ライフサイエンスコーパス: IGF-II

1 IGF-II is a mitogenic peptide that has been implicated i

2 IGF-II isoforms thus possess unique biological propertie

3 IGF-II levels in vivo were detected using immunohistoche

4 IGF-II mRNA as determined by in situ hybridization was p

5 IGF-II mRNA in SSc lung fibroblasts was expressed primar

6 IGF-II stimulates both mitogenesis and myogenesis throug

7 IGF-II triggered the activation of both phosphatidylinos

8 IGF-II up-regulates its own gene expression via the PI3K

9 IGF-II was highly expressed in the epithelium surroundin

10 IGF-II-dependent memory enhancement requires IGF-II rece

11 IGF-II-mediated memory enhancement does not alter memory

12 IGF-II/IGF1R signalling blockade inhibits Nanog expressi

13 architecture and evolution of the domain 11 IGF-II-binding site, and the potential interactions with

14 ains 11-12, 11-12-13-14 and domains 11-12-13/IGF-II complex.

15 After controlling for IGFBP-3, IGF-II was no longer associated (0.99; 0.91-1.08; P(tren

16 IR and expressing solely the IR-A (R-/IR-A), IGF-II is a more potent mitogen than insulin.

17 ctivity is essential for secretion of active IGF-II, thus establishing IGF-II as a client of GRP94.

18 ot respond to the stress by producing active IGF-II.

19 Ad-IGF-II cytokine-treated islets exhibited decreased cell

20 Ad-IGF-II overexpression during cytokine treatment resulted

21 Ad-IGF-II transduction did not affect islet viability or fu

22 ss islet transplant model, the ability of Ad-IGF-II-transduced rat islets to restore euglycemia in no

23 Adding IGF-II or constitutively activating Akt rescues the IGFB

24 is methylated and the methylation may affect IGF-II expression and the survival of ovarian cancer pat

25 In contrast, beta1A does not affect IGF-II levels.

26 llular and secreted IGF-II without affecting IGF-II leader-3, leader-4, c-myc, or beta-actin mRNA lev

27 the minireceptors demonstrated high affinity IGF-II and Man-6-P-ligand binding, suggesting a function

28 Addition of antibody against IGF-II to cell cultures inhibited the proliferative effe

29 IGF-I, but was moderately effective against IGF-II.

30 ular target has been identified as TIP47, an IGF II receptor binding protein.

31 of a luciferase reporter mRNA containing an IGF-II 5'-untranslated region known as leader 3 but not

32 racycline-inhibited adenovirus expressing an IGF-II cDNA in the antisense orientation reversibly inhi

33 t mannose-6-phosphate receptor has gained an IGF-II-binding function and is termed type II IGF recept

34 e in regulation of cell proliferation via an IGF-II-dependent pathway in K562 leukemia cells.

35 tion of PTEN, which was not observed with an IGF-II-analog that does not bind to IGFBPs or in the pre

36 ated in the CD loop, which initially anchors IGF-II.

37 from the P3 promoter of the IGF-II gene, and IGF-II induced both a dose- and time-dependent increase

38 153 cells in vitro was stimulated by GRP and IGF-II and inhibited by JV-1-65.

39 man antibody that neutralizes both IGF-I and IGF-II and inhibits IGF signaling through both the IGF-1

40 We hypothesised that IGF-I and IGF-II are associated with improved, and insulin with wo

41 iologically relevant quantities of IGF-I and IGF-II had no detectable effects on IGFBP expression.

42 We found that IGF-I and IGF-II levels in bronchial tissue specimens containing h

43 demonstrate that the inhibition of IGF-I and IGF-II ligands by MEDI-573 results in potent antitumor a

44 ype of HCC is due to activation of IGF-I and IGF-II signaling that results in over-expression of both

45 directly by forming complexes with IGF-I and IGF-II that prevent them from activating the IGF-I recep

46 hat MEDI-573 blocks the binding of IGF-I and IGF-II to IGF-1R or IR-A, leading to the inhibition of I

47 nic and proliferative potential of IGF-I and IGF-II were significantly reduced.

48 nal force generation stimulated by IGF-I and IGF-II while the effects of the vitreous-type fragment a

49 matrix contraction in response to IGF-I and IGF-II while the IGFBP-3 fragment modulated cell respons

50 Insulin-like growth factors (IGF), IGF-I and IGF-II, are small polypeptides involved in regulating ce

51 apoptotic and mitogenic effects of IGF-I and IGF-II, facilitated the autophosphorylation of the type

52 mediates the biological actions of IGF-I and IGF-II, has emerged in recent years as a promising thera

53 The insulin-like growth factors IGF-I and IGF-II, through their cognate tyrosine kinase receptor (

54 is critical for production of both IGF-I and IGF-II, we ablated glucose-regulated protein 94 (GRP94)

55 of IGF-IR and its ligands, namely IGF-I and IGF-II.

56 (V12) or loss of p53 overexpressed IGF-I and IGF-II.

57 bly insulin-like growth factor I (IGF-I) and IGF-II.

58 rs (insulin-like growth factor I [IGF-I] and IGF-II) exert important effects on growth, development,

59 ing events, we hypothesized that insulin and IGF-II could affect IR-A biological responses by differe

60 retaining responsiveness to both insulin and IGF-II.

61 estingly, AEW541 also inhibited insulin- and IGF-II-stimulated effects in TamR cells.

62 r (IGF)-II-treated C2C12 mouse myoblasts and IGF-II-overexpressing Chinese hamster ovary cells.

63 at surgery, tumor grade, disease stage, and IGF-II or IGFBP-3 expression.

64 oblasts were cultured from lung tissues, and IGF-II mRNA was measured using reverse transcriptase-pol

65 Antiapoptotic IGF-II decreases apoptosis in vitro and significantly im

66 ention strategy in which cells with LOI are "IGF-II addicted" and undergo reduced tumorigenesis in th

67 ibrosis both in vitro and in vivo as well as IGF-II-induced ECM production through both phosphatidyli

68 In multivariate analysis, baseline IGF-II levels were significantly lower in participants w

69 als who developed obesity had lower baseline IGF-II levels (P = 0.006).

70 ry, producer cells do not go extinct because IGF-II acts as a nonlinear public good, creating negativ

71 the IGF-II binding site on the bifunctional, IGF-II cation-independent mannose 6-phosphate receptor.

72 r isoforms of IGF-II, termed "pro" and "big" IGF-II, has been observed.

73 role of unprocessed pro-IGF-II, called 'big'-IGF-II, in GISTs.

74 Down-regulation of either big-IGF-II or IR affected AKT and MAPK signaling and reduced

75 Furthermore, big-IGF-II isoforms bound much more weakly to purified ectod

76 GIST48 cell lines secrete high levels of big-IGF-II as demonstrated by ELISA and Western blotting ana

77 Immunohistochemical analysis of big-IGF-II protein expression was associated with moderate-

78 Disruption of big-IGF-II signaling in combination with imatinib had additi

79 Our data put forth the big-IGF-II/IR isoform A axis as an autocrine survival pathwa

80 has been associated with an ability to bind IGF-II.

81 phosphate receptor, yet only domain 11 binds IGF-II with high specificity and affinity.

82 ed in Western ligand blots with biotinylated IGF-II.

83 tified an association with higher cord blood IGF-II levels (P = 0.05 to 0.0001).

84 terminal Man-6-P-binding sites of the bovine IGF-II/MPR.

85 ernalization, a process modestly affected by IGF-II.

86 uced by visceral adipocytes was corrected by IGF-II/insulin growth factor binding protein-5.

87 PTEN expression is stimulated by IGF-II forming a feedback loop.

88 In these cells, IGF-II gene and protein expression are induced as early

89 cifically suppressed translation of chimeric IGF-II leader-3/luciferase mRNA without altering reporte

90 potentially important roles for circulating IGF-II, IGFBP-2, and IGFBP-3 in PSA-detected prostate ca

91 Our data suggest that circulating IGF-II levels may play a role in body weight regulation

92 ion known as leader 3 but not one containing IGF-II leader 4.

93 he first time an miRNA mechanism controlling IGF-II expression.

94 bers are consistent with a role of deficient IGF-II levels in the cause of the Silver-Russell syndrom

95 cascades, the inhibition of which diminished IGF-II-induced ECM production.

96 NAs were expressed in opposing dorsoventral (IGF-II) and ventrodorsal (IGFBP-5) patterns, with IGF-II

97 To be effective, IGF-II needs to be administered within a sensitive perio

98 5'-untranslated regions consisting of either IGF-II leader 3 or leader 4.

99 recovery patients further revealed elevated IGF-II and IGF binding proteins IGFBP4 and IGFBP6.

100 s study was to employ genetically engineered IGF-II analogs to establish which receptor(s) mediate th

101 The established IGF-II purification protocol allowed for cost-effective

102 ecretion of active IGF-II, thus establishing IGF-II as a client of GRP94.

103 ued the lethal phenotype induced by "excess" IGF-II in type 2 receptor-null mice; mutant IGFBP-5 over

104 pe can be complemented either with exogenous IGF-II or by expression of functional GRP94.

105 cer cells in the presence of CAFs expressing IGF-II can induce Nanog expression and promote stemness.

106 d IR variant that exhibits high affinity for IGF-II as well as for insulin.

107 h factor (IGF)-II, although the affinity for IGF-II is 3-10-fold lower than insulin depending on a ce

108 mRNA levels for IGF-II, IGF receptor-I, GRP receptor, and EGF receptor i

109 ns, with domain 11 primarily responsible for IGF-II binding.

110 duction of PTEN, but IGFBP-2, when free from IGF-II can suppress PTEN.

111 ts received a single injection of 10 micro g IGF-II, and the contralateral muscle received an injecti

112 Relatively higher IGF-II levels were also associated with a reduced risk o

113 protein containing a portion of mature human IGF-II fused to the C terminus of human beta-glucuronida

114 etry to identify the cleavage sites of human IGF-II, TGF-alpha, amylin, reduced amylin, and amyloid-b

115 The addition of recombinant human IGF-II peptide to these cells restored cell proliferatio

116 ponding MS9II cells overexpressing the human IGF-II receptors.

117 , and determined binding kinetics with human IGF-II using isothermal calorimetry and surface plasmon

118 Insulin-like growth factor-I (IGF-I), IGF-II, and insulin have all been implicated in regulati

119 prospective associations of insulin, IGF-I, IGF-II and IGFBP-3 with physical performance in the UK-b

120 IGF-I, IGF-II, and IGF-IR were highly expressed in sensitive ce

121 lar matrix contraction in response to IGF-I, IGF-II, and PDGF.

122 39 men); and cross-sectional insulin, IGF-I, IGF-II, IGFBP-2 and IGFBP-3 in the Boyd Orr cohort (n =

123 iopsy and measurements of blood serum IGF-I, IGF-II, IGFBP-2, and IGFBP-3 obtained at recruitment.

124 he suppression of autocrine/paracrine IGF-I, IGF-II, or GH-RH.

125 an tumor cell-derived growth factors (IGF-I, IGF-II, TGF-alpha and TGF-beta) and angiogenic factors (

126 ency for the IGF1R and IR, inhibited IGF-I-, IGF-II-, and insulin-stimulated Akt phosphorylation, pro

127 EM164 inhibits IGF-I-, IGF-II-, and serum-stimulated proliferation and survival

128 also determined the structures of human IDE-IGF-II and IDE-TGF-alpha at 2.3 A and IDE-amylin at 2.9

129 Our results identify IGF-II (insulin-like growth factor 2), a critical regula

130 o not produce insulin-like growth factor II (IGF-II) grow slowly in pure cultures but have a prolifer

131 injection of insulin-like growth factor II (IGF-II) into the dorsal hippocampus of rats or mice enha

132 Insulin-like growth factor II (IGF-II) is a major embryonic growth factor belonging to

133 Insulin-like growth factor II (IGF-II) mRNA-binding protein 3 (IMP3) is emerging as a u

134 also known as insulin-like growth factor II (IGF-II) mRNA-binding protein-1.

135 f a family of insulin-like growth factor II (IGF-II) mRNA-binding proteins (IMPs), is expressed prefe

136 rm effects of insulin-like growth factor II (IGF-II) on extraocular muscle morphometry and force gene

137 Since insulin-like growth factor II (IGF-II) receptors facilitate the delivery of nascent lys

138 e polypeptide insulin-like growth factor II (IGF-II) reverses all these deficits.

139 nistration of insulin-like growth factor II (IGF-II), a polypeptide that crosses the blood-brain barr

140 target gene, insulin-like growth factor II (IGF-II), was greatly diminished in the presence of PC2 s

141 a fragment of insulin-like growth factor II (IGF-II), with the IGF-II binding site on the bifunctiona

142 t of which is insulin-like growth factor II (IGF-II).

143 administering insulin-like growth factor II (IGF-II, also known as IGF2) significantly enhances memor

144 up-regulates insulin-like growth factor-II (IGF-II) mRNA and protein levels.

145 member of the insulin-like growth factor-II (IGF-II) mRNA-binding protein (IMP) family, is expressed

146 The insulin-like growth factor-II (IGF-II) receptor (IGF2R) regulates the level or activity

147 defective in insulin like growth factor-II (IGF-II) secretion, an autocrine/paracrine factor involve

148 7 regulation, insulin-like growth factor-II (IGF-II).

149 lung fibroblasts had a fourfold increase in IGF-II mRNA and a twofold increase in IGF-II protein com

150 ase in IGF-II mRNA and a twofold increase in IGF-II protein compared with normal lung fibroblasts.

151 results, we propose that NET37 has a role in IGF-II maturation in the secretory pathway during myobla

152 mannose 6-phosphate receptor (IGF2R) include IGF-II and mannose 6-phosphate modified proteins.

153 CRD-BP knockdown markedly increased IGF-II mRNA and protein levels but did not alter transla

154 Immunostaining revealed increased IGF-II expression in fibroblastic foci of SSc lungs.

155 ty to IGF-II signaling, not simply increased IGF-II levels, because in vivo blockade with NVP-AEW541,

156 We exploited this increased IGF-II sensitivity to develop an in vivo chemopreventive

157 We have expressed each individual IGF-II isoform in their proper O-glycosylated format and

158 owed that sumoylation inhibits PLAG1-induced IGF-II expression in reporter assays.

159 At the cellular level, IGF-II receptor overexpression causes localization of AP

160 Our study demonstrates increased local IGF-II expression in SSc-associated pulmonary fibrosis b

161 ght regulation and that individuals with low IGF-II levels may be more susceptible to weight gain and

162 s, resulting in up-regulation of both mature IGF-II mRNA and protein expression.

163 In BTBR mice, IGF-II, via IGF-II receptor, but not via IGF-I receptor,

164 ) and the insulin-like growth factor II/MPR (IGF-II/MPR), recognize a diverse population of Man-6-P-c

165 fibroblast MS cells deficient in the murine IGF-II receptor and corresponding MS9II cells overexpres

166 inding specificity in comparison with native IGF-II.

167 weakly to purified ectodomain of the natural IGF-II scavenging receptor, IGF-IIR.

168 Neither IGF-II nor IGFBP-II concentrations were associated with

169 wn-regulated after prolonged insulin but not IGF-II exposure.

170 -5 (IGFBP-5) promotes the myogenic action of IGF-II.

171 Although autocrine actions of IGF-II are known to initiate myoblast differentiation, t

172 s) mediate the stemness promoting actions of IGF-II on mouse subventricular zone neural precursors.

173 tified IMP-3 as a translational activator of IGF-II leader-3 mRNA.

174 its uptake was inhibited by the addition of IGF-II.

175 our results suggest that a lower affinity of IGF-II for the IR-A promotes lower IR-A phosphorylation

176 F19A, an analog of IGF-II that does not bind the IGF-2R, stimulated an incr

177 1C integrin, of its ligand Laminin-1, and of IGF-II in the tumor microenvironment may promote prostat

178 as no consistent evidence of associations of IGF-II, or IGFBP-3 with physical performance.

179 detailed NMR structural characterization of IGF-II analogs that revealed a link between the altered

180 iation between circulating concentrations of IGF-II and subsequent weight gain and progression to obe

181 When added with low concentrations of IGF-II, IGFBP-5 restores IGF-II expression and myogenic

182 ults highlight the potential contribution of IGF-II receptor to AD pathology not only by regulating e

183 cancer cells do not respond to high doses of IGF-II due to induction of PTEN, but IGFBP-2, when free

184 7 cells were not responsive to high doses of IGF-II due to induction of PTEN, which was not observed

185 KB signaling in LOI(+) cells at low doses of IGF-II, which was reduced in the presence of the inhibit

186 The effects of IGF-II occur via IGF-II receptors, and not IGF-I recepto

187 residue for PTEN to modulate the effects of IGF-II on activating the PI3K/Akt pathway in RMS cells.

188 on and survival by inhibiting the effects of IGF-II.

189 IGFBP-5 is induced before the elevation of IGF-II expression during myogenesis.

190 ignaling pathways for myogenic expression of IGF-II remain elusive.

191 ed 7 and selectively increased expression of IGF-II, proliferating cell nuclear antigen, and aspartyl

192 to an increase in hippocampal expression of IGF-II, which requires the transcription factor CCAAT en

193 Inhibition of IGF-II production impaired the transcriptional actions o

194 le is very responsive to direct injection of IGF-II.

195 sed expression of several longer isoforms of IGF-II, termed "pro" and "big" IGF-II, has been observed

196 Our complex shows that Phe19 and Leu53 of IGF-II lock into a hydrophobic pocket unique to domain 1

197 We found that serum levels of IGF-II (OR per SD increase: 1.16; 95% CI: 1.08-1.24; P(t

198 ng IGF-binding protein (IGFBP) modulation of IGF-II actions on MCF-7 breast cancer cells, we found th

199 Overexpression of IGF-II and IR-A is reported in multiple types of cancer

200 an autocrine pathway involving production of IGF-II and activation of the IGF-I receptor, phosphatidy

201 sm by which mTOR regulates the production of IGF-II, a master switch governing the initiation of skel

202 ning weight (P for trend across quintiles of IGF-II = 0.006).

203 -BP knockdown, suggesting that regulation of IGF-II gene expression, rather than c-myc mRNA levels, m

204 idence that beta1C-mediated up-regulation of IGF-II levels increases adhesion to Laminin-1, a basemen

205 Here, we report the regulation of IGF-II transcription by mTOR, as well as by amino acid s

206 transport capacity consistent with a role of IGF-II in modulating both the placental supply and fetal

207 ults provide novel insights into the role of IGF-II in the pathogenesis of SSc-associated pulmonary f

208 he Toll receptor, inhibited the secretion of IGF-II, affected the conformation of Grp94, and suppress

209 These findings suggest that the timing of IGF-II expression and regulation of its accessibility by

210 F-II expression by inhibiting translation of IGF-II mRNA.

211 Transplantation of IGF-II overexpressing islets under the kidney capsule of

212 ng pathway, as revealed by its dependence on IGF-II and by accelerated malignant progression upon IGF

213 the negative regulatory effects of IGF2R on IGF-II-induced growth can lead to embryonic lethality an

214 an IGFBP-3 mutants that cannot bind IGF-I or IGF-II by substituting alanine for six residues in the p

215 tivation of IGF-IR or inhibition of IGF-I or IGF-II expression but enhanced by overexpression of IGF-

216 ut not insulin-like growth factor (IGF)-I or IGF-II.

217 agment alone or in combination with IGF-I or IGF-II.

218 ferate in response to PDGF, but not IGF-I or IGF-II.

219 ly inhibited the in vivo growth of IGF-I- or IGF-II-driven tumors.

220 with equivalent concentrations of insulin or IGF-II.

221 sed an adenoviral (Ad) vector to overexpress IGF-II in isolated rat islets and investigated its antia

222 e third trimester of pregnancy and placental IGF-II contents at birth (P = 0.03).

223 on of human K562 cells, involving a possible IGF-II-dependent mechanism that appears independent of i

224 We also observed that pro-IGF-II co-immunoprecipitates with NET37.

225 stigate the putative role of unprocessed pro-IGF-II, called 'big'-IGF-II, in GISTs.

226 nteracts physically and transiently with pro-IGF-II intermediates, and its activity is essential for

227 In hippocampal slices, IGF-II promotes IGF-II receptor-dependent, persistent long-term potentia

228 ting and degradation of the growth-promoting IGF-II has been proposed as a mechanism for the tumor su

229 We found that two RNA-binding proteins, IGF-II mRNA-binding protein (Imp) and Syncrip (Syp), dis

230 Structural analysis identifies the putative IGF-II binding site at one end of the beta-barrel whilst

231 rward protocol for production of recombinant IGF-II and prepared six IGF-II analogs with IGF-I-like m

232 Furthermore, injections of recombinant IGF-II into the hippocampus after either training or mem

233 culture of IR-treated cells with recombinant IGF-II partially reversed the effects of IMP-3 knockdown

234 esults suggest that IMP-3 knock down reduced IGF-II expression by inhibiting translation of IGF-II mR

235 ic myeloid leukemia cells because of reduced IGF-II biosynthesis.

236 s to IR-induced apoptosis and led to reduced IGF-II production.

237 cation of a signaling pathway that regulates IGF-II expression in myogenesis and implicate the mTOR-I

238 stimulates colonic myofibroblasts to release IGF-II, which increases proliferation of colonic epithel

239 IGF-II-dependent memory enhancement requires IGF-II receptors, new protein synthesis, the function of

240 w concentrations of IGF-II, IGFBP-5 restores IGF-II expression and myogenic differentiation, whereas

241 creased levels of intracellular and secreted IGF-II without affecting IGF-II leader-3, leader-4, c-my

242 CCD18Co cells secreted IGF-II in response to rhPG(1-80), and conditioned media

243 IGF2R sequesters IGF-II; imbalances occur in cancers and IGF2R is implica

244 een baseline concentrations of fasting serum IGF-II and risk of gaining > or =2.5 kg body wt or devel

245 hosphorylation on Ser473 and Thr308 in seven IGF-II-overexpressing rhabdomyosarcomas (RMS) cells.

246 ction of recombinant IGF-II and prepared six IGF-II analogs with IGF-I-like mutations.

247 In hippocampal slices, IGF-II promotes IGF-II receptor-dependent, persistent lo

248 of IGFBP-5 impairs myogenesis and suppresses IGF-II gene expression.

249 We show that systemic IGF-II treatments reverse the typical defects in social

250 ge progenitors at a lower concentration than IGF-II.

251 that IGF-I would be even more effective than IGF-II.

252 ion during normal early development and that IGF-II can compensate in part for IGF-I actions on myeli

253 ther, these data lead to the conclusion that IGF-II promotes stemness of NSCs via the IR-A and not th

254 Western blot analysis confirmed that IGF-II inhibits apoptosis via activation of the phosphat

255 Here we demonstrate that IGF-II messenger RNA binding protein (Imp) counteracts e

256 Our results show that IGF-II receptor overexpression increases the protein lev

257 Taken together, these results show that IGF-II-initiated signaling through the insulin-like grow

258 al and gene-association studies suggest that IGF-II may influence body weight regulation and that ind

259 We suggest that IGF-II represents a potential novel therapeutic target f

260 ion in affected family members suggests that IGF-II affects postnatal growth in addition to prenatal

261 ressed primarily from the P3 promoter of the IGF-II gene, and IGF-II induced both a dose- and time-de

262 ve way, by increasing the sensitivity of the IGF-II signaling pathway itself, providing a previously

263 with NVP-AEW541, a specific inhibitor of the IGF-II signaling receptor, showed reduction of prolifera

264 lls were non-responsive to high doses of the IGF-II-analog.

265 ermined solvent-exposed loop residues of the IGF-II-binding site of human domain 11, expressed these

266 d an increase in the expression ratio of the IGF-II-sensitive, A isoform of the insulin receptor vers

267 Ligands of the IGF-II/mannose 6-phosphate receptor (IGF2R) include IGF-

268 ce that the two Man-6-P-binding sites of the IGF-II/MPR are structurally similar to each other and to

269 entiation by binding to and switching on the IGF-II auto-regulation loop.

270 juxtaposition of these domains provides the IGF-II-binding unit, with domain 11 directly interacting

271 indicate that IMP-3 acts in part through the IGF-II pathway to promote cell survival in response to I

272 ll as by amino acid sufficiency, through the IGF-II promoter 3 and a downstream enhancer during C2C12

273 ge in mixed cultures, where they can use the IGF-II provided by producer cells.

274 lin-like growth factor II (IGF-II), with the IGF-II binding site on the bifunctional, IGF-II cation-i

275 date, it is ambiguous as to what role these IGF-II isoforms have in initiating and sustaining tumori

276 Mutagenesis analyses confirm this IGF-II 'binding-hotspot', revealing that IGF-binding pro

277 Thus IGF-II may represent a potentially important and effecti

278 Thus, IGF-II may represent a novel potential therapy for ASD.S

279 Thus, IGF-II may represent a novel target for cognitive enhanc

280 of the vitreous-type fragment are limited to IGF-II.

281 IGFBP-3 fragment modulated cell responses to IGF-II only.

282 s, whereas IGFBP-6 reduced cell responses to IGF-II only.

283 OI(+) mice also have enhanced sensitivity to IGF-II signaling, not simply increased IGF-II levels, be

284 analog with IR-A binding affinity similar to IGF-II.

285 ergo reduced tumorigenesis in the colon upon IGF-II pathway blockade.

286 ally supports cell adhesion to Laminin-1 via IGF-II is selectively regulated by the beta1 cytoplasmic

287 In BTBR mice, IGF-II, via IGF-II receptor, but not via IGF-I receptor, reverses th

288 The effects of IGF-II occur via IGF-II receptors, and not IGF-I receptors, and target bo

289 In vivo IGF-II blockade with NVP-AEW541 abrogated this effect, r

290 bility for new learning and also occurs when IGF-II treatment is given in concert with memory retriev

291 tained treatment effect can be achieved with IGF-II and, potentially, other growth factors, the pharm

292 , we show that IMP-3 protein associates with IGF-II leader-3 and leader-4 mRNAs and H19 RNA but not c

293 7a-3, however, was inversely correlated with IGF-II expression and positively with insulin-like growt

294 it, with domain 11 directly interacting with IGF-II and domain 13 modulating binding site flexibility

295 Interference with IGF-II production by a tetracycline-inhibited adenovirus

296 ke growth factor (IGF)-I and negatively with IGF-II (Ptrend=0.006 for both) but not with IGF binding

297 of R-/IR-A cells with insulin, but not with IGF-II, targeted the receptor to a degradative pathway.

298 I) and ventrodorsal (IGFBP-5) patterns, with IGF-II excluded from the rostral, alpha-subunit-expressi

299 in vitro in culture medium supplemented with IGF-II analogs.

300 port that, in mice, systemic treatments with IGF-II given before training significantly enhance the r