ライフサイエンスコーパス: TGFalpha

1 TGFalpha animals heterozygous for both the Ink4a/Arf and

2 TGFalpha causes rapid membrane translocation and subsequ

3 TGFalpha directly activates the EGFR on these cells in v

4 TGFalpha expression can be detected in breast cancer cel

5 TGFalpha increased apoptosis in PE01CDDP cells but decre

6 TGFalpha may play its synergistic role, at least in part

7 TGFalpha treatment in AGS cells led to increases in Pdx1

8 TGFalpha-induced tumors appear stochastically and with r

9 involves the interaction of gurken (grk), a TGFalpha-like protein, with torpedo (top), the Drosophil

10 ifying the spatial distribution of Gurken, a TGFalpha-like EGFR ligand that acts as a morphogen in Dr

11 ntrols the activation of the ligand Spitz, a TGFalpha-like factor.

12 h ADAMs showed substrate preference (ADAM17, TGFalpha and heparin-binding EGF; and ADAM9, NRG), subst

13 Plasma with added TGFalpha stimulated HK migration that reached more than

14 Inhibiting NHE1 activity after TGFalpha stimulation with 10 muM of the NHE1-specific in

15 cteristics of newly proliferated cells after TGFalpha stimulation and/or aminoglycoside damage in the

16 inhibited by neutralizing antibodies against TGFalpha and/or EGFR and by the EGFR-specific inhibitor

17 inhibited by neutralizing antibodies against TGFalpha and/or EGFR.

18 Addition of neutralizing antibodies against TGFalpha to serum or depletion of TGFalpha from serum by

19 ells led to upregulation of the EGFR agonist TGFalpha and subsequently to EGFR activation.

20 wth factor transforming growth factor alpha (TGFalpha) and the nuclear transcription factor c-myc oft

21 autocrine transforming growth factor alpha (TGFalpha) controls the epidermal growth factor receptor

22 e enhanced transforming growth factor alpha (TGFalpha) expression plays an important role in the indu

23 -EGF), and transforming growth factor alpha (TGFalpha) from tumor cells suppress the expression of os

24 ens at the transforming growth factor alpha (TGFalpha) gene in situ.

25 ody versus transforming growth factor alpha (TGFalpha) had no effect on the primary activation of eit

26 effects of transforming growth factor alpha (TGFalpha) in a 6-OHDA Parkinson's disease model when com

27 t oncogene transforming growth factor alpha (TGFalpha) in bitransgenic mice.

28 integrated transforming growth factor alpha (TGFalpha) induced EGFR-gene-protein interaction network.

29 fusions of transforming growth factor alpha (TGFalpha) into forebrain structures.

30 Transforming growth factor alpha (TGFalpha) is a potent inducer of cellular transformation

31 Transforming growth factor alpha (TGFalpha) is a principal molecule in the normal and neop

32 Transforming growth factor alpha (TGFalpha) is widely expressed in malignant as well as no

33 tramucosal transforming growth factor alpha (TGFalpha) levels in the gastric fundus leads to oxyntic

34 duction of transforming growth factor alpha (TGFalpha) mRNA in situ in MDA-MB 231 cells stably transf

35 nd second, transforming growth factor alpha (TGFalpha) mRNA was used as a gene target in situ for sta

36 nfusion of transforming growth factor alpha (TGFalpha) plus insulin.

37 ceptors by transforming growth factor alpha (TGFalpha) results in production of prostaglandin E2, whi

38 tration of transforming growth factor alpha (TGFalpha) to the contused mouse spinal cord can enhance

39 ecursor of transforming growth factor alpha (TGFalpha), as a model cargo protein, we demonstrate in c

40 expressing transforming growth factor alpha (TGFalpha), c-Met is constitutively phosphorylated in the

41 s, EGF and transforming growth factor alpha (TGFalpha), causes MUC5AC expression in airway epithelial

42 2) and for transforming growth factor alpha (TGFalpha), have been cloned downstream of the mouse mamm

43 contained transforming growth factor alpha (TGFalpha), insulin-like growth factor type one (IGF-1),

44 its ligand transforming growth factor alpha (TGFalpha), suggesting that ADAM17 regulates terminal dif

45 in (AREG), transforming growth factor alpha (TGFalpha), syndecan-1 (SDC1), and tumor necrosis factor

46 r (EGF) or transforming growth factor alpha (TGFalpha), which are known activators of Rac.

47 strogen on transforming growth factor alpha (TGFalpha)- and prolactin (PRL)-induced mammary tumorigen

48 ivation of transforming growth factor alpha (TGFalpha)-erbB-1 and neuregulin-erbB-4 signaling pathway

49 cules from transforming growth factor alpha (TGFalpha)-stimulated human keratinoytes, which contained

50 GFR ligand transforming growth factor alpha (TGFalpha).

51 (bFGF) or transforming growth factor alpha (TGFalpha).

52 The transforming growth factor alpha (TGFalpha)/epidermal growth factor receptor (EGFR) signal

53 rs such as transforming growth factor alpha (TGFalpha); however, the mechanisms by which TNF interact

54 Transforming growth factor-alpha (TGFalpha) and fibroblast growth factor-7 (FGF7) exhibit

55 (EGF), and transforming growth factor-alpha (TGFalpha) elicit differential postendocytic processing o

56 (EGF) and transforming growth factor-alpha (TGFalpha) from the plasma membrane.

57 n (Grk), a transforming growth factor-alpha (TGFalpha) homolog) is received by predetermined terminal

58 Transforming growth factor-alpha (TGFalpha) is a ligand for the epidermal growth factor re

59 eport that transforming growth factor-alpha (TGFalpha) may regulate sex- and age-dependent developmen

60 ther human transforming growth factor-alpha (TGFalpha) or simian virus 40 large and small T antigen (

61 induced by transforming growth factor-alpha (TGFalpha) requires PI3K-dependent NHE1-activation and su

62 c-myc and transforming growth factor-alpha (TGFalpha) transgenes in mouse liver induces a state of o

63 , or human transforming growth factor-alpha (TGFalpha), and immunohistochemically stained for phospho

64 ested that transforming growth factor-alpha (TGFalpha), but not the other EGFR ligands EGF, heparin-b

65 s, such as transforming growth factor-alpha (TGFalpha), NRG1alpha, and NRG1beta, the PE01CDDP line wa

66 nding-EGF, transforming growth factor-alpha (TGFalpha), or amphiregulin we have shown that only the a

67 egulin and transforming growth factor-alpha (TGFalpha).

68 alian EGFR ligands including EGF, TGF-alpha (TGFalpha), amphiregulin (AREG), heparin-binding EGF-like

69 mice that overexpression of the c-erbB-2 and TGFalpha genes predisposes the mammary gland to stochast

70 Thus, EGF and TGFalpha are biased agonists, whereas BTC and AREG are b

71 In radioligand binding assays, EGF and TGFalpha exhibited increased affinity for EGFR/ErbB2 het

72 g, revealing collaborative roles for EGF and TGFalpha in mammopoiesis and lactogenesis.

73 of meprinalpha-mediated shedding of EGF and TGFalpha were investigated with human colorectal adenoca

74 EGF and TGFalpha, but not FN fragments, increased Rac1 activity

75 ionally behave as soluble decoys for EGF and TGFalpha, ligands that would otherwise activate downstre

76 Simultaneous stimulation by FGF7 and TGFalpha indicated that the FGF7-induced MAPK(ERK1,2) si

77 In contrast to NHEK, IFN-gamma and TGFalpha are not very effective in inducing TGFalpha or

78 indicating alterations in both IFN-gamma and TGFalpha response pathways.

79 shedding of the ADAM17 substrates CD62-L and TGFalpha is not affected.

80 OS generated by over-expression of c-myc and TGFalpha in the liver are the primary carcinogenic agent

81 Both in vitro and in vivo, PRL and TGFalpha cooperatively enhanced Akt phosphorylation, whi

82 Furthermore, PRL and TGFalpha in combination blocked the mitogenic effects of

83 In combination, prolactin and TGFalpha also increased the incidence and reduced the la

84 Prolactin and TGFalpha cooperated to reduce dramatically the latency o

85 s of the transgene on cell proliferation and TGFalpha expression, the results suggest that Whn modula

86 utralization of TGFalpha function by an anti-TGFalpha antibody or inhibition of MAPK function by MEK1

87 mphiregulin we have shown that only the anti-TGFalpha antibody significantly decreases NT-induced pho

88 se to TSST-1 and is also necessary for AREG, TGFalpha, and TNFR1 shedding.

89 losely related ADAM10, is required for AREG, TGFalpha, and TNFR1 shedding.

90 shedding of other ADAM17 substrates, such as TGFalpha, is not affected in iRhom2(-/-) mEFs but can be

91 The membrane-associated TGFalpha induced higher phosphorylation of EGFR on the c

92 Selective MEK inhibitors attenuated TGFalpha-mediated basal activation of p70S6K (S6K) speci

93 Autocrine TGFalpha is an important growth effector in the transfor

94 It produces autocrine TGFalpha but requires exogenous EGF in the medium for op

95 ments show for the first time that autocrine TGFalpha regulates cell adhesion function by multiple si

96 lpha from its transmembrane precursor before TGFalpha can bind to erbB1 receptors, we sought to deter

97 mphiregulin, and EPR; and (ii) betacellulin, TGFalpha, and epigen.

98 extracellular function of hsp90alpha blocks TGFalpha-induced keratinicyte migration.

99 The interaction of membrane bound TGFalpha precursor with the EGFR caused a slower interna

100 tivation of MAPK(ERK1,2) for 1 h, induced by TGFalpha, was necessary and sufficient to initiate branc

101 opment, the principal lesion type induced by TGFalpha.

102 a, the PE01CDDP line was growth inhibited by TGFalpha and NRG1beta but unaffected by NRG1alpha.

103 The increase in COX-2 mRNA by TGFalpha requires activation of both the extracellular s

104 The increase of c-Met phosphorylation by TGFalpha in A431 cells was inhibited by neutralizing ant

105 and the increase of c-Met phosphorylation by TGFalpha or EGF, in tumor cell lines is the result of th

106 al growth factor receptor transactivation by TGFalpha, whereas acid responses required ErbB4 transact

107 However, MDA 231 and MDA 468 cells, TGFalpha stimulation induced sustained MAPK activation,

108 In MCF-7 cells, TGFalpha stimulation induced only transient MAPK activat

109 ion of TGFalpha in FET cells by constitutive TGFalpha expression abrogated the requirement for IGF-IR

110 e tethered TGFalpha indicates that defective TGFalpha processing provides a mechanism whereby maligna

111 founder cells produce Spitz (the Drosophila TGFalpha homolog) signal, which is passed to the neighbo

112 Daily administration of PX-866 during TGFalpha induction prevented increases in lung collagen

113 EGF, TGFalpha, and betacellulin (BTC) appear to mainly stimul

114 r HER3 by adding the heterodimer ligands EGF/TGFalpha or heregulin.

115 ween membrane receptor and ligand (e.g. EGFR-TGFalpha) results in a constitutive activation of MAPK-E

116 of both TGF promoter activity and endogenous TGFalpha mRNA at 4 h.

117 Falpha to the mammary gland have established TGFalpha overexpression can induce hyperproliferation, h

118 2-Adam17(-/-) mice was restored by exogenous TGFalpha application, confirming the involvement of tran

119 Exposure to exogenous TGFalpha or EGF increased the phosphorylation of c-Met i

120 llowing internalization, while, as expected, TGFalpha stimulates markedly less.

121 moid carcinoma cell line, A431 which express TGFalpha, but not in normal human hepatocytes.

122 astic ducts in response to the growth factor TGFalpha, we performed genetic lineage tracing experimen

123 n of hepatocarcinogenesis characteristic for TGFalpha/c-myc mice.

124 rated a facilitating, proliferative role for TGFalpha in the development of neoplasia and implicated

125 er, deduction of EGF-activated pathways from TGFalpha-activated pathways in the same cells allowed us

126 Activation of erbB-1 receptors by glial TGFalpha has been shown to be a component of the develop

127 (PFCs) competent to receive the Gurken (Grk)/TGFalpha signal emitted by the oocyte to control body ax

128 ransgenic mouse models targeting heterologus TGFalpha to the mammary gland have established TGFalpha

129 ithelial cell cycle to induce cancer and how TGFalpha enhanced the process.

130 -terminal seven amino acid residues of human TGFalpha.

131 Despite evidence implicating TGFalpha in the development of mammary neoplasia, the ac

132 These data show that PI3K is activated in TGFalpha/EGFR-mediated pulmonary fibrosis and support fu

133 d selenoproteins in liver tumor formation in TGFalpha/c-Myc transgenic mice, which are characterized

134 ion that results in a postnatal reduction in TGFalpha gene expression.

135 of the TGFalpha autocrine loop resulting in TGFalpha-mediated EGFr activation which was critical for

136 ale for efforts to inhibit EGFR signaling in TGFalpha-positive colon cancers.

137 ivity in several signaling assays (including TGFalpha shedding, activation of NFAT luciferase, and be

138 d not restore the ability of 4-OHT to induce TGFalpha mRNA.

139 detected after 1 day of doxycycline-induced TGFalpha expression, was blocked by treatment with the P

140 eract to regulate both basal and EGF-induced TGFalpha expression.

141 TGFalpha are not very effective in inducing TGFalpha or COX-2 expression in several squamous carcino

142 Intrastriatal TGFalpha infusion induced significant proliferation, hyp

143 el developmental signaling cascade involving TGFalpha>PI3K>NHE1>pHi alkalization, which leads to a pe

144 ly expressed in the SCN, (2) the EGFR ligand TGFalpha is expressed and apparently locally released in

145 membrane proteins, including the EGFR ligand TGFalpha, from the endoplasmic reticulum (ER) to the Gol

146 ADAM17-mediated shedding of the EGFR ligand TGFalpha.

147 Coexpression of EGFR with its ligand TGFalpha indicates their role in paracrine and autocrine

148 e lung epithelial cells, the pro-EGF ligands TGFalpha, neuregulin 1beta (NRG), and heparin-binding EG

149 s by modulating the shedding of EGFR ligands TGFalpha and HB-EGF and, consequently, EGFR signaling ac

150 is by simultaneous deregulation of EGF-like (TGFalpha) and Wnt growth factors.

151 in ERalpha induced by neu-related lipocalin-TGFalpha.

152 acent cells than equivalent levels of mature TGFalpha.

153 al auto-stimulation by the PLCgamma-mediated TGFalpha-EGFR autocrine network.

154 milar phenotypes are observed in female MMTV-TGFalpha transgenic rats.

155 Furthermore, in an organ culture model, TGFalpha can increase levels of phospho-EGFR and promote

156 lar hyperplasia in both metallothionein (MT)-TGFalpha mice and patients with Menetrier's disease.

157 Overexpression of TGFalpha in MT-TGFalpha mice and Menetrier's disease patients elicits e

158 The distribution of Pdx1 in MT-TGFalpha mice and Menetrier's disease patients was evalu

159 In MT-TGFalpha mice, 8 weeks of zinc treatment elicited nuclea

160 the role of Pdx1-expressing stem cells in MT-TGFalpha transgenic mice, and second, to further charact

161 expression was evaluated in Pdx1(lacZ/+)/MT-TGFalpha bigenic mice treated with zinc.

162 Pdx1(lacZ/+)/MT-TGFalpha bigenics showed up-regulated Pdx1 expression in

163 reatment for 2 to 8 weeks in Pdx1(lacZ/+)/MT-TGFalpha transgenic mice resulted in expression of Pdx1

164 In addition, multiparous TGFalpha-expressing female transgenics frequently develo

165 ed that during hepatocarcinogenesis in c-myc/TGFalpha double transgenic mice, there is increased expr

166 nt branching by suppression of two necessary TGFalpha-induced morphogenetic effectors, matrix metallo

167 tion and Shc-HER2 homodimer binding, but not TGFalpha-induced AKT phosphorylation.

168 NRL-TGFalpha mice acquire proliferative hyperplasias as well

169 el NRL-transforming growth factor alpha (NRL-TGFalpha) transgenic mouse model in which growth factor

170 ammary lesions, p53+/- mice carrying the NRL-TGFalpha transgene developed ER negative/PR negative und

171 This is supported by the ability of TGFalpha to rapidly induce COX-2 and the inhibition of t

172 ion-induced cleavage and autocrine action of TGFalpha.

173 The actions of TGFalpha and NRGs in glia are synergistic and involve re

174 ectively, these data show that activation of TGFalpha-EGFR signaling in colon cancer cells creates a

175 Binding of TGFalpha to the epidermal growth factor receptor (EGFR),

176 Interestingly, the combination of TGFalpha and insulin could duplicate the HK pro-motility

177 es against TGFalpha to serum or depletion of TGFalpha from serum by immunoprecipitation significantly

178 this pathway and prevent the development of TGFalpha-induced neoplasia and tumor formation.

179 cells, we show that PKD1 acts downstream of TGFalpha and Kras, to mediate formation of ductal struct

180 ynthesis prevented the stimulatory effect of TGFalpha on both PGE2 and TGFbeta1 release.

181 Forced expression of TGFalpha in C10 tumor cells led to the generation of aut

182 The inappropriate expression of TGFalpha in growth arrest contributes to malignant progr

183 The expression of TGFalpha, a known regulator of leading edge formation, i

184 n was accompanied by increased expression of TGFalpha, a ligand of epidermal growth factor receptor (

185 d FET cells down-regulated the expression of TGFalpha, EGFr and, in turn, EGFr activation.

186 d activation of EGFR by the tethered form of TGFalpha was reflected by higher activation of Grb2, SHC

187 Given the importance of TGFalpha in malignant progression, this work addressed t

188 ied by an approximate threefold induction of TGFalpha expression along with EGFr activation at 1 h fo

189 h oral PX-866 4 weeks after the induction of TGFalpha prevented additional weight loss and further in

190 in animals with both lesion and infusion of TGFalpha was there a rapid proliferation of forebrain st

191 Both PRL and estrogen reduced the latency of TGFalpha-induced oncogenesis, resulting in tumors that w

192 ated the hypothesis that increased levels of TGFalpha in the fundus induces an antral pattern of cell

193 sing high (C9) or negligible (C10) levels of TGFalpha were implanted into the cecal walls of nude mic

194 ha (Tgfa) mRNA and secreted higher levels of TGFalpha, leading to activation of EGFR signaling in aci

195 f mammary neoplasia, the actual mechanism of TGFalpha-induced transformation is unclear.

196 icate that Muc1 is an important modulator of TGFalpha-dependent tumor progression.

197 Neutralization of TGFalpha function by an anti-TGFalpha antibody or inhibi

198 Overexpression of TGFalpha in MT-TGFalpha mice and Menetrier's disease pat

199 Overexpression of TGFalpha in vivo by intraparenchymal adeno-associated vi

200 These models identify the overexpression of TGFalpha or c-myc as etiological factors in the developm

201 Although processing of TGFalpha has been extensively studied in normal cells, t

202 Therefore, we compared the processing of TGFalpha in two human colon carcinoma cell lines.

203 epithelium and can impact the progression of TGFalpha-mandated mammary tumorigenesis.

204 ssion, this work addressed the regulation of TGFalpha expression in the early stage colon carcinoma c

205 growth arrest associated down-regulation of TGFalpha in FET cells by constitutive TGFalpha expressio

206 colon tumor cells show a down-regulation of TGFalpha in growth arrest and require both nutrients and

207 TNF-induced release of TGFalpha and activation of EGFR signaling were inhibited

208 matrix metalloproteinase-mediated release of TGFalpha and subsequent EGFR transactivation triggers a

209 activation mechanism involves the release of TGFalpha into the medium through activation of the metal

210 TACE-like activity, and enhanced release of TGFalpha.

211 inases (most likely TACE) and the release of TGFalpha.

212 we demonstrate that constitutive shedding of TGFalpha can be reduced by inhibition of Src in several

213 Src(E378G)-stimulated shedding of TGFalpha is abolished in Adam17(-/-) cells, but can be r

214 tro results identify tanycytes as targets of TGFalpha action and demonstrate that activation of erbB-

215 y of the EGF-EGFR interaction versus that of TGFalpha-EGFR in the acidic conditions of sorting endoso

216 that in eyelid closure Get1 acts upstream of TGFalpha in the EGFR/ERK pathway.

217 o determine the effect of Muc1 expression on TGFalpha/EGFR-dependent breast transformation, we crosse

218 e pathways express the ligands HB-EGF and/or TGFalpha.

219 ubated with 10 ng/ml of BDNF, CNTF, FGF2, or TGFalpha for 10 or 30 minutes or 1, 3, or 6 hours and th

220 of recipient breast cancer cells 4-fold over TGFalpha or HB-EGF exosomes and 5-fold over equivalent a

221 vironmental factors such as glucose, oxygen, TGFalpha, VEGF and fibronectin.

222 Five lines of PEPCK-TGFalpha transgenic rats were established, each genetic

223 ngs demonstrate that ADAM17 is the principal TGFalpha sheddase that is activated by Src in a manner t

224 , despite elevated ERalpha levels in NRL-PRL/TGFalpha glands, tumor latency was not reduced with incr

225 esulting in retention of partially processed TGFalpha on the cell surface of both the HCT116a2alphaS3

226 in pancreatic tumor genesis and progression, TGFalpha transgenic mice were crossed onto Ink4a/Arf and

227 of S100A4 using shRNA significantly reduced TGFalpha induced branching and altered E-cadherin locali

228 cells, there is little information regarding TGFalpha cleavage in malignant cells.

229 ontrast, highly progressed cells up-regulate TGFalpha during growth arrest and require only nutrients

230 ctor alpha converting enzyme (TACE) releases TGFalpha from its transmembrane precursor before TGFalph

231 f phosphorylated ERK1/2 compared with single TGFalpha transgenic glands, suggesting that this kinase

232 ge species could differ from that of soluble TGFalpha.

233 lative to the internalization of the soluble TGFalpha/EGFR complexes.

234 ously showed that induction of lung-specific TGFalpha expression in transgenic mice caused progressiv

235 SP stimulated TGFalpha release into the extracellular space that was m

236 noncanonical GLI2 activation with subsequent TGFalpha secretion, activation of EGFR in pancreatic epi

237 The release of other ADAM17 substrates, TGFalpha and sMet, are also regulated this way, pointing

238 gher activation of EGFR by membrane tethered TGFalpha indicates that defective TGFalpha processing pr

239 In addition, the tethered TGFalpha was resistant to the ability of protein-tyrosin

240 ignificantly greater membrane stability than TGFalpha or HB-EGF.

241 Together these experiments indicate that TGFalpha and the EGFR signaling pathway are potentially

242 ined responsive to estrogen, indicating that TGFalpha and PRL in combination can inhibit some, but no

243 al between plasma and serum, we propose that TGFalpha is the physiologic HK pro-motility factor in HS

244 We proposed that TGFalpha and the autocrine activation of its receptor, e

245 Time-lapse studies revealed that TGFalpha and TGFbeta1 have dramatically opposite effects

246 These results suggest that TGFalpha may regulate postpubertal, sex differentiation

247 The TGFalpha-like ligand SPITZ is activated in the neurons,

248 d for excitatory amino acids to activate the TGFalpha-erbB1 signaling module in hypothalamic astrocyt

249 endochondral ossification by activating the TGFalpha/EGFR signaling axis.

250 ere was a defective cleavage pattern for the TGFalpha precursor resulting in retention of partially p

251 S100A4 induced a significant increase in the TGFalpha mediated branching phenotype and a concomitant

252 In summary, the cells in the TGFalpha-induced migratory cellular wave remain undiffer

253 IR activation up-regulates components of the TGFalpha autocrine loop resulting in TGFalpha-mediated E

254 rogenitors directed toward the region of the TGFalpha infusion site.

255 The use of deletion constructs of the TGFalpha promoter in chimeras with chloramphenicol acety

256 basal activity and EGF-responsiveness of the TGFalpha promoter.

257 hese data demonstrate that disruption of the TGFalpha-EGFR-MAPK signaling module represents a strateg

258 show that changes in the distribution of the TGFalpha-like ligand Gurken (GRK), a crucial ligand for

259 also been linked to decreased levels of the TGFalpha-like molecule Gurken, which controls normal egg

260 o-motility activity in HS, although only the TGFalpha, but not insulin, levels increase in serum over

261 e-induced rotations in animals receiving the TGFalpha infusions.

262 ion but minimal migration in response to the TGFalpha infusion.

263 phiregulin (AR) were derived and bred to the TGFalpha-knockout to generate mice lacking various combi

264 tically to potentiate EGFR signaling via the TGFalpha-like ligand Spitz.

265 que TGFalpha/EGF response element within the TGFalpha promoter were similarly induced following IGF-I

266 he localization of a cis-sequence within the TGFalpha promoter which mediates this stimulation.

267 siveness to between -247 and -201 within the TGFalpha promoter.

268 teins, including the precursors of TNFalpha, TGFalpha, several other cytokines, as well as the recept

269 UDCA decreases amount of shed TNFalpha, TGFalpha, and sMet in cell culture media and the phospho

270 and release of ADAM17 substrates, TNFalpha, TGFalpha, and c-Met receptor (or its soluble form, sMet)

271 re incubated with a neutralizing antibody to TGFalpha.

272 ting that the retraction was attributable to TGFalpha-induced TGFbeta1 formation.

273 of the erbB receptor family, and respond to TGFalpha with receptor phosphorylation, release of prost

274 fects on EGFR phosphorylation in response to TGFalpha and EGF in cancer cells.

275 Prolonged (>12 hr) exposure of tanycytes to TGFalpha resulted in focal tanycytic retraction, an effe

276 nse to NRGs and, to a lesser extent, that to TGFalpha and blocked the erbB-dependent, glia-mediated,

277 DNA binding proteins which bind to a unique TGFalpha/EGF response element within the TGFalpha promot

278 Unlike TGFalpha, FGF7 promoted sustained proliferation as well

279 These data demonstrate that unregulated TGFalpha expression in the mammary gland leads to oncoge

280 monary lesions were observed in 28 of 29 WAP-TGFalpha/Muc1(+/+) animals (including one metastatic pul

281 Bitransgenic mice carrying both WAP-TGFalpha and WAP-c-myc displayed a dramatic acceleration

282 cantly suppressed in tumors derived from WAP-TGFalpha/Muc1(-/-) animals compared with those expressin

283 eased approximately 30% in MMTV-infected WAP-TGFalpha transgenic animals compared to noninfected tran

284 was a common occurrence in MMTV-infected WAP-TGFalpha tumors, and some noninfected WAP-TGFalpha tumor

285 We previously reported that multiparous WAP-TGFalpha transgenic mice develop mammary gland carcinoma

286 AP-TGFalpha tumors, and some noninfected WAP-TGFalpha tumors also showed evidence of elevated Wnt-3 t

287 Although 100% of WAP-TGFalpha/Muc1(+/+) mice form mammary gland tumors by 1 y

288 mary gland tumors by 1 year, only 37% of WAP-TGFalpha/Muc1(-/-) form tumors by this time.

289 nt breast transformation, we crossed the WAP-TGFalpha transgenic mouse model of breast cancer onto a

290 WAP-TGFalpha/Muc1(-/-) compared with the WAP-TGFalpha/Muc1(+/+) mice.

291 mas), although none were detected in the WAP-TGFalpha/Muc1(-/-) animals.

292 a doubling of onset time observed in the WAP-TGFalpha/Muc1(-/-) compared with the WAP-TGFalpha/Muc1(+

293 Non-virgin WAP-TGFalpha transgenic mice displayed accelerated mammary d

294 The order of potency was: TGFalpha > insulin > EGF > heparin binding (HB)-EGF > IG

295 Whereas TGFalpha promotes tanycytic outgrowth, TGFbeta1 elicits

296 However, the molecular mechanism by which TGFalpha transcription is activated is poorly understood

297 n mammary gland development, in concert with TGFalpha by activating MMP-3, and increasing invasion in

298 To identify genes that cooperate with TGFalpha in mammary tumorigenesis, we used a retroviral

299 ed several oncogenes that can cooperate with TGFalpha to transform the mammary epithelium.

300 iated-thymidine was infused, with or without TGFalpha plus insulin, into the inner ears of normal or