ライフサイエンスコーパス: cell survival

1 the nucleus can promote genome stability and cell survival.

2 t, roles in organ development and adult stem cell survival.

3 tion lost by these mutations is essential to cell survival.

4 breaks (DSBs) is of critical importance for cell survival.

5 that yielded equivalent levels of clonogenic cell survival.

6 sation supports that the combination reduces cell survival.

7 ion, which bolsters anti-oxidant defense and cell survival.

8 with antibody for RNA clearance and improved cell survival.

9 XO1, which is critical for tumorigenesis and cell survival.

10 argets of these miRNAs, and reduced lymphoma cell survival.

11 an in vivo role of CHK2-induced autophagy in cell survival.

12 ased AKT and mTOR phosphorylation, enhancing cell survival.

13 er than formation promoted HSF1 activity and cell survival.

14 G growth factor (Ccl5) critical for LGG stem cell survival.

15 le to prevent genome instability and promote cell survival.

16 ducing excitability increased early Purkinje cell survival.

17 s critical for maintaining redox balance and cell survival.

18 e lesions that threaten genome stability and cell survival.

19 of mHtt on transcription factor function and cell survival.

20 dulate genes that are fundamental for cancer cell survival.

21 both known to play a crucial role in cancer cell survival.

22 t, associated with defective IL-15-dependent cell survival.

23 ng genes mediating CD8 effector function and cell survival.

24 53BP1 protein stability, and its function in cell survival.

25 such as lipid metabolism, proliferation, and cell survival.

26 nse (ISR) to restore homeostasis and promote cell survival.

27 ress to modulate repair programs and sustain cell survival.

28 ing of growth factor receptors controls beta cell survival.

29 becomes critical for cytokine production and cell survival.

30 e the Na(+)/K(+)-ATPase, a pump required for cell survival.

31 al tract narrowing, and increases intestinal cell survival.

32 TEN protein-phosphatase activity to restrain cell survival.

33 n generates localized signaling required for cell survival.

34 cell cycle progression, DNA replication, and cell survival.

35 vesicle, rather than an effect on progenitor cell survival.

36 al activity to enhance cell cycle arrest for cell survival.

37 ts the critical role of p21 in GNL1-mediated cell survival.

38 nner ear that can mediate nonautonomous hair cell survival.

39 g that stress-induced OPA1 cleavage supports cell survival.

40 olutionarily conserved process essential for cell survival.

41 ulates calcium homeostasis, ER stress, and T cell survival.

42 d cells and stimulate antiviral immunity and cell survival.

43 ing cell death and apoptosis while promoting cell survival.

44 ls and proved critical for TSG silencing and cell survival.

45 ew mechanism for TRAF3 in the restraint of B cell survival.

46 that Galphaq deficiency leads to enhanced NK cell survival.

47 that removes 8-oxoG, but did not compromise cell survival.

48 ynthase (GGPPS), a metalloenzyme crucial for cell survival.

49 L-10 mimicked the effects of advanced age on cell survival.

50 promote angiogenesis, energy metabolism, and cell survival.

51 cessary for maintaining genome integrity and cell survival.

52 gate ROS-induced ER stress to promote cancer cell survival.

53 ndrial calcium uniporter, and are central to cell survival.

54 al cell wall and are therefore important for cell survival.

55 s in ASS1-deficient cancers decreased cancer cell survival.

56 with the selected 3D printing technique and cell survival.

57 profound effects on transcription and tumor cell survival.

58 enable uptake through the cell, facilitating cell survival.

59 on and mTOR activity and thereby reduces HCC cell survival.

60 rafficking can be used to promote islet beta cell survival.

61 signaling, action potential generation, and cell survival.

62 r through which BCR signaling impacts on MCL cell survival.

63 affinity maturation of antibodies and plasma cell survival.

64 g cells deposit fibronectin to promote tumor cell survival.

65 mental stress response (ESR) is critical for cell survival.

66 endent functions, such as NF-kappaB-mediated cell survival.

67 enes that feeds back to regulate glioma stem cell survival.

68 tonomy is critical for ribosome function and cell survival.

69 eactive oxygen species (ROS) are crucial for cell survival.

70 nt protein condensates with roles to promote cell survival.

71 n the DNA damage response may simply enhance cell survival.

72 a mechanism for prolonged epithelioid tumor cell survival.

73 incompatibility between virus production and cell survival.

74 ween sphingolipid metabolism and KSHV+ tumor cell survival.

75 reserve mitochondrial homeostasis and ensure cell survival.

76 cessary for maintaining genome stability and cell survival.

77 er metastasis, and reduced clonogenic cancer cell survival.

78 eading to a dependence on glutaminolysis for cell survival.

79 epression, increasing fatty acids to support cell survival.

80 stroke-induced hippocampal neurogenesis and cell survival.

81 -host disease risk and enhance transferred T cell survival(7,8), and infused these cells prophylactic

82 gesting expression of Tn/STn may offer tumor cell survival advantages through altering DR4 and/or DR5

83 to discover that XRN2 depletion compromised cell survival after additional knockdown of specific DNA

84 r abnormalities, CHD6 loss leads to impaired cell survival after chronic oxidative stress, abnormal c

85 tagenic translesion synthesis (TLS) promotes cell survival after DNA damage but is responsible for mo

86 rapped by PARP inhibitors, thereby promoting cell survival after drug treatment.

87 ure density are much greater determinants of cell survival after exposure.

88 Cell survival after GenX exposure was determined for two

89 C activity via AC modRNA treatment increased cell survival after hypoxia or MI.

90 A recently described mechanism promoting cell survival after ionizing radiation (IR)-induced DNA

91 Sp, but not GOLPH3, is essential for GDR and cell survival after IR-induced DNA-damage in human lymph

92 the oxidative stress response implicated in cell survival after ischemia.

93 mutation and toxicity barriers that prevent cell survival after large-scale genome engineering.

94 ons, suggesting the possibility of a role in cell survival, although a high level of overexpression c

95 of the allograft microenvironment on memory cell survival and activation, as well as new therapeutic

96 Moreover, MDSCs promote tumor cell survival and angiogenesis to support tumors.

97 r lung before transplantation, with a global cell survival and antiapoptotic signature.

98 owever, many NF-kappaB-mediated pathways for cell survival and apoptosis signaling in cancer remain t

99 le machinery and in pathways associated with cell survival and apoptosis.

100 or knocking down SMPDL3b partially restored cell survival and conferred radioprotection.

101 number of physiological processes including cell survival and death, encouraging research into its m

102 role in regulating homeostasis by modulating cell survival and death.

103 through which Bcl-2 family members regulate cell survival and death.

104 ates nutrient-signaling networks to regulate cell survival and development.

105 Robust cell survival and diabetes correction is observed follow

106 naling cascades, with detrimental effects on cell survival and differentiation as well as on the abil

107 B led to significant suppression of leukemic cell survival and disease progression in vivo.

108 lays a nonredundant role in multiple myeloma cell survival and disease progression, and indicate that

109 en ER and mitochondria, with implications in cell survival and diseases associated with mitochondrial

110 sess stemness properties to facilitate tumor cell survival and dissemination.

111 Stem cell therapies are limited by poor cell survival and engraftment.

112 Pappaa as an extracellular regulator of hair cell survival and essential mitochondrial function.

113 n events, facilitating mutant haematopoietic cell survival and expansion as well as contributing to m

114 ATP which is an essential energy source for cell survival and function such as PG biosynthesis.

115 erload in pancreatic islets can improve beta-cell survival and function under GLT stress and thus cou

116 a and as such is a major regulator of immune cell survival and function.

117 d exerting direct protective effects on beta cell survival and function.

118 th as observed in human lesions and supports cell survival and function.

119 t H727 cells remain dependent on the UPS for cell survival and growth despite harboring intrinsic res

120 Apart from single-cell survival and growth, it plays a major role at the g

121 nization and function through regulating the cell survival and Hh signaling.

122 is an essential self-digestion machinery for cell survival and homoeostasis.

123 cell proximity to TAM was linked with tumor cell survival and hypoxia was associated with accumulati

124 er, our data indicate that PIMs support PMBL cell survival and immune escape and identify PIMs as pro

125 that TMPRSS13 plays an important role in CRC cell survival and in promoting resistance to drug-induce

126 eas, knockdown of NO66 resulted in decreased cell survival and increased sensitivity to docetaxel.

127 ession of the DNA MMR pathway prevented club cell survival and increased the severity of viral diseas

128 he activity of EGFR inhibitors by decreasing cell survival and inhibiting bFGF, HGF, and IGF1 growth

129 and beta-catenin are important mediators of cell survival and interaction with the microenvironment,

130 Forced expression of NO66 promoted cell survival and invasion of PCa cells; whereas, knockd

131 romote processes that increase breast-cancer-cell survival and invasion.

132 ivity of these two kinases to the control of cell survival and lipid metabolism.

133 r work implicates c-Rel in both CNS-resident cell survival and lymphocyte responses to HSV-1 infectio

134 D-loop properties appear to be important for cell survival and mating-type switch in haploid yeast.

135 critical mediator of OX40-mediated CD8(+) T cell survival and memory formation following Ag exposure

136 mitochondria via mitophagy is essential for cell survival and neuronal functions.

137 Protein (IAP) family, is required for cancer cell survival and overexpressed in almost all solid tumo

138 on of ACADVL enabled enhanced intratumoral T cell survival and persistence in an engineered mouse mod

139 /FGFR axis is essential for multiple myeloma cell survival and progression by protecting multiple mye

140 a the provision of signals that enable tumor cell survival and proliferation as well as contribute to

141 otein levels to identify mechanisms of tumor cell survival and proliferation in adherent and nonadher

142 l modulator for acute myeloid leukemia (AML) cell survival and proliferation in multiple human leukem

143 ed the enrichment of genes associated with T cell survival and proliferation specifically in beta(2)-

144 EF domain increased leukemogenesis, enhanced cell survival and proliferation, and promoted stem cell

145 of rapamycin (mTOR) kinase is important for cell survival and proliferation, and viruses are known t

146 aling in EBV-infected B cells that optimizes cell survival and proliferation, setting the stage for o

147 mice, the NF-kappaB inhibitor JSH-23 reduced cell survival and proliferation.

148 wild-type counterpart, including superior T-cell survival and proliferation.

149 h lactate environment is detrimental for NKT cell survival and proliferation.

150 lling and metabolic reprogramming to support cell survival and proliferation.

151 sm for the requirement of PRMT5 for leukemia cell survival and provides potential biomarkers for the

152 s and amniotes where Fgf-signaling regulates cell survival and proximodistal patterning.

153 the ER stress pathway, causing enhanced beta-cell survival and reduced diabetes incidence in the face

154 E)-selectin as a novel mediator of malignant cell survival and regeneration which, upon blockade, has

155 rs signaling pathways that promote malignant cell survival and regeneration.

156 target gene and, therefore, may promote PCa cell survival and resistance to AR targeting therapeutic

157 ata highlights the importance of NTAL in APL cell survival and response to treatment.

158 rophages secrete SPP1, which sustains glioma cell survival and stimulates angiogenesis.

159 essential role of NCAM1 in the regulation of cell survival and stress resistance.

160 roles that creatine metabolism has in cancer cell survival and the function of the immune system.

161 polarity factors during ER stress safeguard cell survival and the timely cell-cycle re-entry upon ER

162 tor-kappaB (NF-kappaB), contribute to cancer cell survival and therapeutic resistance under oxidative

163 ng axis that is crucial to pancreatic cancer cell survival and therapeutic resistance, but they also

164 Mechanistically, PTN promoted CML stem cell survival and TKI resistance via induction of Jun an

165 ROCK2-dependent signaling and enhances tumor cell survival and tumor growth.

166 of pancreatic cancer cells without affecting cell survival and viability.

167 genes involved in oxidative stress response, cell survival, and cardiac hypertrophy.

168 A1, had decreased cell cycle progression and cell survival, and decreased feedback repression of the

169 aling pathways, inducing cell proliferation, cell survival, and invasion.

170 peanut-specific IgE response, decreased GCB cell survival, and loss of GC dark zone B cells after pe

171 n development, including cortical progenitor cell survival, and that expression during early neurogen

172 iation, chemotherapy resistance, cancer stem cell survival, and tumor metastasis.

173 lating 19 genes involved in lung endothelial cell survival, angiogenesis and DNA repair including, EP

174 titude of genes, including those involved in cell survival, angiogenesis, glycolysis and invasion/met

175 tch signaling, which are critical for cancer cell survival, apoptosis, proliferation, invasion, and c

176 n of beta-cell mass and, in particular, beta-cell survival/apoptosis.

177 ssion, depletion of UBR5 resulted in reduced cell survival, as a consequence of MYC stabilization.

178 A clonogenic cell survival assay confirmed that these drug-loaded pol

179 he CellTiter-Glo luminescence and clonogenic cell survival assays.

180 lex resulted in Stat5 phosphorylation and NK cell survival at a concentration or density of the compl

181 Through cell survival-based cDNA expression screens in neural pr

182 verrepresented among genes non-essential for cell survival but required for organism development.

183 ngiogenesis by influencing not only vascular cell survival, but also migration and adhesion.

184 esent evidence that S70pBcl2 promotes cancer cell survival by acting as a redox sensor and modulator

185 nteract, Pi-activated AKT signaling promotes cell survival by activating the mammalian target of rapa

186 ction as a tumor promoter, supporting cancer cell survival by counteracting replication stress.

187 olic basis of TRAF3-mediated regulation of B cell survival by employing metabolomic, lipidomic, and t

188 observed that blocking Ship1/2 abrogated EMC cell survival by exerting dual effects on the BCR signal

189 Here we show that NPR1 promotes cell survival by targeting substrates for ubiquitination

190 rotein kinase B (AKT) signaling mediates HCC cell survival caused by moderate heat stress in vitro, b

191 0 (PTEN) plays a critical role in regulating cell survival, cell growth, and proliferation by antagon

192 -alpha (PGC1alpha) expression that maintains cell survival cues by promoting mitochondrial function,

193 costimulatory signal that enhances CD8(+) T-cell survival, cytotoxicity, and mitochondrial activity,

194 hanisms for dependence receptors' control of cell survival/death balance, which may offer new clues f

195 a previously unknown mortalin substrate and cell survival/death effector.

196 , allows inferring the mutation rate and the cell survival/death rate per division.

197 t and substantial inter-patient variation of cell survival/death rates.

198 the molecular mechanisms underpinning cancer cell survival despite the oncogenic stress could provide

199 ogy and activity regulation is essential for cell survival, differentiation, and migration.

200 MSCs of all groups exhibited well-maintained cell survival, distribution and morphology.

201 ever, its application is hindered by limited cell survival due to the harmful dystrophic microenviron

202 However, the mechanisms that drive cell survival during a normally lytic infection remained

203 ted translation adaptation was essential for cell survival during chronic glucose deprivation.

204 ific WRKY transcription factors, and promote cell survival during ETI.

205 ly conserved recycling pathway that promotes cell survival during periods of stress.

206 petitive fitness advantage, likely promoting cell survival during stress.

207 symptomatically in the striatum, implicating cell survival (e.g. Hipk4) intertwined with cell prolife

208 suggesting that DYRK1A expression decreases cell survival efficiency in response to DNA damage and p

209 ably tetrameric PKM2 mutant, K422R, promoted cell survival even in the absence of IB5, and IB5 furthe

210 /Cip1), MSI1 and KLF4 regulates Bmi1-Cre(ER) cell survival, exit from quiescence and regenerative pot

211 cellular and genetic determinants of cancer cell survival following exposure to alpha-particle irrad

212 ht, together with new findings demonstrating cell survival following MOMP, this pro-inflammatory role

213 were biocompatible and able to support stem cell survival following recellularisation.

214 ified in regulating DNA damage responses and cell survival following treatment with DNA-damaging agen

215 iciencies in DNA damage repair and decreased cell survival following x-ray irradiation, particularly

216 In support of a role for JAG1 in cell survival, genes involved in mitochondrial function

217 rdinately modulate oncogenic pathways and/or cell survival/growth across cancers.

218 Still, immune sera inhibited HER2+ SKBR3 cell survival in a dose-dependent fashion.

219 microRNA in hypoxia and is known to promote cell survival in a hypoxic environment.

220 s diminish insulin secretion and reduce beta-cell survival in both major forms of diabetes.

221 uggests a mechanistic link between decreased cell survival in cell culture and severe fever-induced b

222 ver 300 client proteins and is essential for cell survival in eukaryotes.

223 y proposed as a potential factor influencing cell survival in models of Parkinson's disease.

224 was uniquely up-regulated and important for cell survival in primary effusion lymphoma (PEL), which

225 s and that alternative fuel usage may affect cell survival in starved animals.

226 hibition may provide a means to promote beta cell survival in the context of metabolic stress and pre

227 ive catabolic process functioning to promote cell survival in the event of inappropriate living condi

228 se blood vessels in the grafts that promoted cell survival in the grafts.

229 Naive CD8(+) T cell survival in the periphery is critically dependent o

230 arable potency in reduction of breast cancer cell survival in vitro and in growth restriction of orth

231 enes, SD-Foxo1 promoted IL-15-mediated CD8 T cell survival in vitro and survival of short-lived effec

232 PLA2G1B also decreased CD4+ T cell survival in vitro, likely playing a role in CD4 lym

233 is demonstrated to increase retinal ganglion cell survival in vivo in mice of both sexes following op

234 nment account for mantle cell lymphoma (MCL) cells survival in lymphoid organs.

235 ription factor that plays a critical role in cell survival including metabolic adaptation under hypox

236 ted upstream regulator proteins that mediate cell survival, including Pdx1, Ptf1a and p53, which are

237 stinal tract narrowing, increased intestinal cell survival, increased sizes of intestinal luminal spa

238 plet-size increases with aggregate-size, and cell survival is higher the larger the droplet.

239 h, yet how WASp influences DNA damage-linked cell survival is unknown.

240 ial response to drug treatment that promotes cell survival is unknown.

241 agic flux in OXPHOS-competent cells promoted cell survival, it was impaired in OXPHOS-defective cells

242 tress response as a key mechanism for cancer cell survival leading to cancer progression and resistan

243 screens typically use coarse assays such as cell survival, limiting what can be learned about mechan

244 tumor microenvironment that supports cancer cell survival, local invasion and metastatic disseminati

245 c signaling pathways involved in endothelial cell survival, metabolism and migration.

246 PreCon mediated cardioprotection in DM mice, cell survival molecules were screened.

247 ibling OPCs confirmed a pathogenic effect on cell survival of both the CSPG4(A131T) (P = 0.006) and C

248 Although LGP2 has also been linked to cell survival of both tumor cells and T cells, the role

249 p53 selectively activates genes to elicit a cell survival or cell death response.

250 repair stress damage, but the means by which cell survival or death is determined remains unclear.

251 e-binding domain in mortalin was critical to cell survival or death.

252 as a novel effector of the nucleus-to-Golgi cell-survival pathway triggered by IR-induced DNA damage

253 (IECs) to target inflammatory, metabolic and cell survival pathways and establish infection.

254 he decision between initiating cell death or cell survival pathways.

255 t TREM2 signals through PLCgamma2 to mediate cell survival, phagocytosis, processing of neuronal debr

256 t-derived colonoids to leflunomide increased cell survival, polarity, and transport function.

257 ctivator to normally induce inflammatory and cell survival programs.

258 ith sustained expression of inflammatory and cell survival programs.

259 iptional evidence of abnormal phagocytic and cell-survival programs.Conclusions: Our findings offer a

260 Akt activity which may explain the aberrant cell survival, proliferation and invasion associated wit

261 ting primary oligodendrocyte (OL) progenitor cell survival, proliferation, and differentiation in vit

262 factor receptor (PDGFR)-alpha plays roles in cell survival, proliferation, and differentiation; howev

263 on analysis of HIF2alpha expression in situ, cell survival/proliferation, and survival in brain tumor

264 The mTOR pathway, an important regulator of cell survival/proliferation, is upregulated in GBM, but

265 Cell survival rate (CSR) is a very important parameter i

266 the membrane-binding domain provided similar cell survival ratio as the full length PfCCT protein.

267 KC regulation, a molecular target for S1P in cell survival regulation, and a tool to further explore

268 nction is critical for cancer but not normal cell survival, representing an effective approach for hi

269 egulator in the events of growth control and cell survival required for the maintenance of the Drosop

270 In a CRISPR cell survival screen, we discovered two genes, Cmas and

271 d reduced NFkappaB-mediated inflammation and cell survival signaling in cells isolated from the lungs

272 through kinases to initiate inflammatory and cell survival signalling.

273 r Friedreich's ataxia (FRDA), is crucial for cell survival since it critically affects viability of n

274 ression of STAT3-regulated genes involved in cell survival, such as c-Myc, CDC25, and CDK1.

275 ignaling pathway that is vital to the cancer cell survival; the trials were not designed to evaluate

276 ive effects of elevated ceramide and promote cell survival, thereby providing cardioprotection after

277 owing that AMPK activates mTORC2 to increase cell survival, these data provide a potential mechanism

278 ts cytotoxic effects on A549 (p53 wild-type) cell survival through a mechanism that depends on hyalur

279 r growth, resistance to stress, and improved cell survival throughout in vitro expansion.

280 Confirming a link between JAGGED1 and cell survival, transcriptional profiling showed that JAG

281 We showed that CaWss1 promotes cell survival under genotoxic stress conditions that gen

282 These results suggest that increased cell survival under half-field exposure is predominantly

283 During initiation, genetic changes enable cell survival under high ROS levels by activating antiox

284 fatty acids toward respiration and enhanced cell survival under low-glucose conditions.

285 under stress conditions, thus promoting CRC cell survival under metabolic stress in vitro and enhanc

286 ntiation between cell states promotes cancer cell survival under stress and fosters non-genetic heter

287 damaged mitochondria, which is required for cell survival under stress conditions.

288 ffective strategy for promoting transplanted cell survival under the condition of an iron overload.

289 Thus, Hog1 contributes to maximizing cell survival upon stress by regulating mitotic exit.

290 -cells, which modulate Ca(2+)/ion transport, cell survival, vesicle/membrane trafficking, glucose met

291 clustering of beta1 integrin, leading to AML cell survival via activation of p38 MAPK.

292 A20 directly inhibits IKK activation and HL cell survival via its C-terminal linear-ubiquitin bindin

293 In both tissues, cell survival was maximal during early development.

294 global profile of mitochondrial salvage and cell survival was observed in the EVLP lung tissue compa

295 Bioenergetics and cell survival were instead unaffected in normal B lympho

296 ucleic acid degrading machines which ensures cell survival when faced with phage attack.

297 egulation, as they are usually essential for cell survival while potentially destructive.

298 target, is a non-cell autonomous mediator of cell survival, while another unidentified secreted facto

299 Finally, BAFF and APRIL support plasma cell survival, with differential impacts on IgM- and IgG

300 ficient mitochondrial targeting, and in vivo cell survival, with lipid-modulated stability, all of wh