ライフサイエンスコーパス: G1 arrest

1 migration and cellular proliferation due to G1 arrest.

2 ding its half-life, leading to p21-dependent G1 arrest.

3 inactive) to nucleus (active), thus inducing G1 arrest.

4 e mating projection during pheromone-induced G1 arrest.

5 esion, inhibition of Akt phosphorylation and G1 arrest.

6 s in a far1 mutant that is also defective in G1 arrest.

7 MCF-10A cells, parcs deficiency led to early G1 arrest.

8 hypoxic mTOR inhibition and hypoxia-induced G1 arrest.

9 id to late S and G2/M leading to a permanent G1 arrest.

10 ma by siRNA reduced UV-induced p53 level and G1 arrest.

11 owth-rate increase resulting from defects in G1 arrest.

12 beyond the priming phase, still induced the G1 arrest.

13 d the rise of p27Kip1 and rescued cells from G1 arrest.

14 press E2f1-target genes to maintain a stable G1 arrest.

15 expression of p27 kip1, explaining their G0-G1 arrest.

16 R) tyrosine kinase inhibitors, which induced G1 arrest.

17 ation of cyclin D1 and CDK2, contributing to G1 arrest.

18 ion of p21 in cells, consequently leading to G1 arrest.

19 beta is not essential for rapamycin-mediated G1 arrest.

20 body formation in the ensuing G1 phase, and G1 arrest.

21 n D1 protein expression and the induction of G1 arrest.

22 in the S phase entry rather than a sustained G1 arrest.

23 role in mediating the ICI182,780-induced G0/G1 arrest.

24 the Skp2 N terminus prevents Rb from causing G1 arrest.

25 dent kinase 2 (cdk2) activity and induced G0/G1 arrest.

26 latin can effectively induce a p53-dependent G1 arrest.

27 s compared to cells undergoing p53-dependent G1 arrest.

28 7Kip1 in the ability of mevastatin to induce G1 arrest.

29 l participate in the same pathway leading to G1 arrest.

30 e to G2 and mitotic arrests but not during a G1 arrest.

31 in G1 and reduces a further antibody-induced G1 arrest.

32 at 32.5 degrees C because of induction of G0/G1 arrest.

33 t this fusion protein is capable of inducing G1 arrest.

34 g pathway participates in both apoptosis and G1 arrest.

35 2 antibody-induced p27Kip1 up-regulation and G1 arrest.

36 ors halted cell growth and caused a distinct G1 arrest.

37 7Kip1 as a critical mediator of PTEN-induced G1 arrest.

38 lated bcl-2, up-regulated bax, and increased G1 arrest.

39 turn leads to hypophosphorylation of Rb and G1 arrest.

40 al mechanism that contributes to RA-mediated G1 arrest.

41 rrest, implying that p53 is not required for G1 arrest.

42 negative tumor cell lines failed to elicit a G1 arrest.

43 p27 promoter region leading to a subsequent G1 arrest.

44 blocked cells inside S phase in addition to G1 arrest.

45 ion, hypophosphorylation of pRB, or a strict G1 arrest.

46 inhibited cellular proliferation by inducing G1 arrest.

47 found to lack the transient heat-induced G0/G1 arrest.

48 mbryo fibroblasts do not undergo a permanent G1 arrest.

49 esting that it might be the primary cause of G1 arrest.

50 cells and immortalized cells, by inducing a G1 arrest.

51 elieving repression of the cyclin E gene and G1 arrest.

52 horylation attenuation, which resulted in G0/G1 arrest.

53 RNAs-mediated vCyclin depletion resulted in G1 arrest.

54 commitment period where pheromone can impose G1 arrest.

55 lication for the next 4 to 6 h, indicating a G1 arrest.

56 nd haemopoietic stem and progenitor cells in G1 arrest.

57 inhibitory pRB-E2F1 complex and limiting G0/G1 arrest.

58 g p53, it is dispensable for recovery from a G1 arrest.

59 ommitment and ensure a robust signal-induced G1 arrest.

60 tum formation and a significantly protracted G1 arrest.

61 plified neuroblastoma cell lines by inducing G1 arrest.

62 s of cyclin D1, increased levels of p27, and G1 arrest.

63 cle progression; p21 overexpression restored G1 arrest.

64 U) into DNA, an effect proposed to reflect a G1 arrest.

65 a cells to proliferate by promoting a robust G1-arrest.

66 on was associated with a strong induction of G1 arrest accompanied by an increase in Kip1/p27, Cip1/p

67 neuroendocrine differentiation induction and G1 arrest actions of the AGN and KMKKT extracts.

68 cts via a distinct, unknown pathway inducing G1 arrest after IL-7 withdrawal from T cells.

69 tor of cyclin-dependent kinases, and blocked G1 arrest after TBI thereby increasing the number of S p

70 NA damage and abrogated irradiation-mediated G1 arrest along with an increase of S phase in MCF7 cell

71 ference decreased both behaviors by inducing G1 arrest along with Rb hypophosphorylation and increase

72 The suppression of both Rb and S6RP enhances G1 arrest and a phenotype resembling cellular senescence

73 pression of SV40 T/t abolished hSNF5-induced G1 arrest and activation of RB.

74 inhibition, 0-30 Gy), resulting in a loss of G1 arrest and an enhancement of apoptosis to comparable

75 Cell cycle analysis demonstrated that G1 arrest and apoptosis contributed to the action of NVP

76 The prevention of mAb 225-induced G1 arrest and apoptosis in DiFi cells by bFGF was sensit

77 th factor-1 (IGF-1) modulate mAb 225-induced G1 arrest and apoptosis in DiFi cells.

78 Ablation of p21 protein by siRNA prevented G1 arrest and apoptosis in PC3-p53 cells.

79 HPR), which downmodulates cyclin D1, induced G1 arrest and apoptosis in rhabdoid cell lines.

80 ction of a subset of p53 targets involved in G1 arrest and apoptosis, including BTG2, RRM2B and GPX1.

81 Since p53 functions by inducing cell G1 arrest and apoptosis, we investigated the link betwee

82 stabilization of p53, and resulting cellular G1 arrest and apoptosis.

83 ion and survivin downregulation, and reduced G1 arrest and apoptosis.

84 rease in p53 protein, which exacerbated both G1 arrest and apoptosis.

85 1 in rhabdoid cells was sufficient to induce G1 arrest and apoptosis.

86 that induction of p27(KIP1) is required for G1 arrest and cell growth inhibition by erlotinib.

87 Furthermore, miR-193a causes cell cycle G1 arrest and cell proliferation repression through targ

88 pharmacological inhibition of LSD1 triggers G1 arrest and cellular senescence.

89 te, such as growth inhibition, apoptosis, G0/G1 arrest and chemoresistance.

90 We found that mevastatin induced G1 arrest and decreased DNA synthesis in rat PASMCs and

91 that coordinate cellular proliferation with G1 arrest and differentiation have long been of interest

92 n and its family members p107 and p130 in G0/G1 arrest and differentiation in mammalian cells.

93 nstrated that autocrine TGF-beta2 induces G0/G1 arrest and differentiation under nonpermissive cultur

94 In contrast, most LRCs were in G1 arrest and expressed genes that are regulated by the

95 ALK inhibition resulted in cell-cycle G1 arrest and inactivation of ERK1/2, STAT3, and AKT sig

96 of PINCR in CRC cells significantly impaired G1 arrest and induced hypersensitivity to chemotherapeut

97 ed knockdown of p21 abrogated the tetraploid G1 arrest and induced killing that was dependent on p53.

98 VSMC growth by decreasing proliferation via G1 arrest and inducing apoptosis.

99 and activates NF-kappaB/Rel, which leads to G1 arrest and induction of Ig L chain gene rearrangement

100 sociated proteins results in a p53-dependent G1 arrest and leads to defects in processing of the pre-

101 l line that had spontaneously undergone a G0-G1 arrest and least similar to the G2-M arrest stimulate

102 Both effects are critical for FIP200-induced G1 arrest and may contribute to the putative antitumor a

103 tor cells from asynchronous cell division to G1 arrest and neuronal specification at the morphogeneti

104 androgen-induced cell proliferation through G1 arrest and of the ability of androgen to suppress neu

105 Rbx1(+/Gt) MEFs do show retarded growth with G1 arrest and p27 accumulation.

106 It is noteworthy that we found that G1 arrest and p27(KIP1) up-regulation by erlotinib occur

107 ll line U937 leads to loss of clonogenicity, G1 arrest and partial differentiation.

108 proliferation, the compound also caused a G0-G1 arrest and prevented nuclear accumulation of cyclin D

109 trosoguanidine (MNNG) and rescues cells from G1 arrest and promotes cell survival after gamma-irradia

110 r pharmacologic inhibition of Prmt5 causes a G1 arrest and reduced proliferation resulting in extende

111 Smac transfectants displayed significant G0/G1 arrest and reduction in 5-bromo-2'-deoxyuridine (BrdU

112 A reduced cell proliferation rate by causing G1 arrest and restored the expression of the differentia

113 shPKCiota decreased proliferation, caused a G1 arrest and significantly prolonged overall survival i

114 uced activation of the EGF receptor, induces G1 arrest and subsequent cell death via apoptosis.

115 ic splice variant of CDKN1A that facilitates G1 arrest and subsequent DNA repair.

116 4/CDK6 with PD 0332991, which leads to early G1 arrest and synchronous S-phase entry upon release of

117 lts suggest that invasive cell fate requires G1 arrest and that strategies targeting both G1-arrested

118 (PSM)-RB has previously been shown to cause G1 arrest and to interfere with S phase progression.

119 l differentiation, in which ATRA coordinates G1 arrest and transition into differentiation by inducin

120 uman aortic smooth muscle cells by causing a G1-arrest and protected from TNFalpha-induced apoptosis.

121 G1 arrest and that strategies targeting both G1-arrested and actively cycling cells may be needed to

122 normal ionizing radiation resistance in both G1-arrested and cycling pro-B lines.

123 iated from CAK, leading to MAT1 degradation, G1 arrest, and decreased CAK phosphorylation of PML/RARa

124 l decreased cyclin E kinase activity, caused G1 arrest, and decreased DNA synthesis.

125 iferation, increased apoptosis, increased G0/G1 arrest, and decreased tumor growth.

126 helix prevents its phosphorylation, promotes G1 arrest, and enhances Rb's tumor suppressive function.

127 Anti-HER2 antibody-induced p27Kip1 protein, G1 arrest, and growth inhibition persist at least 5 days

128 guanine nucleotides, prevents cell growth by G1 arrest, and induces cell differentiation in a cell-ty

129 on in S. pombe results in growth inhibition, G1 arrest, and induction of fnx1+, a gene whose expressi

130 nin modulate G1 phase cyclins-CDKs-CDKIs for G1 arrest, and the Chk2-Cdc25C-Cdc2/cyclin B1 pathway fo

131 rylation, enhanced RB-E2F-1 association, and G1 arrest, and these events have been shown to protect f

132 hepatocytes, we found that TGF-beta-induced G1 arrest, apoptosis, and epithelial-to-mesenchymal tran

133 respective of the underlying cause mediating G1 arrest, are resistant to apoptosis induced by the pro

134 adhesion of myeloma cells to FN results in a G1 arrest associated with increased p27kip1 protein leve

135 3/Cdkn2b signaling in podocytes specifies G0/G1 arrest associated with podocyte differentiation, wher

136 der replication-53BP1 nuclear body formation-G1 arrest axis as an unanticipated outcome of homologous

137 We hypothesize that the predominance of G1-arrested bacteria in the infectious population, and t

138 d by TGF-beta1 in cells that fail to undergo G1 arrest because of inactivation of the retinoblastoma

139 The few cells that manage to bypass the G1 arrest become tumorigenic and fail to undergo pre-B c

140 human fibroblasts deregulated E2F1 causes a G1 arrest, blocking serum-induced cell cycle progression

141 ata1(low) phenotype (increased apoptosis and G1 arrest both in marrow and spleen and increased osteob

142 ishes that PKR activation in VSMC leads to a G1 arrest brought about by an inhibition of cyclin-depen

143 with p53 family members, as Nutlin-3 induced G1 arrest but did not activate apoptosis in p53(-/-) sar

144 ction of lipid droplets when associated with G1 arrest but do not cause morphological changes.

145 T1 clones were resistant to G1 arrest but more sensitive to cisplatin.

146 led that differentiation is not regulated by G1 arrest but rather by cell spreading and the level of

147 duction in BrdU incorporation reflects not a G1 arrest but rather direct inhibition of the initiation

148 t lead to increased E2F can overcome hypoxic G1 arrest but that additional alterations, promoted by E

149 le in apoptosis, the documented induction of G1 arrest by activation of the p38 MAP kinase pathway ha

150 hibitor-leads to irreversible, p53-dependent G1 arrest by an unknown mechanism.

151 er, these findings suggest that induction of G1 arrest by HA results from down-regulation of cyclin D

152 entry from G1 to S) and to HER1 inhibitors (G1 arrest) by changes in cell cycling.

153 t1-as2) by adding the ATP analog 1-NM-PP1 in G1-arrested cells allows the induction of synchronous me

154 n SYT were detected in confluent cultures of G1-arrested cells but not in sparse cells or during S or

155 A single double-stranded break (DSB) in G1-arrested cells causes phosphorylation of Rad55-S378,

156 These G0/G1-arrested cells express high levels of cyclin-dependen

157 aling pathway in response to a single DSB in G1-arrested cells that activates Mec1 without eliciting

158 duces p27 and Foxo3a levels, thus permitting G1-arrested cells to reenter the cell cycle.

159 In contrast, G1-arrested cells were more sensitive to mitogen-activat

160 wnregulation of RECQ4 expression occurred in G1-arrested cells, both in the absence or presence of ex

161 nd Mec1p, the yeast ATM and ATR homologs; in G1-arrested cells, most gamma-H2AX formation was depende

162 ow frequencies of SSA and gene conversion in G1-arrested cells, suggesting that SSA is not a frequent

163 sistant delta phospho-isoform not present in G1-arrested cells.

164 ha hypophosphorylation occur in ATRA-induced G1-arresting cells undergoing differentiation but not in

165 Although the p53-dependent G1 arrest checkpoint response to gamma-rays in MEFs has

166 seriously compromised in aged cells, and the G1 arrest coincides with massive aggregation of a metast

167 ore robust DNA damage response and increased G1 arrest compared with WT MEFs.

168 G1 arrest-correlated, long-term nitrogen starvation and

169 n under stress and calorie restriction (CR), G1 arrest defects, dedifferentiation, elevated recombina

170 ion of cell proliferation characterized by a G1 arrest dependent on the tumor suppressor p53.

171 ication response, AHR activation leads to G0-G1 arrest, diminished capacity for DNA replication, and

172 oss of eIF2alpha-P induced by UVB diminished G1 arrest, DNA repair, and cellular senescence coinciden

173 data support a model in which Pas1 inhibits G1 arrest downstream of Tsc1 and Tsc2, linking nutrient

174 not associated with its role in mediating G0/G1 arrest during cell cycle progression.

175 gh butyrate and sulindac induce a similar G0-G1 arrest, elevation of beta-catenin-Tcf signaling, and

176 Adult human corneal endothelial cells are G1-arrested, even in response to injury, leading to an a

177 In response to a G1 arrest evoked by the mating pheromone alpha factor th

178 In the Drosophila ectoderm, G1 arrest first appears during the seventeenth embryonic

179 d dThd withdrawal: JH-2 cells have an intact G1 arrest (>72 h) and delayed cell death (>96 h), wherea

180 ded with diminished T-cell proliferation and G1 arrest, hallmarks of IL-35 biological activity.

181 6 oncoprotein, does not prevent PTEN-induced G1 arrest, implying that p53 is not required for G1 arre

182 skeleton has been widely reported to cause a G1 arrest in a variable, and often high, proportion of c

183 f phosphatase activity impaired p53-mediated G1 arrest in arrested human glioblastoma GM cells in res

184 pigenin treatment of LNCaP cells resulted in G1 arrest in cell cycle progression which was associated

185 endent manner, which was largely due to a G0/G1 arrest in cell cycle progression; higher dose and lon

186 re sufficient to mediate p53 interaction and G1 arrest in cells.

187 onstrate for the first time that TKI-induced G1 arrest in CML progenitor cells is mediated by re-acti

188 -particle radiation revealed a total lack of G1 arrest in either p53-/- or p21waf1-/- cells, indicati

189 ing Whi5 and Stb1 allows partial escape from G1 arrest in far1 cln2 cells, along with partial derepre

190 de DOX-induced G2 arrest and instead induced G1 arrest in HL60 and Jurkat, thus propelling these p53-

191 pression of AR, and that the onset of the G0/G1 arrest in LNCaP and CWR22R cells is correlated with t

192 that PKCdelta mediates phorbol ester-induced G1 arrest in lung adenocarcinoma cells and establish an

193 sion of mouse double minute-2 (MDM2) induces G1 arrest in normal cells.

194 of mutated Notch1 receptors and induces a G0/G1 arrest in NOTCH1-mutated human leukemia cells.

195 lear receptor nhr-67/tlx directs the AC into G1 arrest in part through regulation of the cyclin-depen

196 the functions of B-Myb required to overcome G1 arrest in Saos-2 cells induced by the retinoblastoma-

197 c1/Tsc2 complex, we examined the kinetics of G1 arrest in single and double mutant strains.

198 of mTOR activity with rapamycin resulted in G1 arrest in SKOV3 cells, but not in OVCAR4 or OVCAR5 ce

199 , and disruption of centrosomes results in a G1 arrest in some cell types.

200 hrough cell division to induce p53-dependent G1 arrest in the daughter cells.

201 ted that unexpectedly, low PTX did not cause G1 arrest in the first cell cycle and did not prevent ce

202 results indicate the importance of not only G1 arrest in the MF but also appropriate progression thr

203 Interestingly, the failure to maintain G1 arrest in the MF led to the specification of R8 photo

204 e due to a failure to establish and maintain G1 arrest in the morphogenetic furrow (MF) and a defect

205 eye disc, bel mutant cells fail to undergo a G1 arrest in the morphogenetic furrow, delay photorecept

206 Overexpression of p27Kip1 induced G1 arrest in the presence of IL-7, whereas knockdown of

207 ytidine treatment of Rael cells results in a G1 arrest in the total cell population which precedes th

208 G1 arrest in the transformed cells was also linked to an

209 eration and tumor infiltration coincide with G1 arrest in tumor infiltrated Siah2(-/-) Tregs in vivo

210 nchorage-independent growth and facilitating G1 arrest in U251MG cells without inhibiting Akt activit

211 rturbations of centrosomal proteins leads to G1 arrest in untransformed mammalian cells has been a my

212 6 inhibition has been shown to induce potent G1 arrest in vitro and tumor regression in vivo; cdk2/1

213 PKR and that this event is required for the G1 arrest in VSMC.

214 this, we show that excess thymidine induces G1 arrest in wild-type fission yeast expressing thymidin

215 ion of RPS6KA2 reduced proliferation, caused G1 arrest, increased apoptosis, reduced levels of phosph

216 Consistent with a G1 arrest, increased expression of PKC-delta caused rapi

217 ite the fact that p53-dependent p21-mediated G1 arrest induced by DNA damage is well defined, the rol

218 Consistent with the G1 arrest induced by FIP200, we found that FIP200 increa

219 RNA, was found to prevent the senescence and G1 arrest induced by HTLV-1 Tax and vFLIP, respectively.

220 KC-delta expression induced a significant G0/G1 arrest, inhibited anchorage-independent growth (50%,

221 Rapamycin-induced G1 arrest is abrogated by nonspecific GSK3beta inhibitor

222 ires pRB, and it has been proposed that this G1 arrest is mediated by pRB-E2F repressor complexes.

223 We further show that G1 arrest is necessary for the histone deacetylase HDA-1

224 Thus, G1 arrest is not always dependent on Rb family members,

225 ished, the mechanism for the hypoxia-induced G1 arrest is not known.

226 G1 arrest is sufficient for some but not all aspects of

227 We show that G1 arrest is the specific nitrogen starvation-induced ev

228 because of its uniform but readily reversed G1 arrest, its fortified cell walls, heat tolerance, and

229 mponent RAD21(10-12) or CTCF(12,13) in these G1-arrested lines.

230 s during nonhomologous end-joining repair in G1-arrested mammalian cells, characterized by a transien

231 SSA is not a frequent DSB repair pathway in G1-arrested mammalian cells, even in the presence of per

232 MAPK inhibitor) and 69-fold higher Decorin (G1 arrest marker) expression in P4KO versus P4WT.

233 G1 arrest may occur by inhibiting the protein synthesis

234 ine palmitoyltransferase in the transient G0/G1 arrest mediated through Cln3 via a novel mechanism.

235 We demonstrate that G1-arrested melanoma cells, irrespective of the underlyi

236 olution Hi-C spatial organization map of the G1-arrested mouse pro-B cell genome and used high-throug

237 able for joining V(D)J recombination DSBs in G1-arrested mouse pro-B-cell lines, dispensable for join

238 In cells lacking RB, neither G1 arrest nor differentiation occurs; instead, they unde

239 th RING genes, are required for G2 delay and G1 arrest of cdc123-4 and promote G1 delay when over-exp

240 on but necessary for pocket protein-mediated G1 arrest of cycling cells.

241 ependent kinase inhibitor responsible for G0/G1 arrest of human melanoma cells grown on fibrillar col

242 IS inhibits ovarian cancer cells by inducing G1 arrest of the 3+Ecad- subpopulation through the induc

243 viral episome stability and abrogated sub-G1/G1 arrest of the cell cycle while increasing the efficie

244 etinoblastoma (Rb) protein and the resultant G1 arrest of the cells.

245 sm triggers a durable p38- and p53-dependent G1 arrest of the daughter cells despite normal division

246 Further analysis revealed a G0/G1 arrest of the phase cell progression and apoptosis, l

247 nation led to more significant cell cycle G0/G1 arrest of tumor cells.

248 F035 and the avicins induced cell cycle (G1) arrest of the human MDA-MB-453 breast cancer cell li

249 n result in a hypoxia-induced quiescence (G0/G1 arrest) of the cancer cells, making them resistant to

250 STS has been shown to cause RB-dependent G1 arrest or apoptosis; however, expression of PSM-RB di

251 UPR, GRP78 overexpression does not result in G1 arrest or depletion of topoisomerase II.

252 ing activity, which either led to a complete G1 arrest or induced the p53-dependent apoptotic pathway

253 ting-incompetent white cells without causing G1 arrest or shmoo formation.

254 ed human fibroblasts, whose features include G1 arrest, p21 induction, senescence-associated heteroch

255 The conversion is dependent on Tet1, as G1 arrest, p53 knockdown or expression of the reprogramm

256 emperature and a terminal, mating-proficient G1 arrest point.

257 The APC/C degrades dNek2 upon synchronous G1 arrest prior to differentiation, which allows retinal

258 that combined deficiency for PAXX and XLF in G1-arrested pro-B lines abrogates DSB joining during V(D

259 ions in the absence of XLF and vice versa in G1-arrested pro-B-cell lines.

260 We further show that in addition to G1 arrest, RASSF1A promotes growth arrest in the G2/M ph

261 In G1 arrest/release experiments with cdc2.33 cells at the

262 ation transition is induced from cancer cell G1 arrest remains unknown.

263 UVC, in contrast, induces a p53-independent G1 arrest response.

264 tein kinase pathway inhibitor, which induced G1 arrest, resulted in resistance to temozolomide or bor

265 IC1 alone strongly disrupts Far1-independent G1 arrest, revealing that inhibition of B-type cyclin-Cd

266 ing arrays to measure histone H3 turnover in G1-arrested Saccharomyces cerevisiae at single-nucleosom

267 ppressed PKC and MAPK signalling and induced G1 arrest selectively in melanoma cell lines carrying GN

268 fore prestalk cells and later encapsulate as G1-arrested spores.

269 Mirk reinforces the G0/G1 arrest state in which differentiation occurs by direc

270 targeted by UCN-01, and second, a tetraploid G1 arrest that can be targeted by siRNA against p21.

271 In CCl39 cells this promoted a sustained G1 arrest that correlated with decreased expression of c

272 Ansamycins cause RB-dependent G1 arrest that is associated with loss of D-cyclins via

273 Senescence is an irreversible form of G1 arrest that requires the p19ARF/p53 and p16INK4a/pRB

274 erest, although far1 cln2 sic1 cells escaped G1 arrest, they lost viability during pheromone exposure

275 how a role for CDKN2C in inducing cell cycle G1 arrest through inhibition of CDK4/6 associated with t

276 tivation by switching cellular response from G1 arrest to apoptosis.

277 cell-cycle arrest that is distinct from the G1 arrest typically observed in temperature-sensitive cd

278 ffector pathways was able to revert cells to G1 arrest upon Q deprivation.

279 dependent intron splicing partly explain the G1 arrest upon the loss of SpPrp18.

280 RAG scanning to mediate distal V(H) usage in G1-arrested v-Abl pro-B cell lines(9), which undergo rob

281 High p21 levels mediate G1 arrest via CDK inhibition, yet lower levels have no i

282 s identify a novel link between PKCdelta and G1 arrest via p21 up-regulation and highlight the comple

283 Molecular studies showed that G1 arrest was associated with a decrease in cyclin D1, c

284 chanism by which E7 bypasses hypoxia-induced G1 arrest, we applied a proteomic approach and used mass

285 Deltatsc1 and Deltatsc2 yeast had a delay in G1 arrest when compared with wild-type, which was rescue

286 ed, only those expressing pRb demonstrated a G1 arrest when treated with PD 0183812.

287 predominantly unbudded with 1N DNA content (G1 arrest), whereas gcr1delta cln1delta cln2delta cells

288 nsferred into IL-7-deficient hosts underwent G1 arrest, whereas 27Kip1-deficient T cells underwent pr

289 Hypoxic cells underwent G1 arrest, whereas anoxic cells also demonstrated S-phas

290 due to deficient p27(Kip1)-upregulation and G1 arrest, whereas SUDHL-1 cells respond with increased

291 miR-503 in heterologous cancer cells induces G1 arrest, which is also attenuated by overexpression of

292 cells the decline in CYCD3;1 levels leads to G1 arrest, which is overcome by ectopic CYCD3;1 expressi

293 high levels of cyclin A escape MDM2-mediated G1 arrest, which may account for a selective growth adva

294 considered to be the active form and directs G1 arrest, while hyperphosphorylated Rb permits the tran

295 reated with gamma-rays undergo p53-dependent G1 arrest, while oncogene-expressing MEFs treated with a

296 Inhibition of Hh signaling results in G0/G1 arrest with a concomitant reduction in S-phase and G2

297 D on the progress of the cell cycle, namely, G1 arrest with MD and an S phase delay followed by a G2/

298 3-OH kinase (PI 3-kinase), which results in G1 arrest with no effect on apoptosis.

299 reases cellular proliferation and results in G1 arrest without affecting cell size.

300 rations of PTX (low PTX) paradoxically cause G1 arrest (without mitotic arrest).