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1                                              PDGF receptor alpha mRNA correlated with CCN2 and other
2                                              PDGF receptor beta (PDGFRbeta) is highly expressed in ac
3                                              PDGF receptor beta-positive myofibroblasts isolated from
4                                              PDGF, but not VEGF, peptides caused mechanical hypersens
5                                              PDGF-alpha-syn transgenic (tg) male and female mice were
6                                              PDGF-BB levels decreased significantly in samples collec
7                                              PDGF-BB maintained ERK activation in the presence of rux
8                                              PDGF-DD engagement of NKp44 triggered NK cell secretion
9                                              PDGF/VEGF ligands regulate a plethora of biological proc
10 tion include c-MYC, KRAS, c-KIT, HIF-1alpha, PDGF-A and hTERT.
11 ansiently increases with elevation of Ang-2, PDGF-BB, and blood glucose; is rapidly reversed on a tim
12       Nintedanib targets VEGF receptors 1-3, PDGF receptors alpha and beta, FGF receptors 1-3, and Sr
13 h factor]), and cluster 4 (n=37; IL-8, IL-4, PDGF-beta [platelet-derived growth factor beta], IL-6, C
14 rovide the first evidence in a metazoan of a PDGF/VEGF ligand acting as a myokine that regulates syst
15 igration (IC(5)(0) congruent with 1 nM) to a PDGF gradient and reduced TNF-alpha-stimulated p65 trans
16                                      Using a PDGF-B-driven proneural glioma mouse model, we assessed
17 its ligand platelet-derived growth factor A (PDGF-A) are co-expressed in migrating cranial NC.
18  MCP-1, MIP-1alpha, IL-12p70, IL-18, VEGF-A, PDGF-BB and IL-1RA significantly correlated with disease
19   Ectopic platelet-derived growth factor-AA (PDGF-AA) protein induces new tenocyte production while i
20 ed upon JAK2 inhibition in vivo, and PDGF-AA/PDGF-BB production persisted in the setting of JAK inhib
21 adient of platelet-derived growth factor-AB (PDGF-AB) expedites migration through native tissue.
22 or [EGF], platelet-derived growth factor AB [PDGF-AB], and albumin) were measured in fresh and lyophi
23 ion of genes associated with Wnt activation, PDGF- and integrin-binding.
24                                       Active PDGF-AA/alphaalpha signaling results in phosphorylation
25 b mesylate and a monoclonal antibody against PDGF receptor-alpha enhanced myocardial damage evidenced
26                  In mouse cardiac allografts PDGF receptor-beta, but not -alpha intragraft messenger
27 ed diminished expression of integrin alpha1, PDGF-R1beta and connexin-43.
28  stimulated with IL (interleukin)-1alpha and PDGF (platelet-derived growth factor)-BB with SMILR knoc
29 actors, including IGF-1, FGF2, IL-1beta, and PDGF-A, was altered in TLR4-deficient injured spinal cor
30 hers showed that P130CAS mediates VEGF-A and PDGF signalling in vitro, but its cardiovascular functio
31               UB cells synthesize VEGF-A and PDGF-BB proteins and RNA, whereas the MM cells express t
32 n wounds in diabetic mice with VEGF-A165 and PDGF-BB incorporated within VWF A1 HBD-functionalized fi
33  similar observations with EGF, PDGF-AA, and PDGF-BB.
34  TFF3, Serpin E-1, VCAM-1, Vitamin D BP, and PDGF-AA, were significantly upregulated in cancer surviv
35 t, the controlled release of collagenase and PDGF-AB increases cellularity at the interface and withi
36 inflammatory genes, such as CXCL1, CXCL6 and PDGF-A in plaque.
37 mbrane proteins, and members of ERK, FGF and PDGF signaling pathways, which play key roles in glandul
38 GF and PDGF, we embed VEGF in fibrin gel and PDGF in a heparin-based coacervate that is distributed i
39 ponse to C. trachomatis infection, IL23A and PDGF were significantly upregulated in scarring progress
40 h mesangial cell markers alpha8-integrin and PDGF receptor-beta but not with endothelial, podocyte, o
41 tic interaction between FGF-induced MAPK and PDGF-induced PI3K signaling.
42 F2, IGFBP-3 binds bFGF, HGF, neuregulin, and PDGF AB with nanomolar affinity.
43 B:R2 KD = 110 pM, PDGF-BB:R2 KD = 40 nM, and PDGF-CC:R2 KD = 70 pM.
44 f pro-regenerative factors including OSM and PDGF-AA.
45 ly observed increases in PTP1B oxidation and PDGF receptor phosphorylation in TrxR1 knockout cells.
46 e collagenase (to increase ECM porosity) and PDGF-AB (to attract endogenous cells) in a localized and
47 inase inhibitor which inhibits both VEGF and PDGF receptors.
48    To achieve sequential release of VEGF and PDGF, we embed VEGF in fibrin gel and PDGF in a heparin-
49 7 following surgery, mean levels of VEGF and PDGF-BB at sites treated with PRGF and PRF were not sign
50  30 after therapy for evaluation of VEGF and PDGF-BB levels.
51 nhanced autocrine signaling through VEGF and PDGF.
52 including the proangiogenic factors VEGF and PDGF.
53  activated upon JAK2 inhibition in vivo, and PDGF-AA/PDGF-BB production persisted in the setting of J
54 beta antibody, iii) by administering an anti-PDGF-AB/BB aptamer, and iv) by using small chemical inhi
55 hances PDGF-driven gliomas in vivo, augments PDGF-induced Akt and STAT3 signaling in vitro, while nex
56    Because platelet-derived growth factor B (PDGF-B) signaling has a pivotal role in mesangial cell p
57 that platelet-derived growth factor (PDGF)-B/PDGF receptor beta (PDGFRbeta) signalling is critical in
58 oped label-free electrochemical C-MEMS based PDGF-BB aptasensor is highly sensitive, selective, and r
59 with both platelet-derived growth factor-BB (PDGF-BB) and vascular endothelial growth factor (VEGF-16
60 levels of platelet derived growth factor-BB (PDGF-BB) in gingival crevicular fluid (GCF) during early
61 GF-A) and platelet-derived growth factor-BB (PDGF-BB) that were engineered to have a syndecan-binding
62 lpha) and platelet-derived growth factor-BB (PDGF-BB) were reduced.
63 forms and platelet-derived growth factor-BB (PDGF-BB), mainly through the heparin-binding domain (HBD
64  agonist, platelet-derived growth factor-BB (PDGF-BB)-induced p21Cip1 degradation and HASMC prolifera
65 PGZ on i) platelet-derived growth factor-BB (PDGF-BB)-stimulated proliferation of human venous smooth
66 ection of platelet-derived growth factor-BB (PDGF-BB).
67 GF-A) and platelet-derived growth factor-BB (PDGF-BB).
68 ressing platelet-derived growth factor beta (PDGF-B), constitutive HRAS, and shRNA-p53 respectively.
69 a], and platelet-derived growth factor-beta [PDGF-beta]) and blood-brain barrier (BBB) occludin and z
70  difference in capillary rarefaction between PDGF-CC-neutralized mice and mice with intact PDGF-CC.
71                           In vitro, blocking PDGF signaling decreased elastogenic gene expression ass
72 c deletion of host IL-33 in mice also blocks PDGF-BB-induced TAM recruitment and metastasis.
73 ts appropriate ligand-mediated activation by PDGF-AA.
74 iferation and its expression is decreased by PDGF-B.
75 without a concurrent increase in fibrosis by PDGF application.
76 nt malignant cell heterogeneity modulated by PDGF-DD signaling in pancreatic neuroendocrine tumors (P
77 h was delayed in the absence of signaling by PDGF-DD.
78 y reduces fibroblast migration stimulated by PDGF-BB and reduced in vivo lung fibrosis in mice.
79                                 HSV carrying PDGF siRNA was established and intrathecally injected in
80  and platelet-derived growth factor B chain (PDGF-BB), to stimulate MM cell differentiation.
81             Sunitinib also inhibited chronic PDGF-A and -B and VEGF-A and -B expressions.
82                       Conversely, continuous PDGF-B infusion in healthy rats induced DbpA expression
83 inflammatory response, such as CXCL1, CXCL6, PDGF-A, MCP-1 and IL-6.
84 organ-specific metabolic roles of Drosophila PDGF/VEGF-like factors (Pvfs).
85       We made similar observations with EGF, PDGF-AA, and PDGF-BB.
86 GFR activation loop that involved endogenous PDGF.
87                             TrkB.T1 enhances PDGF-driven gliomas in vivo, augments PDGF-induced Akt a
88 e biopsy samples from DMD patients expressed PDGF-BB.
89 olled the dissemination of tumors expressing PDGF-DD more effectively than control mice, an effect en
90                   Finally, the growth factor PDGF induced CAP1 dephosphorylation, suggesting CAP1 may
91              Platelet-derived growth factor (PDGF) acts through two conserved receptor tyrosine kinas
92 tors such as platelet-derived growth factor (PDGF) and the activation of the ERK1/2 are major regulat
93 sion of both platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) is i
94 ride-induced platelet-derived growth factor (PDGF) and Wnt signaling pathways.
95 York, NY), a platelet-derived growth factor (PDGF) antagonist, administered in combination with the a
96          The Platelet Derived Growth Factor (PDGF) family of ligands have well established functions
97 TNF-alpha or platelet-derived growth factor (PDGF) followed by evaluation of ECM production and depos
98 tative being platelet-derived growth factor (PDGF) isoforms (PDGF-AA, -BB, and -AB), insulin-like gro
99 l model of a platelet-derived growth factor (PDGF) protein and its DNA aptamer, which was selected in
100          The platelet-derived growth factor (PDGF) receptor (PDGFR) family of receptor tyrosine kinas
101        While platelet-derived growth factor (PDGF) receptor alpha (PDGFRalpha) has well-documented fu
102 r (VEGF) and platelet-derived growth factor (PDGF) receptors, has single-agent activity in non-small-
103  gradient of platelet-derived growth factor (PDGF) requires signaling through the phospholipase C (PL
104  to enhanced platelet-derived growth factor (PDGF) signaling are commonly observed in the proneural s
105 receptor for platelet-derived growth factor (PDGF) signaling recruits the p85 subunit of Phosphoinosi
106 how that the platelet-derived growth factor (PDGF) signalling pathway is activated in mutant iPSC-CMs
107  insulin and platelet-derived growth factor (PDGF) using the Aptamer-SWNT hybrids and the Aptamer-Anc
108 A) targeting platelet-derived growth factor (PDGF) was used to alleviate bone cancer pain.
109              Platelet-derived growth factor (PDGF), a potent mitogen for cells of mesenchymal origin,
110  gradient of platelet-derived growth factor (PDGF), together with other spatial cues.
111 a (TGFbeta), platelet-derived growth factor (PDGF), WNT and hedgehog signalling drive disease progres
112     In vitro platelet-derived growth factor (PDGF)- and tumor necrosis factor-alpha (TNF-alpha)-induc
113 , including platelet- derived growth factor (PDGF)-AA/alphaalpha, are linked to primary cilia.
114 we show that platelet-derived growth factor (PDGF)-B/PDGF receptor beta (PDGFRbeta) signalling is cri
115              Platelet-derived growth factor (PDGF)-BB belongs to a family of growth factors that regu
116 rand factor, platelet-derived growth factor (PDGF)-BB, angiopoietin-1, and lysyl oxidase-2 and the ce
117 treated with platelet-derived growth factor (PDGF)-BB.
118 ta 2 (FOG2), platelet-derived growth factor (PDGF)-beta, and phosphatidic acid phosphatase 2b (PPAP2B
119 r PDGFRbeta, platelet-derived growth factor (PDGF)-DD, opened the possibility of a previously unident
120 mors produce platelet-derived growth factor (PDGF)-DD, which promotes cellular proliferation, epithel
121 ivation in a platelet-derived growth factor (PDGF)-dependent manner.
122 nt two novel platelet-derived growth factor (PDGF)-driven mouse models of pediatric supratentorial HG
123 27 inhibited platelet-derived growth factor (PDGF)-induced migration in human VSMCs.
124 es and mice, platelet-derived growth factor (PDGF)-like signaling induced mesencephalic astrocyte-der
125 ombined VEGF/platelet-derived growth factor (PDGF)/FGF receptor inhibitors, paracrine ERK activation
126 VEGF) and 2) platelet-derived growth factor (PDGF-BB) in gingival crevicular fluid (GCF) from localiz
127 that the presence of fibrotic growth factor, PDGF-AA, results in increased proliferation of PDGFRalph
128             Platelet-derived growth factors (PDGF) have an ambiguous role in this deleterious cascade
129             Platelet-derived growth factors (PDGFs) and their receptors (PDGFRs) make profound contri
130 We computationally predict that cross-family PDGF binding could contribute up to 96% of VEGFR2 ligati
131 erated from exogenous stimulation with FGF2, PDGF, and hGF and readily prevented MBC cell growth indu
132 ficant difference in proliferation following PDGF exposure.
133  PI3K recruitment of ZC3H14 is necessary for PDGF-induced neuroprotection and that this interaction i
134 hese results show that CRMP2 is required for PDGF-directed cell migration in vitro.
135 ion in rats, suggesting a conserved role for PDGF and VEGFR-2 signaling in regulating mechanical noci
136 ion, consistent with an instructive role for PDGF signaling.
137                                   A role for PDGF-BB in vasculogenesis in the 3D MM/UB co-culture sys
138 ion strategies provided high selectivity for PDGF-BB and high stability of 90.34% after 10 days.
139 f TGF-beta upregulated invadosome formation, PDGF-B mRNA expression, and phosphorylation of PDGFR.
140 tly bound to and activated Usp1 Furthermore, PDGF-mediated expression of USP1 led to the stabilizatio
141                        Moreover, we generate PDGF-BB- and VEGFA-hypersecreting hMSC lines as short-te
142                                 On one hand, PDGF may exert vascular stabilizing and antiapoptotic ac
143 osstalk in the heart; and on the other hand, PDGF signaling mediates neointimal formation and exacerb
144 r, we demonstrate activity for heterodimeric PDGF-AB ligand in the vigorous activation of PDGFR-beta
145                                     However, PDGF-B/PDGFRbeta signalling is expendable for maintainin
146                                     However, PDGF-BB stimulated MM cell proliferation, migration, and
147 membrane (CM) treated with recombinant human PDGF-BB (rhPDGF-BB).
148 -mediated gene transfer of recombinant human PDGF-BB upregulated messenger RNA expression of anti-mes
149 tional mouse mutagenesis, we here identified PDGF-PDGFRbeta signaling as critical functional mediator
150                                We identified PDGF-D as a CMV-induced factor essential for pericyte re
151      In mice challenged with angiotensin II, PDGF receptor alpha-positive cells were increased in the
152 receptor-beta cell interactions to implicate PDGF-BB as a primary effector of MM cell vasculogenesis.
153 sphatase inhibitor okadaic acid, implicating PDGF-induced activation of protein phosphatase 1 (PP1) i
154                      In NSCLC alterations in PDGF receptors are markers of worst prognosis and effici
155 c small interfering RNA induced apoptosis in PDGF-activated fibroblasts, but not in quiescent fibrobl
156 roliferation and migration and is crucial in PDGF-BB pathway in VSMCs.
157 a large (Bcl-xL) as a key survival factor in PDGF-activated human and mouse fibroblasts.
158 h activation of SOX7 transcription factor in PDGF-BB-stimulated pericytes.
159 old in HGF, 2.9-fold in VEGF and 8.7-fold in PDGF-B higher gene expressions compared to BMSCs.
160 xpanding the range of proteins implicated in PDGF signalling pathways.
161  loss of expression of oncogenes involved in PDGF, EGFR, VEGF, insulin/IGF/MAPKK, FGF, Hedgehog, TGFb
162 cytes, PI3Kalpha was selectively involved in PDGF-B expression, whereas both PI3Kalpha and PI3Kdelta
163       We found that Prx2 becomes oxidized in PDGF-treated fibroblasts, but only when TrxR1 has first
164                                This includes PDGF secretion from alveolar type I and type II cells, c
165       Heparin, which binds ligands including PDGF and SCF, and imatininib which blocks downstream tyr
166  gut development and regeneration, including PDGF-A, IGFBP-3, IGFBP-2, and IGF-1.
167                      However, both increased PDGF ligand abundance and enhanced PDGFRalpha pathway ac
168 r proneural glioblastoma featuring increased PDGF signaling.
169 ing regeneration, acts as a decoy to inhibit PDGF signalling and to prevent FAP over-activation.
170 RK1/2 inhibitors are effective at inhibiting PDGF-mediated proliferation, collagen production, and IL
171   Thus, miR-125a-5p in this context inhibits PDGF-BB pathway and is therefore a potential regulator o
172    Our results indicate that NOTCH2 inhibits PDGF-B-dependent proliferation and its expression is dec
173  Subsequent experiments revealed that intact PDGF-B signaling, mediated via Olfml3 binding, is requir
174 DGF-CC-neutralized mice and mice with intact PDGF-CC.
175 telet-derived growth factor (PDGF) isoforms (PDGF-AA, -BB, and -AB), insulin-like growth factor bindi
176 rowth factor], sCD40L [soluble CD40 ligand], PDGF [platelet-derived growth factor], RANTES [regulated
177    By selective activation of PI3K and MAPK, PDGF and FGF cooperate with and oppose each other to bal
178 ce plasmon resonance to identify and measure PDGF-to-VEGFR binding rates, establishing cut-offs for b
179                            We discovered new PDGF:VEGFR2 interactions with PDGF-AA:R2 KD = 530 nM, PD
180 R2 interactions with PDGF-AA:R2 KD = 530 nM, PDGF-AB:R2 KD = 110 pM, PDGF-BB:R2 KD = 40 nM, and PDGF-
181                    Surprisingly, ablation of PDGF-DD did not affect the vasculature or stroma of PanN
182 reased Akt phosphorylation in the absence of PDGF-AA stimulation, which we show is due to impaired de
183 proteomics study, using a SILAC approach, of PDGF-stimulated mouse embryonic fibroblasts (MEFs).
184           The rules governing the binding of PDGF ligand to the receptor to produce activation and do
185 strocytic growth by intravitreal delivery of PDGF-A was sufficient to block retinal vascular pruning
186 ferentiation and implicate downregulation of PDGF signaling as a critical event in the transition fro
187      RhoG is activated by Trio downstream of PDGF in a PI3K- and Src-dependent manner.
188 s describe a signaling cascade downstream of PDGF that sustains proneural glioblastoma cells and sugg
189 d VCAM-1 appear to be involved downstream of PDGF-PDGFRbeta.
190 gial cells confirmed a stimulatory effect of PDGF-B on DbpA transcript numbers and protein levels.
191 ration, we examined the regulatory effect of PDGF-B on DbpA.
192                 Independent of the effect of PDGF-CC neutralization on renal fibrosis, we found no di
193 e is known about the downstream effectors of PDGF signaling in glioblastoma.
194 tro experiments to understand the effects of PDGF-BB on myoblasts involved in the pathophysiology of
195 d on days 3, 7, 14, and 30 for evaluation of PDGF-BB levels and alkaline phosphatase (ALP) levels.
196 d TRIM27 knockdown reduced the expression of PDGF receptor-beta (PDGFRbeta) and the phosphorylation o
197                            The expression of PDGF-AA and BMP2 was positively regulated by the p38 MAP
198 cells, likely due to decreased expression of PDGF-AA and BMP2.
199                We analyzed the expression of PDGF-BB in muscle biopsy samples from controls and patie
200             However, the precise function of PDGF-DD in tumor growth and invasion remains elusive.
201 roblasts responding to a shallow gradient of PDGF, signifying polarization.
202 Depletion of CRMP2 resulted in impairment of PDGF-mediated cell migration in an in vitro wound healin
203         Our data indicate that inhibition of PDGF signaling presents an attractive therapeutic approa
204                                Inhibition of PDGF-A/PDGFRalpha blocks NC migration by inhibiting N-ca
205 tic potential of crenolanib, an inhibitor of PDGF receptor signaling, in cultured fibroblasts and in
206                     Intrathecal injection of PDGF siRNA and morphine reversed thermal and mechanical
207 odel of DMD with repeated i.m. injections of PDGF-BB.
208                                PDE levels of PDGF-AA, platelet glycoprotein VI, integrin-linked kinas
209                                    Levels of PDGF-BB and VEGF were higher in the PRGF-treated group,
210 ys 3 and 7 following surgery, mean levels of PDGF-BB at sites treated with PRF membrane or CM incorpo
211 th rhPDGF-BB showed comparable GCF levels of PDGF-BB initially with PRF showing more sustained levels
212 d [Ca(2+) ] levels, affecting mRNA levels of PDGF-BB, RICTOR, and MIR17HG as mediators of Ca(2+) -sig
213 ory elements in the widely accepted model of PDGF activity.
214 synoviocytes that involves the production of PDGF-B induced by TGF-beta.
215  Here we show that endothelial production of PDGF-CC during white adipose tissue (WAT) angiogenesis r
216        Thus, while cancer cell production of PDGF-DD supports tumor growth and stromal reaction, it c
217 b axis in osteoclasts, with the promoters of PDGF-AA and BMP2 having Creb binding sites.
218 DGFB) plays a crucial role in recruitment of PDGF receptor beta-positive pericytes to blood vessels.
219   In addition, helix-structural refolding of PDGF binding aptamers (PBA) indirectly wrapped on the SW
220                                  The role of PDGF-BB in muscle regeneration in humans has not been st
221   A distinctive transcriptional signature of PDGF-DD-induced cytokines and the downregulation of tumo
222 ults indicate that DbpA is a novel target of PDGF-B signaling and a key mediator of mesangial cell pr
223  are key to a more complete understanding of PDGF ligand-receptor interactions and their downstream s
224 nderlying collagen and migrated dependent on PDGF or serum.
225 ing imaginal disc by activating the oncogene PDGF/VEGF-receptor (Pvr).
226            Among the PDGF-A-D isoforms, only PDGF-B was found both significantly elevated in FLS line
227        Interference with PDGFR activation or PDGF neutralization inhibited invadosome formation in RA
228                                 TNF-alpha or PDGF significantly (P < 0.001) increased ECM deposition
229                   Furthermore, TNF-alpha- or PDGF-induced ECM gene expression in ASM cells was signif
230 dated by direct interference with PDGF-BB or PDGF receptor-beta cell interactions to implicate PDGF-B
231 aracteristics when exposed to cholesterol or PDGF (platelet-derived growth factor).
232 bone morphogenetic protein 4 (BMP4), EGF, or PDGF was unaffected by the TAT-SNX9 peptide.
233 EB), and cAMP response element (CRE)-Luc, or PDGF-induced cyclin D1 expression.
234 F-AA:R2 KD = 530 nM, PDGF-AB:R2 KD = 110 pM, PDGF-BB:R2 KD = 40 nM, and PDGF-CC:R2 KD = 70 pM.
235  cells revealed that melanoma cells produced PDGF-BB and TGFbeta, which blocked PEDF production in fi
236               Our results lead us to propose PDGF-A/PDGFRalpha signalling as a tissue-autonomous regu
237 in MCMV+ mice, inhibiting MCMV reactivation, PDGF-D expression, pericyte recruitment, and tumor angio
238 binding, e.g., VEGFs bind to VEGF receptors, PDGFs bind to PDGF receptors, etc.
239  cells and innate lymphoid cells, recognizes PDGF-DD.
240 which was recently identified as a requisite PDGF-gradient-sensing pathway, with the goal of identify
241                        Based on our results, PDGF-BB may play a protective role in muscular dystrophi
242  to provide early instructive cue and retain PDGF-B along newly formed vessels to achieve optimal ang
243                 We demonstrated that the RTK PDGF/VEGF receptor (Pvr) and its ligands (Pvfs 2 and 3)
244 t once NC cells have undergone EMT, the same PDGF-A/PDGFRalpha works as an NC chemoattractant, guidin
245 only weakly amplifies signaling in a shallow PDGF gradient, but it synergizes with other feedback mec
246 ncluding toll-like receptor (TLR) signaling, PDGF- and angiotensin-regulated airway remodeling, the J
247               These results demonstrate that PDGF siRNA can effectively treat pain induced by bone ca
248 parative transcriptomics, we determined that PDGF signaling upregulated ubiquitin-specific peptidase
249               Mechanistically, we found that PDGF signaling regulated the expression of the E2F trans
250                 In this study, we found that PDGF-BB-induced synthetic SMCs suppressed EC proliferati
251  or stroma of PanNET; instead, we found that PDGF-DD stimulated bulk tumor cell proliferation by indu
252                         We further show that PDGF-CC stimulation upregulates UCP1 expression and acqu
253 ious contexts of infection, and suggest that PDGF BB and NEDD9 play important roles in this interacti
254                     Our results suggest that PDGF-B signaling may play a role in endothelial and card
255 in zebrafish pdgfra mutants, suggesting that PDGF signaling steers cardiomyocytes toward the midline
256                                          The PDGF receptor tyrosine kinase inhibitor imatinib mesylat
257                                    Among the PDGF-A-D isoforms, only PDGF-B was found both significan
258 e (PD) that expresses GFP-ASYN driven by the PDGF-beta promoter, we investigated how accumulation of
259 us uncover a novel mode of signaling for the PDGF family during vertebrate development.
260 ngitudinal live imaging of the retina in the PDGF-alpha-syn::GFP mice might represent a useful, non-i
261 xpression levels or decreased binding of the PDGF ligand to PDGFRbeta.
262  findings suggest that the activation of the PDGF pathway contributes to the pathogenesis of LMNA-rel
263 rmacological and molecular inhibition of the PDGF signalling pathway ameliorated the arrhythmic pheno
264 oma cells and suggest that inhibition of the PDGF-E2F-USP1-ID2 axis could serve as a therapeutic stra
265 gfr/MEK-induced tumor growth and produce the PDGF- and VEGF-related factor 1 (Pvf1) ligand to non-aut
266 onstrate that, after ligand stimulation, the PDGF beta receptor (PDGFRbeta) becomes ubiquitinated in
267 anNET characterized by signaling through the PDGF-DD/PDGFRbeta axis.
268                                        These PDGF receptor alpha-positive cells co-localized with PDG
269  several proteins, including human thrombin, PDGF-BB, Avidin, and His-tagged recombinant protein, wer
270  VEGFs bind to VEGF receptors, PDGFs bind to PDGF receptors, etc.
271 athogenesis of LMNA-related DCM and point to PDGF receptor-beta (PDGFRB) as a potential therapeutic t
272     The results suggest that, in response to PDGF stimulation, PDGFR activity is evenly distributed a
273 gulated and 45 down-regulated in response to PDGF stimulation.
274  showed decreased P-Akt(S473) in response to PDGF-AA upon anterograde transport disruption.
275 s well as with the PDGFRbeta, in response to PDGF-BB stimulation.
276 enuates PDGFRalpha activation in response to PDGF-BB, and reduced phosphorylation of extracellular si
277  PI3K/AKT signaling and dampened response to PDGF-induced mitochondrial fission and reactive oxygen s
278 ollagen deposition, partially in response to PDGFs.
279  and Cbl-b were more prone to migrate toward PDGF-BB, whereas no reproducible effect on cell prolifer
280 s (PHH3(+) mitotic cells, YAP translocation, PDGF secretion) or increase collagen presence.
281 ion and CAF-induced tumor cell invasion upon PDGF-BB stimulation.
282 ative response of Olfml3(-/-) pericytes upon PDGF-B stimulation was significantly diminished.
283  increase in P-Akt(S473) or P-Akt(T308) upon PDGF-AA stimulation.
284 vation, and that combined inhibition of VEGF/PDGF/FGF receptors is sufficient to inhibit mitogenic si
285                                    In vitro, PDGF-BB attracted myoblasts and activated their prolifer
286      FOG2 regulates VEGF expression, whereas PDGF-beta and PPAP2B regulate Akt activity.
287                       The mechanism by which PDGF regulates pain was also investigated by comparing t
288 ll as reduced tumour growth (associated with PDGF-BB delivery) and vascular permeability (triggered b
289 discovered new PDGF:VEGFR2 interactions with PDGF-AA:R2 KD = 530 nM, PDGF-AB:R2 KD = 110 pM, PDGF-BB:
290                            To interfere with PDGF-B signaling, we injected nephritic rats with PDGF-B
291 em was validated by direct interference with PDGF-BB or PDGF receptor-beta cell interactions to impli
292 eptor alpha-positive cells co-localized with PDGF receptor beta, procollagen, and periostin.
293       Consistently, in VSMCs pretreated with PDGF-BB, calpastatin induction and calpains inhibition s
294 B signaling, we injected nephritic rats with PDGF-B neutralizing aptamers or the MEK/ERK inhibitor U0
295              In response to stimulation with PDGF, CRMP2 was dephosphorylated on Thr514, an event kno
296              In wild-type cells treated with PDGF-AA, c-Cbl becomes enriched in the cilium, and the r
297 -to-mesenchymal transition when treated with PDGF-BB and TGFbeta1, resulting in vascular SMCs that di
298 sis of muscles from the animals treated with PDGF-BB showed an increased population of satellite cell
299  period of serum deprivation, treatment with PDGF leads to the rapid formation of dramatic, actin-ric
300 pillary rarefaction in mice with and without PDGF-CC neutralization (using genetically deficient mice

 
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