ライフサイエンスコーパス: checkpoint control

1 phase and functions in radiation-induced G2 checkpoint control.

2 d kinetochore proteins in mitotic timing and checkpoint control.

3 MDC1 regulates BRCA1 function in DNA damage checkpoint control.

4 microtubule-independent function in mitotic checkpoint control.

5 to function as sensors in the DNA integrity checkpoint control.

6 cal components of cell cycle progression and checkpoint control.

7 rly to their replication counterparts during checkpoint control.

8 3-related kinase (ATR), which function in G2 checkpoint control.

9 l material, indicating relaxation of spindle checkpoint control.

10 mediator protein involved in DNA replication checkpoint control.

11 quired for DNA synthesis and S-M replication checkpoint control.

12 le, indicating that Spc24p has a function in checkpoint control.

13 slesion DNA synthesis (TLS) and a DNA damage checkpoint control.

14 ls do not arrest in metaphase in response to checkpoint control.

15 ein that plays a critical role in cell cycle checkpoint control.

16 and could function as a sliding clamp during checkpoint control.

17 +), three genes essential for the DNA damage checkpoint control.

18 death and another that regulates cell cycle checkpoint control.

19 pombe homolog has been implicated in G(2)/M checkpoint control.

20 al regulation, DNA repair, and/or cell cycle checkpoint control.

21 Swe1 being the primary downstream target of checkpoint control.

22 uploidy, apparently by compromising the G(2) checkpoint control.

23 fied novel proteins such as p53 in executing checkpoint control.

24 xyurea resistance, as well as S and G2 phase checkpoint control.

25 ional regulation, DNA repair, and cell cycle checkpoint control.

26 nucleolus, aging, cell cycle regulation, and checkpoint control.

27 of radiation-induced G(2)/M, but not G(1)/S, checkpoint control.

28 vival following gamma-irradiation and G(2)-M checkpoint control.

29 a compound which is known to induce loss of checkpoint control.

30 functions such as DNA repair and cell cycle checkpoint control.

31 DNA damage that has the effect of enhancing checkpoint control.

32 ng that hRAD17 may have a role in cell cycle checkpoint control.

33 ng a block in entry into S phase and loss of checkpoint control.

34 ian female meiosis lacks chromosome-mediated checkpoint control.

35 ogenesis and may also be a target of meiotic checkpoint control.

36 ished by caffeine, an agent which attenuates checkpoint control.

37 ction between Bub1 and hBubR1 with hBub3 for checkpoint control.

38 ude effects on cell viability and cell cycle checkpoint control.

39 ferently than do normal cells in terms of G1 checkpoint control.

40 otic divisions; it may also be a target of a checkpoint control.

41 d sensitivity to x-rays and UV and a loss of checkpoint control.

42 ionizing radiation and defects in cell-cycle checkpoint control.

43 nce for a putative role of cyclin G1 in G2/M checkpoint control.

44 atively different from that of G2 DNA damage checkpoint control.

45 es involved in DNA metabolism and cell-cycle checkpoint control.

46 a new ATR activator involved in replication checkpoint control.

47 ion partner choice, DSB repair pathways, and checkpoint control.

48 phosphorylation is unnecessary for cell size checkpoint control.

49 ally interact and participate in replication checkpoint control.

50 dissect the contributions of Chk1 and MK2 to checkpoint control.

51 s required for Crb2 localization to DSBs and checkpoint control.

52 has an unexpected early role in replication checkpoint control.

53 end resection and DNA damage-induced G(2)/M checkpoint control.

54 sites of DNA damage and is required for G2/M checkpoint control.

55 anism to regulate cell cycle progression and checkpoint control.

56 mit APC activity for substrate selection and checkpoint control.

57 damage response, participating in cell cycle checkpoint control.

58 chanism downstream of ATM/ATR activation for checkpoint control.

59 amage sites and functions with BRCA1 in G2/M checkpoint control.

60 rotein hnRNPA0 is the "successor" to p53 for checkpoint control.

61 lication and have been linked to replication checkpoint control.

62 f p53 transcription contributes to defective checkpoint control.

63 roper cell cycle progression and replication checkpoint control.

64 k repair (DSBR) and intra-S phase DNA damage checkpoint control.

65 s essential functions to both cell cycle and checkpoint control.

66 and allow transformed pre-B cells to bypass checkpoint control.

67 required for chromosome motility and spindle checkpoint control.

68 ollowing DNA damage and participates in G2/M checkpoint control.

69 n a manner that is distinct from its role in checkpoint control.

70 and also plays a critical role in cell cycle checkpoint control.

71 amage response and is involved in cell cycle checkpoint control.

72 or involved in DNA repair and damage-induced checkpoint controls.

73 the loss of key components of ATR-dependent checkpoint controls.

74 ay be involved in DNA damage and replication checkpoint controls.

75 e required for DNA damage and/or replication checkpoint controls.

76 s and not through deficiencies in cell cycle checkpoint controls.

77 o gamma-rays and UV light, without affecting checkpoint controls.

78 that information to the parasite cell cycle checkpoint controls.

79 a-rays and UV light and eliminate associated checkpoint controls.

80 delayed in interphase through the action of checkpoint controls.

81 ing NIMA kinase is thus a target for S-phase checkpoint controls.

82 integrity and from Mec1- and Tel1-dependent checkpoint controls.

83 e separable from the conventional DNA damage checkpoint controls.

84 sruption of DNA replication or by defects in checkpoint controls.

85 ous aspects of DNA repair, recombination and checkpoint control [2][3].

86 plicated the protein kinase Mec1p in S-phase checkpoint control [5].

87 ion to roles in apoptosis [6] and cell-cycle checkpoint control [7] in response to DNA damage, p53 pr

88 ing modules believed to be crucial for their checkpoint control activities.

89 erved in checkpoint control mutants, loss of checkpoint control activity is associated with a reducti

90 e inappropriate expression of the DNA damage checkpoint control activity of UmuD(2)C.

91 This osteoblast-induced enhanced G(0)-G(1) checkpoint control affected the chemosensitivity of LNCa

92 Abrogation of checkpoint control after cdk1 depletion or inhibition in

93 nducible gene product involved in cell cycle checkpoint control after DNA damage.

94 and results in attenuated apoptosis and G1-S checkpoint control, allowing Brca1Delta11/Delta11 cells

95 287 phosphorylation is a major locus of G2/M checkpoint control, although several checkpoint-independ

96 is effect was associated with a loss of G1-S checkpoint control, although the cyclin D1-overexpressin

97 machinery plays additional roles in S phase checkpoint control, although the identities of the repli

98 s serves as both a damage sensor to activate checkpoint control and a component of base excision repa

99 s serves as both a damage sensor to activate checkpoint control and a component of the BER.

100 tion, whereas ATR controls damage-induced G2 checkpoint control and apoptosis in proliferating cells.

101 pathway plays a critical role in cell-cycle checkpoint control and apoptosis, whereas Rho family sma

102 fic downregulation of genes involved in G2/M checkpoint control and contained tetraploid cells that w

103 t lack the RB homolog MAT3 show loss of size checkpoint control and deregulated cell-cycle progressio

104 gh kinase cascades that result in cell cycle checkpoint control and DNA repair.

105 tivity and plays central roles in cell cycle checkpoint control and DNA repair.

106 BRCA1 has important functions in cell cycle checkpoint control and DNA repair.

107 Many of the gene products involved in checkpoint control and DSBR have been studied in great d

108 in how Hec1 plays a crucial role for spindle checkpoint control and faithful chromosome segregation.

109 We find that Bub1 is essential for checkpoint control and for correct chromosome congressio

110 DC gene products participate in a DNA damage checkpoint control and in translesion DNA synthesis.

111 phaly, plays an important role in DNA damage checkpoint control and mitotic entry.

112 Thus, p21 coupled p53-dependent checkpoint control and preservation of chromosomal stabi

113 ca1 show genetic instability, defective G2-M checkpoint control and reduced homologous recombination.

114 Centrosomes integrate G2/M checkpoint control and repair signals in response to gen

115 as markedly increased in the absence of TP53 checkpoint control and significantly modulated by the ce

116 y CK2, is a relevant target of CK2 in G(2)/M checkpoint control and that both molecules participate i

117 coproteins results in the loss of cell cycle checkpoint control and the accumulation of chromosomal a

118 ce, providing a firm link between cell cycle checkpoint control and tissue regeneration.

119 ation of wild-type p53 leads to loss of G1/S checkpoint control and to genomic instability, including

120 ne products participate in both a DNA damage checkpoint control and translesion DNA synthesis.

121 e yeast Saccharomyces cerevisiae that affect checkpoint control and/or viability in response to a sin

122 nction is well known to influence cell cycle checkpoint controls and apoptosis.

123 SFN also has a marked effect on cell cycle checkpoint controls and cell survival and/or apoptosis i

124 The tumor suppressor p53 is involved in such checkpoint controls and is also required to avoid a high

125 upstream of p53 in mediating G1-S cell cycle checkpoint control, and both atm and p53 are believed to

126 ge response comprises DNA repair, cell-cycle checkpoint control, and DNA damage-induced apoptosis tha

127 ted with transcriptional activation, meiotic checkpoint control, and DNA double-strand break (DSB) re

128 e required for DNA damage resistance, G(2)-M checkpoint control, and DNA repair.

129 ion, DNA double-strand break repair, meiotic checkpoint control, and histone deacetylation.

130 help to explain how p53 mediates growth and checkpoint control, and how members of the p300/CBP fami

131 re due to enhanced DSB repair, robust G(2)-M checkpoint control, and resistance to IR-induced apoptos

132 n DNA double-strand break repair, cell cycle checkpoint control, and telomere length maintenance.

133 lopment is associated with the loss of these checkpoint controls, and this provides an approach for t

134 t prometaphase; (b) participating in spindle checkpoint control; and (c) moving poleward at anaphase.

135 BT, including the addition of gap phases and checkpoint controls, are accompanied by activation of th

136 It has been implicated in mitotic checkpoint control, as an active kinase at unattached ki

137 p53 mediates checkpoint control at G(1) by transcriptional regulation

138 nes controlling mitotic spindle assembly and checkpoint control at the 40-h time point as regulated a

139 The dissociation of checkpoint control at the level of Cdc25 indicates that

140 nsitive pds1 allele, pds1-128, defective for checkpoint control at the permissive temperature and ess

141 The p53-mediated checkpoint controls become important when differentiatio

142 of G(1)/S CDK complexes is important in the checkpoint control blocking mitotic onset when DNA repli

143 cate CtIP as a critical player in cell cycle checkpoint control but also provide molecular mechanisms

144 1 mutants are partially defective in S-phase checkpoint control but are proficient in DNA damage and

145 HPV-16 E7 involves attenuation of DNA damage checkpoint control by accelerating the proteolytic turno

146 We propose that Ddk modulates the S-phase checkpoint control by attenuating checkpoint signaling a

147 ycle machinery and are subject to cell cycle checkpoint control by cyclin-dependent kinase (CDK) inhi

148 of human Rad9 protein is important for G(2) checkpoint control by operating the transport of the hRa

149 ination of DNA repair with the p53-dependent checkpoint control by sensing UV damage and releasing p5

150 lyzed the role of the protein kinase Chk1 in checkpoint control by using cell-free extracts from Xeno

151 und to possess a glucose-sensitive metabolic checkpoint controlled by the energy sensor AMP-activated

152 ngs raise the possibility that the signaling checkpoints controlled by proteases could be useful targ

153 ore, our findings support the notion that G1 checkpoint control can be restored in tumor cells contai

154 AC invasion as a model for understanding key checkpoints controlling cell invasion.

155 Consistent with altered mitotic checkpoint control, cells expressing T displayed elevate

156 Checkpoint controls coordinate entry into mitosis with t

157 HU-induced checkpoint control could not be uncoupled from drug resi

158 Moreover, HRAD1 complements the checkpoint control defect of this strain after UV exposu

159 and whether the sensitivities correlate with checkpoint control deficiencies.

160 sing link between p53 activation and S phase checkpoint control designed to eliminate replicating pre

161 sigma is linked to p53-regulated cell cycle checkpoint control, detailed mechanisms of how cell cycl

162 ings identify JAB1 as an important factor in checkpoint control during early B cell development, as w

163 through S phase, but also for maintenance of checkpoint control during S phase.

164 lated and is required for DNA damage-induced checkpoint control during the transition from G2 to M ph

165 ated and is essential for DNA damage-induced checkpoint control during the transition from the G(2) p

166 ociated with stress response, and cell cycle checkpoint control (e.g., YB-1, DBPA, and ATF4), and gen

167 Critical checkpoints controlling early thymic T-cell development

168 rther, the translation of ccnd1 mRNA, a G1/S checkpoint control element, was impaired by microinjecti

169 Checkpoint controls ensure that events of the cell-divis

170 PV-16 E7, decreased the fidelity of multiple checkpoints controlling entry into and exit from mitosis

171 Checkpoint controls exist in eukaryotic cells to ensure

172 Together, these data reveal that a checkpoint control exists in early but not late prophase

173 We show here that, similar to the DNA checkpoint controls, expression of vpr promotes subcellu

174 diation sensitivity, and aberrant cell-cycle-checkpoint control following exposure to ionizing radiat

175 ection, the gustatory system acts as a final checkpoint control for food acceptance or rejection beha

176 ith UmuD(2)C is important for the DNA damage checkpoint control function of the umuDC gene products.

177 b1 is functionally linked to the replication checkpoint control gene cds1.

178 of the Schizosaccharomyces pombe DNA damage checkpoint control gene rad1(+) and its Saccharomyces ce

179 RNA levels corresponding to HRAD17, another checkpoint control gene, demonstrated a similar pattern,

180 e 14-3-3sigma gene has been reported to be a checkpoint control gene, since it promotes G(2) arrest f

181 ss of BRCA1 was 14-3-3 sigma, a major G(2)/M checkpoint control gene.

182 nserved mammalian HRAD9 and Mrad9 cell cycle checkpoint control genes have been isolated and called H

183 Mutations in checkpoint control genes therefore may contribute to the

184 ed induction of several G1/S as well as G2/M checkpoint control genes upon SAG withdrawal.

185 suppressor loci, and based on the biology of checkpoint control genes, HRAD9 should be considered a s

186 iated repression of p53 and other cell cycle checkpoint-control genes.

187 the correlation among a dysfunctional G(2)/M checkpoint control, genomic instability, and loss of tel

188 A direct role for TopBP1/Mus101 in checkpoint control has been difficult to prove, however,

189 This checkpoint control has been the subject of intensive gen

190 apoptotic signals but its role in cell cycle checkpoint control has not been elucidated.

191 gulators have been identified in plants, and checkpoint control has not been observed during plant me

192 unction of Pds1p, independent of its role in checkpoint control, has not been elucidated.

193 Defects in checkpoint control have been seen in certain hereditary

194 es, including transcription, ubiquitination, checkpoint control, homologous recombination, and DNA re

195 ification of Tyr(20) may serve in a cellular checkpoint controlling IFITM3 trafficking and degradatio

196 and Ddi1p renders cells defective in S-phase checkpoint control, implicating UBA domains in checkpoin

197 PK signaling and p21 can regulate cell cycle checkpoint control in carcinoma cells at the G(1)/S tran

198 olutionarily conserved proteins required for checkpoint control in fission yeast.

199 and identify Cdc25C as a potential target of checkpoint control in human cells.

200 active Chk2 monomers that proceed to enforce checkpoint control in irradiated cells.

201 in kinase, has been implicated in cell cycle checkpoint control in lower eukaryotes.

202 lly critical role for Claspin in replication checkpoint control in mammalian cells.

203 on the proteins mediating G1/S, S, and G2/M checkpoint control in mammalian cells.

204 amage, which coincides with defective G(2)/M checkpoint control in response to DNA damage.

205 tion of p53 protein, and exhibit an impaired checkpoint control in response to DNA damage.

206 cating the involvement of Chk1/Grapes in the checkpoint control in response to overreplication.

207 B11 is essential for DNA replication and S/M checkpoint control in Saccharomyces cerevisiae.

208 2 contributes to the loss of mitotic spindle checkpoint control in the E7 cells.

209 consistent with a loss of normal cell cycle checkpoint control in these cells.

210 nsitions at the five-blob stage and activate checkpoint controls in the oocyte that arrest Grk synthe

211 l aspects of the DNA damage response besides checkpoint control, including inhibition of septum forma

212 with proteins involved in DNA damage-induced checkpoint control, including the DNA helicase BACH1 and

213 These results suggest that diminished G1 checkpoint control is an early event in the process of c

214 e lymphoblastic leukemia, the BACH2-mediated checkpoint control is compromised by deletions, rare som

215 Loss of this checkpoint control is detrimental to the developing embr

216 One important target of checkpoint control is ribonucleotide reductase (RNR), wh

217 The target of the checkpoint control is the anaphase-promoting complex (AP

218 p53-mediated checkpoint control is unperturbed in ARF-null fibroblast

219 erved mitotic regulator critical for spindle checkpoint control, kinetochore functionality, and cell

220 Whether partial loss of checkpoint control leads to more subtle rates of chromos

221 n pathway in mammalian cells that provides a checkpoint control, linking amino acid sufficiency to th

222 nteraction with MAD1 is required for mitotic checkpoint control, MAD2B does not interact with MAD1, s

223 /2 cell clones to examine whether loss of G1 checkpoint control may be an early event in tumor develo

224 at the process of replication initiation and checkpoint control may be fundamentally different in mit

225 human genes, suggesting that aspects of the checkpoint control mechanism are conserved between fissi

226 ting a critical role of CE in the elongation checkpoint control mechanism during promoter clearance.

227 tokine- and pre-BCR signaling and how normal checkpoint control mechanisms are circumvented in pre-B

228 Moreover, by overwhelming checkpoint control mechanisms that may prevent cells wit

229 nimal systems, including transcriptional and checkpoint control mechanisms.

230 rating chromosome damage and undermining the checkpoint control mechanisms.

231 lls are largely independent of G1 cell cycle checkpoint control mediated by p21.

232 ssion, nuclear import/export, and cell cycle checkpoint control) might be subject to regulation by ex

233 ntly suggested that a morphogenesis/polarity checkpoint control monitors bud emergence in order to ma

234 e progression is resumed and, as observed in checkpoint control mutants, loss of checkpoint control a

235 rogression beyond this apparent PIC assembly checkpoint control occurs only in the presence of Pol II

236 lls, including DNA repair and recombination, checkpoint control of cell cycle, and transcription.

237 cycle programme, and disrupt DNA-replication checkpoint control of cell-cycle progression.

238 R responses to DNA damage and their links to checkpoint control of DNA replication.

239 is proposed in which proteolytically driven checkpoint control of ER mannosidase I contributes to th

240 Furthermore, checkpoint control of Sld3 impacts fork progression unde

241 e of Cdc25 phosphatase-dependent pathways in checkpoint control, oncogenesis, and apoptosis.

242 This checkpoint control operated at the level of inhibition o

243 Here, we show that a DNA replication checkpoint control operates during meiosis in fission ye

244 estigated whether cdc20+ is required for the checkpoint control operating in fission yeast, and our d

245 mitosis prematurely as a result of a lack of checkpoint control or in embryos with elevated Cdk1 acti

246 yeast genetically altered to lack DNA damage checkpoint control or that constitutively promote cell c

247 y directly inducing DNA damage, inactivating checkpoint controls, or manipulating repair processes.

248 The data demonstrate that lack of checkpoint control over mitosis can secondarily cause de

249 In addition to restoring checkpoint control, overexpression of sum1+ inhibits the

250 (UPS) to be required in mammalian DNA damage checkpoint control, particularly the G(1) cell cycle che

251 defects in the DNA damage aspect of the rad checkpoint control pathway had an increased frequency of

252 of S. Pombe is an essential component of the checkpoint control pathway which responds to both DNA da

253 an important protein family associated with checkpoint control pathways, 14-3-3, is involved in cell

254 regulate signal transduction, apoptotic, and checkpoint control pathways.

255 that participate in signal transduction and checkpoint control pathways.

256 s playing roles in DNA repair and cell cycle checkpoint control pathways.

257 tivation of the cell cycle and repression of checkpoint control pathways.

258 The spindle assembly checkpoint controls proper chromosome segregation during

259 We have characterized the Drosophila mitotic checkpoint control protein Bub1 and obtained mutations i

260 cell-cycle control: Nud1p binds the spindle checkpoint control proteins Bfa1p and Bub2p to the SPB,

261 ns of the HUS1-encoded protein and two other checkpoint control proteins, RAD1p and RAD9p, implicated

262 at interacts with multiple, known cell cycle checkpoint control proteins.

263 it, Cdc55p, a protein recently implicated in checkpoint control regulation.

264 is important for understanding mechanisms of checkpoint control, repair and cell death following such

265 Moreover, whereas checkpoint control requires kinetochores, the regulation

266 Here we provide evidence that a checkpoint control requiring the mitotic DNA-damage chec

267 During this interval, S-phase checkpoint controls restrain mitosis until replication i

268 nd UmuC together participate in a cell cycle checkpoint control; second, UmuD'(2)C enables translesio

269 EN(+/+) cells recapitulated the lack of size checkpoint control seen in PTEN(-/-) cells.

270 icipates in DNA damage repair and cell-cycle checkpoint control, serving as a tumor susceptibility ge

271 nt discovery of Ran's involvement in spindle checkpoint control suggested a potential new arena for i

272 uman CDC2 mutants in fission yeast abolishes checkpoint control, suggesting that these residues could

273 ential component of a previously unsuspected checkpoint control system that couples the completion of

274 in response to DNA damage as part of the SOS checkpoint control system.

275 Interference with inhibitory immunological checkpoints controlling T cell activation provides new o

276 regulation of the transcriptional elongation checkpoint control (TECC) stage of gene expression and h

277 tenance factor, raising the possibility that checkpoint control, telomere maintenance and aging may b

278 nd that one of these proteins is part of the checkpoint control that ensures accurate chromosome segr

279 fect in T cell developmental programming and checkpoint control that permits a subset of the normal o

280 in response to ER stress is a mechanism for checkpoint control that prevents cell-cycle progression

281 hese microtubular structures contribute to a checkpoint control that retains the equatorial position

282 pombe, respectively, and also participate in checkpoint controls that ensure DNA replication is compl

283 Thus, Pxr serves as a major checkpoint controlling the transition from growth to dev

284 elangiectasia mutated and Rad3 related-Chk1) checkpoint controls the timing of cell division in the f

285 highly regulated processes involving several checkpoints controlling the resolution of inflammation.

286 o function in mutation avoidance, cell cycle checkpoint control, the cytotoxicity of various DNA-dama

287 at least in part by compromising the mitotic checkpoint control through inactivation of BubR1.

288 dence suggests that Rad53 exerts its role in checkpoint control through regulation of the Polo kinase

289 st a novel pathway involving HDAC1 in G(2)/M checkpoint control through the interaction with a functi

290 nce, and depend upon an intact morphogenesis checkpoint control to survive.

291 -cleavage of UmuD (which participates in the checkpoint control) to yield UmuD' (which enables TLS).

292 pair, microsatellite instability, cell cycle checkpoint control, transcription-coupled nucleotide exc

293 have roles in DNA damage repair, cell cycle checkpoint control, transcriptional regulation and ubiqu

294 Loss of DNA damage-induced checkpoint control was caused by a reduction in formatio

295 regulators and/or effectors involved in size checkpoint control, we employed a novel endogenous epito

296 To better understand the role of p34cdc2 in checkpoint control, we have screened for more mutations

297 To further study the role of Chk1 in G2 checkpoint control, we identified a potent and selective

298 A replication, mitosis, and spindle assembly checkpoint control were all highly represented in the mu

299 flammation, Hsp27 regulation, and cell cycle checkpoint control with a focus on brain pathologies.

300 A role for MLH1 in G2-M cell cycle checkpoint control, without alteration in G1, after IR w