ライフサイエンスコーパス: normal cell

1 ic factor, have a hyperacidic pH compared to normal cells'.

2 itions, including hypoxia, in tumor, but not normal cells.

3 y cancerous, somatic mutations can reside in normal cells.

4 in PIK3CA-mutant cancer cells while sparing normal cells.

5 tion of cancer cells while being nontoxic to normal cells.

6 rhythm, collagen synthesis, and ER stress in normal cells.

7 and transcriptional regulation in cancer and normal cells.

8 on processivity, and respiratory function in normal cells.

9 lly increased mutational burdens relative to normal cells.

10 ces cisplatin resistance in melanoma but not normal cells.

11 tic-resistant mutants at comparable rates to normal cells.

12 ere found to exhibit RNA-DNA interactions in normal cells.

13 fluorescence lifetime in cancer relative to normal cells.

14 IH/3T3 fibroblast cells, and SV-HUC1 bladder normal cells.

15 me and utilize glucose at a higher rate than normal cells.

16 ectively kills tumor cells, without damaging normal cells.

17 y that is required for cell proliferation of normal cells.

18 re epigenetically repressed in virtually all normal cells.

19 neoplastic cells without similarly affecting normal cells.

20 cancer cells of different origins as well as normal cells.

21 ressed at different levels by neoplastic and normal cells.

22 be cellular metabolic activity in cancer and normal cells.

23 n turnover in HGPS-derived cells compared to normal cells.

24 t is not required for division in almost all normal cells.

25 cleavage of PARP in tumor cells compared to normal cells.

26 mechanism of action also may be occurring in normal cells.

27 ixtures of cancer subpopulations, as well as normal cells.

28 oxicity in some types of cancer cell but not normal cells.

29 l lymphoma types and low cytotoxicity toward normal cells.

30 ntly more DNA damage in cancer cells than in normal cells.

31 trigger cancer cell apoptosis while sparing normal cells.

32 g indiscriminate IKK/NF-kappaB inhibition in normal cells.

33 ivity of new agents for fungal pathogens and normal cells.

34 fferently compared with unselected tumor and normal cells.

35 hibits proliferation in cancer cells but not normal cells.

36 l settings are always mixtures of cancer and normal cells.

37 over tumor cells and minimize toxicity over normal cells.

38 y of cancer cell lines but have no effect on normal cells.

39 without modeling the effect of the drugs on normal cells.

40 neoantigens that distinguish malignant from normal cells.

41 ivery in lung cancer cells and its impact on normal cells.

42 ree proteins without causing toxicity toward normal cells.

43 t were more extreme than those observed with normal cells.

44 ee of aberrant CpG island DNA methylation in normal cells.

45 umour type, but it was almost never found in normal cells.

46 FBXO44/SUV39H1 were dispensable in normal cells.

47 antly more DNA damage in the cancer cells vs normal cells.

48 ctively kills cancer cells, while protecting normal cells.

49 centrations-a condition that generally kills normal cells.

50 However, chimeric RNAs can also be found in normal cells.

51 or samples would always be contaminated with normal cells.

52 rowth, thereby distinguishing them from most normal cells.

53 cytotoxic mechanism against cancer cells vs. normal cells.

54 t, and pancreatic cancers, but is limited in normal cells.

55 otoxicity in mixed populations of cancer and normal cells.

56 in acute myeloid leukemia (AML), but not in normal cells.

57 contains exosomes produced by malignant and normal cells.

58 ating discrete differences between tumor and normal cells.

59 rom a more depolarized potential compared to normal cells.

60 lls exclusively with minimal side effects to normal cells.

61 to target at cancer cells without disrupting normal cells.

62 ams in genome instability disorders and even normal cells.

63 ng DNA replication in tumor cells but not in normal cells.

64 ated expression of HUWE1 in MM compared with normal cells.

65 sed dependency in leukemia cells compared to normal cells.

66 perinuclear, trans-Golgi pattern observed in normal cells.

67 ferentially cytotoxic to cancer cells versus normal cells.

68 bladder cancer cells was higher than that in normal cells.

69 tumors that are sufficiently separated from normal cells.

70 -hyperactive cancer cells while sparing ErbB-normal cells.

71 llular superoxide anion in cancerous but not normal cells.

72 R5 in a wide range of cancers, while sparing normal cells.

73 10 most significant RNA-DNA interactions in normal cells, 5 colocalized with the gene pairs that for

74 ntly because of their widespread presence in normal cells across every species ranging from yeast to

75 ted in diverse tissues, including apparently normal cells adjacent to tumors.

76 nique target differentiating cancer from the normal cell, affording the potential for very sensitive

77 could constitute a "stemness marker" of the normal cell and a possible target for immunotherapeutic

78 ity, CPPB does not show cytotoxicity against normal cells and a series of cancer cell lines.

79 uman embryonic kidney 293 cells (HEK 293) as normal cells and Au/Fc-PAMAM(G2)/FA electrode showed two

80 ds AGS cancer cells when compared to HEK 293 normal cells and bone marrow mesenchymal stem cells (BM-

81 omain of PI3K, resulting in proliferation of normal cells and cancer cells.

82 Currently, PHGDH regulation in normal cells and cancer is not well understood.

83 rneath a stiff hydrogel, conditions in which normal cells and cells with reduced levels of Ras-ERK si

84 erein, we review the regulation of 2OGDDs in normal cells and how that regulation is corrupted in can

85 ls and tissues following counterselection on normal cells and identified a panel of human antibodies

86 r examples of NTCP in both a simple model of normal cells and in a model of normal and damaged cells.

87 ndex PI=40-60), while remaining non-toxic to normal cells and normal cell spheroids, even after photo

88 hibitor with dual selectivity: leukemia over normal cells and NOTCH1 mutants over wild-type receptors

89 D47, which is a protein broadly expressed on normal cells and often overexpressed on cancer cells, an

90 osure to low dose ionising radiation affects normal cells and organisms, even though our cells are co

91 cule with pleiotropic physiological roles in normal cells and pathophysiological roles in cancer.

92 eracting pathways restrains proliferation in normal cells and prevents tumor initiation is still poor

93 Cell-cell interactions between normal cells and RasV12 cells trigger ephrin-A-EphA2 sig

94 e most tumors are a heterogeneous mixture of normal cells and subpopulations of cancer cells, or clon

95 roach to effectively kill ERPC cells sparing normal cells and suggest that development of a long-term

96 ingle E2F cis-element mediates repression in normal cells and that expression is activated by its mut

97 signaling important for stress adaptation by normal cells and the survival of cancer cells.

98 function of such biomolecular condensates in normal cells and their roles in contexts ranging from de

99 e perform whole genome methyl-seq on diverse normal cells and tissues and three cancer types.

100 quires better insight into the metabolism of normal cells and tumour cells in vivo.

101 dual modeling of drug responses to tumor and normal cells and utilize them to design targeted combina

102 /or virally infected cells, although sparing normal cells, and has been implicated in the pathogenesi

103 ole in regulating basic energy metabolism in normal cells, and that this function of Tgifs is amplifi

104 ntracellular iron trafficking, and egress in normal cells, and their perturbations in cancer have bee

105 igher levels of reactive oxygen species than normal cells, and this can serve as a possible therapeut

106 rand breaks (DSBs) form and are processed in normal cells, and whether they predispose to cancer-asso

107 Interestingly, normal cells are much more resistant to the treatment du

108 To test whether RNA-DNA interactions in normal cells are predictive of fusion RNAs, we analyzed

109 de that transformed cells engage surrounding normal cells as active and essential microenvironmental

110 rticles were approved by FR-negative HEK 293 normal cells as FR-negative cells through cellular uptak

111 ch reduces nonspecific, geometric capture of normal cells as typically observed in vertical filters.

112 nt on RB and an intact DREAM complex in both normal cells as well as in palbociclib-sensitive cancer

113 ithium surface by electrolyte wetting during normal cell assembly.

114 e NIR-ASM to differentiate cancer cells from normal cells based on NQO1 activity using fluorescence m

115 To determine smoking effect on FSTL1, normal cell BEAS2B and lung cancer cell lines was treate

116 romosome instability (CIN) is deleterious to normal cells because of the burden of aneuploidy.

117 pression is tolerated in adult mice, sparing normal cells but allowing for an enhanced p53 response t

118 Both caspases exist as inactive zymogens in normal cells but are activated during apoptosis and are

119 mpounds 1 and 2 (Pac 1 and 2) did not affect normal cells but selectively induced cell death in cance

120 in is dispensable for V(D)J recombination in normal cells, but because of functional redundancy, it i

121 valent promoters is only lowly methylated in normal cells, but frequently shows elevated methylation

122 er CpG islands are typically unmethylated in normal cells, but in cancer a proportion are subject to

123 exhibit shorter telomere length compared to normal cells, but it is not fully understood how WRN def

124 otic proteins (IAPs) enters cancer cells and normal cells by caveolin-dependent endocytosis and macro

125 nstrate that A3B expression is suppressed in normal cells by repressive E2F complexes and that viral

126 nce of CH25H in defense against education of normal cells by TEV and argue for the use of reserpine i

127 n by a131 causes reversible growth arrest in normal cells by transcriptionally upregulating PIK3IP1,

128 In contrast to normal cells, cancer cells coopt this pathway to propaga

129 Compared to normal cells, cancer cells have an increased antioxidant

130 ling process can occur in both cancerous and normal cells, cancer-selective labelling needs to be ach

131 sed susceptibility to CD40 killing, while in normal cells CD40 signalling is cytoprotective.

132 ALDH(+)/CD49f(+)/EpCAM(+) tumor and normal cells clustered differently compared with unselec

133 NNs targeting Plk1 generate less toxicity in normal cells compared to the small molecule Plk1 inhibit

134 nificant degree by their subject genes under normal cell conditions.

135 V-induced mutation frequencies compared with normal cells, consistent with their GGR deficiency.

136 Cerebrospinal fluid testing showed normal cell counts, a negative result on reverse-transcr

137 loop was formed by CTCF self-dimerisation in normal cells (CTCF binds to both unmethylated CTCF-BS3 a

138 of Rad51 requires TCTP in MCF-7 cells under normal cell culture conditions.

139 in LF differentiation despite maintenance of normal cell cycle exit.

140 K20) and its function has been implicated in normal cell cycle progression and cancer metastasis.

141 , and that restoring of DBC1 is required for normal cell cycle progression in vitro and in vivo.

142 that DBC1/DN-DBC1 transitions play a role in normal cell cycle progression in vivo after cells leave

143 ctive mitochondria, lower apoptotic markers, normal cell cycle regulations, moderately lowered ROS, b

144 arent in single fission yeast cells during a normal cell cycle.

145 l division during pollen development and for normal cell-cycle progression and endoreplication during

146 nowledge regarding the role of FBXO31 during normal cell-cycle progression is restricted to its funct

147 catalytic domain, and hence interfering with normal cell-cycle progression, did not affect virus repl

148 timulation of T-PLL cells evoked higher-than-normal cell-cycle transition and profiles of cytokine re

149 s: melanoma cell-derived exosomes (MTEX) and normal cell-derived exosomes (non-MTEX).

150 nd stability of our genomes is essential for normal cell division, tissue homeostasis, and cellular a

151 KAP1, but not the SKAP1 S31 mutant, restored normal cell division.

152 ve higher reactive oxygen species (ROS) than normal cells, due to genetic and metabolic alterations.

153 6 is required for normal cell production and normal cell elongation, and its natural genetic variatio

154 utations are typically required to transform normal cells enabling growth in soft agar or in immunode

155 n that these observations were identified in normal cells exhibiting minimal cell stress and death ph

156 be exploited in cancer therapy because most normal cells express STING, while many tumor cells do no

157 selectively lethal to tumor and immortalized normal cells expressing the mutant kinase B-Raf(V600E) o

158 drive self-reinforced recruitment, derailing normal cell-fate control during development and leading

159 are histone demethylases that both regulate normal cell fates during development and contribute to t

160 We analyzed 420 tumor cells and 284 adjacent normal cells for expression of 93 genes that included a

161 YAP/TAZ-regulated autophagy is essential in normal cells for YAP/TAZ-mediated dedifferentiation and

162 ostine may not only protect in multiple ways normal cells from radiation-induced DNA damage but also

163 When taken up by normal cells from the stroma EN2 induces the expression

164 Adequate protein folding is necessary for normal cell function and a tightly regulated process tha

165 lts demonstrate that scaling is required for normal cell function and delineate possible rules for ce

166 echanosensitive ion channels are crucial for normal cell function and facilitate physiological functi

167 or PI3K catalytic and regulatory subunits in normal cell function and in disease.

168 n is an essential micronutrient required for normal cell function and physiological processes.

169 es in specific SGs are sufficient to disrupt normal cell function and point to a possible role for SG

170 ce because of the critical role of folate in normal cell function and the wide range of disorders, in

171 on of essential client proteins critical for normal cell function as well as cancer initiation and pr

172 al response, which has implications for both normal cell function as well as disease.

173 tals, and proteins is required to understand normal cell function, and ultimately, elucidate the mech

174 iseases but also recognized as a key part of normal cell function, signaling, and death (ferroptosis)

175 modifications in humans and is essential for normal cell function.

176 ification of proteins or SUMOylation ensures normal cell function.

177 ion, is crucial for cellular homeostasis and normal cell function.

178 ed proteins, which ultimately interfere with normal cell function.

179 chines may lead to striking perturbations in normal cell function.

180 n prolyl 4-hydroxylase, and is essential for normal cell function.

181 ing MYC at homeostatic levels is critical to normal cell function; overexpression drives many cancers

182 y and flow cytometry, we also evaluated some normal cell functions that could be modulated by our com

183 s of these proteins including their roles in normal cell growth and differentiation and in human dise

184 multiple cancer cell lines without affecting normal cell growth and survival.

185 d to decreased neuronal marker staining, and normal cell growth as judged by phosphohistone H3 staini

186 cle fusion kinetics, diffusion could support normal cell growth rates.

187 lecular Cell, Sharma et al. (2019) show that normal cell growth requires conversion of an arginine re

188 ed growth would be significantly slower than normal cell growth.

189 s increase the frequency of apoptosis during normal cell growth.

190 Our circuit analysis showed that while normal cells have an oxidative state and a glycolytic st

191 CMLD-2-treated normal cells, HuR-regulated mRNAs and proteins albeit sh

192 dative, proteotoxic, and metabolic stress in normal cells, hyperactivation of NRF2 is oncogenic, alth

193 3.59 microM, but they are less cytotoxic on normal cells (IC50 > 100 microM).

194 (including normal-karyotype AML cells) from normal cells, identify expression signatures associated

195 the gene expression programs responsible for normal cell identity and pathogenic state.

196 A significant difference is that normal cells in a multicellular organism have evolved in

197 Cancer cells differ from normal cells in both gain of functions (i.e., upregulati

198 e proteomes of virus-infected and uninfected normal cells in response to cell-intrinsic dsDNA sensing

199 s with nuclear YAP compared with the DLC1(+) normal cells in the adjacent tissue.

200 in a proliferative disadvantage relative to normal cells in the population.

201 AF V600 monomers, but spares RAF function in normal cells in which CRAF homodimers can drive signalin

202 rotein 1) that acts to supress apoptosis in "normal" cells in the fly.

203 mediated killing of cancer cells, but not of normal cells, in vitro.

204 lopment and in many physiologic processes of normal cells, in which it regulates growth, apoptosis, a

205 ignalling cascade and emphasize its roles in normal cells (including coordinating cell metabolism and

206 er cells have altered metabolism compared to normal cells, including dependence on glutamine (GLN) fo

207 We show that RCC1 overexpression in normal cells increased cellular RanGTP levels and accele

208 Loss of RIalpha LLPS in normal cells increases cell proliferation and induces ce

209 CA) and that the experimental deciliation of normal cells induces a malignant-like phenotype with inc

210 a process that drives the transformation of normal cells into malignant cells.

211 plex, a component of the spliceosome that in normal cells is found in the cell.

212 ses and consequences of somatic mutations in normal cells is limited.

213 How somatic mutations accumulate in normal cells is poorly understood.

214 Thus, endogenous MCAK/Kif2C activity in normal cells is tuned to a mean level to achieve maximal

215 hey are resistant to tumorigenesis, and most normal cells isolated from them grow slowly in culture.

216 In normal cells, it suppresses tumorigenesis by maintaining

217 In normal cells, KCC2 undergoes developmental dephosphoryla

218 In normal cells, Ki-67 was a late marker of cell-cycle entr

219 fficacy.SIGNIFICANCE STATEMENT Understanding normal cell kinetics of adult neurogenesis and the type

220 r NAD+ preferentially in cancer cells versus normal cells, leading to depletion of ATP and robustly i

221 enes, BRAF(V600E) causes oncogenic stress to normal cells, leading to growth arrest (senescence) or a

222 MBD1-deficient stem cells may interfere with normal cell lineage commitment and cause the accumulatio

223 ainst Jurkat, K562, U937, and HL60 tumor and normal cell lines and induction of apoptosis.

224 Normal cell lines and tissue were unstained by mAb-A4.

225 lso 4a was found to be less cytotoxic toward normal cell lines as compared to cancer cell lines.

226 screening on a unique pair of matched cancer/normal cell lines obtained from a single patient.

227 -1143 and HCC-1187) along with their matched normal cell lines to great sequencing depths (up to 278x

228 structurally and functionally different from normal cell mitochondria.

229 intaining sensitivity below a threshold over normal cell models.

230 ressed on malignant cells, but expression on normal cells must be absent or limited.

231 the cytosol of cancer cells, but rescues the normal cells (namely, HS-5 cells) by trafficking the BTZ

232 a cell depends is typically consistent among normal cells of a particular phenotype, Bcl-2 family dep

233 tients with advanced cancers without harming normal cells or tissues.

234 mutant mice do not accumulate mutant p53 in normal cells, our study on a mutant p53 mouse model of L

235 rian cancer (HGSOC) cell lines compared with normal cells-ovarian surface epithelia cells and fallopi

236 Forced-expression of MICU1 in normal cells phenocopies the metabolic aberrations of ma

237 ations in NS levels are required to maintain normal cell physiology and are dysregulated in disease.

238 impede advances in our deep understanding of normal cell physiology and disease pathogenesis.

239 ophagic systems ensures basal catabolism and normal cell physiology, and failure of either system cau

240 ite their well-known function in maintaining normal cell physiology, how inorganic elements are relev

241 This has potential consequences in normal cell physiology, where the chromatin environment

242 growth and genomic stability is critical for normal cell physiology.

243 CpG methylation status in normal cells points to locally active regulatory sites a

244 pattern of H3K4me1 at CpG island borders in normal cells predicts the different modes of cancer CpG

245 are initially present at low frequencies in normal cells preferentially expand in the altered tumor

246 However, the genetic events that occur in normal cells prior to tumorigenesis are still unknown.

247 AAK6 is required for normal cell production and normal cell elongation, and i

248 ced ROS generation can provide insights into normal cell proliferation in cerebellar development and

249 t cancer cell growth, but is dispensable for normal cell proliferation.

250 and which, we hypothesize, is a hallmark of normal cell proliferation.

251 -cell genomics of breast tumors and adjacent normal cells propagated for a short duration under growt

252 tion stress, low basal replication stress in normal cells protected them from DNA damage and toxicity

253 ells in a large dynamic range, we found that normal cells rejuvenated with a lag time distribution th

254 age to the malignant cells while leaving the normal cells relatively unharmed.

255 scription factors ARX and PDX1 specify these normal cells, respectively(5,6), and 84% of 142 non-func

256 During G1-phase of the cell cycle, normal cells respond first to growth factors that indica

257 y conditions; however, only RlpA can support normal cell separation in low-salt media.

258 e metabolic pathways is required to maintain normal cell shape in E. coli.

259 In normal cells, signal transduction pathways control core

260 n percent of insertions were also present in normal cells, similar to findings in genomic DNA from no

261 hile remaining non-toxic to normal cells and normal cell spheroids, even after photo-irradiation.

262 erentiation and a defect in maintenance of a normal cell state.

263 roadly cytotoxic, causing cell death also in normal cells such as dermal fibroblasts and endometrial

264 In normal cells, such metabolic stress leads to inhibition

265 ifferences in the lysosomes of cancer versus normal cells suggest that they could be targets for drug

266 is prevalent in human cancers, but absent in normal cells, suggesting that proteins involved in the c

267 icient ER export is not sufficient to enable normal cell-surface expression of TREM2.

268 some function is critical for cancer but not normal cell survival, representing an effective approach

269 repair activities and impairs tumour but not normal cell survival.

270 signaling network unrelated to that seen in normal cells, sustaining the expression of unique sets o

271 The model accounts for tumour and normal cells that are both nested in a vascular system t

272 ust also correctly detects a small number of normal cells that are mixed in a cancer cell population.

273 Due to the infiltration of tumor surrounding normal cells, the expression data derived from tumor sam

274 In normal cells, this pathway is restrained by p53 protein

275 In normal cells, this provides a kind of electrostatic lubr

276 MENs distinguish cancer cells from normal cells through the membrane's electric properties;

277 In this study, we show that in normal cells, TLR2 limits RV-induced IFN responses by at

278 e, cell cycle surveillance mechanisms enable normal cells to arrest and undergo repair processes.

279 ion) and the accommodation (or tolerance) of normal cells to bound antibody, activation of complement

280 Cancer cells utilize more glucose than normal cells to meet the energy demand arising due to th

281 that causes the related gene instability and normal cells to transform into tumor cells.

282 These processes enable normal cells to tune energy production in variable micro

283 g the intracellular pH (pH(i)) from ~7.1 (in normal cells) to ~7.5 (in cancer cells).

284 The absence of toxicity toward normal cells, together with the small molecular weight (

285 In comparison with normal cells, TRAK1-deficient fibroblasts showed irregul

286 cts of normal brain architecture but without normal cell-type regionalization, these spheroids bore a

287 In contrast, a panel of normal cell types did not express MC2 mRNA, and similar

288 RDs at oncogenes tend to be conserved across normal cell types.

289 l strategy can be applied to other cancer or normal cell types.

290 y significant differences between cancer and normal cells using MB concentrations as low as 0.05 and

291 However, normal cells usually have to progress through a precance

292 cytoplasmic vesicles and it is required for normal cell wall composition and integrity, affecting ad

293 regulate transcriptional isoform activity in normal cells, we predicted the highly dysregulated patte

294 and targets, compared to other genes and to normal cells were observed.

295 pipeline by detecting subtle alterations in normal cells when subjected to small mechano-chemical pe

296 rcation of CpG island methylation borders in normal cells, which become eroded in cancer.

297 affinity to ICAM-1 to avoid cytotoxicity in normal cells with basal levels of ICAM-1 expression.

298 d STAT3 cancer cells without cytotoxicity to normal cells with dormant STAT3.

299 an alternating electric field on cancer and normal cells within an in vivo-like microenvironment wit

300 The normal cells within the tissue serve as internal positiv