ライフサイエンスコーパス: TGF-alpha

1 TGF-alpha and amphiregulin secretion by GRP stimulation

2 TGF-alpha and cripto-1 were also overexpressed in Smad7/

3 TGF-alpha antisense transfection of HCT116 cells showed

4 TGF-alpha antisense-transfected cells also showed attenu

5 TGF-alpha did not disrupt a non-behavioral rhythm, the r

6 TGF-alpha is expressed in the suprachiasmatic nucleus (S

7 TGF-alpha reversibly inhibits wheel-running activity dur

8 TGF-alpha, compared with EGF, is a more potent activator

9 this in a developmental model, MT-42 (CD-1) TGF-alpha mice were treated with vehicle or PD0325901 (2

10 A TGF-alpha/EGFR-RhoA module initiates one of these networ

11 o regulate their proliferation mediated by a TGF-alpha-dependent signal transduction pathway.

12 Reconstitution of bone marrow cells into a TGF-alpha transgenic mouse model demonstrated that fibro

13 astrocyte mitogen through the induction of a TGF-alpha/EGFR signaling pathway.

14 ation with an EGFR-neutralizing Ab or with a TGF-alpha-neutralizing Ab, implicating ligand (TGF-alpha

15 These stimuli induced TACE activation, TGF-alpha release, and mucin expression, effects that we

16 In addition, TGF-alpha regulated the function of TLR5 and TLR9, becau

17 Co-localised images of diaphragm after TGF-alpha overexpression revealed a layered fibrotic app

18 or ligands transforming growth factor alpha (TGF alpha) and amphiregulin are delivered to the basolat

19 its ligand transforming growth factor-alpha (TGF alpha), the downstream enzyme phospholipaseC-gamma (

20 , although transforming growth factor alpha (TGF-alpha) and epidermal growth factor (EGF) share the s

21 release of transforming growth factor alpha (TGF-alpha) by matrix metalloproteinases (MMPs).

22 duction of transforming growth factor alpha (TGF-alpha) expression, or tumor necrosis factor alpha-in

23 GF) and by transforming growth factor alpha (TGF-alpha) in NIH3T3 cell lines expressing EGFR with and

24 ithelia of transforming growth factor alpha (TGF-alpha) or c-myc.

25 es secrete transforming growth factor alpha (TGF-alpha) to trigger proliferation of cancer cells.

26 zed murine transforming growth factor alpha (TGF-alpha) transgenic hepatocyte (TAMH) cells, derived f

27 tor (EGF), transforming growth factor alpha (TGF-alpha), EGF receptor (EGFR), phosphorylated EGFR (pE

28 s Spitz, a transforming growth factor alpha (TGF-alpha)-like ligand that triggers epidermal growth fa

29 GFR ligand transforming growth factor alpha (TGF-alpha).

30 ceptor and transforming growth factor alpha (TGF-alpha)/epidermal growth factor (EGF) receptor activa

31 ls secrete transforming growth factor-alpha (TGF-alpha) and brain-derived neurotrophic factor (BDNF).

32 release of transforming growth factor-alpha (TGF-alpha) and interleukin-1 (IL-1) family ligands.

33 ion of the transforming growth factor-alpha (TGF-alpha) and of the epidermal growth factor receptor (

34 levels of transforming growth factor-alpha (TGF-alpha) and platelet-derived growth factor-BB (PDGF-B

35 leavage of transforming growth factor-alpha (TGF-alpha) by matrix metalloproteinases mediated GRP-ind

36 autocrine transforming growth factor-alpha (TGF-alpha) controls the expression of integrin alpha2, c

37 autocrine transforming growth factor-alpha (TGF-alpha) expression plays an important role in colon c

38 (EGF) and transforming growth factor-alpha (TGF-alpha) has been studied meticulously, with the forme

39 Transforming growth factor-alpha (TGF-alpha) is a candidate output signal of the hypothala

40 m by which transforming growth factor-alpha (TGF-alpha) is a more potent activator of epidermal growt

41 Transforming growth factor-alpha (TGF-alpha) is the major autocrine EGF receptor ligand in

42 (EGF) and transforming growth factor-alpha (TGF-alpha) ligands.

43 s, such as transforming growth factor-alpha (TGF-alpha) or heparin-binding EGF (HB-EGF), is also ofte

44 GF)-II and transforming growth factor-alpha (TGF-alpha) over IGF-I and epidermal growth factor, respe

45 hysiologic transforming growth factor-alpha (TGF-alpha) sheddase, and we also demonstrated enhanced s

46 ulation of transforming growth factor-alpha (TGF-alpha) shedding by reactive oxygen species (ROS) thr

47 Transforming growth factor-alpha (TGF-alpha) transduces its signal through the epidermal g

48 at express transforming growth factor-alpha (TGF-alpha), a liver mitogen, and Bcl-2.

49 ression of transforming growth factor-alpha (TGF-alpha), established by the presence of pleural and p

50 release of transforming growth factor-alpha (TGF-alpha), interleukin-1alpha (IL-1alpha), and IL-1 rec

51 (NRG), and transforming growth factor-alpha (TGF-alpha), is important in many cellular signaling path

52 d oncogene transforming growth factor-alpha (TGF-alpha), PRL induced mammary tumors in 100% of male b

53 to soluble transforming growth factor-alpha (TGF-alpha), pro-TGF-alpha.

54 release of transforming growth factor-alpha (TGF-alpha).

55 ediated by transforming growth factor-alpha (TGF-alpha).

56 (EGF) and transforming growth factor-alpha (TGF-alpha).

57 (EGF) and transforming growth factor-alpha (TGF-alpha).

58 ription of transforming growth factor-alpha (TGF-alpha).

59 e.g., transforming growth factor type alpha (TGF-alpha)] and EGFR phosphorylation are implicated in m

60 of ADAM17 substrates TNF-alpha, TNFR1-alpha, TGF-alpha, amphiregulin (AREG), HB-EGF and IL-6Ralpha, f

61 Altered TGF-alpha/beta signaling drives cooperation between brea

62 R30 reduced the expression of both GLT-1 and TGF-alpha and abrogated the G1-induced increase in GLT-1

63 the induction of IL-6, IL-1beta, IL-1ra, and TGF-alpha mRNA in WT-->WT mice but not in A2A-KO-->WT mi

64 variants but failed to restore TNF-alpha and TGF-alpha release in the shedding-defective CHO cell lin

65 ch provide a model of enhanced TGF-alpha and TGF-alpha self-induction, mutating the core AP2 site of

66 estored ectodomain shedding of TNF-alpha and TGF-alpha, suggesting that defects in the TACE gene cont

67 vels of PAR-2-induced p-AKT, HIFs-alpha, and TGF-alpha; our results suggest that ILK is involved in t

68 hology of 18-month-old wild-type, AR-/-, and TGF-alpha-/- mice were examined.

69 of the EGFR ligands amphiregulin (AREG) and TGF-alpha, which rely upon the cell surface protease TAC

70 of ADAM17 substrates TNFR1-alpha, AREG, and TGF-alpha (4-15-fold reductions, p<0.0001 for all three)

71 Ras-CM and TGF-alpha also increase PI3-K activity downstream of the

72 Both Ras-CM and TGF-alpha stimulated EGFR phosphorylation, and exogenous

73 usion, mechanical strain releases HB-EGF and TGF-alpha and promotes fetal type II cell differentiatio

74 Additionally, although both EGF and TGF-alpha have been shown to effectively induce initial

75 e (AP)-tagged ligands shed mature HB-EGF and TGF-alpha into the supernatant and promoted type II cell

76 ed that strain-induced release of HB-EGF and TGF-alpha is mediated via integrin-ADAM17/TACE interacti

77 rough EGFR (ErbB1) via release of HB-EGF and TGF-alpha ligands.

78 how that herstatin expression alters EGF and TGF-alpha signaling profiles, culminating in inhibition

79 lial cells actives TACE, releases HB-EGF and TGF-alpha, and promotes differentiation.

80 tic beads activated TACE and shed HB-EGF and TGF-alpha.

81 ir ability to migrate in response to EGF and TGF-alpha.

82 iation via ectodomain shedding of HB-EGF and TGF-alpha.

83 lls, in which the overexpression of EGFR and TGF-alpha constitute the major autocrine mitogenic signa

84 n excess of cold epidermal growth factor and TGF-alpha but not by an irrelevant molecule.

85 reactive oxygen species (ROS) generation and TGF-alpha-dependent epidermal growth factor receptor (EG

86 ults in apical mislocalization of Naked2 and TGF-alpha.

87 was reduced with aging in nontransgenic and TGF-alpha mice, indicating that some growth and death re

88 led to significant cleavage of only NRG and TGF-alpha and was inhibited by BB94; only LPA-induced NR

89 HB-EGF, NRG, and TGF-alpha cleavage was not dependent on PKC, and only HB

90 (TPA) -induced cleavage of HB-EGF, NRG, and TGF-alpha was dependent on PKC and sensitive to BB94 inh

91 completely blocked EGFr phosphorylation and TGF-alpha release.

92 enesis, which is then facilitated by PRL and TGF-alpha cross talk.

93 elial growth factor, PDGF, EGF receptor, and TGF-alpha, have recently become available.

94 F, leptin, G-CSF, GM-CSF, LIF, NGF, SCF, and TGF-alpha.

95 nar cell metaplasia to ductal structures and TGF-alpha-induced expression of ductal markers in ex viv

96 hepatocyte proliferation by combined TNF and TGF-alpha treatment is self-limited through antiprolifer

97 sis are both governed by a self-antagonizing TGF-alpha-IL-1alpha/beta-IL-1ra autocrine cascade in vit

98 uld be largely replaced by expression of any TGF-alpha ligand, including spitz (spi), in the endogeno

99 olonged (>24 h) and, though not as robust as TGF-alpha/EGF, did increase beta-cell proliferation.

100 ression and nuclear localization, as well as TGF-alpha mRNA and protein levels.

101 In addition, Slug attenuated TGF-alpha-induced acinar cell metaplasia to ductal struc

102 This network is activated by autocrine TGF alpha secretion, and the EGFR-dependent downstream s

103 omotion signaling is controlled by autocrine TGF-alpha.

104 Moreover, autocrine TGF-alpha-mediated epidermal growth factor receptor acti

105 ome by treating cells with TGF-alpha because TGF-alpha stimulates EGFR endocytosis, but not degradati

106 valuate the cooperative interactions between TGF-alpha and signature mutations in pancreatic tumor ge

107 Although both TGF-alpha and EGF were able to induce EGFR internalizati

108 upregulated and 3 downregulated DEGs in both TGF-alpha- and insulin-stimulated HKs.

109 3) changed the cellular localization of both TGF-alpha and EGFR and inhibited ligand-dependent phosph

110 d AP2 occur downstream of EGFR activation by TGF-alpha and are required for TGF-alpha self-induction.

111 SH, activation of the EGF receptor (EGFR) by TGF-alpha is required for the development of parathyroid

112 P and subsequent mucin production induced by TGF-alpha.

113 sible for most of the total mucin induced by TGF-alpha.

114 t astrocytes, an effect that was mediated by TGF-alpha.

115 tivation by TGF-beta and activin, but not by TGF-alpha.

116 also increased by IGF-1/glucose, but not by TGF-alpha/EGF, despite upstream PKB activation.

117 rowth factor (TGF)-beta, but not promoted by TGF-alpha.

118 ssed by OCT-based indentation was reduced by TGF-alpha at both left and right lateral locations (p <

119 ional organ bath studies was also reduced by TGF-alpha overexpression (p < 0.01).

120 In NCI-H292 cells, TGF-alpha stimulation induced two phases of EGFR phospho

121 In NHBE cells, TGF-alpha-induced EGFR activation did not lead to signif

122 In knock-out cells, TGF-alpha, a ligand for EGFR, was not released by stretc

123 toplasmic tail of TGF-alpha, thereby coating TGF-alpha-containing exocytic vesicles and directing the

124 through the integrated activity of a coupled TGF-alpha-IL-1alpha/beta-IL-1ra autocrine cascade.

125 isoform of TGF-alpha and increased cytosolic TGF-alpha immunoreactivity.

126 of matrix metalloproteinase (MMP) decreased TGF-alpha secretion and TxB-induced EGFR and ERK activat

127 e of tubulogenic growth factors such as EGF, TGF-alpha, IGF-I, and hepatocyte growth factor.

128 on for mammalian EGFR ligands including EGF, TGF-alpha (TGFalpha), amphiregulin (AREG), heparin-bindi

129 ated EGF-R in EGF/TGF-alpha-positive and EGF/TGF-alpha-negative lesions from mice treated with PKI 16

130 ed down-regulation of activated EGF-R in EGF/TGF-alpha-positive and EGF/TGF-alpha-negative lesions fr

131 ated endothelial cells was found only in EGF/TGF-alpha-positive tumors.

132 d identified the common genes and eliminated TGF-alpha- or insulin-specific genes.

133 s ERK/MAPK signaling activated by endogenous TGF-alpha as one of the mechanistic features controlling

134 431 cells, which provide a model of enhanced TGF-alpha and TGF-alpha self-induction, mutating the cor

135 Here we examined TGF-alpha processing in a physiologically relevant cell

136 Exogenous TGF-alpha can either enhance or diminish apoptosis in ad

137 imulated EGFR phosphorylation, and exogenous TGF-alpha mimicked the effects of Ras-CM to increase rad

138 activity induced by endogenous or exogenous TGF-alpha.

139 rmal growth factor (EGF)-like growth factors TGF-alpha, heparin binding-EGF, amphiregulin, and EGF re

140 ng mobilization of 2 crucial growth factors, TGF-alpha and amphiregulin.

141 kidney cells; however, membrane staining for TGF alpha is restored on silencing expression of this mu

142 loss-of-function mutations in the genes for TGF-alpha and EGFR.

143 gulation, generating a feed-forward loop for TGF-alpha activation of its receptor, EGFR receptor (EGF

144 tigotes present two classes of receptors for TGF-alpha with different binding affinities.

145 activation by TGF-alpha and are required for TGF-alpha self-induction.

146 Here, we report a new role for TGF-alpha in modulating the direct cellular proliferatio

147 ll interfering RNA prevented ROS generation, TGF-alpha release, and mucin expression by these stimuli

148 oxidase 1-->reactive oxygen species-->TACE-->TGF-alpha-->EGFR phosphorylation pathway.

149 most resistant to calcitriol therapy, higher TGF-alpha activation of the EGFR was associated with an

150 However, TGF-alpha was determined to be a key factor for promotin

151 ion, mutating the core AP2 site of the human TGF-alpha promoter markedly impaired promoter activity i

152 (125)I-TGF-alpha binding was competed by an excess of cold epid

153 d the structures of human IDE-IGF-II and IDE-TGF-alpha at 2.3 A and IDE-amylin at 2.9 A.

154 cell-derived growth factors (IGF-I, IGF-II, TGF-alpha and TGF-beta) and angiogenic factors (VEGF and

155 identify the cleavage sites of human IGF-II, TGF-alpha, amylin, reduced amylin, and amyloid-beta by h

156 Additional studies implicated TGF-alpha as the active EGFR ligand cleaved by TACE duri

157 us AP2 DNA sequence preceded the increase in TGF-alpha induced by high dietary phosphate.

158 death regulatory mechanisms remain intact in TGF-alpha epithelia.

159 ese findings and the requirement for TACE in TGF-alpha shedding is proposed.

160 Increased TGF-alpha/EGFR activation induced the synthesis of liver

161 factor independence was due to the increased TGF-alpha expression and EGFR activation of these cells

162 This increased TGF-alpha expression in quiescent HCT116 cells was assoc

163 ed that EGFR activation was due to increased TGF-alpha expression.

164 human airway epithelial cells HNE increases TGF-alpha release, EGFR phosphorylation, and MUC5AC muci

165 ine activation of EGFR and protein A-induced TGF-alpha was neither required nor sufficient to activat

166 ATP-induced TGF-alpha shedding required calcium and was independent

167 Moreover, ATP-induced TGF-alpha shedding was completely inhibited by scavenger

168 ACE inhibited PMA-, PA sup-, and LPS-induced TGF-alpha shedding, EGFR phosphorylation, and mucin prod

169 TGF-alpha, but not the production of latent TGF-alpha, whereas engineered overexpression of RHBDF1 m

170 lacking TACE activity shed dramatically less TGF-alpha as compared with wild-type cultures and that T

171 E maturation and shedding of the EGFR ligand TGF-alpha in Rhbdf2-deficient cells.

172 upts GRP-stimulated secretion of EGFR ligand TGF-alpha, but not the production of latent TGF-alpha, w

173 ow that EGFR activation by its potent ligand TGF-alpha induces reactivation of EGFR via binding of en

174 F-alpha-neutralizing Ab, implicating ligand (TGF-alpha)-dependent EGFR phosphorylation in mucin produ

175 es, stimulation with the potent EGFR ligand, TGF-alpha, yielded a significant downregulation of compl

176 dition, mutant HER2 induced the EGFR ligands TGF-alpha and amphiregulin at the mRNA and protein level

177 Like TGF-alpha, NRG-1 caused a significant weight loss.

178 and TACE cDNAs increased shedding of mature TGF-alpha with concomitant conversion of cell-associated

179 roximal (C-terminal) sites to release mature TGF-alpha.

180 of TGF-alpha, with release of soluble mature TGF-alpha in various epithelial tissues.

181 t that ILK is involved in the PAR-2-mediated TGF-alpha via an HIF-alpha-dependent pathway.

182 Double transgenic mice, TGF-alpha and Bcl-2 single transgenics, and wild type re

183 GF-alpha compared to bigenic MMTV-DNIIR/MMTV-TGF-alpha was the marked suppression of tumor invasion b

184 difference in mammary tumors arising in MMTV-TGF-alpha compared to bigenic MMTV-DNIIR/MMTV-TGF-alpha

185 re similar to those expressing only the MMTV-TGF-alpha transgene (<10 months median latency).

186 ation-defective (G2A) NKD2, neither NKD2 nor TGF alpha appears at the basolateral plasma membrane of

187 cient to attenuate DCA-induced AREG, but not TGF-alpha shedding.

188 TACE and AREG, but not TGF-alpha, were overexpressed in both colorectal cancer

189 Interestingly, both NRL-TGF-alpha/PRL and NRL-PRL males demonstrated increased d

190 Binary Tet-On transgenic Krt12(rtTA)/tet-O-TGF-alpha mice were subjected to doxycycline (Dox) induc

191 ope suggests that mAb 13A9 mediates observed TGF-alpha blocking effects through conformational pertur

192 Processing and cell-surface delivery of TGF alpha are accelerated in NKD2-overexpressing Madin-D

193 D2, i.e., myristoylation-dependent escort of TGF alpha to the basolateral plasma membrane of polarize

194 al sorting motifs in the cytoplasmic tail of TGF alpha.

195 sults identify an EGFR-independent action of TGF-alpha, in which it protects Naked2 from proteasomal

196 Conversely, excessive activities of TGF-alpha/EGFR result in hairless phenotypes and skin ca

197 Upon binding of TGF-alpha to amastigotes, the ligand is internalized, in

198 Blockade of TGF-alpha or EGFR, abrogated Stat5 activation.

199 14D that is required for ADAM17 cleavage of TGF-alpha, heparin-binding EGF, and amphiregulin.

200 HB-EGF and NRG but only moderate cleavage of TGF-alpha.

201 sis and counteracted the enhancing effect of TGF-alpha.

202 PRAS40) as the unique downstream effector of TGF-alpha but not EGF signaling via threonine 308-phosph

203 Here we examined the effects of TGF-alpha overexpression on adult ocular surface homeost

204 d ligand, and EGFRvIII-induced expression of TGF-alpha and HB-EGF suggests that EGFRvIII plays a role

205 hyperparathyroidism, enhanced expression of TGF-alpha in the parathyroid leads to its own upregulati

206 ytoplasmic tail of a Golgi-processed form of TGF-alpha and that TGF-alpha is not detected at the baso

207 re proper delivery, tethering, and fusion of TGF-alpha-containing vesicles to a distinct region at th

208 ctivator protein 2alpha (AP2), an inducer of TGF-alpha gene transcription, in the upregulation of par

209 cancer progression through the induction of TGF-alpha expression by ILK/HIFs-alpha, as well as throu

210 Inhibition of TGF-alpha receptor suppressed the G1-induced increase in

211 deed, in A431 cells, erlotinib inhibition of TGF-alpha self-induction caused parallel reductions in A

212 ng erlotinib, a highly specific inhibitor of TGF-alpha/EGFR-driven signals, reduced AP2 expression do

213 d by addition of pharmacologic inhibitors of TGF-alpha signaling or neutralizing antibodies to macrop

214 We also show that an acute injection of TGF-alpha inhibits activity (ICV, 5 microl, 3.3 microM o

215 uction in the 16-kDa cell surface isoform of TGF-alpha and increased cytosolic TGF-alpha immunoreacti

216 116b subcompartment showed similar levels of TGF-alpha expression as HCT116 when cells were in expone

217 IF inhibitor, resulted in depleted levels of TGF-alpha protein.

218 yte (TAMH) cells, derived from the livers of TGF-alpha transgenic mice.

219 were found to cooperate was by modulation of TGF-alpha and TGF-beta signaling.

220 Overexpression of TGF-alpha in the corneal epithelium induces changes in a

221 ies have demonstrated that overexpression of TGF-alpha in the developing eye leads to anterior segmen

222 d2, and we have shown that overexpression of TGF-alpha reduces binding of AO7 to Naked2.

223 Overexpression of TGF-alpha stabilizes Naked2 protein in an EGF receptor (

224 In Menetrier disease, overexpression of TGF-alpha, a ligand for the RTK EGFR, results in selecti

225 me (TACE) is reported to cleave precursor of TGF-alpha, with release of soluble mature TGF-alpha in v

226 ls, the HCT116 cells showed up-regulation of TGF-alpha expression during growth arrest as a result of

227 mammary tumor progression via regulation of TGF-alpha, MSP, and HGF signaling pathways.

228 ways by facilitating cleavage and release of TGF-alpha and amphiregulin in HNSCC.

229 SCC are mediated by extracellular release of TGF-alpha and require the activation of an EGFR-dependen

230 by p38 MAP kinase results in the release of TGF-alpha family ligands, which activate EGF receptor si

231 mulation resulting from increased release of TGF-alpha family ligands.

232 adhesion molecule E-cadherin and release of TGF-alpha, which was accompanied by transactivation of t

233 surface, resulting in increased secretion of TGF-alpha, amphiregulin, and heregulin.

234 RHBDF1 markedly accelerates the secretion of TGF-alpha.

235 thesized that TACE increases the shedding of TGF-alpha, resulting in EGFR phosphorylation and inducin

236 interaction between the cytoplasmic tail of TGF-alpha and Naked2 is necessary and sufficient for thi

237 ked1, interacts with the cytoplasmic tail of TGF-alpha, thereby coating TGF-alpha-containing exocytic

238 hable intracellular signaling networks, only TGF-alpha stimulation causes exosome-mediated secretion.

239 e (DN) mutant overexpression blocks not only TGF-alpha- but also hypoxia- and H2O2-induced exosome se

240 In hepatocellular carcinomas of TGF-beta1 or TGF-alpha/c-myc transgenic mice, we observed constitutiv

241 s its signaling cascade elicited upon EGF or TGF-alpha stimulation.

242 BMP-4, but not EGF or TGF-alpha, accelerates opening of the eyelid explants is

243 ptor downregulation induced by either EGF or TGF-alpha.

244 o doxycycline (Dox) induction to overexpress TGF-alpha in the corneal epithelium.

245 d that double-transgenic mice overexpressing TGF-alpha manifested peripheral anterior synechiae.

246 ity of the hyperplasia driven by parathyroid TGF-alpha self-upregulation in secondary hyperparathyroi

247 cription, in the upregulation of parathyroid TGF-alpha in secondary hyperparathyroidism.

248 h-phosphate diets, inhibition of parathyroid TGF-alpha self-induction using erlotinib, a highly speci

249 ib prevented the upregulation of parathyroid TGF-alpha, the progression of growth, and the reduction

250 ves peptides and a soluble form of precursor TGF-alpha (proTGFecto) at the N-terminal site but not th

251 forming growth factor-alpha (TGF-alpha), pro-TGF-alpha.

252 oncomitant conversion of cell-associated pro-TGF-alpha to a processed form.

253 Purified TACE accurately cleaved pro-TGF-alpha in vitro at the N-terminal site and also cleav

254 F-alpha-converting enzyme (TACE) cleaves pro-TGF-alpha into soluble TGF-alpha and can be activated by

255 size that Duox1 activates TACE, cleaving pro-TGF-alpha into soluble TGF-alpha, resulting in mucin exp

256 site and also cleaved a soluble form of pro-TGF-alpha containing only the ectodomain at the C-termin

257 ROS generation, resulting in cleavage of pro-TGF-alpha, EGFR activation, and MUC5AC mucin expression

258 y when combined with substitution of the pro-TGF-alpha P2-P2' sequence, markedly increased BTC sheddi

259 Conversely, substitution of the pro-TGF-alpha stalk or lengthening of the pro-BTC stalk, esp

260 juxtamembrane stalk or truncation of the pro-TGF-alpha stalk to match the pro-BTC length reduced TGF-

261 ction of TACE-deficient fibroblasts with pro-TGF-alpha and TACE cDNAs increased shedding of mature TG

262 rine cascade involving the pro-proliferative TGF-alpha and IL-1 receptor antagonist (IL-1ra) ligands

263 atment of A17(DeltaKC) mice with recombinant TGF-alpha significantly improved TGM activity and decrea

264 ha stalk to match the pro-BTC length reduced TGF-alpha shedding from transfected cells to background

265 ution of the pro-BTC P2-P2' sequence reduced TGF-alpha shedding less dramatically.

266 Hydrogen peroxide restored TGF-alpha shedding after calcium chelation.

267 me (TACE) cleaves pro-TGF-alpha into soluble TGF-alpha and can be activated by ROS.

268 es TACE, cleaving pro-TGF-alpha into soluble TGF-alpha, resulting in mucin expression.

269 These stimuli induced release of soluble TGF-alpha, EGFR phosphorylation, and MUC5AC expression,

270 or alpha (proTGF-alpha) and releases soluble TGF-alpha as a ligand that binds and activates epidermal

271 We report that ATP stimulates TGF-alpha proteolysis with concomitant EGFR activation a

272 3 channel activity, which in turn stimulates TGF-alpha release.

273 servation, we found the effects of long-term TGF-alpha infusion (ICV, 12 microl/day, 3.3 microM) to b

274 50-fold more efficiently than the C-terminal TGF-alpha peptide.

275 binant TACE cleaves TNF-alpha and N-terminal TGF-alpha peptides 50-fold more efficiently than the C-t

276 as compared with wild-type cultures and that TGF-alpha cleavage was partially restored by infection o

277 a Golgi-processed form of TGF-alpha and that TGF-alpha is not detected at the basolateral surface of

278 These findings provide evidence that TGF-alpha up-regulates TLR expression and function, augm

279 We found that TGF-alpha, a growth and differentiation factor that is p

280 These results suggest that TGF-alpha/EGFR-mediated autocrine growth of transformed

281 sment, provides new evidence suggesting that TGF-alpha overexpression produces impairment in diaphrag

282 pression and transcriptional activity at the TGF-alpha promoter determine the severity of the hyperpl

283 an intracrine regulatory loop connecting the TGF-alpha/EGFR/RhoA-c-Jun and JNK-c-Jun-AP-1 pathways in

284 osophila Egfr has four ligands: three of the TGF-alpha-type and a single neuregulin-like called vein

285 After internalization of the TGF-alpha/EGFR complex, EGFR recycles back to the plasma

286 In addition to TGF-alpha release, GRP induced amphiregulin, but not EGF

287 Neutralizing antibodies to TGF-alpha and to BDNF abrogated the ability of EBD-condi

288 Furthermore, exposure of macrophages to TGF-alpha induced increased amastigote proliferation.

289 In contrast, when the WAP-TGF-alpha transgene was carried on the FVB/N strain, con

290 nd -2 in a glucose-dependent manner, whereas TGF-alpha/EGF did not.

291 ons predict that when EGFR is activated with TGF-alpha, receptor activation is biased toward the cell

292 ation can be overcome by treating cells with TGF-alpha because TGF-alpha stimulates EGFR endocytosis,

293 ant channels, forms a signaling complex with TGF-alpha/EGFR.

294 roid AP2 expression strongly correlated with TGF-alpha levels and with the rate of parathyroid growth

295 hermore we stimulated HKs independently with TGF-alpha or insulin and identified the common genes and

296 growth factor receptor tyrosine kinase with TGF-alpha induced phosphorylation of the MUC1 cytoplasmi

297 EGFRs stimulated with TGF-alpha recycled back to the plasma membrane, where th

298 Thus, stimulation with TGF-alpha prolongs EGFR signaling compared with EGF.

299 s, proinflammatory cytokines synergized with TGF-alpha to induce GM-CSF expression.

300 ctivated EGFR after stable transfection with TGF-alpha cDNA.