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1 ed by administration of the lung ILC product amphiregulin.
2 n the shedding rate of any ligand, including amphiregulin.
3 f Ras in response to constitutively produced amphiregulin.
4 n of 2 crucial growth factors, TGF-alpha and amphiregulin.
5 ILC2 subset is enriched in cells expressing amphiregulin.
6 oter and thereby suppressed the induction of amphiregulin.
7 f the growth factors regenerating gene I and amphiregulin.
8 perplasia by the cAMP-dependent induction of amphiregulin.
9 he SCID mouse is mediated, in large part, by amphiregulin.
10 th proximal tubule cell-specific knockout of amphiregulin.
11 the mechanism by which tobacco smoke induces amphiregulin.
12 e H55a#1 contained a library insert encoding amphiregulin.
13 with a >/= 3 h delay relative to HB-EGF and amphiregulin.
14 and their tumorigenic potential by secreting amphiregulin.
15 n recipient Foxp3(+) cells were deficient in amphiregulin.
16 AFs through an autocrine process mediated by amphiregulin.
17 sue repair, including IL-7, Ccl2, Ptgs2, and Amphiregulin.
18 , and AREG, which codes for the EGFR ligand, amphiregulin.
19 2 expression of IL-5 and IL-13 and increased amphiregulin.
20 avage of TGF-alpha, heparin-binding EGF, and amphiregulin.
21 HT of human stroke are described, including amphiregulin, a growth factor that regulates matrix meta
22 roteinase (ADAM) 17) to cleave transmembrane amphiregulin, a ligand for the epidermal growth factor r
25 (H)2), but not other T cell subsets, express amphiregulin, a member of the epidermal growth factor (E
27 models of lung tumors in mice, we found that amphiregulin, a member of the epidermal growth factor fa
30 yrosine kinase or a neutralizing antibody to amphiregulin abrogated the increase in DNA synthesis med
31 c hyperplasia and suggest that inhibition of amphiregulin activity could be an efficacious therapeuti
32 strogen growth factor receptor (EGFR) ligand amphiregulin acts as an important stage-specific effecto
33 in ADAM17 hypomorphic mice; injected soluble amphiregulin also reversed the corresponding protective
34 lling and is inhibited by antibodies against amphiregulin, an EGFR ligand concentrated on these vesic
35 ralizing antibody to EGFR, or an antibody to amphiregulin, an EGFR ligand, also blocked tobacco smoke
40 vealed that PTH stimulates the expression of amphiregulin, an epidermal growth factor (EGF)-like liga
41 ed transmembrane molecule: the precursor for amphiregulin, an epidermal growth factor-related molecul
42 fter stimulation with heparin-binding EGF or amphiregulin and alters the rate of recruitment of the a
43 dermal growth factor receptor (Egfr) ligands amphiregulin and beta-cellulin, as well as Egfr and phos
46 ription of HB-EGF (epidermal growth factor), amphiregulin and epiregulin, resulting in autocrine acti
47 bited with neutralization antibodies against amphiregulin and HB-EGF, the heparin-binding growth fact
48 NA levels of two other EGF receptor ligands, amphiregulin and heparin binding-EGF, however, in the sk
49 CE-deficient cells increased the shedding of amphiregulin and heparin-binding EGF (HB-EGF) proteins.
51 show that during infection, the EGFR ligands amphiregulin and heparin-binding EGF-like growth factor
54 igh gene expression levels of epiregulin and amphiregulin and patients with wild-type K-ras are more
55 ss both transforming growth factor alpha and amphiregulin and require autocrine signaling through the
59 m by which TS activated EGFR, the release of amphiregulin and transforming growth factor alpha, two l
62 the epidermal growth factor receptor ligand amphiregulin and tumor necrosis factor receptor I (TNFRI
63 release of the endogenous ADAM17 substrates, amphiregulin and tumor necrosis factor-alpha, metallopro
64 pigen, TGFalpha), which also require soluble amphiregulin and YAP1 to induce sustained EGFR activatio
65 evels of two ectopic EGFR ligands (HBEGF and amphiregulin) and the FGFR2(IIIb) receptor ligand KGF, f
67 recognized HB-EGF as well as the EGFR ligand amphiregulin, and bound specifically to human HB-EGF, bu
68 owth factors TGF-alpha, heparin binding-EGF, amphiregulin, and EGF receptor tyrosine phosphorylation
69 l into two major groups as follows: (i) EGF, amphiregulin, and EPR; and (ii) betacellulin, TGFalpha,
70 ression of transforming growth factor-alpha, amphiregulin, and gastrin; and activation of extracellul
71 h factor vascular endothelial growth factor, amphiregulin, and glucose metabolism-involved gene insul
72 tor (EGF), transforming growth factor alpha, amphiregulin, and heparin-binding EGF in regenerating li
73 piregulin, transforming growth factor alpha, amphiregulin, and heparin-binding EGF-like growth factor
74 r, Wnt, Hh, transforming growth factor beta, amphiregulin, and hepatocyte growth factor) to their res
76 tor receptors (eg, hepatocyte growth factor, amphiregulin, and insulin-like growth factor 1 receptor)
77 genes revealed that caveolin 1, caveolin 2, amphiregulin, and melanoma growth stimulatory activity a
78 s effect allows plasma components, including amphiregulin, and other mitogens to enter the CSF and pr
80 B1 [transforming growth factor-beta1], AREG [amphiregulin], and HGF [hepatocyte growth factor]) coupl
81 tor, AG1478, 2) neutralizing HB-EGF, but not amphiregulin, antibodies, heparin, or CM197, and 3) phar
83 nd we also demonstrated enhanced shedding of amphiregulin (AR) and heparin-binding (HB)-EGF upon rest
84 ic polypeptide-expressing metaplasia (SPEM), amphiregulin (AR) and transforming growth factor-alpha-d
94 pidermal growth factor (EGF) receptor ligand amphiregulin (AR) is reported to be an 84-amino acid res
96 a saline extract of tobacco smoke stimulated amphiregulin (AR) transcription resulting in increased a
101 e A pathway, which induced the expression of amphiregulin (AR), an epidermal growth factor family mem
102 in-binding epidermal growth factor (EGF) and amphiregulin (AR), and activation of the EGF receptor an
103 protein, and mRNA transcripts for TGFalpha, amphiregulin (AR), and heparin-binding EGF-like growth f
104 es EGFR ligands heparin-binding (HB)-EGF and amphiregulin (AR), and reduces betacellulin mRNA levels.
105 ting hormone (FSH) and the EGF-like peptide, amphiregulin (AR), are potent inducers of maturation in
106 ming growth factor (TGF)-alpha, but not with amphiregulin (AR), betacellulin (BTC) or epiregulin (EPR
107 actor (TGF)-alpha, heprin-ding (HB)-EGF, and amphiregulin (AR), have been shown to stimulate events a
108 pidermal growth factor (EGF) family hormones amphiregulin (AR), transforming growth factor-alpha (TGF
109 epidermal growth factor-like growth factor, amphiregulin (AR), which was not expressed by untreated
115 sforming growth factor alpha (TGF alpha) and amphiregulin are delivered to the basolateral surface of
116 gh levels of the EGFR ligands epiregulin and amphiregulin are more likely to have disease control wit
117 sine kinase (DDR1) and the ErbB1 receptor of amphiregulin are, for example, required for ductal branc
118 genes repressed by BRCA1, we have identified amphiregulin (AREG) and early growth response-1 (EGR1).
119 dermal growth factor receptor (EGFR) ligands amphiregulin (AREG) and epiregulin (EREG), and systemic
121 idermal growth factor receptor (EGFR)-ligand amphiregulin (AREG) and sensitize epithelial cells for e
122 ving ectodomain shedding of the EGFR ligands amphiregulin (AREG) and TGF-alpha, which rely upon the c
123 is study evaluated the diagnostic utility of amphiregulin (AREG) as a pancreatic cyst fluid biomarker
124 ve identified the EGF receptor (EGFR) ligand amphiregulin (AREG) as an important mediator of inflamma
125 idermal growth factor receptor (EGFR) ligand Amphiregulin (AREG) by co-activating the transcription f
126 ermal growth factor (EGF)-like growth factor amphiregulin (AREG) engages EGFR on Treg cells and, in d
129 se fragment complementation imaging studies, amphiregulin (AREG) functioned as a partial agonist, ind
131 here is a large body of literature regarding amphiregulin (AREG) in human cancer, most knowledge focu
132 with IL-33, expression of the growth factor amphiregulin (AREG) is a dominant functional signature o
134 everal ligands, and we provide evidence that amphiregulin (AREG) is important for activating this sig
135 rian and lung cancer patients and found that amphiregulin (AREG) is the most abundant and generalized
136 how that silencing of the EGF-related factor amphiregulin (AREG) markedly inhibits the expansion of h
137 ession of EGFR ligands epiregulin (EREG) and amphiregulin (AREG) may correlate with EGFR-targeted the
138 epidermal growth factor (EGF)-like molecule Amphiregulin (AREG) might be a critical component of typ
139 tissue-protective ILC2 responses, defective amphiregulin (AREG) production and increased susceptibil
141 e epidermal growth factor (EGF)-like protein amphiregulin (AREG) was highly expressed in ExeR cells b
142 owth factor 7, hepatocyte growth factor, and amphiregulin (AREG) were elevated in the extracellular e
145 study shows that AGR2 induces expression of amphiregulin (AREG), a growth promoting EGFR ligand.
147 K by derepressing miR-200 targets, including amphiregulin (AREG), betacellulin (BTC), and the transcr
148 We evaluated the role of the EGFR ligand, amphiregulin (AREG), during cholestatic liver injury and
149 th factor receptor (EGFR) pathway, including amphiregulin (AREG), epiregulin (EREG), and ectodomain c
150 ubstrates TNF-alpha, TNFR1-alpha, TGF-alpha, amphiregulin (AREG), HB-EGF and IL-6Ralpha, from IGROV1-
151 factor (EGF)-like growth factors, including Amphiregulin (AREG), heparin-binding EGF (HB-EGF), and t
152 ligands including EGF, TGF-alpha (TGFalpha), amphiregulin (AREG), heparin-binding EGF-like growth fac
153 -mediated silencing of one of these ligands, amphiregulin (AREG), results in keratinocyte growth arre
154 alpha to regulate directly the expression of amphiregulin (Areg), the progesterone receptor (Pgr) and
155 evealed that the ADAM17 proteolytic targets, amphiregulin (AREG), transforming growth factor alpha (T
156 ratinocytes (KCs) is strongly dependent upon amphiregulin (AREG), whereas blockade of heparin-binding
157 growth factor receptor (EGFR) and its ligand amphiregulin (AREG), which generally must be cleaved fro
160 in AD, and we found dendritic cell (CLEC7A, amphiregulin/AREG, EREG) and macrophage products (CCL13)
163 elated evidence led to the identification of amphiregulin as a major autocrine factor for keratinocyt
165 s a cause of sustained expression of uterine amphiregulin before the initiation of implantation.
167 n addition to TGF-alpha release, GRP induced amphiregulin, but not EGF, secretion into HNSCC cell cul
169 in blood and multiple tissue types produced amphiregulin, but this was neither a unique feature of T
170 tissue repair by producing the growth factor amphiregulin, but whether similar tissue-reparative Treg
173 fter injury; however, the mechanism by which Amphiregulin contributes to wound repair remains unknown
174 combination of F115 and Y123 determined the amphiregulin cross-reactivity and that F115 accounted fo
175 that the addition of recombinant epiregulin, amphiregulin, CX3CL1, and interleukin-11 significantly e
176 inflammation (interleukin-6), lung stretch (amphiregulin), damage to epithelial (surfactant protein
179 e epithelial cell proliferation, and lack of amphiregulin delayed expulsion of the nematode Trichuris
180 am as well as downstream of ErbB1 to promote amphiregulin-dependent autocrine stimulation of NHKs and
181 pressor gene, a transcriptional activator of amphiregulin, did not parallel amphiregulin transcript l
183 ding of transforming growth factor alpha and amphiregulin does not require ADAM17, even though ADAM17
184 iated proteins appear to act as cofactors in amphiregulin-driven mitogenesis mediated by the epiderma
186 monstrated that specific proteins, including amphiregulin, effectively predict COVID-19 severity from
188 signaling cascade of GRP-Src-PI3-K-PDK1-TACE-amphiregulin-EGFR with multiple points of interaction, t
190 factors and immune modulation-especially via amphiregulin-epidermal growth factor receptor (EGFR) sig
192 bFGF, IL-8, and ANGPTL-2), as well as ErbB (amphiregulin, epiregulin, and neuregulins) and TGF-ss, w
193 pha, heparin-binding EGF-like growth factor, amphiregulin, epiregulin, betacellulin, or heregulin bet
194 exhibited TCR-independent, IL-33-stimulated amphiregulin expression and a heightened ability to indu
195 echanisms: protection from fatal immunity by amphiregulin expression and augmentation of antileukemic
197 g miR-149, epidermal growth factor (EGF) and amphiregulin expression levels were strongly reduced, re
198 naling via IL-33 induces type 2 cytokine and amphiregulin expression, and increases ILC2 migration.
199 or-beta signaling, the extracellular matrix, amphiregulin expression, and the growth hormone/insulin-
200 ceptor-deficient mice is driven by decreased amphiregulin expression, which IFN signaling can up-regu
203 lar smooth muscle cells, particularly COX-2, amphiregulin, follistatin, inhibin-beta-A, and CYR61.
204 mutant mice suggests a compensatory role of amphiregulin for uterine loss of HB-EGF, preventing comp
205 th factor receptor (EGFR) and of its ligand, amphiregulin, for the formation of a signaling complex b
206 emonstrate that PTH increases the release of amphiregulin from osteoblastic cells, which acts on the
211 The epidermal growth factor receptor ligand Amphiregulin has a well-documented role in the restorati
214 nds including epidermal growth factor (EGF), amphiregulin, heparin-binding EGF and beta-cellulin.
215 as well as transforming growth factor-alpha, amphiregulin, heparin-binding epidermal growth factor-li
216 In addition, three ErbB1 ligand transcripts (amphiregulin, heparin-binding epidermal growth factor-li
217 ) ligands (transforming growth factor-alpha, amphiregulin, heregulin, heparin binding EGF-like ligand
218 stromal lymphopoietin, and the growth factor amphiregulin in a human bronchial epithelial cell line.
220 In this study, we investigated the role of amphiregulin in breast cancer cell proliferation using h
222 ional psoriatic epidermis, the importance of amphiregulin in hyperproliferative skin diseases has bee
224 ll RNA sequencing identifies upregulation of amphiregulin in leukocyte populations during sepsis, whi
225 binding EGF-like growth factor (HB-EGF); and amphiregulin in NHBECs, and when administered exogenousl
226 or gradient 2, yes-associated protein 1, and amphiregulin in OPA tumor cells, indicating a role for t
227 r, these data indicate an important role for amphiregulin in psoriatic hyperplasia and suggest that i
231 py induces the expression of the EGFR ligand amphiregulin in tumour cells, which reprogrammes EGFR-ex
233 not transforming growth factor (TGF)alpha or amphiregulin, in young adult mouse colon cells and ADAM1
234 e secretion of EGF family ligands, including amphiregulin, independent of metalloprotease a disintegr
235 on on mesenchymal stromal cells (pericytes), Amphiregulin induced their differentiation into myofibro
238 terminal differentiation in adult breast and amphiregulin is critical to normal embryonic breast deve
241 e finding that proximal tubule cell-specific amphiregulin knockout mice were protected from fibrosis
242 trate that selective Treg cell deficiency in amphiregulin leads to severe acute lung damage and decre
244 tion, resulting in impaired IL-5, IL-13, and amphiregulin levels, despite undiminished numbers of Th2
245 er EGFR ligands EGF, heparin-binding EGF, or amphiregulin, mediates SP-induced EGFR transactivation.
246 actor, transforming growth factor-alpha, and amphiregulin mRNA and protein in lesional psoriasis comp
248 9, an EP2-specific agonist, strongly induced amphiregulin mRNA levels in a protein kinase A-dependent
250 genomic responses, since both calcitonin and amphiregulin mRNAs were increased after progesterone tre
253 induces expression of either the EGFR ligand amphiregulin or the transcription factor CDX2, only the
254 ncentration that neutralized the function of amphiregulin, or antibodies against TGFalpha or HB-EGF a
255 tivity, high levels of ERBB2 (P = 0.036) and amphiregulin (P = 0.026) predicted sensitivity to lapati
257 t the cytoplasmic carboxy-terminal domain of amphiregulin plays an important role in regulating autoc
260 h factor receptor (EGFR) phosphorylation and amphiregulin production were examined by Western blot an
261 s showed that IGF-1 transactivation required amphiregulin production, whereas LPA was dependent on mu
263 The WT1(-KTS) isoform binds directly to the amphiregulin promoter, resulting in potent transcription
266 dermal growth factor and 10-fold increase in amphiregulin, respectively) in HELUs compared with TDLUs
267 entified macrophages as a critical source of Amphiregulin, revealing a direct effector mechanism by w
269 by the epidermal growth factor receptor, but amphiregulin's immunolocalization to keratinocyte nuclei
270 th proximal tubule cell-specific deletion of amphiregulin's releasing enzyme, the transmembrane cell-
272 defect in tTreg cells caused by the lack of amphiregulin secretion, which could contribute to the ma
273 0 and ADAM17, reduces in vitro HER-2/neu and amphiregulin shedding, confirming that it interferes wit
274 mphiregulin transcript and protein amplifies amphiregulin signaling in a positive feedback loop.
278 cific pattern of WT1 itself, and recombinant Amphiregulin stimulates epithelial branching in organ cu
279 e observation of normal induction of uterine amphiregulin surrounding the blastocyst at the time of a
281 ytes secrete soluble EGFR ligands (including amphiregulin) that are processed from membrane-bound pro
284 d protein 1 (YAP1)-dependent upregulation of amphiregulin transcript and protein amplifies amphiregul
285 activator of amphiregulin, did not parallel amphiregulin transcript levels, suggesting that another
286 SUM-149PT and H55a#1 cells overexpressed amphiregulin transcripts, and secreted moderate EGF-like
287 PRIP-deficient glands expressed increased amphiregulin, transforming growth factor-alpha, and beta
290 lonal antibody capable of neutralizing human amphiregulin was examined for anti-proliferative effects
291 ntrols, the percentage of ILCs that produced amphiregulin was higher in females than in males, and pe
292 teral ureteral obstruction demonstrates that amphiregulin was necessary for the development of fibros
293 nsforming growth factor-alpha (TGFalpha), or amphiregulin we have shown that only the anti-TGFalpha a
294 GF-alpha), heparin binding-EGF (HB-EGF), and amphiregulin were analyzed for their ability to mediate
297 (EGF), transforming growth factor alpha, and amphiregulin were used to identify roles for these EGF r
298 uscle Treg cells expressed the growth factor Amphiregulin, which acted directly on muscle satellite c
299 EGF receptor stimulation by TGF-alpha and/or amphiregulin, which are known to be elevated in psoriati
300 xtures is dependent on transient exposure to amphiregulin, which is exclusively secreted by non-tumor