ライフサイエンスコーパス: defective cell

1 PARP1 is hyperactivated in replicating BRCA2-defective cells.

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

3 of nucleotide excision repair-proficient and defective cells.

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

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

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

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

8 aneous chromosomal aberrations seen in BRCA2-defective cells.

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

10 luciferase reporter assay employing DNA-PKcs defective cells.

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

12 us macromolecules had reduced levels in CLN3-defective cells.

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

14 estabilization especially in mismatch repair-defective cells.

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

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

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

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

19 ferential abundance between control and CLN3-defective cells.

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

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

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

23 ls in PMA-treated wild-type or uracil repair-defective cells.

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

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

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

27 ll proliferation was enhanced in endocytosis-defective cells.

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

29 ns such as killing cancer cells or replacing defective cells.

30 e cells, we used OXPHOS-competent and OXPHOS-defective cells.

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

32 egradation and chromosomal breakage in BRCA2-defective cells.

33 frequency and chromosome integrity in BRCA2-defective cells.

34 utophagy in both OXPHOS-competent and OXPHOS-defective cells.

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

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

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

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

39 consequences of ribonucleotides in RNase H2-defective cells.

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

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

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

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

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

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

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

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

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

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

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

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

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

53 lls, this apoptotic response occurred in p53-defective cells and cell killing was not blocked by a pa

54 gene encoding the hemoglobin beta subunit in defective cells and CRISPR-Cas9, transcription activator

55 or the PV industry by reducing the number of defective cells and improving the overall efficiency of

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

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

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

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

60 induced (CDI) ferroptosis, even in autophagy-defective cells, and subsequently discovered that clathr

61 RC-induced replication failure in checkpoint-defective cells, and the presence of methylated H3K4 slo

62 XRCC4-defective cells are extremely sensitive to ionizing radi

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

64 Finally, we show that BRCA-defective cells are hypersensitive to CldU, either alone

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

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

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

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

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

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

71 ted cell survival, it was impaired in OXPHOS-defective cells because of inhibition of autophagosome-l

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

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

74 t only did supplementary Pgk1 enhance NOM in defective cells, but injection of Pgk1 rescued denervati

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

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

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

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

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

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

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

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

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

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

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

86 ing resulted from impaired cell motility and defective cell-cell adhesion, with damaged cells additio

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

88 Fgfr1/2 conditional null mutants showed defective cell-cell and cell-matrix adhesion, both of wh

89 iptional defects in memory B-cells mirroring defective cell-cell communication upon activation.

90 els lacking Sun1b had aberrant junctions and defective cell-cell connections.

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

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

93 Defective cell cycle checkpoint function has been linked

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

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

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

97 during DNA damage, which was associated with defective cell cycle control caused by FLCN knockdown.

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

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

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

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

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

103 ollowing injury, with aberrant SC expansion, defective cell cycle exit, and failure to transition eff

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

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

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

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

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

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

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

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

112 Although defective cell cycle-checkpoint regulation and associate

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

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

115 of aberrant cell death pathways coupled with defective cell death clearance mechanisms that promote e

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

117 Defective cell death pathways have recently been suggest

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

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

120 nts that displayed loss of ERK signaling and defective cell differentiation, Etv deficiency augmented

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

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

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

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

125 h demand on the cell division machinery, and defective cell division can cause microcephaly and other

126 We hypothesize that defective cell division during kidney development and/or

127 pathological condition often associated with defective cell division that results in severe brain dev

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

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

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

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

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

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

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

135 Because defective cell elongation is the earliest and most unive

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

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

138 erved two types of cellular behavior: growth-defective cells exhibited a mathematically predicted tra

139 likely cause of ATRi sensitivity, and SMG8/9-defective cells exhibited a reduced level of ATRi-induce

140 In addition, defective cells exhibited disorganized phragmoplast MT a

141 n the absence of exogenous DNA damage, PBRM1-defective cells exhibited elevated levels of replication

142 ablishment of apical cAMP gradients in Myo5b-defective cells exposed to physiological levels of gluco

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

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

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

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

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

148 in physical forces are coordinated to remove defective cells for homeostatic maintenance of living ep

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

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

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

152 ll division and if not maintained results in defective cell function caused by the abnormal distribut

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

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

155 ften lead to infertility, but replacement of defective cells has been limited by the inability to dep

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

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

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

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

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

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

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

163 e) scars are lost from the chromatin of ARH3-defective cells in the prolonged presence of PARP inhibi

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

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

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

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

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

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

170 gous-recombination-deficient BRCA1- or BRCA2-defective cells is synthetically lethal(11,12), and aber

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

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

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

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

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

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

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

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

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

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

181 ERAD-defective cell lines likewise exhibited reduced quantiti

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

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

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

185 Complementation of defective cell lines with the appropriate transcription

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

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

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

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

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

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

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

193 Together, our data suggest that defective cell-matrix interactions are linked to Wnt sig

194 characterized by hypergammaglobulinemia and defective cell-mediated immunity.

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

196 three distinct pathological mechanisms: (i) defective cell membrane expression; (ii) impaired LGI1-b

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

198 otility and invasive potential and show that defective cell migration and invasion stem from alterati

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

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

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

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

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

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

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

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

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

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

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

210 still impaired ATR/CHK1 signaling in SMG8/9-defective cells, other characteristic responses to ATRi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

225 AhR-defective cells reconstituted with an AhR containing the

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

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

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

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

230 aKGDH and impaired autophagic flux in OXPHOS-defective cells resulted in pronounced cell death in res

231 Checkpoint-defective cells show premature sister-chromatid separati

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

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

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

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

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

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

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

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

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

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

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

243 They raise the possibility that defective cell surface exposure of PtdSer may be respons

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

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

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

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

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

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

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

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

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

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

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

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

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

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

258 ed with brain calcification, suggesting that defective cell-to-cell adhesion and dysfunction of the m

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

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

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

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

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

264 o cell wall-acting antimicrobials suggesting defective cell wall biosynthesis.

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

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

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

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

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

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

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

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

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

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

275 controlling viral infections and eliminating defective cells, we explored the phenotypic and function

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

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

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

279 d that all non-homologous end joining (NHEJ) defective cells (whether deficient in components of the

280 tely downstream of ES-linked VSGs in RNase H defective cells, which also have an increased amount of

281 nd glycosphingolipids were decreased in CLN3-defective cells, which were also impaired in the recycli

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

283 tranded DNA and synthetic lethality in 53BP1-defective cells whilst the inhibition of DNA nucleases t

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

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

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

287 Cdc42-defective cells with restored transcriptional induction

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

289 nificant overlap of upregulated genes in NMD-defective cells with those in the brain tissues, micro-d

290 eostasis of both OXPHOS-competent and OXPHOS-defective cells, with Ca(2+) regulation of alphaKGDH act