ライフサイエンスコーパス: proliferative signal

1 s translation, allowing a tightly controlled proliferative signal.

2 with blocked apoptosis and the induction of proliferative signal.

3 alpha371beta were incapable of transducing a proliferative signal.

4 IL-12Rbeta2 alone is capable of delivering a proliferative signal.

5 ntinuously in the germ line to transduce the proliferative signal.

6 x of extracellular calcium and abrogates the proliferative signal.

7 t together with the APL does not result in a proliferative signal.

8 requires a beta chain for transduction of a proliferative signal.

9 ta1 receptor is involved in transmitting the proliferative signal.

10 ial cells from responding to hormone-induced proliferative signals.

11 ll survival in response to a wide variety of proliferative signals.

12 -term responses to chronic drug treatment or proliferative signals.

13 idative stress and altered responsiveness to proliferative signals.

14 and possibly other activators in response to proliferative signals.

15 autocrine production of proinflammatory and proliferative signals.

16 critical intermediate in the transduction of proliferative signals.

17 to both TCR/CD28-mediated and IL-2R-mediated proliferative signals.

18 pon reentry of the cell cycle in response to proliferative signals.

19 active state, thereby relaying uncontrolled proliferative signals.

20 sion Kinase phosphorylation and induction of proliferative signals.

21 ncy disorder whose B cells oppose EBV-driven proliferative signals.

22 esis by inducing Erf and Etv3l to antagonize proliferative signals.

23 olyinosinic-polycytidylic acid-induced acute proliferative signals.

24 d during cell cycle arrest responses to anti-proliferative signals.

25 , aimed to deprive CLL cells of survival and proliferative signals.

26 etic modification of proteins in response to proliferative signals.

27 re of progenitor nuclei to neurogenic versus proliferative signals.

28 adherin engagement to transduce stretch into proliferative signals.

29 -1 (MKP-1), which attenuates ERK1/2-mediated proliferative signals.

30 ll adhesion to the extracellular matrix into proliferative signals.

31 he JAK2 kinase alone might be sufficient for proliferative signaling.

32 inase activity and the box2 region initiated proliferative signaling.

33 ession of ERK-specific phosphatases sustains proliferative signaling.

34 that receptor dimerization is sufficient for proliferative signaling.

35 HPTP1, PTP1C, and SHP1) have been defined in proliferative signaling.

36 rotein-coupled receptors promotes downstream proliferative signaling.

37 tes DNA damage-induced G(2)-M checkpoint and proliferative signaling.

38 G12/13-stimulated pathway implicated in cell proliferative signaling.

39 t effects on cell cycle progression and cell proliferative signaling.

40 growth and fueling their own growth via Fas proliferative signaling.

41 way leading us to broaden our exploration of proliferative signaling.

42 ivity is not required, for sPLA2-IIA-induced proliferative signaling.

43 ry structural determinants of IL-4R-mediated proliferative signaling.

44 t whether the PI3K pathway is sufficient for proliferative signaling, a tamoxifen-regulated form of P

45 pe from cell death pathways, evasion of anti-proliferative signals, a decreased reliance on exogenous

46 Pharmaceutical inhibition of proliferative signaling also induced CD133 expression in

47 tive expression of MCT-1 results in a strong proliferative signal and is associated with deregulation

48 omised Stat5 activation also compromised the proliferative signal and revealed a quantitative correla

49 ey determinant of the magnitude of the IL-15 proliferative signal and that IL-15R occupancy functione

50 protease potentially deadly to the cell for proliferative signaling and demonstrate a functional con

51 ngs define EEA1 endosomes as major sites for proliferative signaling and establish that Galphas and G

52 mbined targeting of PP2A and mTOR suppresses proliferative signaling and induces cell death and impli

53 lity of tyrosine-deficient IL-4Rs to mediate proliferative signaling and STAT phosphorylation was abs

54 promoting WNT/beta-CATENIN and AKT/GSK3beta proliferative signaling and that its inhibition induces

55 From sustained proliferative signaling and the activation of invasion a

56 R is critical for the transduction of normal proliferative signals and contributes to differentiative

57 They are also refractory to proliferative signals and show a repressed canonical Wnt

58 ment and we also investigate the predominant proliferative signals and the on-going research addressi

59 Conversely, c-myc is a strong proliferative signal, and overexpression of Myc is frequ

60 ued to produce vimentin, exhibited vicarious proliferative signaling, and expressed less vascular end

61 er that promotes both pro-apoptotic and anti-proliferative signaling, and they highlight the utility

62 chanism through which tumor cells evade anti-proliferative signals, and provides insight into how RB-

63 g and sustained relative to that produced by proliferative signals, and the growth inhibitory effects

64 bcl family genes and delivery of a competent proliferative signal are not sufficient to promote cell

65 scribes a novel mechanistic paradigm for how proliferative signals are counterbalanced in regeneratin

66 eration of AMPs, which demonstrates that pro-proliferative signals are transduced from enterocytes to

67 -myc is a major target that transduces Myb's proliferative signal, as shown by the ability of a c-Myc

68 FLT3 activation leads to antiapoptotic and proliferative signals, but little is known about the imp

69 that fumarate accumulation confers a chronic proliferative signal by disrupting cellular iron signali

70 Proliferative signaling by a receptor mutant with a weak

71 Although increased proliferative signaling by a representative G-CSFR trunc

72 TGF-beta opposes proliferative signaling by IL-2 through mechanisms that

73 t the sensitivity of cells to non-estrogenic proliferative signaling by increasing cellular levels of

74 f T3 to stimulate ERK1/2 phosphorylation and proliferative signaling by inhibiting expression of the

75 that ectopically expressed SOCS-3 suppresses proliferative signaling by not only ER-HY343 but also c-

76 as a transcription factor, the mechanism of proliferative signaling by Shc is poorly defined.

77 y, surface gangliosides are known to enhance proliferative signaling by the epidermal growth factor (

78 Proliferative signaling by the IL-2R can occur through t

79 ls mediated by IRF-1, IFN-gamma may activate proliferative signals by phosphorylation of Stat1 and St

80 rapamycin (mTOR) pathway, causing sustained proliferative signals, can lead to exhaustion of HSC rep

81 This proliferative signalling cascade is upregulated in breas

82 manner by activating pro-apoptotic and anti-proliferative signaling cascades that results in strengt

83 Prior investigations document that proliferative signaling cascades, under some circumstanc

84 ian cells by intracellular and extracellular proliferative signals combined with blocked apoptosis.

85 primary cilia presents a conundrum: how are proliferative signals conveyed through an organelle that

86 Interruption of these homing and proliferative signals could have therapeutic potential f

87 ation of Ha-Ras, which is required for eIF4E proliferative signaling, did not suppress Myc-induced ap

88 vitro evidence that PKCdelta is required for proliferative signaling downstream of the ErbB2 receptor

89 tional programs in combination with abnormal proliferative signaling drive leukemic transformation.

90 related protein 1 (SFRP1) as a candidate pro-proliferative signal during prostatic development and ca

91 tivation of NFkappaB/Rel provides a critical proliferative signal early in the cellular transformatio

92 tion increases the stimulation of downstream proliferative signaling effectors MEK1/2 and p38-MAPK in

93 cells and their microenvironment to sustain proliferative signaling, evade growth suppressors, resis

94 ce of cancer hallmarks, including sustaining proliferative signaling, evading growth suppression, res

95 ctivation through which tumour cells sustain proliferative signalling even under conditions of limite

96 tPA triggered sequential proliferative signaling events involving Erk1/2, p90RSK,

97 ells (IEC), by regulating their responses to proliferative signals following intestinal injury.

98 growth response-1 (EGR-1) protein is an anti-proliferative signal for certain tumor cells and is requ

99 in part, to activation of IL-6 expression, a proliferative signal for cholangiocytes.

100 (FGF) signaling, originally identified as a proliferative signal for oligodendrocyte precursor cells

101 This study identifies Shh as an essential proliferative signal for the cerebellar ventricular germ

102 Three distinct proliferative signals for multiple myeloma (MM) cell lin

103 Thus, Stat5 is a critical component of the proliferative signal from Tyr510 of the IL-2R and regula

104 n and determine the duration and strength of proliferative signaling from this compartment.

105 GSCs further derive pro-proliferative signals from broadly utilized monoclonal a

106 Our work identifies a mechanism by which proliferative signals from Cdk1 are removed in response

107 ting on JNK and p38, and thereby transducing proliferative signals from Galpha(q) to the nucleus inde

108 se studies indicated that anti-apoptotic and proliferative signals from IGF-1 bifurcate downstream of

109 by Tgfbeta2 in the developing eye to dampen proliferative signals from Pdgfrbeta, which effect ultim

110 esponder lymphocytes receiving the strongest proliferative signals from vaccines experienced the grea

111 involved not only in the transmission of the proliferative signal generated by ligand binding but als

112 that GATA2 may be upregulated to thwart the proliferative signal generated by PML-RARA and that its

113 athway plays a critical role in transmitting proliferative signals generated by cell surface receptor

114 he actin cytoskeleton in the transduction of proliferative signals has been established through the u

115 tion of both positive and "negative" or anti-proliferative signals has emerged as a common paradigm f

116 dies assessing the role of Stat5 in the IL-2 proliferative signal have produced contradictory, and th

117 These data demonstrate that (a) proliferative signaling (i.e., inhibition of cell cycle

118 antly, we demonstrate that leptin provides a proliferative signal in BAF-3 cells and increases the pr

119 We show that leptin provides a proliferative signal in hematopoietic cells.

120 dentified higher B-cell content and a strong proliferative signal in subgroup A and enriched T-cell,

121 By contrast, FGFR1 transmits a proliferative signal in various cell types in vivo.

122 ls, we attempted to determine if the altered proliferative signaling in a tumor cell might effect the

123 type cyclins are essential components of Shh proliferative signaling in CGNPs.

124 resulted in the inhibition of G-CSF-induced proliferative signaling in DT40GR cells.

125 nhibitory activity of the p38 pathway in Ras proliferative signaling in experimental NIH 3T3 cells.

126 onin release from dense granules, triggering proliferative signaling in hepatocytes.

127 convergence point of anti-proliferative and proliferative signaling in mammary tumor cells.

128 To determine how dasatinib blocks proliferative signaling in osteoblasts, we analyzed the

129 e cyclin D1 and its promoter were targets of proliferative signaling in prostate cancer cell lines, a

130 and WNT/beta-CATENIN as well as AKT/GSK3beta proliferative signaling in three different types of non-

131 N-gamma-JAK2-STAT1/3-dependent migratory and proliferative signaling in VSMCs.

132 investigated the role of AP-1 in controlling proliferative signals in breast cells, and have previous

133 preferentially induced by growth factors and proliferative signals in cultured cells.

134 ium as a central integrator of metabolic and proliferative signals in Drosophila intestinal stem cell

135 Thus, RelA antagonizes TNFR1-JNK proliferative signals in epidermis and plays a nonredund

136 ith suboptimal anti-CD3 stimulation augments proliferative signals in FasL+ but not FasL- CTLs.

137 A20 enhances IL-6/STAT3 pro-proliferative signals in hepatocytes by down-regulating

138 ulation, promoting vascular inflammatory and proliferative signals in other cells to drive disease.

139 of tumor suppressor genes provide continuous proliferative signals in part by adjusting the state of

140 player in transduction of antiapoptotic and proliferative signals in T cells.

141 player in transduction of anti-apoptotic and proliferative signals in T cells.

142 The interleukin 2 receptor (IL-2R) generates proliferative signals in T lymphocytes by ligand-induced

143 player in transduction of antiapoptotic and proliferative signals in T-cells, we investigated whethe

144 rated excessively, suggesting that increased proliferative signals in the LN3alphabeta thymus compens

145 ate adhesive events with neighbors into anti-proliferative signals in the nucleus.

146 ce on surface receptors and matrix for their proliferative signals in vivo and provide a therapeutic

147 clin kinase inhibitor p21/WAF-1 and positive proliferative signals including c-myc and cyclin DI were

148 Although both damage and proliferative signals increase XRCC1 levels, the mechani

149 ne, which means that the proinflammatory and proliferative signals independently regulate the express

150 investigated the role of AP-1 in transducing proliferative signals induced by peptide and steroid gro

151 CD133-deficient cells are more sensitive to proliferative signal inhibition in livers and intestinal

152 ts to test the possibility that the positive proliferative signal initiated by oncogenes might change

153 This proliferative signal is critically dependent upon cytopl

154 quickly returns to its normal size when the proliferative signal is removed.

155 y known mitogenic pathways, we show that Shh proliferative signaling is mitogen-activated protein kin

156 coprotein integral to cell-cell adhesion and proliferative signaling, is increased in several maligna

157 t the VEGF HBD contributes to angiogenic and proliferative signaling, is required for accelerated com

158 r by downregulating CXCR3-B and by promoting proliferative signals, likely through CXCR3-A.

159 uction of inflammation by microbiota sustain proliferative signaling, limit cell death, and induce an

160 odeling suggested that decoupling growth and proliferative signaling may facilitate cell cycle entry

161 rapeutic effect by suppressing AKT and other proliferative signaling mechanisms.

162 egulated, presumably as a consequence of the proliferative signal mediated by the increased level of

163 all cytoplasmic tyrosines, revealed a robust proliferative signal mediated through Shc.

164 ignal transduction is abrogated, whereas pro-proliferative signaling mediated through NH(2)-terminal

165 pamycin plays a critical role in transducing proliferative signals mediated through the phosphatidyli

166 tivation may provide both anti-apoptotic and proliferative signals mediated via its transcriptional t

167 ences diverse hallmarks of cancer, including proliferative signaling, metastasis, and resistance to c

168 e at least certain of these factors modulate proliferative signaling, mutated Epo receptor forms lack

169 able to bind erythropoietin and transduce a proliferative signal normally.

170 al tail of the class I G-CSFR down-modulates proliferative signaling, not only in myeloid cell lines,

171 We show here that EGF-induced, proliferative signaling occurs from EEA1 endosomes and i

172 We reasoned that the proliferative signal of cE alpha was transduced either t

173 and interfering with anti-adhesive and anti-proliferative signaling of HKa.

174 hether the IL-7 receptor actually delivers a proliferative signal or whether, by promoting survival,

175 arrest provoked in somatic cells by aberrant proliferative signals or by cumulative population doubli

176 V(H)14 IgH chains did not provide increased proliferative signals or exhibit enhanced poly- or autor

177 is reactivated in these adult cell types by proliferative signals or oxidative stress.

178 O A and R1 are involved in the c-Myc-induced proliferative signaling pathway in the presence of serum

179 denomatous polyposis coli (APC)/beta-catenin proliferative signaling pathway in vivo.

180 through a pathway that is distinct from the proliferative signaling pathway utilized by tyrosine kin

181 ssion without interfering with the cytosolic proliferative signaling pathway.

182 awareness that some GPCRs can also regulate proliferative signaling pathways and that chronic stimul

183 iffer from those of oncogenes which activate proliferative signaling pathways in NIH3T3 cells.

184 tory factor in the activation of mTOR in the proliferative signaling pathways of animal cells.

185 and with Src and other partners to influence proliferative signaling pathways often activated in ADPK

186 d, we observed activation of prosurvival and proliferative signaling pathways, including phosphorylat

187 minimizes the activation of inflammatory and proliferative signaling pathways, including the NF-kappa

188 urvival (P = 0.01) and greater activation of proliferative signaling pathways, proliferation, wound h

189 ed FLT3 signaling leads to antiapoptotic and proliferative signaling pathways.

190 in numerous developmental, morphogenic, and proliferative signaling pathways.

191 ra and important epithelial inflammatory and proliferative signaling pathways.

192 69-83 of the Mpl cytoplasmic domain enhances proliferative signaling, perhaps mediated by a decrease

193 inhibition of Hh pathway mainly by enhancing proliferative signals, possibly mediated through TCF4 ac

194 tablishes a chromatin state that limits EGFR proliferative signaling, preventing tumor-like stem cell

195 ; this outcome is clearly separable from the proliferative signal produced by most receptor tyrosine

196 Together, our results suggest that Shh proliferative signaling promotes synthesis of regulatory

197 and Bcl-x(L), can be elevated only after the proliferative signal provided by Egr3 has subsided.

198 sponsive to both early activation events and proliferative signals provided via the TCR and 4-1BB.

199 replication forks and due to the continuous proliferative signaling, providing an exploitable therap

200 JAK2V617F transgenic mice exhibited enhanced proliferative signals, relative resistance to cell death

201 y, TBX5c antagonizes TBX5a activation of pro-proliferative signals such as IGF-1, FGF-10, and BMP4.

202 By having shown previously that proliferative signals, such as epidermal growth factor (

203 e Ras which results in downregulation of its proliferative signals, such as reduced phosphorylation o

204 king this sequence do not transmit effective proliferative signals, suggesting that this receptor fun

205 he cascade by IGF-IR may constitute a potent proliferative signaling system and is possibly a mechani

206 as well as providing granulosa cells with a proliferative signal that requires oocyte-somatic cell b

207 pon the LAM cell-metabolic reprogramming and proliferative signals that drive uncontrolled growth and

208 es (e.g. resisting cell death and sustaining proliferative signaling) that explain the biological cap

209 nic factor for activated T cells, delivers a proliferative signal through ligation of the heterotrime

210 itogenesis, mp110*ER enhanced Stat5-mediated proliferative signaling through a mechanism independent

211 o elucidate the molecular events involved in proliferative signaling through heterotrimeric G protein

212 ure T cells exhibit a diminished response to proliferative signals through CD3.

213 ance, favoring the active form and promoting proliferative signaling, thus rendering KRAS an appealin

214 of mesenchyme FGF-10 requires an associated proliferative signal to induce bud migration.

215 GATA2 additionally conferred a proliferative signal to primitive erythroid progenitors.

216 e of the wound, suggesting that VEGF sends a proliferative signal to these cells.

217 that IL-7 provides potent anti-apoptotic and proliferative signals to early thymocyte progenitors.

218 PAEC-activated human DC provided proliferative signals to the naive autologous CD4+ T cel

219 Endothelial lesions trigger intense proliferative signals to the SMCs of the subintima, stim

220 newly described POX-mediated suppression of proliferative signaling together with the previously rep

221 ubiquitin ligase involved in attenuation of proliferative signals transduced by activated receptor t

222 ates a link between IR-induced activation of proliferative signal transduction pathways and enhanced

223 cal dose levels activates both pro- and anti-proliferative signal transduction pathways, the balance

224 have shown that these targeted inhibitors of proliferative signal transduction provide well-tolerated

225 odimer of h-erb-B-3-erb-B-2 was required for proliferative signal transduction to the nucleus.

226 mmatory signaling and PI3K-Akt-mTor survival/proliferative signaling underlies the transforming poten

227 way functions as a negative regulator of Ras proliferative signaling via a feedback mechanism.

228 Proliferative signaling via nicotinic acetylcholine rece

229 Studies of proliferative signaling via type 1 cytokine receptors ha

230 s, constitutes a conduit for transmission of proliferative signals via post-translational modificatio

231 ating factor-1 (CSF-1)-mediated survival and proliferative signaling, we compared the CSF-1 responses

232 s to the cytoplasm in response to stress and proliferative signals, where it stabilizes or modulates

233 elayed proliferation and lower activation of proliferative signals, which correlated with overactivat

234 HLA Abs and cytokines in the transduction of proliferative signals, which stimulate the development o

235 tween the insulin receptor, PI3'-kinase, and proliferative signaling while enhancing other signaling

236 ls (such as MCF7), require AP-1 to transduce proliferative signals, while other breast cancer cells (

237 roups is overactive RAS/ERK signaling, a pro-proliferative signal whose contributions to cell differe

238 h as from TGF-beta and insufficient survival/proliferative signals within the tumor microenvironment