ライフサイエンスコーパス: defective cell

1 shift mutations are strongly elevated in Clp-defective cells.

2 aneous chromosomal aberrations seen in BRCA2-defective cells.

3 sphorylation, however, was attenuated in NER-defective cells.

4 luciferase reporter assay employing DNA-PKcs defective cells.

5 in cell mass and an elimination of excess or defective cells.

6 ics compared with WT, BER-defective, and NER-defective cells.

7 estabilization especially in mismatch repair-defective cells.

8 ty of DNA-damaging agents selectively in p53-defective cells.

9 e topoisomerase I inhibitor SN38 only in p53-defective cells.

10 ike gain of Rga8 function, is lethal to Shk1-defective cells.

11 mutant cell lines, including XPF- and ERCC1-defective cells.

12 en in rad6 and rad18 cells as well as in NER-defective cells.

13 rictive temperature, a hallmark of secretion-defective cells.

14 ld confer some repair to extracts from ERCC1-defective cells.

15 te DNA sequences are high in mismatch repair-defective cells.

16 ear loci was impaired in the internalization-defective cells.

17 re obtained with extracts from polA- or polB-defective cells.

18 ll proliferation was enhanced in endocytosis-defective cells.

19 ent because induction does not occur in Arnt-defective cells.

20 , a type 1 topoisomerase inhibitor) in FANCB-defective cells.

21 oD is less accessible in the differentiation-defective cells.

22 n, invasion and apoptotic resistance of Tsc2-defective cells.

23 ication stress and genome instability in RER-defective cells.

24 consequences of ribonucleotides in RNase H2-defective cells.

25 nly shown in p53 wild-type cells, not in p53-defective cells.

26 e entry points for fork degradation in BRCA2-defective cells.

27 in ARF6-activated cells but impaired in ARF6-defective cells.

28 egradation and chromosomal breakage in BRCA2-defective cells.

29 nuclei, and DNA was overreplicated in export-defective cells.

30 frequency and chromosome integrity in BRCA2-defective cells.

31 PARP1 is hyperactivated in replicating BRCA2-defective cells.

32 rDNA GCI, although not to the extent of BLM defective cells.

33 of nucleotide excision repair-proficient and defective cells.

34 in a reporter construct is impaired in ERCC1-defective cells.

35 that mutagenesis is elevated 50-fold in Clp-defective cells.

36 sion of beta1 integrin in JAM-A dimerization-defective cells.

37 PMS2), as compared with HEC-1-A (hMSH6/hPMS2-defective) cells.

38 In contrast, yeast BER-defective cells accumulate endogenous damage preferentia

39 ated in the perinuclear region, resulting in defective cell adhesion and directional migration.

40 Genetic ablation of PLD1 led to defective cell adhesion and migration of inflammatory ce

41 lin-1 protein in keratinocytes, resulting in defective cell adhesion and migration.

42 deficient glands, which may result from the defective cell adhesion between the cap and body cell la

43 ere FACS sorted, GFP-expressing cells showed defective cell adhesion on tissue culture surfaces and s

44 The BER/NER-defective cells also possess increased levels of intrace

45 h wild type (WT) or NER-defective cells, BER-defective cells and BER/NER-defective cells possess elev

46 st, overexpression of rga8 is lethal to shk1-defective cells and causes morphological and cytokinesis

47 luciferase reporter assay employing both Ku-defective cells and Ku small interfering RNA knock-down

48 tory pathway that may be involved in killing defective cells and that has been evolutionarily conserv

49 ion of environmental factors that affect MMR-defective cells and their propensity for oncogenic trans

50 romoter driving E1A expression in Rb pathway-defective cells, and furthermore, that its oncolytic act

51 XRCC4-defective cells are extremely sensitive to ionizing radi

52 The BER/NER-defective cells are genetically unstable, exhibiting mut

53 Thus, CMA-defective cells are more sensitive to stressors, suggest

54 Here, we show that BRCA2-defective cells are not completely impaired in HR by str

55 hesis in Drosophila or Caenorhabditis causes defective cell arrangements and embryonic death.

56 elerated and pronounced way in the NF-kappaB-defective cells, as soon as 6 h after infection, when vi

57 In ATG14 homo-oligomerization-defective cells, autophagosomes still efficiently form b

58 In p53 or ATM defective cells, AZD6738 treatment resulted in replicati

59 th, when compared with wild type (WT) or NER-defective cells, BER-defective cells and BER/NER-defecti

60 when the HLA-DRA promoter is inactive in Rb-defective cells but not when the promoter is converted t

61 s HR repair by strand invasion also in BRCA2-defective cells, but less efficiently.

62 Treatment of these defective cells, but not cells with functional MutY, wit

63 We observed that RB-defective cells, but not the RB-reconstituted clones, de

64 es such as cancer require the elimination of defective cells by apoptosis.

65 They recognize defective cells by binding to peptides presented on the

66 ically inhibits the G(2)/M checkpoint in p53-defective cells by down-regulation of two critical check

67 Remarkably, PDS reduces proliferation of HR-defective cells by inducing DSB accumulation, checkpoint

68 n vitro by the action of PKC and in the MutY-defective cells by phorbol-12-myristate-13-acetate but t

69 uced G(2) checkpoint most selectively in p53-defective cells, by primarily targeting Chk1.

70 ions typically lead to arrest in S-phase but defective cells can also progress through the cell cycle

71 tic elimination of p53 mutant and DNA-repair defective cells caused by UVA radiation.Oncogene advance

72 The cellular basis of this phenotype is defective cell-cell adhesions of developing germ cells t

73 Analysis of transformation-defective cell clones generated after mutagenesis of the

74 ptibility to UVB-induced skin SCCs involving defective cell cycle arrest in response to UVB.

75 Defective cell cycle checkpoint function has been linked

76 These data indicate that defective cell cycle checkpoints and chromosomal instabi

77 g cellular responses to DNA damage caused by defective cell cycle checkpoints and/or DNA repair.

78 was carried through into mitosis because of defective cell cycle checkpoints, resulting in cell deat

79 Defective cell cycle control in the absence of Mnt is li

80 proteins occur frequently in tumor cells and defective cell cycle control is a common and perhaps uni

81 ation stress, impaired checkpoint signaling, defective cell cycle control, and genomic instability, w

82 ping, (2) there was no enhanced apoptosis or defective cell cycle entry in Csx/Nkx2.5 null cardiac my

83 lin E knock-in HSCs that was associated with defective cell cycle exit and the emergence of chromosom

84 es p27 levels in Schwann cells, which causes defective cell cycle progression and aberrant differenti

85 tion, BAX- and BAK-deficient B cells display defective cell cycle progression to B cell receptor cros

86 cellular proliferation, increased apoptosis, defective cell cycle progression, a diminished ability t

87 ryonic fibroblasts (MEFs) is impaired due to defective cell cycle progression, associated with reduce

88 ssion in human endothelial cells resulted in defective cell cycle progression.

89 ibutes to accumulation of CRL substrates and defective cell cycle progression.

90 t cells had elevated genomic instability and defective cell cycle reentry following replication stres

91 ctive MmRad51-mediated DNA repair and not by defective cell cycle regulation.

92 Although defective cell cycle-checkpoint regulation and associate

93 d by cellular sensitivity to mitomycin C and defective cell-cycle progression.

94 Because defective cell death (too little or too much) is implica

95 port showing the role of CD24 in the delayed/defective cell death in sepsis.

96 s, we show that HR events occurring in BRCA2-defective cells differ from HR events in wild-type cells

97 The combination of defective cell differentiation and lamination led to ret

98 Thus, RECQL5 and BLM impact FANCB-defective cells differently in response to replication s

99 p62/SQSTM1, which accumulates in autophagy-defective cells, directly binds to and inhibits nuclear

100 We show that BLM-defective cells display a higher frequency of anaphase b

101 d-type cells leading to mitotic catastrophe, defective cell division and apoptosis.

102 nsfections, cells undergo both apoptosis and defective cell division.

103 genesis revealed a tight correlation between defective cell divisions and SCR expression in cells tha

104 ges, but larval organs show asynchronous and defective cell divisions, and imaginal discs arrest earl

105 evels of SSBs, and PAR polymers formed in HR-defective cells do not colocalize to replication protein

106 esponse-dependent gene expression in editing-defective cells during amino acid stress.

107 s that allows recognition and elimination of defective cells during the early stages of development a

108 Mutations in CSI1 cause defective cell elongation in hypocotyls and roots and re

109 Because defective cell elongation is the earliest and most unive

110 overexpression of Mad2 protein in checkpoint-defective cells enhances paclitaxel sensitivity.

111 their signal peptides displays an identical defective cell envelope phenotype.

112 In addition, defective cells exhibited disorganized phragmoplast MT a

113 In MutY-defective cell extracts, but not extracts with functiona

114 glucose metabolism, which correlates with a defective cell fate decision.

115 thelial cells hyperproliferative, and caused defective cell fate specification or differentiation bot

116 ly increased casapse-3 activation in the NER-defective cells following cisplatin treatment.

117 altered cell cycle arrest pattern of the NER-defective cells following cisplatin treatment.

118 developmental pathways or completely remove defective cells from a population is a widespread strate

119 The elimination of unnecessary or defective cells from metazoans occurs during normal deve

120 sion or delamination can remove apoptotic or defective cells from the epithelial sheet and can restor

121 ddition, maturation of OCLs was abrogated by defective cell fusion of pre-OCLs depleted of Orai1, con

122 from mutant elo1-1 (designated as elongation defective) cells grown with long or medium chain fatty a

123 We also documented that yeast BER-defective cells have significantly higher levels of endo

124 In VHL-defective cells, HIF alpha-subunits are constitutively s

125 show that inactivation of Cdc2 in gamma-H2A-defective cells impairs Crb2-dependent signaling to the

126 nuclear translocation is not affected in Ku defective cells, implying Ku functionality may be mainly

127 To identify the defective cells in BXD2 mice, mouse synovial fibroblasts

128 ulations consisting of normal and E-cadherin defective cells in monolayer cell culture.

129 ted to an increased apoptosis of replication-defective cells in the C/EBPbeta-null epithelium.

130 ults in the same phenotypes observed in ssrA-defective cells, including a variety of phage developmen

131 We show that Zpr1 defective cells initiate lumen formation, but are blocke

132 GA treatment pushed irradiated p53 signaling-defective cells into a premature mitosis characterized b

133 of ribosome and tRNA synthesis in secretion-defective cells involves activation of the cell integrit

134 STAT activation in JAK2- and TYK2-defective cells is also normal, and the tyrosine phospho

135 The arrest in cdc20 defective cells is dependent on the BUB2 checkpoint and

136 This effect was not seen in a caspase 3-defective cell line (MCF-7) and was abrogated in Bak-sen

137 An ataxia-telangiectasia defective cell line also shows elevated rDNA GCI, althou

138 duced increase in nuclear Rad51 in the Brca2-defective cell line Capan-1.

139 Irs-20 is a DNA-PKcs-defective cell line with milder gamma-ray sensitivity th

140 An SSB repair-defective cell line, EM9 with an XRCC1 mutation, has an

141 Moreover, in VHL-defective cell lines (RCC4 and RCC10) derived from spora

142 cantly more tumor cells from the parental RB-defective cell lines and the RB revertants than from the

143 Consistent with this, APTX-defective cell lines are sensitive to agents that cause

144 rtant for recombinational repair, as paralog-defective cell lines exhibit spontaneous chromosomal abe

145 The Fanconi-defective cell lines Hs766T, PL11, and CAPAN1 were hyper

146 ERAD-defective cell lines likewise exhibited reduced quantiti

147 te-binding site SLO mutants and carbohydrate-defective cell lines revealed that glycan recognition is

148 (b) on the surface of the antigen processing defective cell lines RMA-S and T2.

149 gest that the extreme sensitivity of paralog-defective cell lines to cross-linking agents is owing to

150 Complementation of defective cell lines with the appropriate transcription

151 an normal fibroblasts and two individual XPC-defective cell lines, 486 genes were identified as XPC-r

152 HIF-alpha subunits has been described in VHL-defective cell lines, leading to HIF activation and up-r

153 ysts of patients with VHL disease and in VHL-defective cell lines.

154 ploidy, and reduced cell survival in the p53-defective cell lines.

155 H is not observed in several mismatch repair-defective cell lines.

156 an be obtained through cultivation in sLe(x)-defective cell lines.

157 CMA-defective cells maintain normal rates of long-lived prot

158 gressive depletion of CD4+ T lymphocytes and defective cell-mediated immunity.

159 cause a novel syndrome of tissue fragility, defective cell migration and chromosome instability in C

160 n of integrin beta1 at the cell surface, and defective cell migration and tubulogenesis.

161 orly galactosylated, which may contribute to defective cell migration during convergent extension mov

162 Mutation of cfz-2 causes defective cell migration, disorganization of head neuron

163 cretion of nonbulky proteins, ER stress, and defective cell morphology are secondary consequences of

164 exhibited severe growth defects, as well as defective cell motility in response to PDGF, lamellipodi

165 ed formation of sarcolemmal protrusions, and defective cell motility.

166 sed cell-cell adhesion, which contributes to defective cell movements in the gastrula.

167 The pob1-defective cells no longer elongate but swell gradually a

168 us infection, we infected wild-type and RNAi-defective cells of the nematode C. elegans with vesicula

169 ast, migration of alpha(4)beta(1) activation-defective cells on VCAM-1 alone was enhanced at higher V

170 her increase with CCT knockdown in autophagy-defective cells/organisms, implying surprisingly that th

171 nal differentiation of the root meristem and defective cell patterning.

172 regulation of actin patch stability; septin-defective cells permitted to enter isotropic growth lost

173 By using ATM- and ATR-defective cells, phosphorylation on Chk1, Chk2, and p53

174 ze the polarity determinant Par3 and display defective cell polarity, resulting in mislocalized junct

175 ibited slower growth, reduced migration, and defective cell polarization, traits common to all ODDD f

176 embryonic lethal (earlier than E6.5) due to defective cell positioning and structure formation of th

177 ctive cells, BER-defective cells and BER/NER-defective cells possess elevated levels of unrepaired, s

178 ness-sensing process that usually eliminates defective cells, pre-cancerous lesions signal the death

179 In addition to defective cell proliferation and survival, genome-wide t

180 ndent, TRAF6/TAK1/p38 signaling pathway; and defective cell proliferation in the palatal mesenchyme.

181 This is not simply due to defective cell proliferation or impaired recombinase exp

182 y mismatch repair leads to telomere loss and defective cell proliferation.

183 horylation of BLM during mitosis, as well as defective cell proliferation.

184 As expected, NER defective cells (rad4 and rad14 strains) are extremely s

185 AhR-defective cells reconstituted with an AhR containing the

186 These defective cells resembled double negative (DN) T cells i

187 As is the case with MMR-defective cells, resistance of Med1-/- MEF to MNNG was d

188 ve intracellular domain of Notch in microRNA-defective cells restored proper activation of Notch.

189 Reintroduction of DNMT3a in DNMT3a-defective cells restores EPAS1 epigenetic silencing, pre

190 Checkpoint-defective cells show premature sister-chromatid separati

191 The LA2 (ARNT-defective) cells showed a major difference between CYP1B

192 DNA-PK inhibitor NU7026 and DNA-PKcs or Ku80 defective cells shown to be sensitive to PARP inhibitors

193 ring adolescence, particularly in those with defective cell signaling mechanisms that control memory,

194 In PC2-defective cells, sorafenib inhibits B-Raf but paradoxica

195 uced pHi had attenuated FAK-pY397 as well as defective cell spreading and focal adhesions.

196 Primary KO oral keratinocytes showed defective cell spreading and robust focal adhesions.

197 zymatically glycated matrix are altered with defective cell spreading, reduced phosphorylation of foc

198 covering that genetic complementation of MMR defective cells stabilizes the MMR deficiency-associated

199 se levels increases CSR efficiency in C-NHEJ-defective cells, suggesting enhanced use of an A-EJ path

200 activation of ERK were also observed in ATM-defective cells, suggesting that 2,3-DCPE-induced these

201 kinetochore localization of hMPS1 in CENP-E defective cells suggests that their interaction with the

202 All 3 mutant SLITRK6 proteins displayed defective cell surface localization.

203 wn to increase the activity of wild-type and defective cell-surface CFTR in vitro.

204 opment in vivo and in vitro, associated with defective cell survival and proliferation.

205 e of PAR polymers can be used to identify HR-defective cells that are sensitive to PARP inhibitors, w

206 Cells mutant for N pathway components, or hh-defective cells that express reduced levels of the Notch

207 PDS toxicity extends to HR-defective cells that have acquired olaparib resistance t

208 b-binding protein 1a is transfected into AhR-defective cells that have been reconstituted with an AhR

209 a kinase autophosphorylation defect in LIG4-defective cells that was corrected by ectopic expression

210 In PC2-defective cells, the interaction of STIM-1 with Orai cha

211 at in the diploid population of proofreading defective cells there exists a transiently hypermutable

212 cle checkpoints, a mechanism that eliminates defective cells to ensure the integrity of the genome.

213 tations in either cut12 or plo1 enable Cdc25-defective cells to enter mitosis.

214 te that the reason for the sensitivity of HR-defective cells to PARP inhibitors is related to the hyp

215 regulation on the ability of excision repair-defective cells to replicate irreparably UV-damaged DNA.

216 -encapsidation, CMV failed to complement the defective cell-to-cell movement of BMV.

217 epithelial cells and macrophages but caused defective cell-to-cell spread and strong attenuation in

218 ivity of p34cdc2 in wild-type and checkpoint-defective cells treated with a DNA synthesis inhibitor.

219 , and not epithelial cells, appear to be the defective cell type in nitrofen-induced hypoplastic lung

220 ivation, or changes in the AKT pathway, this defective cell volume control is specifically associated

221 dylglycerolphosphate synthase (Pgs1p), has a defective cell wall due to decreased beta-1,3-glucan.

222 s, including reduction in ADH2 derepression, defective cell wall integrity and increased sensitivity

223 n a perturbation of TORC2 functions, causing defective cell wall integrity, aberrant actin organizati

224 the presence of ethidium bromide was due to defective cell wall integrity, not from "petite lethalit

225 elta Saccharomyces cerevisiae cells restored defective cell wall separation during proliferation.

226 ene from the E.coli chromosome, resulting in defective cell wall synthesis and diaminopimelic acid au

227 Our findings reveal defective cell wall synthesis as an unexpected initiator

228 class of Arabidopsis root hair mutants with defective cell walls.

229 IFN gamma-induced apoptosis in RB-defective cells was enhanced by serum stimulation, which

230 Using SWI/SNF-defective cells, we demonstrated that Brahma-related gen

231 n adducts in mismatch repair-proficient and -defective cells were found.

232 BRCA2-defective cells were not found to have increased levels

233 nt with kinetoplast dispensability, V-ATPase defective cells were oligomycin resistant, suggesting AT

234 dder following IFN-gamma treatment of the RB-defective cells while higher molecular weight DNA was pr

235 tations were observed, including respiration-defective cells with decreased viability, dominant-negat

236 sphorylation was wortmannin-sensitive in ATM-defective cells with depleted ATR.

237 Treatment of CAF-I- or RCAF-defective cells with methyl methanesulfonate increased t

238 Cdc42-defective cells with restored transcriptional induction

239 petent state, induced by treatment of the Rb-defective cells with the HDAC inhibitor, trichostatin A.