ライフサイエンスコーパス: cell survival

1 control the pathophysiological processes of cell survival.

2 nment plays a critical role in promoting AML cell survival.

3 s, and pose a threat to genome stability and cell survival.

4 (ADT) to prevent androgen-independent tumor cell survival.

5 arly stages of SCI and affects prognosis and cell survival.

6 rly universal role of this pathway in cancer cell survival.

7 orward signaling circuit that promoted tumor cell survival.

8 ion, translation, cell cycle regulation, and cell survival.

9 ins, and this increase is thought to promote cell survival.

10 an unlinked monomeric state is essential to cell survival.

11 fferent times, modulate DNA TLS for improved cell survival.

12 in malignancies, leading to increased cancer cell survival.

13 nuclear factor kappaB (NF-kappaB)-dependent cell survival.

14 ptotic effectors, BAX and BAK, and promoting cell survival.

15 cts as a gain-of-function mutation enhancing cell survival.

16 that persistent signaling supports senescent cell survival.

17 ethylation of the CENP-A tail contributes to cell survival.

18 ion worsens genome instability, compromising cell survival.

19 imulated PNKP activity and promoted SSBR and cell survival.

20 ry response to EGFR inhibition that mediates cell survival.

21 aneously to target autoreactive or malignant cell survival.

22 ion to T-cell-independent antigens but not B-cell survival.

23 ncrease in DNA damage load and impairs tumor cell survival.

24 the pluripotency marker Oct3/4 and increased cell survival.

25 essor and other proteins critical for tumour cell survival.

26 forks, thereby ensuring genome stability and cell survival.

27 nicity and may play a role in shaping cancer cell survival.

28 ate cyclase (GC) signaling and photoreceptor cell survival.

29 ter chromatid cohesion to redundantly ensure cell survival.

30 nding GTPase and is required for cancer stem cell survival.

31 cells and their microenvironment, promoting cell survival.

32 mechanisms, both rather associated with host cell survival.

33 gh inhibition of APC, ensuring smooth muscle cell survival.

34 d fission, similarly affect retinal ganglion cell survival.

35 s highly diverse and essential for mammalian cell survival.

36 ve damage from reaching levels that threaten cell survival.

37 unexpectedly, Par3 is essential for mammary cell survival.

38 ial for HIV-1 infection, but dispensable for cell survival.

39 as a BET target gene essential for melanoma cell survival.

40 the goal of identifying genes essential for cell survival.

41 bsence alternative repair mechanisms promote cell survival.

42 isorder regulates events that are crucial to cell survival.

43 A localization at the lysosome and increased cell survival.

44 mage to complete the cell cycle and maintain cell survival.

45 w that BCR signalling is required for tumour cell survival.

46 s triggering cell cycle arrest and promoting cell survival.

47 state, and impact DNA repair and subsequent cell survival.

48 S and G2 when productive TLS is critical for cell survival.

49 understanding of the mechanisms that govern cell survival.

50 ocyst docking, membrane-protein delivery and cell survival.

51 , an oxysterol stress responder, to optimize cell survival.

52 only inhibited Cav1.3 function but increased cell survival.

53 ng the MTA1-SGK1 axis for the benefit of the cell survival.

54 on, and plays a critical role in controlling cell survival.

55 cell counterparts, consequently enhancing B cell survival.

56 4, instigating autophagy gene activation and cell survival.

57 n had a long-lasting effect in promoting rod cell survival.

58 urther substantiating a role for ST6Gal-I in cell survival.

59 no detectable effect on nonmalignant CD34(+) cell survival.

60 including cell proliferation, metabolism and cell survival.

61 ion, metabolic regulation, and SOD1-mediated cell survival.

62 volved a switch from BCL2 to BCLXL-dependent cell survival.

63 that increase metastasis, proliferation, and cell survival.

64 olved in axon guidance, cell patterning, and cell survival.

65 site-specific inhibitors reduce cancer stem cell survival.

66 activities and impairs tumour but not normal cell survival.

67 s critical for mitochondrial homeostasis and cell survival.

68 role for ACC enzymes in redox regulation and cell survival.

69 and minimalizing toxicity and thus ensuring cell survival.

70 ked PI3K/Akt/Mdm2 pathway and suppressed HCC cell survival.

71 identify small molecule inhibitors affecting cell survival.

72 tream of Tolls can drive either apoptosis or cell survival.

73 of Akt and promoting p53 function, effecting cell survival.

74 uirement in neuronal differentiation but not cell survival.

75 s critical for triple-negative breast cancer cell survival.

76 acellular domain (CD74-ICD), which regulates cell survival.

77 for inducing a metabolic shift essential for cell survival.

78 tion to environmental stress is critical for cell survival.

79 rating tumor immune escape and supporting RS cell survival.

80 keratinocyte proliferation, epithelial stem cell survival, adipocyte biology, and inflammatory skin

81 pacity while providing a glutamine-dependent cell survival advantage, strongly suggests a metabolic s

82 promotes DNA end resection, increases HR and cell survival after ionizing radiation, and prevents cel

83 nd its transcriptional targets in outer hair cell survival after noise damage.

84 /or S514 are important for damage bypass and cell survival after UV irradiation.

85 is an essential cytokine known to promote T cell survival and activate the effector function of memo

86 oteins is a fundamental cellular process for cell survival and adaptation to environmental stimuli.

87 n tumor suppressor, can contribute to cancer cell survival and adaptation to low-glutamine conditions

88 d two novel pro-tumorigenic roles (promoting cell survival and altering cell polarity) for genetic al

89 RM3 activation in colon cancer cells reduces cell survival and anchorage-independent growth in vitro

90 emerging roles of CIB1 in regulating cancer cell survival and angiogenesis, although the mechanisms

91 ns of the BCL-2 family are key regulators of cell survival and are frequently overexpressed in malign

92 ulfoxide reductase A to modulate liposarcoma cell survival and ASC differentiation state.

93 d XIAP and cyclin D1, suggesting its role in cell survival and cell cycle.

94 ainst TrkA, p75(NTR), and sortilin decreased cell survival and cell migration through decreased SRC a

95 ing of receptors to the axon is critical for cell survival and circuit formation.

96 in the TNF signaling pathway that integrates cell survival and cytokine production.

97 regulates the splicing of genes involved in cell survival and death, insulin secretion, and c-Jun N-

98 optosis are cellular processes that regulate cell survival and death, the former by eliminating dysfu

99 wn about how the choice is made between germ cell survival and death.

100 Furthermore, knockdown of KLF15 reduced cell survival and destabilized the actin cytoskeleton in

101 tterns, with activation of genes involved in cell survival and down-regulation of genes involved in a

102 NFE2L2 leading to NRF2 accumulation promote cell survival and drug resistance in cancer cells.

103 a the AKT signaling pathway and increased NK cell survival and effector function.

104 In conclusion, irisin can promote beta-cell survival and enhance GSIS and may thus participate

105 with CD80 in lymphoid tissue promoted CD8+ T cell survival and expansion, thereby enhancing the GVL r

106 EL ), which is associated with an enhanced B-cell survival and expressed in humans, but not in mice.

107 ed process that is essential for appropriate cell survival and function, and the ubiquitin pathway ha

108 invade and metastasize without affecting the cell survival and growth.

109 pression by RNAi caused a decrease in cancer cell survival and growth.

110 e that is responsible for peripheral naive T cell survival and homeostasis.

111 uced autophagy provides nutrients for cancer cell survival and identifies novel cotreatment strategie

112 thropoietin by the kidney; reduced red blood cell survival and iron deficiency; and mineral bone dise

113 cellular response to hypoxia is critical for cell survival and is fine-tuned to allow cells to recove

114 have exposed a critical role for BCL-W in B cell survival and lymphomagenesis.

115 en implicated in different aspects of cancer cell survival and metastasis.

116 merous human diseases, including cancer stem cell survival and metastatic phenotype.

117 LKB1 deficiency disrupted Treg cell survival and mitochondrial fitness and metabolism,

118 TSPAN1 is an androgen-driven contributor to cell survival and motility in prostate cancer.

119 (CSE) and smokeless tobacco extract (STE) on cell survival and motility of periodontal ligament (PDL)

120 stimuli, including significant reductions in cell survival and myofibroblast differentiation.

121 role in dorsal root ganglion (DRG) neuronal cell survival and neurotransmission by transporting mito

122 lucose levels and increases concomitant beta-cell survival and number in a streptozotocin-induced dia

123 1 is critical for OGT-mediated regulation of cell survival and of lipid synthesis, as overexpression

124 ses and biological functions associated with cell survival and organismal death rather than inflammat

125 ting beta-catenin/SHH signals in mesenchymal cell survival and outgrowth of the mandible during devel

126 T (Tfh) cells promote germinal center (GC) B cell survival and proliferation and guide their differen

127 ese PA scaffolds support myogenic progenitor cell survival and proliferation and they can be optimize

128 ranscription factors that play a key role in cell survival and proliferation in many hematological ma

129 e, we show that Pax6 controls eye progenitor cell survival and proliferation through the activation o

130 rtance of PTEN S-nitrosylation in supporting cell survival and proliferation under conditions of ener

131 ng and activating chemokines and controlling cell survival and proliferation.

132 tor (BCR) signaling, resulting in aberrant B-cell survival and proliferation.

133 uR multimerization modules and reduces tumor cell survival and proliferation.

134 -catenin directly altered immediate CD49f(+) cell survival and proliferation.

135 ges revealed the molecular networks defining cell survival and proliferation.

136 r, has an important role in gene expression, cell survival and promoting hypoxic response.

137 during development, adult hematopoietic stem cell survival and quiescence, and terminal maturation of

138 as an important player in the regulation of cell survival and recovery from stress.

139 ability, a key player associated with cancer cell survival and recurrence, however, remains poorly un

140 Protein glycosylation is essential for cell survival and regulates many cellular events.

141 on Cardiac CEST imaging can be used to image cell survival and rejection in preclinical models of cel

142 ssion was shown to be essential for CML stem cell survival and self-renewal during imatinib mesylate

143 scle growth, myofiber maturation, and muscle cell survival and that alterations in its activity resul

144 se element-binding protein pathway mediating cell survival and the G protein-coupled receptor --> Gs

145 of the IL-32gamma isoform, leading to tumor cell survival and thus favoring tumor progression.

146 and, specifically, Smarcal1 in hematopoietic cell survival and tumor development.

147 adiosensitivity was determined by clonogenic cell survival and tumor growth delay assays.

148 s treatment synergistically reduced melanoma cell survival and tumor growth.

149 e have important roles in maintaining cancer cell survival and uncover a previously unappreciated rol

150 P(H) cofactors, which is critical for cancer cells survival and progression.

151 and promote lysosomal biogenesis, autophagy, cell survival, and brain tumorigenesis.

152 a2-AMPK in modulating ribosome biosynthesis, cell survival, and cardioprotection.

153 s, display an immature morphology, promote T-cell survival, and enhance proliferation and IFNgamma pr

154 P response element-binding protein-dependent cell survival, and ERK-dependent neuritogenesis, respect

155 o, but enhanced ECM-mediated signaling, LUAD cell survival, and micrometastasis expansion in hyaluron

156 d keratinocytes, Edaradd rescues DNA damage, cell survival, and proliferation of Gata6 knockout cells

157 , inhibited cell growth without compromising cell survival, and suppressed tube morphogenesis of ECs,

158 s play key roles in insulin release and beta cell survival, and their dysfunction may contribute to t

159 ct this has on reactive remodeling, ganglion cell survival, and visual function after experimental gl

160 l-mesenchymal transition (EMT) and promoting cell survival, anoikis resistance, invasion, and metasta

161 e/threonine kinase, plays important roles in cell survival, apoptosis, and oncogenes.

162 osin receptor kinase C (TrkC) is involved in cell survival, apoptosis, differentiation, and tumorigen

163 The stress response and cell survival are necessary for normal pancreatic beta-c

164 site) signaling and regulating smooth muscle cell survival, as well as differentiation in advanced at

165 iologic processes involved in the control of cell survival (B-cell lymphoma 2 [BCL2]), cell prolifera

166 tion of ced-11 does not cause an increase in cell survival but can enhance cell survival in other cel

167 We evaluated cell survival by a clonogenic assay; apoptosis by Annexi

168 Given SGK3 inhibition reduces AI-resistant cell survival by eliciting excessive EnR stress and also

169 demonstrate that HSP90 inhibition impairs BL cell survival by interfering with tonic BCR signaling, t

170 e a variety of cytokines that promote plasma cell survival by regulating antiapoptotic members of the

171 s, whereas miR-451a overexpression repressed cell survival by targeting and downregulating c-Myc.

172 -155 was associated with increased levels of cell survival, colony formation, cell migration and decr

173 endence through the production of the plasma cell survival cytokine interleukin-6 (IL-6).

174 high-throughput and high accuracy clonogenic cell-survival data for therapeutic scanned proton beams.

175 liferation and differentiation of stem cell, cell survival/death, and cellular metabolism under both

176 Thymic maturation and peripheral T cell survival depend on several signaling cascades, but

177 al to the neurotrophic factors that regulate cell survival, differentiation, and neuron-specific char

178 SspA is essential for cell survival during acid-induced stress, and we found t

179 NKT cell survival during development requires signal process

180 cell survival, resulting in increased cancer cell survival during DNA damage.

181 e focus on the mechanisms that regulate germ cell survival during embryonic development in Drosophila

182 satory signaling mechanism that promotes AML cell survival during FLT3 inhibition.

183 1 (THBS1) was recently shown to promote beta-cell survival during lipotoxic stress.

184 criptional network governing pancreatic beta-cell survival during stress.

185 differentiated phenotype may facilitate beta-cell survival during the stresses associated with islet

186 tailored to manipulate cell death to limit T-cell survival (eg, autoimmunity and transplantation) or

187 toimmunity and transplantation) or enhance T-cell survival (eg, vaccination and immune deficiency).

188 of ERalpha stimulates cell proliferation and cell survival, ERbeta promotes apoptosis.

189 rrent dogma, Mdm2 expression is required for cell survival even in the absence of p53.

190 and CD40, blockade of B cell function and B cell survival factors, and disruption of the formation o

191 Continued activation of cell survival factors, Atf6 and Ire1alpha during chronic

192 utoantibody production, including IL-6 and B cell survival factors, but also reactive oxygen intermed

193 y from checkpoint activation is critical for cell survival following DNA damage.

194 the self-folded hydrogel-based tubes support cell survival for at least 7 d without any decrease in c

195 edistribution of MTA1, SGK1 upregulation and cell survival functions were compromised by a pharmacolo

196 xt-dependent, the role of autophagy in tumor cell survival has attracted great interest in targeting

197 mplement, extracellular matrix (ECM), lipid, cell survival, immune system, metabolism, or unknown/oth

198 not only in MGE differentiation, but also in cell survival, implying that other adapters mediate at l

199 und that Shikonin binds PKM2 and inhibits BC cell survival in a dose-dependent but pyruvate kinase ac

200 Thus, naive T cells regulate B cell survival in a SLAMF6- and SAP-dependent manner.

201 umor cells with blood cells to augment tumor cell survival in circulation.

202 al clinically relevant mechanism to increase cell survival in cystinosis.

203 The pathways regulating pancreatic beta cell survival in diabetes are poorly understood.

204 rstanding of essential pathways regulating B-cell survival in health and disease.

205 nd ROS generation, thereby sustaining cancer cell survival in hypoxia.

206 KR-mediated hyperinduction of iNOS decreases cell survival in mouse embryonic fibroblasts via mechani

207 rkers and normal ultrastructure and improves cell survival in murine podocytes.

208 an increase in cell survival but can enhance cell survival in other cell-death mutants, indicating th

209 RADD to DSBs into the nucleus contributes to cell survival in response to DNA damage through an activ

210 the G1 phase of the cell cycle and improves cell survival in response to growth-induced pressure.

211 induces NRF2 activation and promotes cancer cell survival in response to oxidative stress.

212 n vitro, silencing the LDLR led to decreased cell survival in serum-starved conditions, associated wi

213 pt repression, cell-cell contact abrogation, cell survival in suspension, STAT3 phosphorylation and w

214 urther, we show that RECQL5 is essential for cell survival in the absence of WRN.

215 type JAK1 or STAT3 was sufficient to promote cell survival in the cells that had either JAK1or STAT3

216 is important for ER remodelling dynamics and cell survival in the face of recursive, transient ER str

217 blation of BLM rescues genomic integrity and cell survival in the presence of DNA double-strand break

218 ionally modulated homeostasis and ultimately cell survival in the retina and brain.

219 tissue, influence inflammatory responses and cell survival in vitro.

220 Treg cell activity and increased effector T cell survival into an efficient CD4(+) T cell response.

221 d pyrimidine known to promote embryonic stem cells survival, is robustly adipogenic and induces postn

222 lymerase-1 (a key molecule in DNA repair and cell survival), leading to SMC apoptosis.

223 depletion of memory B cells despite normal B cell survival ligand concentrations.

224 gnalling as a novel key pathway coordinating cell survival, lineage allocation, and specification and

225 way recently shown to be critical for cancer cell survival, may explain the excess lactate generation

226 This dynamic change in B cell survival mechanisms is unique to virus-infected cel

227 CME that alters signaling to enhance cancer cell survival, migration, and proliferation.

228 e ATX-LPA signaling pathway is implicated in cell survival, migration, and proliferation; thus, the i

229 zone of lymph nodes (LNs) are pivotal for T cell survival, mobility, and peripheral tolerance.

230 g that adaptation mechanisms contributing to cell survival must be in place.

231 inase receptor that is required for pericyte cell survival; N-cadherin, the key adherens junction pro

232 concepts and information surrounding plasma cell survival niches, and consider two opposing models t

233 x adhesion is required for normal epithelial cell survival, nutrient uptake and metabolism.

234 ge is crucial to ensure genome stability and cell survival of all organisms.

235 sing concentration of TiO2 NPs increased the cell survival of Bacillus subtilis in autolysis-inducing

236 (TNFR1) death receptor by TNF induces either cell survival or cell death.

237 pro- or anti-apoptotic factors which mediate cell survival or death.

238 , different Tolls can preferentially promote cell survival or death.

239 n the presence of C1q alters macrophage foam cell survival or function.

240 without affecting androgen-mediated luminal cell survival or regeneration.

241 be serially and noninvasively used to probe cell survival or rejection after intramyocardial implant

242 eptor, TNFR1, can drive cytokine production, cell survival, or cell death.

243 athways control polarization: epigenetic and cell survival pathways that prolong or shorten macrophag

244 affects cellular DNA content and is a novel cell survival phosphatase preventing both thermal and ox

245 of RAF dimers and ERK signaling promotes HCC cell survival, prevents apoptosis via downregulation of

246 at integrates environmental cues to regulate cell survival, proliferation and metabolism, and is ofte

247 ngly, we find that it is also required for B cell survival, proliferation, and cytokine secretion in

248 IL-15-activated CD40L(+) ILC3s helped B-cell survival, proliferation, and differentiation of IL-

249 PAK4 plays critical roles in cell survival, proliferation, and morphology.

250 ibroblasts demonstrated that Gal-3 regulates cell survival, proliferation, and type I collagen synthe

251 increased surface IgM but did not enhance B cell survival, proliferation, or altered NF-kappaB respo

252 that activate signaling cascades controlling cell survival, proliferation, protein synthesis, and ves

253 normal HSPCs and AML cells and inhibits AML cell survival/proliferation.

254 lutaminase (TG2) is an important cancer stem cell survival protein that exists in open and closed con

255 We observed higher hair cell survival rates and lower auditory brainstem respons

256 The relative cell survival (RCS), i.e. the ratio of normalized cell p

257 Although it is clear that plasma cell survival requires cell extrinsic signals, the natur

258 both required to enact DNA damage repair and cell survival, resulting in increased cancer cell surviv

259 echanisms of posttranslational regulation on cell survival signaling proteins.

260 s required for maintaining autocrine Schwann cell survival signaling, and inactivation of Schwann cel

261 cases, we also demonstrate that the PI3K/Akt cell survival signalling pathway is dysregulated in both

262 mOGT is also critical for cell survival; siRNA-mediated knockdown of endogenous mO

263 ted transcriptional pause-release, promoting cell survival specifically in vivo.

264 Remarkably similar to patterns known from cell survival studies, LET-dependencies with pronounced

265 t that SET1B/COMPASS, which is essential for cell survival, surprisingly has a cytoplasmic variant.

266 ure accounts for the correlation between the cell-survival, the absorbed (physical) dose and the prot

267 en developed in the last 10 years to enhance cell survival, they showed limited efficacy.

268 ediated mitogenic signaling, promoting tumor cell survival through an androgen-independent signaling

269 20 pulses (300 ns, 20 Hz, 6 kV/cm) decreased cell survival to 34% compared with 51% in control cells

270 hat DNTs and Tolls can switch from promoting cell survival to death in the central nervous system (CN

271 odeling, and (3) increasing angiogenesis and cell survival to protect against and limit damage associ

272 and energy balance and plays a vital role in cell survival under adverse conditions, including nutrie

273 vering physiologic mechanisms promoting beta-cell survival under conditions of inflammation and stres

274 ondrial metabolism was necessary to maintain cell survival under drug stress.

275 at controls expression of genes critical for cell survival under hyperosmotic conditions.

276 p collagen fragments, which can promote PDAC cell survival under nutrient limited conditions, and tha

277 The ROS-signaling responses necessary for cell survival under oxidative stress conditions remain i

278 HSR promotes cell survival under proteotoxic conditions by maintainin

279 HSP essential for nucleolus homeostasis and cell survival under proteotoxic stress.

280 Autophagy is essential for cell survival under stress and has also been implicated

281 so a target of Pdx1 and is critical for beta-cell survival under stress conditions.

282 53 activity to ensure LT-HSC maintenance and cell survival under stress.

283 ation, proliferation, effector function, and cell survival upon binding to its ligand, CD70.

284 (ER) unfolded protein response and promotes cell survival upon ER stress.

285 that tumor-associated mutp53 promotes cancer cell survival upon glutamine deprivation both in vitro a

286 f PAX2 in PAX2-null human HGSC cells reduced cell survival via apoptosis.

287 stages of kidney repair and promotes tubular cell survival via IL-13 receptor alpha2 (IL13Ralpha2)-me

288 Toll-6 promotes cell survival via MyD88-NF-kappaB and cell death via Wek

289 -cell loss and shows that exendin-4 improves cell survival via restoration of lysosomal function and

290 Whether GLP-1 mediates beta-cell survival via the key lysosomal-mediated process of

291 General anesthetics may control cell survival via their effects on autophagy by activati

292 by neurotrophin (NT) ligands, which promote cell survival via their Trk and p75(NTR) receptors and c

293 more, dendritic cell- and IL-2/7-dependent T cell survival was found to be independent of coronin 1.

294 No difference in therapeutic effect or cell survival was observed between labeled and non-label

295 the context-selective role of TBK1 in cancer cell survival, we employed a combination of broad-scale

296 established role of GLP-1 in promoting beta-cell survival, we hypothesized that IL-6 may also direct

297 tly, TrkC-miR2 overexpression promoted SW480 cell survival, which was detected by flow cytometry, MTT

298 ctional role for ST6Gal-I in fostering tumor cell survival within the serum-depleted tumor microenvir

299 lular response to TNF and may promote cancer cell survival within TNF-rich tumor microenvironments.

300 tatic liver-infiltrating MDSCs induced tumor cell survival without involvement of innate or adaptive