ライフサイエンスコーパス: survival signal

1 sm of the Xenopus laevis egg provides a cell survival signal.

2 cellular stressors and is an important cell survival signal.

3 d infiltrates, STAT3 activity, and increased survival signal.

4 eration signaling, whereas Pi3k mediates the survival signal.

5 ligation of BAFF-R by BAFF delivers a potent survival signal.

6 of PLK1, which is sufficient to mediate this survival signal.

7 ll receptor signaling, a putative CLL-growth/survival signal.

8 ence of stromal co-culture or cytoprotective survival signals.

9 romoting inflammation and promoters of tumor survival signals.

10 lation of the B-cell receptor (BCR) triggers survival signals.

11 cell lymphoma (DLBCL) and mediate essential survival signals.

12 iRs in the malignant B cell resulting in pro-survival signals.

13 indirect response to cell proliferation and survival signals.

14 inating antigen and microenvironment-derived survival signals.

15 erein, we examine a role for MFB-derived CCA survival signals.

16 ies for PTLD through targeting of EBV-driven survival signals.

17 T(CM) development largely through providing survival signals.

18 ed to migrate into the white pulp to receive survival signals.

19 eptors, thereby depriving tumor cells of pro-survival signals.

20 r multiple non-RTKs and drives leukemic cell survival signals.

21 vely respond to specific, proximal death and survival signals.

22 cells rely on B-cell receptor (BCR)-mediated survival signals.

23 critical regulator of inflammatory and cell survival signals.

24 actor availability and regulating homing and survival signals.

25 acent neurons, and this entry amplified cell survival signals.

26 als act through a form of positive feedback--survival signals.

27 with pronounced dependence on extracellular survival signals.

28 heir surveying task for both foreign Ags and survival signals.

29 f apoptosis in response to extracellular pro-survival signals.

30 n mutual exclusion and may compete for local survival signals.

31 E2F1 apoptotic activity under the control of survival signaling.

32 mation via its effects on focal adhesion and survival signaling.

33 K2 appears to be an important mediator of Hh survival signaling.

34 n ATM-driven DDR-like response and NF-kappaB survival signaling.

35 ing AKT is critical in PTK6 and FAK-mediated survival signaling.

36 targeted therapies through proliferative and survival signaling.

37 extrinsic apoptosis and increasing NF-kappaB survival signaling.

38 n, and subsequent down-regulation of myocyte survival signaling.

39 nt apoptotic signaling and PI3K-AKT-mediated survival signaling.

40 s enhanced degradation of a key component of survival signaling.

41 n MET-independent activation of BCL-2/BCL-XL survival signaling.

42 complex processes such as cell adhesion and survival signaling.

43 ctivated activity could down-regulate the IR survival signaling.

44 ed kinase activity, which impairs downstream survival signaling.

45 ctive tissue growth factor and activated ERK survival signaling.

46 ll-ECM adhesion regulates Src activation and survival signaling.

47 F-kappaB2, an essential component for BAFF-R survival signaling.

48 ith Src and contributes to cell-ECM-mediated survival signaling.

49 lator of lipid biosynthesis and Akt-mediated survival signaling.

50 to evade therapy through increased PI3K/AKT survival signaling.

51 tabilization of EGFR and consequent ERK/MAPK survival signaling.

52 a cytotoxin, which interferes with integrin survival signaling.

53 LXND1-dependent) activation of PI3K-mediated survival signaling.

54 ng BECN1 and blunting IGF1 receptor and mTOR survival signaling.

55 ng complex and enhancing downstream PI3K/Akt survival signaling.

56 oxic insults by binding EGFR and stimulating survival signaling.

57 ns between NF-kappaB and p300 that reinforce survival signaling.

58 cluding proliferation, growth, invasion, and survival signaling.

59 to chemotherapy through the induction of pro-survival signalling.

60 e examine the death signals and compensatory survival signals activated during B cell activation and

61 lts demonstrated that CRAG enhances the cell survival signal against the accumulation of unfolded pro

62 ulture media promoted NF-kappaB activity and survival signal, Akt activation, in HC11 cells, whereas

63 l regulatory loop between cell death and the survival signal and may provide guidance for the develop

64 on constitute a locus for cross-talk between survival signaling and cell motility pathways.

65 eptor tyrosine kinase has been implicated in survival signaling and chemoresistance in many human can

66 E2-induced estrogen receptor-dependent cell survival signaling and gene expression.

67 and retinal ganglion cells (RGCs) differ in survival signaling and global gene expression.

68 Doxorubicin also reduced pro-survival signaling and increased apoptosis in WT hearts.

69 ine kinase 3 expression and stromal-mediated survival signaling and led to the stabilization of key N

70 te growth factor-cMet-Akt-mTor proliferation/survival signaling and PAR-2-Galphai-NFkappaB inflammato

71 K1 plays a key role in regulating neutrophil survival signaling and thus may prove a valuable therape

72 zation, which in turn triggers dysfunctional survival signaling and UPR/ER stress.

73 otectal projection via its regulation of pro-survival signalling and axonal mitochondrial homeostasis

74 esion, migration, and invasion by activating survival signals and conferring resistance to anoikis.

75 nduced signaling and overcame stroma-induced survival signals and migratory stimuli from CXCL12.

76 BLyS levels affect survival signals and selective apoptosis of autoantibody

77 r proteins that are activated upon decreased survival signals and/or increased cellular stress.

78 -8 functions as an angiogenic factor and pro-survival signal, and ICAM-1 has been implicated in tumor

79 activation of macrophages it also provides a survival signal, and the potential for the caspases to p

80 dually stimulates sustained, downstream Akt survival signaling, and dampens NHE1 activity through co

81 uired for maintaining autocrine Schwann cell survival signaling, and inactivation of Schwann cell STA

82 zation, mobility, and function of molecules, survival signaling, and migration.

83 s, mitochondrial ATP synthase activity, cell survival signaling, and other changes.

84 ne protein kinase mediates growth factor and survival signalling, and cooperates potently with c-MYC

85 ons, by facilitating optimal pre-TCR-induced survival signals, and by promoting thymocyte proliferati

86 initiate downregulation of adhesion-related survival signals, and further affect cell engraftment af

87 on and degradation of PDGF-BB, augmented its survival signals, and promoted cell survival after nutri

88 signaling pathways required to transmit this survival signal are poorly understood.

89 tivity and the resulting aberrant growth and survival signaling are a common driving force of cancer.

90 Cell survival signals are modulated by many different recepto

91 all, these studies define N-domain-dependent survival signaling as an Achilles heel of persistent STA

92 balance proliferation, differentiation, and survival signals, as well as to remodel local and distan

93 e in the CDCP1 molecule completely abrogated survival signaling associated with the 70-kDa CDCP1, and

94 in cell cycle were accompanied by diminished survival signals because of impaired IRS/Akt signaling.

95 ings highlight differential requirements for survival signals between primary and secondary effector

96 We found that, in response to survival signals, BimEL was rapidly phosphorylated on th

97 abolism, is insensitive to inhibition of BCR survival signaling but is functionally undefined.

98 veal a parallel requirement for TCR-mediated survival signaling, but an asymmetric requirement for TC

99 K and Akt, and PKG Ialpha contributes to pro-survival signaling by directly phosphorylating BAD.

100 inhibitors (pan-AKIs) disrupts TRAIL-induced survival signaling by effectively reducing Aurora-IKK ki

101 Survival signaling by the erythropoietin (Epo) receptor

102 ng cell delivery and harnessing the power of survival signaling cascades for ex vivo genetic modifica

103 Because of their involvement in growth and survival signaling cascades, the sigma(1) receptors (sig

104 ver, activation of iNKT cells overrides this survival signal, causing marked apoptosis of monocytes i

105 the signaling pathways that mediate neuronal survival signaling could lead to new therapeutic targets

106 rk has shown that mature B cells depend upon survival signals delivered to the cells by their antigen

107 ed without the need to compete for extrinsic survival signals derived from other cell types.

108 ough a population-autonomous competition for survival signals derived from other interneurons.

109 ve pathway in addition to the cone viability survival signals derived from rods.

110 CAL-101 reduces survival signals derived from the BCR or from nurse-like

111 and the misbalance between proapoptotic and survival signaling detected in STZ-DM rats.

112 Identification of microenvironment-specific survival signaling determinants is critical for the rati

113 Therefore, VEGF164 provides survival signals directly to developing GnRH neurons, in

114 CC cells, suggesting that dasatinib inhibits survival signals distinct from other oncogenic receptor

115 roprotectin D1 (NPD1), a potent activator of survival signaling, down-regulated oxidative stress-indu

116 aintenance in this model, even after loss of survival signals driven by the MYC oncogene.

117 s from pre-B cells that critically depend on survival signals emanating from a functional pre-BCR.

118 sistance to venetoclax is by kinase-mediated survival signals encountered in proliferation centers th

119 We propose a model in which OPN provides a survival signal for a precursor T(FH) cell subset, which

120 els of p38alpha kinase, providing a specific survival signal for Lgr6(+) cells as mediated by increas

121 f BBRs on B cells may provide a tonic and/or survival signal for the maintenance of peripheral B cell

122 NFR family member GITR can provide important survival signals for CD8 T cells.

123 ors probably provides both proliferative and survival signals for cells in the B-cell development pat

124 de evidence that fibronectin-mediated matrix survival signals for hepatocytes are transduced through

125 covalently cross-linked matrix could promote survival signals for hepatocytes in adult tissue remodel

126 f the B cell receptor, provides constitutive survival signals for latently infected cells through Syk

127 e blockage of IGF1R results in inhibition of survival signal from Bcl-x(L) and cell death in the sens

128 BCR) stimulation, which is another important survival signal from the leukemic microenvironment.

129 SPHK1 inhibition was associated with reduced survival signaling from S1P receptor 2, resulting in sel

130 cells that have preferentially responded to survival signals from self-Ags or cytokines.

131 of early combination therapy to target early survival signals from the bone marrow microenvironment,

132 fective against CLL cells that have received survival signals from the microenvironment.

133 omas again use paracrine IL-6 signaling as a survival signal, highlighting the ability of tumor cells

134 d via inhibition of downstream NF-kappaB pro-survival signalling however the upstream drivers of BTK

135 For long-lasting immunity, growth and survival signals imparted through the Akt/protein kinase

136 lasmic reticulum (ER), provides an essential survival signal in glioblastoma multiforme cells.

137 CREB also induces an antiapoptotic survival signal in monocytes and macrophages.

138 iated signaling may abrogate a TLR9-mediated survival signal in prognostically unfavorable IGHV unmut

139 educed the phosphoinositide 3-kinase and Akt survival signal in rod photoreceptors.

140 through HIF-1 and VEGF provides an autocrine survival signal in the developing cardiac OFT and that p

141 calmodulin levels at least partially control survival signaling in Amo and that restoration of GM-CSF

142 induced apoptotic signaling and Trk-mediated survival signaling in brain neurons.

143 gen synthase kinase-3 (GSK3) as important in survival signaling in CTCL.

144 am of Ub, whether enhanced Ub contributes to survival signaling in early PO, and if loss of this mech

145 Herein, we assess the mechanism of Syk survival signaling in EBV+ B cell lymphomas from post-tr

146 alternate RTKs in maintaining progrowth and survival signaling in HNSCC cells in the setting of FGFR

147 regulate the lipid phosphatase SHIP2 for Akt survival signaling in keratinocytes.

148 bs) against Tyro3 to examine their effect on survival signaling in melanoma cell lines.

149 ix production/remodeling, and, consequently, survival signaling in melanoma cells via beta1-integrin,

150 inhibition of Akt activation and downstream survival signaling in myotubularin-deficient cells is ca

151 of Src-ERK signaling pathways, which promote survival signaling in pancreatic cancer cells.

152 ed the molecular mechanisms of Fas-activated survival signaling in pancreatic cancer cells.

153 E-19 cells and that NPD1 is part of an early survival signaling in RPE cells.

154 I3K/AKT (phosphatidylinositol 3'-kinase/AKT) survival signaling in the melanoma cells following BRAF

155 ity negatively regulated the neuroprotective survival signaling in the retina.

156 th a number of critical proteins involved in survival signaling in tumor cells, we hypothesized that

157 d IL-34 provide powerful neuroprotective and survival signals in brain injury and neurodegeneration i

158 phosphatase and tensin homolog proliferation/survival signals in FL-fibroblasts, which were reversed

159 kinases (RTKs) provides critical growth and survival signals in high risk acute myeloid leukemia (AM

160 3 (Stat3) is involved in aberrant growth and survival signals in malignant tumor cells and is a valid

161 ata indicate that Tyro3 may confer increased survival signals in melanoma cells and can be stymied us

162 yrosine kinase Zap70 is required to transmit survival signals in naive CD8 T cells.

163 and decreasing available water places these survival signals in overdrive and may be accelerating th

164 equired during early somite stages to convey survival signals in the developing vertebrate head.

165 by dynein motors, supplies cell bodies with survival signals in the form of 'signaling endosomes'.

166 her for limiting amounts of gammac-dependent survival signals in the thymus.

167 pathway is a key driver of proliferation and survival signals in tumor cells and has been the focus o

168 ependent, L5 impairs Akt-mediated growth and survival signals in vascular ECs by way of LOX-1.

169 p85alpha-induced maturation, and growth and survival signals, in mast cells can be uncoupled.

170 m molecules involved in B-cell proliferation/survival signaling including STAT1, NFATC2, c-Fos, c-Myc

171 tered on decreased mTOR-regulated growth and survival signaling, including increased expression of le

172 es harboring MYD88 L265P, by down-modulating survival signals, including NF-kappaB and autocrine IL-6

173 Loss of Pals1 blocks essential cell survival signals, including the mammalian target of rapa

174 tegrates upstream growth, proliferation, and survival signals, including those transmitted via ERK1/2

175 rt an in-depth analysis of the apoptotic and survival signals induced by the 3 HexAbs in Burkitt lymp

176 s, maintain vascular integrity, and transmit survival signals into the cell.

177 tPA triggered a cascade of survival signaling involving extracellular signal-regula

178 first evidence that the IGF-1R/NFkappaB cell survival signal is a crucial regulator of the level of c

179 This "tonic" BCR survival signal is distinct from that induced by antigen

180 This starvation survival signal is independent of ascarosides, a class o

181 After a survival signal is successfully executed, a cell must de

182 Survival signaling is critical for the metastatic progra

183 We now report that CD28 pro-survival signaling is dependent upon downstream activati

184 e essential for apoptosis induction, whereas survival signaling is initiated by TNFR1 at the plasma m

185 e determination, yet its contribution in pro-survival signaling is largely unknown.

186 it is directly involved in hypertrophic and survival signaling is not known.

187 However, little is known about how survival signalling is regulated in CML stem cells.

188 death, but how the balance between death and survival signals is regulated to prevent immunodeficienc

189 tumor cell proliferation by activating cell survival signaling mainly via NF-kappaB, but this signal

190 This simultaneous reduction in survival signaling markedly decreases the anchorage-inde

191 ress kinases activation and (2) restored the survival signals (mediated by Akt and ERK pathways).

192 mpts have been made to explore the host cell survival signals modulated by the bacterium Enterococcus

193 y itself, alterations in cell cycle and cell survival signaling molecules, and the activation of esca

194 can be negatively regulated by activation of survival signals, mostly dependent on tyrosine kinase ac

195 cubation with GST-PEX9 induced intracellular survival signals, namely Lyn phosphorylation and Mcl-1 u

196 ent kidney tumors and drives a metabolic and survival signaling network necessary to cope with impair

197 NMDAR-NFATc4-BDNF pathway contributes to the survival signaling network that supports cortical develo

198 rect Notch3-regulated gene that mediates the survival signal of Notch3 in ovarian cancer.

199 tection and Alzheimer disease by controlling survival signaling of neuronal EGFR.

200 ding partner dendrin and antagonizes the pro-survival signaling of the downstream Hippo pathway effec

201 ence, targeting the convergence of oncogenic survival signals on translation initiation is an effecti

202 and show no epidermal growth factor-induced survival signaling or protection against excitotoxicity,

203 hes of the UPR can activate adaptive and pro-survival signals, or induce apoptotic cell death.

204 We identified a pro-survival signaling pathway activated in cardiomyocytes i

205 amycin treatment triggers activation of cell survival signaling pathway by activating the prosurvival

206 eceptor transcription and suggest a new cell survival signaling pathway mediated by PI 3-kinase and C

207 control in this critical metabolic and cell survival signaling pathway.

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

209 Paradoxically, interleukin 6 promotes a pro-survival signalling pathway through activation of signal

210 sulin-like growth factor-1 receptor (IGF-1R) survival-signaling pathway.

211 d activation of caspase-8 and caspase-3) and survival signaling pathways (BclxL) were examined.

212 Cell death and survival signaling pathways have opposed but fundamental

213 ggesting that CS1 induces central growth and survival signaling pathways in MM cells.

214 effectively blocks microenvironment-mediated survival signaling pathways in primary CLL cells.

215 Identification of critical survival signaling pathways in tumor cells might unveil

216 ce resulting from constitutive activation of survival signaling pathways is a fundamental pathogenic

217 Cross-talk between apoptosis and survival signaling pathways is crucial for regulating ti

218 genous cardiac repair and enhancement of pro-survival signaling pathways that antagonize senescence w

219 s effect was caused by interference with the survival signaling pathways triggered by MSCs.

220 Specific cell death and survival signaling pathways were assessed by Western blo

221 Survival signaling pathways were concurrently up-regulat

222 re important regulators of apoptosis and pro-survival signaling pathways whose deregulation is often

223 ell growth and survival via activation of MM survival signaling pathways, including the MEK-extracell

224 Using RPPA, we confirmed that multiple survival signaling pathways, including the phosphatidyli

225 amage, cancer cells can sustain/activate pro-survival signaling pathways, leading to apoptotic resist

226 tend to display elevated activity of several survival signaling pathways.

227 gnaling from betaARs and also stimulate cell survival signaling pathways.

228 oxidative stress by activating multiple cell survival signaling pathways.

229 for the feed-forward amplification of cancer survival signaling pathways.

230 and phosphatidylinositol 3-kinase (PI3K)/AKT survival signaling pathways.

231 are key regulators of anti-apoptotic and pro-survival signaling pathways.

232 ondrial biogenesis and activates ERK and Akt survival signalling pathways, thereby driving neuroprote

233 ay offering previously unrecognized layer of survival signal processing and integration.

234 isms of posttranslational regulation on cell survival signaling proteins.

235 mic T-cell development, and it is one of the survival signals provided by follicular dendritic cells

236 Furthermore, MI-2 abrogated survival signals provided by stromal cells and BCR cross

237 vated oncogenes and to proliferative and pro-survival signals provided by the abnormal tumor microenv

238 w that it also depends on T cell-independent survival signals provided by the B cell-activating facto

239 f CLL cells in vitro, and effectively blocks survival signals provided externally to CLL cells from t

240 CP1 cleavage upstream from CDCP1-induced pro-survival signaling provides a potential mechanism for th

241 il apoptosis and its temporary inhibition by survival signals provides a target for anti-inflammatory

242 revealed a recurrent theme-the engagement of survival signals redundant to those transduced by the ta

243 We also demonstrate that survival signalling relies on neuronal, but not endothel

244 switching of carcinoma cells and subsequent survival signaling results in activation of canonical su

245 coreceptors, a balance between apoptosis and survival signals results in outcomes as divergent as clo

246 ation of mitochondrial Bax following loss of survival signaling sensitizes cells to proapoptotic BH3

247 monstrate that disrupting adhesion-dependent survival signals slows the rate of Bax's dissociation fr

248 ing through calreticulin-LRP1 activates cell survival signals such as PI3-kinase.

249 ociated deleterious signalling and decreases survival signalling suggesting that p75NTR could be a va

250 to the loss of integrin-related 'outside-in' survival signals, Terada and colleagues demonstrate a no

251 Lasting B cell persistence depends on survival signals that are transduced by cell surface rec

252 h the lumen; however, cells with upregulated survival signals that extrude basally could potentially

253 ssion of a functional EPOR and provides cell survival signals that may contribute critically to persi

254 In leukemias, KV11.1 regulates pro-survival signals that promote resistance to chemotherapy

255 er this response is associated with distinct survival signals that protect T and B cells.

256 ribed trophic factors that elicit retrograde survival signaling, the precursor forms of neurotrophins

257 We demonstrate that disruption of downstream survival signaling through antiapoptotic Bcl-2 proteins

258 Taken together, we propose that survival signaling through Bcl-xL is a critical and intr

259 ssociated death promoter, thereby permitting survival signaling through BCL-XL.

260 he first BH3-only protein linked to proximal survival signals through phosphorylation by survival kin

261 s to persistent inflammation by conferring a survival signal to alpha4beta1 expressing proinflammator

262 ptotic AKT kinase, which provides a powerful survival signal to antigen-stimulated CLL cells.

263 , suggesting that the dying daughters send a survival signal to protect their stem cells for future r

264 , indicating that OX40 delivers an important survival signal to T reg cells after activation.

265 (PI3K) by nitration and diverts the PI3K-Akt survival signal to the p38-mitogen-activated protein kin

266 RIP shuttles between CD95/Fas death and FAK survival signaling to mediate anoikis.

267 suggests that BM stromal cells that provide survival signals to autoreactive memory T cells and STAT

268 ucing ligand (TRAIL) and thus rely on potent survival signals to circumvent cell death by TRAIL.

269 L) and, therefore, are dependent upon potent survival signals to circumvent TRAIL cytotoxicity.

270 ecently been explored for providing putative survival signals to CML stem/progenitor cells (SPCs) wit

271 and CD4(+) cells provides costimulatory and survival signals to effector T cells.

272 l and mitochondria, enabling fluctuations in survival signals to finely adjust apoptotic sensitivity.

273 d metabolic products (uric acid) function as survival signals to help reduce water loss and store fat

274 B-cell receptor (BCR) mimic known to provide survival signals to infected B cells.

275 acrine FGF signaling is to provide essential survival signals to lens placode cells.

276 llicular helper T (Tfh) cells, which provide survival signals to the B cell.

277 cally, IL-2 was capable of providing crucial survival signals to the Tregs upon inhibitor treatment i

278 (+)CD19(-) progenitors and IL-7 by providing survival signals to these progenitors.

279 suggest that antigen stimulation may provide survival signals to tumor cells and that there is a sele

280 downstream of an IGF-1R/NFkappaB coordinate survival signal, to regulate caspase-3 activity.

281 l DNA, shifting the balance of pro- and anti-survival signals toward apoptosis via induction of mitoc

282 ular domain as a scaffold for recruitment of survival signal-transducing kinases.

283 include vasoconstriction, modulation of pro-survival signal transduction pathways, and endothelial c

284 that was recently demonstrated to provide a survival signal upon binding to its unique receptor CX3C

285 Targeting survival signaling using CpG(A)-siRNAs inhibits the grow

286 n of Amo with exogenous calmodulin increased survival signaling via GM-CSF and PI-3K and reduced ROS

287 Recent work has established that Akt cell survival signaling via the epidermal growth factor recep

288 genesis in vivo by promoting both growth and survival signaling via the promotion of tumor vasculogen

289 udies demonstrated that Syk transduces BAFFR survival signals via ERK and PI3 kinase.

290 Talin1-regulated cell survival signals via phosphorylation of focal adhesion c

291 To identify the molecular nature of this survival signal, we have developed a genetic approach in

292 To gain better insight into TBK1 survival signaling, we searched for altered phosphoprote

293 riggers BTK, IRAK1/IRAK4, and HCK growth and survival signaling, whereas CXCR4 mutations promote AKT

294 Tak1 mediates a critical survival signal, which protects against both TNF-alpha/F

295 LM11A-31 restored striatal AKT and other pro-survival signalling while inhibiting c-Jun kinase (JNK)

296 port alteration may further impair BDNF-TrkB survival signaling within the corticostriatal connection

297 consistent with the idea that DOCK8 mediates survival signals within a specialized niche.

298 Essential survival signals within hematopoietic stem cell (HSC) an

299 Predicting that survival signals would be delivered by phosphoinositide-

300 post-GC plasmablasts undergoing constitutive survival signaling, yet knowledge of the mechanisms that