairing cell cycle arrest in response to Actinomycin D.

209 Cellular senescence, a state of stable cell cycle arrest in response to cellular stress, is an

210 ds to activation of CHK1 or CHK2 kinases and cell cycle arrest in S or G2/M phases.

211 sufficient to activate damage signaling and cell cycle arrest in the absence of DNA damage.

212 1 reduced in vitro colony formation, induced cell cycle arrest in the G2/M phase and cleavage of casp

213 fect of these compounds was the induction of cell cycle arrest in the G2/M phase as a direct conseque

214 Moreover, 5f induced cell cycle arrest in the G2/M phase of the cell cycle in

215 methoxy)-9H-purin-2-amine] leads to G1-phase cell cycle arrest in the marine diatom, Phaeodactylum tr

216 etinoblastoma tumour suppressor, inducing G1 cell cycle arrest in tumour cells.

217 criptional changes that induce apoptosis and cell-cycle arrest in leukemia cells and finally demonstr

218 nd TORC2, the compound induced apoptosis and cell-cycle arrest in multiple myeloma cell lines and pre

219 uction of GLI2 protein levels and subsequent cell-cycle arrest in myofibroblasts.

220 dyskerin suppression caused p53-dependent G1 cell-cycle arrest in p53 wild-type cells, and a p53-inde

221 ctivity conferred increased apoptosis and G1 cell-cycle arrest in primary cutaneous anaplastic T-cell

222 6 inhibitors that induce reversible G1-phase cell-cycle arrest in retinoblastoma-positive tumor model

223 -forming ability, while transiently delaying cell-cycle arrest in vitro The prometastatic activity of

224 transcriptional upregulation with associated cell-cycle arrest, increased DNA damage, and cell death.

225 conserved cell-cycle state characterized by cell-cycle arrest, increased stress resistance, enhanced

226 ene transcription to control a reversible G1 cell-cycle arrest, independent of p21(CIP) function.

227 er, 53BP1 can transduce prolonged mitosis to cell cycle arrest independently of the spindle assembly

228 onal antibody suppresses DNA damage and also cell cycle arrest, indicating that pneumolysin oligomeri

229 ated the apoptotic effects, but not the G2/M cell cycle arrest induced by JA.

230 Senescence is a form of cell cycle arrest induced by stress such as DNA damage a

231 also found that the ability of Tax to induce cell cycle arrest inhibits its fundamental function of a

232 These results imply that cell cycle arrest inhibits Tax-mediated activation of se

233 it can paradoxically promote an irreversible cell cycle arrest known as oncogene-induced senescence.

234 telomeric DNA and eventually a specific G2/M cell-cycle arrest known as senescence.

235 We propose that cell cycle arrest leading to apoptosis is a strategy tha

236 evels of D2 PSII subunits, or RbcL; however, cell cycle arrest leads to unbalanced growth whereby pho

237 However, PI3K inhibitors primarily induce cell cycle arrest, leaving a significant reservoir of tu

238 ransformed HBECs with specific mimics led to cell-cycle arrest mediated in part through transcription

239 S concentration (10 muM) stimulated myoblast cell cycle arrest, migration and sprouting, which were i

240 xA8 siRNA recapitulated exposure to FR, with cell cycle arrest, neuronal transdifferentiation, and co

241 rial membrane potential, mitochondrial mass, cell cycle arrest, nuclear size, and cell number.

242 n of DNA damage response (DDR) and permanent cell cycle arrest of cardiomyocytes.

243 (shRNA) in embryonic rat brains, we observe cell cycle arrest of proliferating neural progenitors at

244 The (N+C)-LP was also able to induce cell cycle arrest of the cells, specifically in the G1 p

245 novel 'one PGC' phenotype as a result of G2 cell cycle arrest of the P4 blastomere.

246 tumor suppressor is a stress sensor, driving cell cycle arrest or apoptosis in response to DNA damage

247 arious DNA damage-induced adducts to trigger cell cycle arrest or apoptosis.

248 d downregulating gene expression, leading to cell cycle arrest or apoptosis.

249 Often described as a mediator of cell cycle arrest or as a pro-apoptotic factor in stress

250 tic silencing of S-phase genes and permanent cell cycle arrest or cellular senescence.

251 sites can survive drug treatment by entering cell cycle arrest or dormancy.

252 mens tested, without the induction of either cell-cycle arrest or apoptosis.

253 aled that CDK4/6 inhibition failed to induce cell-cycle arrest or senescence.

254 moted ROS production, enhanced apoptosis and cell cycle arrests particularly.

255 have developed a new approach that utilizes cell cycle arresting patterns as unique molecular signat

256 Cellular senescence is a stress-responsive cell-cycle arrest program that terminates the further ex

257 arcomas lacking p53 induced apoptosis and G2 cell-cycle arrest, prolonging survival of mice with thes

258 es and anaphase bridges and positive for the cell-cycle arrest protein p21.

259 in RAS mutant organoids induced a transient cell-cycle arrest rather than cell death.

260 Cell cycle arrest/release experiments of MCF7/SKBR3 brea

261 Functional p53 elicits a cell cycle arrest response, whereas, in p53-null transfo

262 ecome critically short, inducing a permanent cell cycle arrest (senescence).

263 c progenitor cells caused severe DNA damage, cell cycle arrest, senescence, and cell death.

264 Although p53-mediated cell-cycle arrest, senescence and apoptosis serve as cri

265 lation-defective mutant that fails to induce cell-cycle arrest, senescence and apoptosis, fully retai

266 Although p53-mediated cell-cycle arrest, senescence, and apoptosis remain crit

267 toxic stress, p53 levels increase and induce cell-cycle arrest, senescence, or apoptosis, thereby pre

268 Cellular senescence is a terminal cell cycle arrested state, assumed to be involved in tum

269 e flies, their transmission being enabled by cell-cycle arrested 'stumpy forms' that are generated in

270 d with, and can promote, cardiomyocyte G0/G1 cell cycle arrest suggesting that centrosome disassembly

271 ce of cell death, impaired proliferation, or cell cycle arrest, suggesting that ALT activation may pr

272 hich involved the induction of apoptosis and cell cycle arrest, supporting the development of bioengi

273 Cellular senescence, a form of stable cell cycle arrest that is traditionally associated with

274 Cellular senescence is a stable cell cycle arrest that occurs in response to sublethal s

275 Consistent with the ability of Tax to induce cell cycle arrest, this population was arrested in G(0)/

276 Knockdown of MGAT4A induces cell cycle arrest through decreasing CCND1 levels.

277 t the RR inhibitor 3-AP actively induces PEL cell cycle arrest through inhibiting the activity of the

278 th drugs were mediated by induction of G0/G1 cell cycle arrest through upregulation of p27 and downre

279 d to apoptosis, knockdown in GBMNS led to G1 cell cycle arrest through upregulation of p27 and hypoph

280 somes via p53 stabilisation and p21-mediated cell-cycle arrest, thus ensuring the maintenance of norm

281 H-GJA4-CDKN1B axis that promotes endothelial cell cycle arrest to enable arterial gene expression.

282 ecule-1, calbindin), followed by a marker of cell cycle arrest (urine insulin-like growth factor-bind

283 adiation, the tumour suppressor p53 mediates cell cycle arrest via expression of the CDK inhibitor, p

284 ed proliferation of GBM cells through a G2/M cell cycle arrest via inhibition of polo-like kinase 1 (

285 necroptosis was linked to increased mitotic cell cycle arrest via Per1/2-controlled Wee1, resulting

286 y and DNA double-strand breaks, resulting in cell cycle arrest via the phosphorylated p53 (Ser-15)-de

287 differentiation, and orchestrated epithelial cell-cycle arrest via SMAD3-mediated connective tissue g

288 Cell cycle arrest was followed by cell death.

289 Arginine deprivation-induced cell cycle arrest was mediated in part by Rictor/mTORC2,

290 Cell cycle arrest was reversible at any point by exogeno

291 Coincident with the ATR-dependent cell cycle arrest, we find increased DNA damage that is

292 Deletion of Ecd in cells causes cell cycle arrest, which is rescued by exogenous ECD, de

293 An enhanced G2 cell cycle arrest with activation of DNA damage response

294 AP1 in vascular smooth muscle cells leads to cell cycle arrest with decreased proliferation and incre

295 lgae enter cellular quiescence, a reversible cell cycle arrest with drastic changes in metabolism all

296 hepatocyte proliferation due to G1 /S-phase cell cycle arrest with overexpression of p27 and emergen

297 a specific CDK4/6 inhibitor, rapidly induces cell cycle arrest within 24 hours and continued exposure

298 TMG decreased tumor cell growth and enhanced cell cycle arrest without impairing cytotoxicity.

299 solid tumors, ABBV-075 triggers prominent G1 cell-cycle arrest without extensive apoptosis.

300 tates and later antagonizes TGFbeta-mediated cell cycle arrest, yet remains critical for the patholog