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1 TGF-beta enhanced the expression of ARHGEF1, while a sma
2 TGF-beta has been implicated as a major pathogenic facto
3 TGF-beta inhibition rescued abnormalities in fibrillin-1
4 TGF-beta is a multifunctional cytokine affecting many ce
5 TGF-beta is an anti-inflammatory cytokine whose signalin
6 TGF-beta is pro-metastatic for malignant cancer cells.
7 TGF-beta is pro-metastatic for the late-stage breast can
8 TGF-beta is regulated at the level of activation, but ho
9 TGF-beta is synthesized as a precursor molecule and prot
10 TGF-beta is synthesized as a proprotein that dimerizes i
11 TGF-beta pre-treatment amplified the effects of BK on Rh
12 TGF-beta signaling components were expressed in most HCC
13 TGF-beta signaling has been associated with the tumorige
14 TGF-beta signaling maintains CD103 expression, promotes
15 TGF-beta signaling mediated by pSMAD2, bone morphogeneti
16 TGF-beta was identified as the factor mediating suppress
17 TGF-beta-induced beta-catenin also regulates NR4A1 expre
18 TGF-beta/Fc and nonlytic IL-2/Fc exert a synergistic eff
19 h (SM16, a selective inhibitor of the type 1 TGF-beta receptor activin receptor-like kinase 5, orally
20 (RTA-408) results in the induction of HO-1, TGF-beta, and IL-10, as well as the repression of NF-kap
21 yet tolerogenic phenotype, expressing IL-10, TGF-beta, IL-27, and aldehyde dehydrogenase 1A2 but not
23 ts independently of the GLP-1/Notch or DAF-7/TGF-beta pathways but together with the DAF-2/insulin IG
26 xtracellular matrix protein and delivering a TGF-beta mAb resulted in a relatively focal uptake in th
28 that a pharmacological compound that abates TGF-beta signalling and enhances ERK5 signalling may be
30 , podocyte injury, fibronectin accumulation, TGF-beta expression, and, most notably, age-related impa
31 pulation by secreting products that activate TGF-beta signalling, but the identity of the active mole
32 n cancers and that oncogenic K-RAS activates TGF-beta signaling to promote tumor invasion and metasta
33 cell types, suggesting a possible activation TGF-beta receptor signaling in tumor cells in response t
36 f growth factors, such as IGF-1, VEGF-alpha, TGF-beta, and Wnt proteins that regulate epithelial and
38 y this enigmatic family of membrane-anchored TGF-beta family signaling regulators and link membrane a
39 genase 1A2 but not IL-12 or IL-35; IL-10 and TGF-beta together drove their suppression of TH2 cell pr
42 cortical expression of IL-18, IL-1beta, and TGF-beta, despite a gradual decline in TNF-alpha express
45 y that combined serum and tissue activin and TGF-beta ligand levels predicts outcome in CRC patients
46 , IL-4 upward arrow, IL-10 upward arrow, and TGF-beta upward arrow) and enhanced regeneration of dama
48 rfering RNA suppressed the effects of BK and TGF-beta on RhoA-GTP content, RhoA translocation and MYP
50 n is essential for vascular development, and TGF-beta signaling plays a critical role in this process
51 cular impacts of altered KLF4 expression and TGF-beta signaling were determined using immunofluoresce
56 tion-induced reduction of bone formation and TGF-beta gene expression, we measured mRNA levels of TGF
57 eactions culminate in antibody formation and TGF-beta secretion, respectively, leading to fibrosis.
59 at the combination of shRNAs against HBV and TGF-beta could be developed into a viable treatment for
61 down-regulating Wnt (beta-catenin, LEF1) and TGF-beta (Smad2/3, collagen type I, alpha-SMA) signaling
64 identified an interaction between moesin and TGF-beta receptor II (TbetaRII) that allows moesin to co
66 f oncogenic mutations in Wnt, EGFR, P53, and TGF-beta signaling pathways facilitates efficient tumor
67 f transcriptional regulation during Ras- and TGF-beta-induced EMT that involves alterations of access
69 dings demonstrate that the absence of apical TGF-beta signaling in normal epithelia is primarily a re
70 and induced by COPD-related stimuli, such as TGF-beta, cigarette smoke (CS), and cellular senescence.
71 es given that blockade of exosome-associated TGF-beta or inhibition of exosome release abrogated Tfr
72 antly reduced Col-1 secretion and attenuated TGF-beta induced increment in Col-1 localization at cell
74 instability or KRAS mutations; (ii) CRIS-B: TGF-beta pathway activity, epithelial-mesenchymal transi
75 that blocks transforming growth factor beta (TGF beta) superfamily inhibitors of erythropoiesis, givi
76 increase in transforming growth factor beta (TGF-beta) and concomitantly an increase in T regulatory
79 pe I and II transforming growth factor beta (TGF-beta) receptors (TbetaRI and TbetaRII, respectively)
81 mediated by transforming growth factor beta (TGF-beta)-containing exosomes released from HCV-infected
86 tivation of transforming growth factor-beta (TGF-beta) signaling pathway is a common feature of hepat
87 al role for transforming growth factor-beta (TGF-beta) signals in safe-guarding specific Treg cell fu
88 mber of the transforming growth factor-beta (TGF-beta) superfamily and has been implicated in various
89 ABSTRACT: Transforming growth factor-beta (TGF-beta), RhoA/Rho-kinase and Src-family kinases (SrcFK
91 induced by transforming growth factor-beta (TGF-beta), we identified the TF musculin (MSC) as being
95 erall, Shenks inhibited fibrosis by blocking TGF-beta pathway and modulating the oxidant/antioxidant
98 a superfamily pathways that can inhibit both TGF-beta and activin signals while enhancing bone morpho
99 gands mimics the hypertrophy seen with broad TGF-beta blockers, while avoiding the adverse effects du
100 Smad transcription factors activated by TGF-beta or by BMP receptors form trimeric complexes wit
101 erin abundance and stress fiber formation by TGF-beta, gene ontology analysis showed that genes encod
107 a molecular switch that controls the cardiac TGF-beta axis and its early transcriptional effects that
111 we report a novel finding that, in TM cells, TGF-beta-induced increase in collagen expression is asso
117 on was found to be a novel pathway of direct TGF-beta-dependent Treg-cell suppression of mast cell ac
119 nesins, KIF5A was notably upregulated during TGF-beta induced mesothelial-mesenchymal transition (Mes
120 neurogenesis and the TGF-beta pathway (i.e. TGF-beta; SMAD-2, -3, and -7; and SMURF-2) in the rat hi
121 fine the relative contribution of endogenous TGF-beta proteins to the negative regulation of muscle m
123 naling is a prerequisite for PAR2 to enhance TGF-beta signaling, we investigated the effects of PAR2-
124 ivity as wild-type (WT) Arkadia in enhancing TGF-beta signaling responses, while W972R does not.
125 en transferred into mice bearing established TGF-beta-OVA-expressing thymomas, produce high amounts o
128 eposition, collagen 1 and 3 mRNA expression, TGF-beta production, and activation of alternatively act
129 bined blocking M2 macrophage-derived factors TGF-beta, VEGF and SDF-1 abolished VEGFR1(+) myeloid cel
130 latory cytokine fusion proteins of IL-10/Fc, TGF-beta/Fc, or IL-2/Fc would enhance allogeneic bone ma
131 Thus, we reveal an unrecognized function for TGF-beta signaling as an upstream factor controlling Tre
132 diomyocyte-specific regulatory mechanism for TGF-beta production by PAI-1, which explains the paradox
133 for binding the other receptor required for TGF-beta signaling, the TGF-beta type II receptor (Tbeta
135 involvement of tolerogenic molecules (HLA-G, TGF-beta, and IL-10) were tested on a mixed lymphocyte r
136 d human airway smooth muscle cells (hASMCs), TGF-beta pre-treatment enhanced the protein expression o
142 8 modeled molecular mediators, we identified TGF-beta and the matrix metalloproteinases as therapeuti
143 their cognate ligands to type I and type II TGF-beta receptors, indicating that Cripto-1 and Cryptic
144 3 phosphorylation levels and SBE activity in TGF-beta-induced fibroblasts were dramatically decreased
145 se changes could be attributed to changes in TGF-beta and matrix metalloproteinase-9, the downstream
146 h prevented Smad3 from binding to SBE DNA in TGF-beta-responsive SMC gene promoters, resulting in sup
147 sels become dependent on a small increase in TGF-beta signaling via activin receptor-like kinase 5 to
149 advanced stages of these cancers, increased TGF-beta expression is linked to high metastasis and poo
155 a rationale to pursue a means of increasing TGF-beta signaling as a potential therapy for Parkinson'
156 t contained rSBEs also effectively inhibited TGF-beta/Smad3 signaling, suggesting that lncRNA-rSBE ma
158 suppresses macrophage activity by inhibiting TGF-beta-activated kinase (TAK1) signaling to NF-kappaB,
164 provide a new avenue to probe and manipulate TGF-beta signaling and may inform similar modifications
165 rotein levels of fibrosis signaling mediator TGF-beta remained the same and the second messenger, Sma
166 ed that both KL and FGF23 signaling modulate TGF beta-induced IL-8 secretion in CF bronchial epitheli
167 red an lncRNA-based mechanism that modulates TGF-beta/Smad3 signaling during SMC differentiation.
168 etained the same overall structure of native TGF-beta monomers and bound TbetaRII in an identical man
169 nal transcription factor that mediates Nodal/TGF-beta signaling, with cis-regulatory modules (CRMs) d
170 wound healing though increased expression of TGF beta leading to enhanced formation of granulation ti
171 mune diabetes, here we show that ablation of TGF-beta receptor II (TbetaRII) in T cells, but not Foxp
174 pressed in most HCC cells, and activation of TGF-beta signaling promoted cell migration and invasion.
179 growth factor (TGF)-beta because blockade of TGF-beta significantly reversed NK anti-fibrotic functio
180 eous stroke because of myeloid deficiency of TGF-beta (transforming growth factor-beta) signaling.
181 models with induced conditional deletion of TGF-beta signaling in the entire eye, the retinal pigmen
183 In turn, cell-intrinsic deregulation of TGF-beta signaling is associated with increased function
185 phorylated SMAD2/3, a downstream effector of TGF-beta Furthermore, in the PD parietal arterioles, C1q
187 ion, but minimally influenced the effects of TGF-beta on cofilin expression and phosphorylation.
189 a RhoGEF inhibitor prevented the effects of TGF-beta on RhoA and Rho-kinase activity and contraction
190 nuclear export results in nuclear export of TGF-beta-induced beta-catenin, which then undergoes prot
191 al inflammation, including the expression of TGF-beta, NFkappaB, MCP-1, IL-1, IL-6, ICAM-1, VCAM-1 an
193 ppo pathway target genes and marker genes of TGF-beta signaling, including biomarkers of renal diseas
197 ced inflammation, lower expression levels of TGF-beta and proteases associated with tissue remodeling
198 nervation-induced decrease in mRNA levels of TGF-beta group, while dexamethasone (DEX) decreased TGF-
199 gene expression, we measured mRNA levels of TGF-beta in denervation mouse bone and found decreased m
202 el predicted that simultaneous modulation of TGF-beta and matrix metalloproteinases would be more eff
203 emical events that lead to overproduction of TGF-beta, oxidative stress, and limited bioavailable nit
204 le of Th1 differentiation in the presence of TGF-beta, suggesting a novel approach to adoptive cell t
207 ARalpha up-regulation leads to repression of TGF-beta signaling, specifically by inhibiting TGF-beta-
210 essential for the expression of a subset of TGF-beta target genes in hepatic stellate cells, and the
212 n PTC samples from patients, upregulation of TGF-beta, p27, p65 and cyclin D1 mRNA were significantly
214 inhibition of CD4(+) T cells is dependent on TGF-beta, whereas inhibition of CD8(+) T cells is depend
216 CC may contribute to activation of oncogenic TGF-beta signaling and subsequent tumor progression.
217 data indicate that KLF4 suppresses oncogenic TGF-beta signaling by activation of Smad7 transcription,
222 ermore, while the TAT-SNX9 peptide prevented TGF-beta's profibrotic activity in vitro as well as in 2
223 inhibition or knockout bone marrow prevents TGF-beta activation and protects against PH development.
224 d by reactive oxygen species (ROS), prevents TGF-beta activation of Smad2, therefore limiting Th17 ce
225 interface stabilize a specific integrin/pro-TGF-beta orientation that defines the pathway through th
226 owth factor (GF) domain in each monomer, pro-TGF-beta is secreted and stored in latent complexes.
228 g the TAT-SNX9 peptide inhibited profibrotic TGF-beta activity in murine cells and human lung fibrobl
230 combined functions of the two most prominent TGF-beta superfamily members activin and TGF-beta in adv
231 iation in human and mouse cells by promoting TGF-beta activation, which in turn was mediated by upreg
234 udy, we show that STAT3 negatively regulates TGF-beta signaling via ERBB2-interacting protein (ERBIN)
235 t mice exhibited changes in genes regulating TGF-beta/BMP/FGF signaling, as well as in genes controll
236 However, to produce cell-specific responses, TGF-beta pathways are heavily regulated by secondary fac
242 A growth arrest-specific 5 (GAS5) suppresses TGF-beta/Smad3 signaling in smooth muscle cell different
243 driver of thoracic aortic disease, and that TGF-beta overactivity in diseased aortas is a secondary,
247 eta in murine bronchiolitis obliterans; that TGF-beta and the C' cascade present signaling interactio
251 of proteins involved in neurogenesis and the TGF-beta pathway (i.e. TGF-beta; SMAD-2, -3, and -7; and
252 in, the neuropeptide receptor NPR-1, and the TGF-beta peptide DAF-7 each have stage-specific effects
254 via targeting Frizzled receptor 4/6 and the TGF-beta-induced activation of lung fibroblasts by inhib
255 eration, migration, tubule formation and the TGF-beta-induced AKT, SMAD- and ERK-dependent phosphoryl
256 a structural motif essential for binding the TGF-beta type I receptor (TbetaRI) but dispensable for b
257 eals that OTUD1 directly deubiquitinates the TGF-beta pathway inhibitor SMAD7 and prevents its degrad
259 /CD24- cells, constitutive activation of the TGF-beta axis was both necessary and sufficient to reduc
260 iation factor-15 (GDF-15) is a member of the TGF-beta cytokine superfamily that is widely expressed a
264 onses and attenuated the upregulation of the TGF-beta signaling pathway and alpha1-antitrypsin protei
265 so explored the potential implication of the TGF-beta signalling pathway in the pathogenesis of suici
267 protein (KCP) is a secreted regulator of the TGF-beta superfamily pathways that can inhibit both TGF-
269 related to loss-of-function mutation of the TGF-beta/BMP receptor complex and the second to increase
270 ministration of the bispecific DVD-Ig or the TGF-beta mAb (1-10 mg/kg) but not the FnEDA mAb attenuat
273 These findings demonstrate that shifting the TGF-beta superfamily signaling with a secreted protein c
274 eceptor required for TGF-beta signaling, the TGF-beta type II receptor (TbetaRII), as an alternative
279 and the Wnt pathway acting together with the TGF-beta pathway in mesendodermal differentiation of mou
280 -37 induces pro-angiogenic responses through TGF-beta, which may act as the bridging molecule that me
282 s that CD4(+) T(Pam3) cells are resistant to TGF-beta-mediated gene expression through Akt activation
287 m induction relies on the combination of two TGF-beta-related signals: maternal and ubiquitous Vg1, a
288 arly tumor development in many cancer types, TGF-beta acts as a tumor suppressor, whereas in the adva
291 ed that IL-17A induces epithelial injury via TGF-beta in murine bronchiolitis obliterans; that TGF-be
294 ogressive kidney disease in association with TGF-beta overexpression, administration of SRT3025 atten
299 ioned medium (MF-CM) or MFs, with or without TGF-beta signaling inhibitor - SB431542 and/or JAK2/STAT
300 scription factor pathways (for example, Wnt, TGF-beta, mir200, ZEB1, OVOL2, p63 and p300) and transla
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