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1 f Ras in response to constitutively produced amphiregulin.
2 n of 2 crucial growth factors, TGF-alpha and amphiregulin.
3 oter and thereby suppressed the induction of amphiregulin.
4 f the growth factors regenerating gene I and amphiregulin.
5 perplasia by the cAMP-dependent induction of amphiregulin.
6 he SCID mouse is mediated, in large part, by amphiregulin.
7 the mechanism by which tobacco smoke induces amphiregulin.
8 , and AREG, which codes for the EGFR ligand, amphiregulin.
9 e H55a#1 contained a library insert encoding amphiregulin.
10 with a >/= 3 h delay relative to HB-EGF and amphiregulin.
11 sue repair, including IL-7, Ccl2, Ptgs2, and Amphiregulin.
12 2 expression of IL-5 and IL-13 and increased amphiregulin.
13 avage of TGF-alpha, heparin-binding EGF, and amphiregulin.
14 ed by administration of the lung ILC product amphiregulin.
15 n the shedding rate of any ligand, including amphiregulin.
16 HT of human stroke are described, including amphiregulin, a growth factor that regulates matrix meta
17 roteinase (ADAM) 17) to cleave transmembrane amphiregulin, a ligand for the epidermal growth factor r
19 (H)2), but not other T cell subsets, express amphiregulin, a member of the epidermal growth factor (E
21 models of lung tumors in mice, we found that amphiregulin, a member of the epidermal growth factor fa
24 yrosine kinase or a neutralizing antibody to amphiregulin abrogated the increase in DNA synthesis med
25 c hyperplasia and suggest that inhibition of amphiregulin activity could be an efficacious therapeuti
26 strogen growth factor receptor (EGFR) ligand amphiregulin acts as an important stage-specific effecto
27 ralizing antibody to EGFR, or an antibody to amphiregulin, an EGFR ligand, also blocked tobacco smoke
32 vealed that PTH stimulates the expression of amphiregulin, an epidermal growth factor (EGF)-like liga
33 ed transmembrane molecule: the precursor for amphiregulin, an epidermal growth factor-related molecul
34 fter stimulation with heparin-binding EGF or amphiregulin and alters the rate of recruitment of the a
35 dermal growth factor receptor (Egfr) ligands amphiregulin and beta-cellulin, as well as Egfr and phos
38 ription of HB-EGF (epidermal growth factor), amphiregulin and epiregulin, resulting in autocrine acti
39 bited with neutralization antibodies against amphiregulin and HB-EGF, the heparin-binding growth fact
40 NA levels of two other EGF receptor ligands, amphiregulin and heparin binding-EGF, however, in the sk
41 CE-deficient cells increased the shedding of amphiregulin and heparin-binding EGF (HB-EGF) proteins.
43 show that during infection, the EGFR ligands amphiregulin and heparin-binding EGF-like growth factor
45 igh gene expression levels of epiregulin and amphiregulin and patients with wild-type K-ras are more
46 ss both transforming growth factor alpha and amphiregulin and require autocrine signaling through the
50 m by which TS activated EGFR, the release of amphiregulin and transforming growth factor alpha, two l
53 the epidermal growth factor receptor ligand amphiregulin and tumor necrosis factor receptor I (TNFRI
54 release of the endogenous ADAM17 substrates, amphiregulin and tumor necrosis factor-alpha, metallopro
55 evels of two ectopic EGFR ligands (HBEGF and amphiregulin) and the FGFR2(IIIb) receptor ligand KGF, f
57 recognized HB-EGF as well as the EGFR ligand amphiregulin, and bound specifically to human HB-EGF, bu
58 owth factors TGF-alpha, heparin binding-EGF, amphiregulin, and EGF receptor tyrosine phosphorylation
59 l into two major groups as follows: (i) EGF, amphiregulin, and EPR; and (ii) betacellulin, TGFalpha,
60 ression of transforming growth factor-alpha, amphiregulin, and gastrin; and activation of extracellul
61 h factor vascular endothelial growth factor, amphiregulin, and glucose metabolism-involved gene insul
62 tor (EGF), transforming growth factor alpha, amphiregulin, and heparin-binding EGF in regenerating li
63 piregulin, transforming growth factor alpha, amphiregulin, and heparin-binding EGF-like growth factor
64 r, Wnt, Hh, transforming growth factor beta, amphiregulin, and hepatocyte growth factor) to their res
66 tor receptors (eg, hepatocyte growth factor, amphiregulin, and insulin-like growth factor 1 receptor)
67 genes revealed that caveolin 1, caveolin 2, amphiregulin, and melanoma growth stimulatory activity a
68 s effect allows plasma components, including amphiregulin, and other mitogens to enter the CSF and pr
70 tor, AG1478, 2) neutralizing HB-EGF, but not amphiregulin, antibodies, heparin, or CM197, and 3) phar
72 nd we also demonstrated enhanced shedding of amphiregulin (AR) and heparin-binding (HB)-EGF upon rest
73 ic polypeptide-expressing metaplasia (SPEM), amphiregulin (AR) and transforming growth factor-alpha-d
83 pidermal growth factor (EGF) receptor ligand amphiregulin (AR) is reported to be an 84-amino acid res
85 a saline extract of tobacco smoke stimulated amphiregulin (AR) transcription resulting in increased a
90 e A pathway, which induced the expression of amphiregulin (AR), an epidermal growth factor family mem
91 in-binding epidermal growth factor (EGF) and amphiregulin (AR), and activation of the EGF receptor an
92 protein, and mRNA transcripts for TGFalpha, amphiregulin (AR), and heparin-binding EGF-like growth f
93 es EGFR ligands heparin-binding (HB)-EGF and amphiregulin (AR), and reduces betacellulin mRNA levels.
94 ting hormone (FSH) and the EGF-like peptide, amphiregulin (AR), are potent inducers of maturation in
95 ming growth factor (TGF)-alpha, but not with amphiregulin (AR), betacellulin (BTC) or epiregulin (EPR
96 actor (TGF)-alpha, heprin-ding (HB)-EGF, and amphiregulin (AR), have been shown to stimulate events a
97 pidermal growth factor (EGF) family hormones amphiregulin (AR), transforming growth factor-alpha (TGF
98 epidermal growth factor-like growth factor, amphiregulin (AR), which was not expressed by untreated
104 sforming growth factor alpha (TGF alpha) and amphiregulin are delivered to the basolateral surface of
105 gh levels of the EGFR ligands epiregulin and amphiregulin are more likely to have disease control wit
106 sine kinase (DDR1) and the ErbB1 receptor of amphiregulin are, for example, required for ductal branc
107 genes repressed by BRCA1, we have identified amphiregulin (AREG) and early growth response-1 (EGR1).
108 dermal growth factor receptor (EGFR) ligands amphiregulin (AREG) and epiregulin (EREG), and systemic
110 ving ectodomain shedding of the EGFR ligands amphiregulin (AREG) and TGF-alpha, which rely upon the c
111 is study evaluated the diagnostic utility of amphiregulin (AREG) as a pancreatic cyst fluid biomarker
112 idermal growth factor receptor (EGFR) ligand Amphiregulin (AREG) by co-activating the transcription f
113 ermal growth factor (EGF)-like growth factor amphiregulin (AREG) engages EGFR on Treg cells and, in d
114 se fragment complementation imaging studies, amphiregulin (AREG) functioned as a partial agonist, ind
116 here is a large body of literature regarding amphiregulin (AREG) in human cancer, most knowledge focu
117 with IL-33, expression of the growth factor amphiregulin (AREG) is a dominant functional signature o
119 rian and lung cancer patients and found that amphiregulin (AREG) is the most abundant and generalized
120 how that silencing of the EGF-related factor amphiregulin (AREG) markedly inhibits the expansion of h
121 ession of EGFR ligands epiregulin (EREG) and amphiregulin (AREG) may correlate with EGFR-targeted the
122 epidermal growth factor (EGF)-like molecule Amphiregulin (AREG) might be a critical component of typ
124 e epidermal growth factor (EGF)-like protein amphiregulin (AREG) was highly expressed in ExeR cells b
125 owth factor 7, hepatocyte growth factor, and amphiregulin (AREG) were elevated in the extracellular e
126 study shows that AGR2 induces expression of amphiregulin (AREG), a growth promoting EGFR ligand.
128 K by derepressing miR-200 targets, including amphiregulin (AREG), betacellulin (BTC), and the transcr
129 th factor receptor (EGFR) pathway, including amphiregulin (AREG), epiregulin (EREG), and ectodomain c
130 ubstrates TNF-alpha, TNFR1-alpha, TGF-alpha, amphiregulin (AREG), HB-EGF and IL-6Ralpha, from IGROV1-
131 factor (EGF)-like growth factors, including Amphiregulin (AREG), heparin-binding EGF (HB-EGF), and t
132 ligands including EGF, TGF-alpha (TGFalpha), amphiregulin (AREG), heparin-binding EGF-like growth fac
133 -mediated silencing of one of these ligands, amphiregulin (AREG), results in keratinocyte growth arre
134 alpha to regulate directly the expression of amphiregulin (Areg), the progesterone receptor (Pgr) and
135 evealed that the ADAM17 proteolytic targets, amphiregulin (AREG), transforming growth factor alpha (T
136 ratinocytes (KCs) is strongly dependent upon amphiregulin (AREG), whereas blockade of heparin-binding
137 growth factor receptor (EGFR) and its ligand amphiregulin (AREG), which generally must be cleaved fro
140 elated evidence led to the identification of amphiregulin as a major autocrine factor for keratinocyt
142 s a cause of sustained expression of uterine amphiregulin before the initiation of implantation.
144 n addition to TGF-alpha release, GRP induced amphiregulin, but not EGF, secretion into HNSCC cell cul
148 combination of F115 and Y123 determined the amphiregulin cross-reactivity and that F115 accounted fo
149 that the addition of recombinant epiregulin, amphiregulin, CX3CL1, and interleukin-11 significantly e
151 e epithelial cell proliferation, and lack of amphiregulin delayed expulsion of the nematode Trichuris
152 am as well as downstream of ErbB1 to promote amphiregulin-dependent autocrine stimulation of NHKs and
153 pressor gene, a transcriptional activator of amphiregulin, did not parallel amphiregulin transcript l
155 ding of transforming growth factor alpha and amphiregulin does not require ADAM17, even though ADAM17
156 iated proteins appear to act as cofactors in amphiregulin-driven mitogenesis mediated by the epiderma
159 signaling cascade of GRP-Src-PI3-K-PDK1-TACE-amphiregulin-EGFR with multiple points of interaction, t
161 bFGF, IL-8, and ANGPTL-2), as well as ErbB (amphiregulin, epiregulin, and neuregulins) and TGF-ss, w
162 pha, heparin-binding EGF-like growth factor, amphiregulin, epiregulin, betacellulin, or heregulin bet
163 echanisms: protection from fatal immunity by amphiregulin expression and augmentation of antileukemic
165 naling via IL-33 induces type 2 cytokine and amphiregulin expression, and increases ILC2 migration.
166 or-beta signaling, the extracellular matrix, amphiregulin expression, and the growth hormone/insulin-
169 lar smooth muscle cells, particularly COX-2, amphiregulin, follistatin, inhibin-beta-A, and CYR61.
170 mutant mice suggests a compensatory role of amphiregulin for uterine loss of HB-EGF, preventing comp
171 th factor receptor (EGFR) and of its ligand, amphiregulin, for the formation of a signaling complex b
172 emonstrate that PTH increases the release of amphiregulin from osteoblastic cells, which acts on the
178 nds including epidermal growth factor (EGF), amphiregulin, heparin-binding EGF and beta-cellulin.
179 In addition, three ErbB1 ligand transcripts (amphiregulin, heparin-binding epidermal growth factor-li
180 as well as transforming growth factor-alpha, amphiregulin, heparin-binding epidermal growth factor-li
181 ) ligands (transforming growth factor-alpha, amphiregulin, heregulin, heparin binding EGF-like ligand
182 stromal lymphopoietin, and the growth factor amphiregulin in a human bronchial epithelial cell line.
183 In this study, we investigated the role of amphiregulin in breast cancer cell proliferation using h
185 ional psoriatic epidermis, the importance of amphiregulin in hyperproliferative skin diseases has bee
186 binding EGF-like growth factor (HB-EGF); and amphiregulin in NHBECs, and when administered exogenousl
187 r, these data indicate an important role for amphiregulin in psoriatic hyperplasia and suggest that i
191 not transforming growth factor (TGF)alpha or amphiregulin, in young adult mouse colon cells and ADAM1
192 e secretion of EGF family ligands, including amphiregulin, independent of metalloprotease a disintegr
193 terminal differentiation in adult breast and amphiregulin is critical to normal embryonic breast deve
196 trate that selective Treg cell deficiency in amphiregulin leads to severe acute lung damage and decre
198 tion, resulting in impaired IL-5, IL-13, and amphiregulin levels, despite undiminished numbers of Th2
199 er EGFR ligands EGF, heparin-binding EGF, or amphiregulin, mediates SP-induced EGFR transactivation.
200 actor, transforming growth factor-alpha, and amphiregulin mRNA and protein in lesional psoriasis comp
202 9, an EP2-specific agonist, strongly induced amphiregulin mRNA levels in a protein kinase A-dependent
204 genomic responses, since both calcitonin and amphiregulin mRNAs were increased after progesterone tre
207 induces expression of either the EGFR ligand amphiregulin or the transcription factor CDX2, only the
208 ncentration that neutralized the function of amphiregulin, or antibodies against TGFalpha or HB-EGF a
209 tivity, high levels of ERBB2 (P = 0.036) and amphiregulin (P = 0.026) predicted sensitivity to lapati
211 t the cytoplasmic carboxy-terminal domain of amphiregulin plays an important role in regulating autoc
213 h factor receptor (EGFR) phosphorylation and amphiregulin production were examined by Western blot an
214 s showed that IGF-1 transactivation required amphiregulin production, whereas LPA was dependent on mu
216 The WT1(-KTS) isoform binds directly to the amphiregulin promoter, resulting in potent transcription
219 dermal growth factor and 10-fold increase in amphiregulin, respectively) in HELUs compared with TDLUs
221 by the epidermal growth factor receptor, but amphiregulin's immunolocalization to keratinocyte nuclei
223 0 and ADAM17, reduces in vitro HER-2/neu and amphiregulin shedding, confirming that it interferes wit
226 cific pattern of WT1 itself, and recombinant Amphiregulin stimulates epithelial branching in organ cu
227 e observation of normal induction of uterine amphiregulin surrounding the blastocyst at the time of a
228 ytes secrete soluble EGFR ligands (including amphiregulin) that are processed from membrane-bound pro
231 activator of amphiregulin, did not parallel amphiregulin transcript levels, suggesting that another
232 SUM-149PT and H55a#1 cells overexpressed amphiregulin transcripts, and secreted moderate EGF-like
233 PRIP-deficient glands expressed increased amphiregulin, transforming growth factor-alpha, and beta
236 lonal antibody capable of neutralizing human amphiregulin was examined for anti-proliferative effects
237 nsforming growth factor-alpha (TGFalpha), or amphiregulin we have shown that only the anti-TGFalpha a
238 GF-alpha), heparin binding-EGF (HB-EGF), and amphiregulin were analyzed for their ability to mediate
240 (EGF), transforming growth factor alpha, and amphiregulin were used to identify roles for these EGF r
241 uscle Treg cells expressed the growth factor Amphiregulin, which acted directly on muscle satellite c
242 EGF receptor stimulation by TGF-alpha and/or amphiregulin, which are known to be elevated in psoriati
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