ライフサイエンスコーパス: survival signal

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

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

3 cellular stressors and is an important cell survival signal.

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

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

6 eration signaling, whereas Pi3k mediates the survival signal.

7 d that basement membrane attachment provided survival signals.

8 brane protein activates NF-kappaB to provide survival signals.

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

10 romoting inflammation and promoters of tumor survival signals.

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

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

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

14 indirect response to cell proliferation and survival signals.

15 inating antigen and microenvironment-derived survival signals.

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

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

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

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

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

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

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

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

24 lent cells that drive integrin-dependent pro-survival signals.

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

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

27 s, (ii) targets bone, and (iii) induces "pro-survival" signal.

28 a cytotoxin, which interferes with integrin survival signaling.

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

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

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

32 oxic insults by binding EGFR and stimulating survival signaling.

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

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

35 E2F1 apoptotic activity under the control of survival signaling.

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

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

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

39 provided by combined interception in TCR and survival signaling.

40 extrinsic apoptosis and increasing NF-kappaB survival signaling.

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

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

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

44 ng more effective inhibition of TLR-mediated survival signaling.

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

46 complex processes such as cell adhesion and survival signaling.

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

48 ed kinase activity, which impairs downstream survival signaling.

49 ctive tissue growth factor and activated ERK survival signaling.

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

51 its activity in supporting EMT and NF-kappaB survival signaling.

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

53 targeted therapies through proliferative and survival signaling.

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

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

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

57 gh kinases to initiate inflammatory and cell survival signalling.

58 ression and has a prominent function in cell survival signalling.

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 sation signal for LRRK2, analysis of the PSP survival signal and eQTLs for LINC02555 in the eQTLGen b

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

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

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

67 merization, thereby blocking HSP27-regulated survival signaling and client-oncoprotein interactions.

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

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

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

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

72 ansformative potential to promote downstream survival signaling and leukemogenesis.

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

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

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

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

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

78 ely inhibits BCR-dependent proliferation and survival signals and has emerged as a breakthrough thera

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

80 with a small-molecule RET agonist activates survival signals and reduces neuronal death significantl

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

82 -8 functions as an angiogenic factor and pro-survival signal, and ICAM-1 has been implicated in tumor

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

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

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

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

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

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

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

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

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

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

93 Cell survival signals are modulated by many different recepto

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

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

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

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

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

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

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

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

102 Survival signaling by the erythropoietin (Epo) receptor

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

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

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

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

107 effectively inhibits this niche-mediated pro-survival signaling, dampens AML blast regeneration, and

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

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

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

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

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

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

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

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

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

117 c phosphatase known to facilitate growth and survival signaling downstream of numerous receptor input

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

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

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

121 Lastly, evaluation of survival signaling following daunorubicin treatment iden

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

139 These findings uncover a key survival signal in CRC through convergent repression of

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

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

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

143 The overall survival signal in the subgroup of patients with EGFR se

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

145 uced NFkappaB-mediated inflammation and cell survival signaling in cells isolated from the lungs of s

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

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

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

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

150 underlying MERTK-mediated Akt activation and survival signaling in kidney cancer.

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

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

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

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

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

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

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

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

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

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

161 This pathway mediates essential LMP1 survival signals in EBV-transformed human B cells and po

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

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

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

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

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

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

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

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

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

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

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

173 s6 activates its receptor Axl and downstream survival signals including Akt and STAT3, which was acco

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

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

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

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

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

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

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

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

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

183 nvironment as well as utilize mitophagy as a survival signal is still not well understood.

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

185 Survival signaling is critical for the metastatic progra

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

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

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

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

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

191 However, the role of Bmal1 in cellular- survival, signaling, its interaction with intracellular

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

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

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

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

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

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

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

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

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

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

202 and pDm8 neurons do not normally compete for survival signals or R7 partners, but can be forced to do

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 The survival signaling pathway phosphoinositide-3-kinase/pro

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

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

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

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

210 Cell death and survival signaling pathways have opposed but fundamental

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

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

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

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

215 Survival signaling pathways were concurrently up-regulat

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

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

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

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

220 vers, thus activating cell proliferation and survival signaling pathways, ultimately reducing injury

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

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

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

224 oxidative stress by activating multiple cell survival signaling pathways.

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

226 AM83A expression maintains essential MEK/ERK survival signalling, preventing cell death in pancreatic

227 eered murine T cells exhibited increased pro-survival signaling, proliferation, antitumor function, a

228 nter and have finite life spans dependent on survival signals propagated by the BCR and the BAFFR.

229 isms of posttranslational regulation on cell survival signaling proteins.

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

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

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

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

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

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

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

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

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

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

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

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

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

243 at targeting this pathway with inhibitors of survival signaling such as venetoclax may prove efficaci

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

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

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

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

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

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

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

251 ng to E-selectin and enable promotion of pro-survival signaling through AKT/NF-kappaB pathways.

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

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

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

255 Moreover, VCP overexpression restored pro-survival signaling through regulating alternative splici

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

257 1 (PD-1) and an agonist of OX40 (provides a survival signal to activated T cells) in mice with pancr

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

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

260 demonstrate that mk acts as both a critical survival signal to control the expansion and function of

261 Erythropoietin (EPO) provides the major survival signal to maturing erythroid precursors (EPs) a

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

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

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

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

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

267 how that anti-inflammatory IL-2C can deliver survival signals to CD4 T cells responding to influenza

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 th kinase inhibition could deplete oncogenic survival signals to reduce tumor growth.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

291 Macrophage homing/survival signals were determined at 14 days after injury

292 egs can effectively transduce IL-15-mediated survival signals when they are provided.

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