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1 TGF-beta depends on RAS and mitogen-activated protein ki
2 TGF-beta is a master regulator of fibrosis, driving the
3 TGF-beta is extensively implicated in the pathogenesis o
4 TGF-beta is long known to require Ras activation to indu
5 TGF-beta is used routinely for expansion of conventional
6 TGF-beta regulates iTreg cell outcomes through 2 distinc
7 TGF-beta treatment increased glycolysis in PASMCs, but d
8 TGF-beta, activins, and growth differentiation factors e
9 TGF-beta-driven fibrosis is mediated through Smad-depend
10 gingiva (IL-6, IL-17A, IL-17F, RANKL, IL-10, TGF-beta and GITR; P < 0.05), and the proliferation of b
11 s and stimulated the cells to produce IL-10, TGF-beta, or both at the immunization site, which might
12 TNF-alpha in REC group and INF-gamma, IL-2, TGF-beta and TNF-alpha in the C-PRO group were also dimi
17 se (HMGCR) and ATP-citrate lyase (ACLY) in a TGF-beta receptor/PI3K/protein kinase B-dependent manner
20 mote itching during skin would healing via a TGF-beta-IL-31 axis with implications for treatment of w
22 AgRP neurons, suggesting a role for aberrant TGF-beta signaling in the development of this phenotype.
24 sults suggest that shaking culture activates TGF-beta expression and Wnt signaling to promote chondro
25 duces H19 expression which in turn activates TGF-beta signaling and EndMT via a TET1-dependent epigen
28 e absence and overexpression of SMAD7 affect TGF-beta signaling and modulates beta-cell proliferation
31 < 0.05), decreasing apoptosis (p < 0.05) and TGF-beta-positive signal (p < 0.05) in surrounding tissu
38 ued P2RX7-deficient Trm cell generation, and TGF-beta sensitivity was dictated by P2RX7 agonists and
40 arkers, Rae-1 expression was notably low and TGF-beta receptor II was high in tx-MDSCs when compared
41 In addition to overexpression of p53 and TGF-beta pathway genes, we identified high levels of MYC
43 B1 provides a molecular link between RAS and TGF-beta pathways for coordinated induction of developme
47 expression of several integrin subunits and TGF-beta receptors, and nuclear translocation of p-SMAD2
49 ive function and that inactivation of ARID1A/TGF-beta axis promotes migration and invasion of PTEN-de
50 collagens in cardiac fibroblasts as well as TGF-beta (transforming growth factor-beta)-activated myo
51 integrin alphaVbeta6 association as well as TGF-beta-mediated permeability across alveolar epithelia
52 M induction, we propose that eCRT attenuates TGF-beta-mediated fibrosis/scarring to achieve tissue re
53 n the appreciation of the roles of autocrine TGF-beta signaling in normal physiological responses to
55 ration, and transforming growth factor beta (TGF-beta and BMP signaling through SMAD members has dist
57 upregulates transforming growth factor beta (TGF-beta) expression, whose signaling pathway synergizes
62 ted a novel transforming growth factor beta (TGF-beta) R2-41BB chimeric receptor that improved solid
66 between the transforming growth factor beta (TGF-beta) signaling proteins, SMAD family member 2 (SMAD
70 d paracrine transforming growth factor beta (TGF-beta) signals to TICs, inducing invasive and drug-re
71 ream of the transforming growth factor beta (TGF-beta) Sma/Mab pathway in the hypodermis to control r
73 ctor (FGF), transforming growth factor beta (TGF-beta), and WNT pathways, we derived PSCs from mice,
74 ase (iNOS), transforming growth factor beta (TGF-beta), NADPH oxidase isoform 4 (Nox4), caspase-3 and
77 (MSTN) is a transforming growth factor-beta (TGF-beta) family member that normally acts to limit musc
79 f enhancing transforming growth factor-beta (TGF-beta) mediated tenogenesis in human adipose-derived
80 (IL-10) and transforming growth factor-beta (TGF-beta) production and inhibited signal transducer and
82 e stress or transforming growth factor-beta (TGF-beta) stimulated EMT in a manner that depended on TG
83 found that transforming growth factor-beta (TGF-beta) superfamily member activin A is increased in t
84 inding that transforming growth factor-beta (TGF-beta) suppresses T helper 2 (T(H)2)-cell-mediated ca
85 L-1RA), and transforming growth factor-beta (TGF-beta)) with incident hospitalization with major infe
86 eases where transforming growth factor-beta (TGF-beta)-induced epithelial-mesenchymal transition (EMT
87 ng, suggesting reciprocal regulation between TGF-beta and EGFR signaling during chlamydial infection.
88 spatially restricted generation of bioactive TGF-beta from latent stores requires the cooperation of
89 ation and function were enhanced by blocking TGF-beta signalling, promoting bone morphogenic protein
90 ed cancer immunity(9), we show that blocking TGF-beta signalling in CD4(+) T cells remodels the tumou
91 cules and peptide modulators to inhibit BMP, TGF-beta (SMAD), and canonical Wnt pathways that reduced
92 perturbing DNA binding by various STFs (BMP/TGF-beta-directed SMADs or WNT-induced TCFs) and affecti
94 cellular and molecular pathways activated by TGF-beta, which determine the suppressor or enhancing ac
95 the transcriptional programme controlled by TGF-beta followed by an unbiased gain-of-function screen
98 EMT and stemness characteristics induced by TGF-beta might be associated with epigenetic regulation
99 ues and diseases and was strongly induced by TGF-beta, particularly in fibroblasts and fibroblast-rel
104 ing how integrins interact with signaling by TGF-beta and/or other growth factors (GFs) within the te
106 ed including cell cycle, pathways in cancer, TGF-beta signaling, FoxO signaling, fatty acid biosynthe
108 hans cells; analysis of BMP versus canonical TGF-beta signaling in DCs and Treg cells; and modeling o
111 rap, 4T-Trap selectively inhibited T(H) cell TGF-beta signalling in tumour-draining lymph nodes, caus
114 ral-memory cells, T-follicular-helper cells, TGF-beta response, and CD4( +) T memory resting cells, b
115 n that ubiquitin E3 ligases potently control TGF-beta signaling through targeted degradation of key r
116 effect of calcitriol on homeostatic (M-CSF, TGF-beta-treated) and proinflammatory (GM-CSF-treated) h
118 Anti-inflammatory TAMs secreted the cytokine TGF-beta that, upon engagement of its receptors in breas
119 induced mouse and human cardiomyocyte death, TGF-beta-induced cardiac fibroblast Smad2/3 activation,
121 VDeltamiR-US5-2 mutant resulted in decreased TGF-beta expression and restoration of myelopoiesis.
122 ts of these microRNAs implicated derepressed TGF-beta signaling as a shared seizure-modifying mechani
124 tures with miR-200 knockdown showed elevated TGF-beta expression, mitotic spindle disorientation, inc
125 ngs reveal a new requirement for endothelial TGF-beta signaling in OFT morphogenesis and suggest an i
128 was evaluated in transforming growth factor (TGF-beta)-incubated LX-2 cells and culture-activated pri
129 ion and clonogenic growth behavior following TGF-beta stimulation, although they exhibited difference
130 ealed that H19X was an obligatory factor for TGF-beta-induced ECM synthesis as well as differentiatio
131 d Scleraxis was a potential intermediate for TGF-beta-regulated expression of Fibromodulin and Adamts
133 factors, including IDO-1, arginase-1, Foxp3, TGF-beta, IL-10, and decreased levels of proinflammatory
134 TGF-beta while protecting infected HPCs from TGF-beta-mediated effects on viral latency and reactivat
136 al interposition surgery targets the hepatic TGF-beta pathway, influencing gluconeogenesis and mitoch
143 regions were enriched near genes involved in TGF beta (TGFB) and BMP signaling, both of which are key
145 ice with chronic infection and a decrease in TGF-beta levels and collagen content in cardiac tissue.
147 tem, manifested by a significant increase in TGF-beta, which weakened the therapeutic effect of micel
148 ch as Calponin (CNN1), and genes involved in TGF-beta signaling, such as AKT Serine/Threonine Kinase
149 pathway blockade can result in reduction in TGF-beta expression, thus, a PLGA microsphere encapsulat
150 ective role for ERbeta-specific signaling in TGF-beta-dependent regulatory T cell (Treg) differentiat
153 Both Smad-dependent and Smad-independent TGF-beta signaling induced HK2 accumulation in murine an
154 fection, and specifically miR-US5-2, induces TGF-beta secretion, which inhibits myelopoiesis in uninf
156 M-driven TGFBR2 expression, while inhibiting TGF-beta signaling decreased tECM-mediated expression of
157 s via LRP1 signaling subsequently initiating TGF-beta receptor signaling for intracellular CRT (iCRT)
161 bound to and repressed the expression of key TGF-beta signaling genes by deacetylating SMAD family me
164 ectodomain and its intact natural ligand, L-TGF-beta, as well as two different inhibitory antibody f
166 re TGF-beta signals within the confines of L-TGF-beta and the release and diffusion of TGF-beta are n
167 addition to collagens, such as Ltbp2 (latent TGF-beta-binding protein 2) and Sulf1 (sulfatase 1), whi
168 vated lipid biosynthesis and suppressed MAPK/TGF-beta gene expression, resulting in endogenous ERK in
169 echanism of TGF-beta activation where mature TGF-beta signals within the confines of L-TGF-beta and t
172 ent stiffness leads to stromal cell-mediated TGF-beta family signaling relying on the induction and u
176 may be a potential candidate for modulating TGF-beta signaling to reduce multiorgan fibrosis during
177 A study from Kiepas et al. revealed a new TGF-beta-dependent role for Src homology/collagen adapto
180 its executionary molecules, accentuation of TGF-beta signaling, Smads and XBP1 nuclear translocation
181 work we show that the profibrotic actions of TGF-beta are mediated, at least in part, through a metab
182 aired progenitor capacity, and activation of TGF-beta (transforming growth factor-beta)/SMAD signalin
183 s the link between endothelial activation of TGF-beta signaling, induction of endothelial-to-mesenchy
188 iously, we showed that embryonic deletion of TGF-beta type 2 receptor in mouse sclerotome resulted in
190 e a major source of IL-22, but the effect of TGF-beta signaling on the production of IL-22 in CD4+ T
197 rotein 1 (RREB1) as a critical integrator of TGF-beta and Ras signals during both developmental and c
199 trate that ARID1A-deficiency lead to loss of TGF-beta tumor suppressive function and that inactivatio
201 beta in fibrosis, highlighting mechanisms of TGF-beta activation and signaling, the cellular targets
202 ptional effector(20,21), as a key partner of TGF-beta-activated SMAD transcription factors in EMT.
203 were then differentiated in the presence of TGF-beta, whereas IL-17-producing effector T cells were
204 ce that this H19/TET1-mediated regulation of TGF-beta signaling and EndMT occurs in mouse pulmonary m
209 lung cells for high-throughput screening of TGF-beta signaling via high-content imaging of nuclear t
210 em cell homeostasis by inducing secretion of TGF-beta while protecting infected HPCs from TGF-beta-me
211 ration by enhancing CD8(+) T cell sensing of TGF-beta, which was necessary for tissue residency.
213 ood-allergic sensitization are suggestive of TGF-beta-mediated compensation for chronic inflammation.
214 ation and signaling, the cellular targets of TGF-beta actions, and the challenges of therapeutic tran
215 Although fibroblasts are major targets of TGF-beta, some fibrogenic actions may reflect activation
217 king groups, CI-iPSCs showed upregulation of TGF-beta and Wnt signaling-related genes, which are know
219 stimulated EMT in a manner that depended on TGF-beta-activated kinase 1 binding protein 1 (TAB1) and
222 underlying these effects with an emphasis on TGF-beta and nuclear receptor subfamily 4 group A member
225 pe was independent of the effect of IL-15 or TGF-beta on mTOR, as the culture of NK cells in the pres
227 els of IL-6 and TNF-alpha, but not IL-1RA or TGF-beta, were significantly associated with increased r
230 at exposure to high extracellular glucose or TGF-beta stimulates phosphorylation of ACTN4 at S159 in
231 g, focal adhesion kinase (FAK) signaling, or TGF-beta signaling independently led to compromised pro-
237 ignaling, p53 signaling, Jak-STAT signaling, TGF-beta and notch signaling), rap1-signaling, axon-guid
238 de, inflammation, complement, WNT signaling, TGF-beta and BMP signaling, lipid metabolism, iron homeo
244 s from PH versus control specimens, and that TGF-beta treatment would phenocopy these metabolic chang
249 Taken together, these results highlight that TGF-beta influences the trajectory of early T-cell activ
257 mily member 2 (SMAD2) and 3 (SMAD3), and the TGF-beta-inhibiting SMAD, SMAD7, seems to play a vital r
258 a bispecific receptor decoy by attaching the TGF-beta-neutralizing TGFBR2 extracellular domain to iba
263 blockade of IL-6R signaling exacerbated the TGF-beta-induced dysregulation of tight junction protein
264 RT6 binding to the promoters of genes in the TGF-beta signaling pathway decreased significantly with
265 cluding genes encoding key components in the TGF-beta, GDNF, AKT, and JAK-STAT signaling pathways.
266 ormation, we generated zebrafish lacking the TGF-beta receptor Alk5 and found a strikingly specific d
267 hogenetic proteins (BMPs) are members of the TGF-beta family that signal via the BMP receptor (BMPR)
268 ome epigenetically reprograms members of the TGF-beta family, including neuronal regeneration-related
269 es(10,11), inducible genetic deletion of the TGF-beta receptor II (TGFBR2) in CD4(+) T cells suppress
270 review dissects the genetic landscape of the TGF-beta superfamily genes in HCC and discusses the esse
271 strate that the Activin/Nodal pathway of the TGF-beta superfamily, but not the BMP pathway, is the pr
272 ic-derived T(REG) cells and potentiating the TGF-beta-dependent differentiation of T(EFF) cells to pe
273 In vitro, the SMAD3 mutations stimulated the TGF-beta pathway in osteoblasts, enhanced nuclear transl
274 erestingly, RNAseq analysis reveals that the TGF-beta and the FGF2 pathways are overexpressed in resp
278 we show that infected HPCs are refractory to TGF-beta signaling as another HCMV miRNA, miR-UL22A, dow
279 that HCMV-infected cells become resistant to TGF-beta signaling through targeting of SMAD3 by miR-UL2
284 marker to identify cells that have undergone TGF-beta signaling, we compared the HIV RNA/DNA contents
285 e conventional CD4(+) T cells that underwent TGF-beta-mediated conversion in the periphery (called pe
286 iated host invasion by chlamydia upregulated TGF-beta expression and signaling, which cooperated with
287 results revealed that Chlamydia upregulated TGF-beta expression as early as 6 h postinfection of epi
288 ) and neonatal fibroblasts (HFFs) mainly via TGF-beta canonical signaling and Smad2/3 activation; RAP
291 ion and invasion, but the mechanism by which TGF-beta signaling converts into cell motility is not co
292 n these results, we propose a model in which TGF-beta regulates Scleraxis via ERK1/2 and then Sclerax
295 rated directly from cultured BM treated with TGF beta-1 was pursued for insights into possible functi
296 h zymosan or LPS during differentiation with TGF-beta and 1,25diOHvitD3, full-length Dicer became abu
298 sis of BEAS-2B and A549 cells incubated with TGF-beta were analyzed through next-generation sequencin