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1 ounding endocardium (Cx40(-), VEGFR2(-), and endoglin(+)).
2 nase 14 (MMP-14) as the cleavage protease of endoglin.
3 is an essential receptor in angiogenesis, or endoglin.
4  signaling can compensate for the absence of endoglin.
5 tor studies showed no involvement of ALK5 or endoglin.
6 Z binding motif in the cytoplasmic domain of endoglin.
7 ith GIPC-promoting cell surface retention of endoglin.
8 evel for accessory molecules beta-glycan and endoglin.
9 l specific TGF-beta superfamily co-receptor, endoglin.
10 roduced similar effects to the inhibition of endoglin.
11  marker expression similar to that seen with endoglin.
12 in hemangioblast frequency in the absence of endoglin.
13 ugh the direct transcriptional regulation of Endoglin.
14 ants was clearly enhanced in the presence of endoglin.
15  interact, and that each also interacts with endoglin.
16  increased motility was inhibited by soluble endoglin.
17        Interestingly, Src phosphorylation of endoglin-(612)YIY(614) was also an important process for
18 ngineering multiple tumor models deprived of endoglin, a co-receptor for TGF-beta in endothelial cell
19  factor beta (TGF-beta) type I receptor, and endoglin, a TGF-beta co-receptor, play an essential role
20 -like tyrosine kinase receptor 1 and soluble endoglin, a TGF-beta signaling inhibitor, we investigate
21 cyte migration by regulating the function of endoglin, a TGF-beta1 accessory receptor.
22                                              Endoglin, a transforming growth factor-beta co-receptor,
23              We previously demonstrated that endoglin, a type III transforming growth factor beta (TG
24                     Here we demonstrate that endoglin abrogates TGFbeta-mediated cell motility, but d
25             TRC105, along with several other endoglin Abs tested, enhance endoglin shedding through d
26 avage substrates tissue transglutaminase and endoglin accompanied MMP-14 suppression.
27 merous vascular conditions, the mechanism of endoglin action remains poorly understood.
28 ncer progression; furthermore, they show how endoglin acts to support the viability of tumor-infiltra
29                            The importance of endoglin, ALK-1, and ALK-5 in endothelial biology is und
30 ar diseases both support essential roles for endoglin, ALK-1, and ALK-5 in the vasculature.
31                                  Blocking of endoglin-ALK1-SMAD1/5 might be a good candidate for ther
32 n increase Smad1/5/8 signalling by promoting endoglin/ALK1 cell surface complex formation.
33                         Here, we report that endoglin also plays an important role early in developme
34                           Here we identified endoglin, an EC-specific TGF-beta co-receptor essential
35                                 Mutations in endoglin and activin-like kinase receptor 1 (ALK1) cause
36 ation via the TGF-beta superfamily receptors endoglin and activin-like kinase-1 (ALK1).
37                             RNA knockdown of endoglin and ALK1 impaired SDF1/CXCR4 regulation by BMP9
38 remodeling, acting via the HHT target genes, endoglin and ALK1.
39        Although prior studies indicated that endoglin and Alk5 were not directly involved in epitheli
40 ition of pericyte migration was dependent on endoglin and alphaV integrin.
41 l therapeutics to reduce circulating soluble endoglin and ameliorate the clinical features of severe
42 oglin internalization and co-accumulation of endoglin and beta-arrestin2 in endocytic vesicles.
43 demonstrate the specific interaction between endoglin and beta-arrestin2 in endothelial cells, enhanc
44 ities of biologically active STBM associated endoglin and Flt-1/sFlt-1 could contribute to the increa
45  missing for the endothelial cell coreceptor endoglin and for the ALK1 type I receptor, which enables
46    Here we report a novel mechanism in which endoglin and Galpha-interacting protein C-terminus-inter
47 h demonstrate a specific interaction between endoglin and GIPC in endothelial cells, mediated by a cl
48 studies define a novel non-Smad function for endoglin and GIPC in regulating endothelial cell functio
49 Here we describe a novel interaction between endoglin and GIPC, a scaffolding protein known to regula
50 hing mammosphere-initiating cells, including endoglin and prion protein, will facilitate the elucidat
51               SPARC interacted directly with endoglin and reduced endoglin interaction with alphaV in
52   Placental growth factor increased, whereas endoglin and soluble vascular endothelial growth factor
53 endoglin shedding through direct coupling of endoglin and the membrane-type 1 matrix metalloproteinas
54   Here we define a novel interaction between endoglin and the scaffolding protein beta-arrestin2.
55                          We established that endoglin and type II receptors bind to overlapping sites
56      In this project, the redundancy between endoglin and vascular endothelial growth factor (VEGF) s
57          Moreover, combined targeting of the endoglin and VEGF pathway, with the VEGF receptor kinase
58    These studies define a novel function for endoglin, and further expand the roles mediated by the u
59 ncluding VE-cadherin, von Willebrand factor, endoglin, and intercellular adhesion molecule-2.
60 ptor type 2, activin receptor-like kinase 1, endoglin, and mothers against decapentaplegic 9.
61 rmed expression of alpha(v)beta(3) integrin, endoglin, and VEGFR2 on tumor vascular endothelial cells
62 pression levels of alpha(v)beta(3) integrin, endoglin, and VEGFR2, which vary during tumor growth in
63 l EC-restricted genes including VE-cadherin, endoglin, and von Willebrand factor, and a negative regu
64 on either Smad 2/3 or Smad 1/5/8 activation, endoglin antagonized TGF-beta-mediated ERK signaling, al
65 detect angiogenesis using anti-VEGF and anti-endoglin (anti-CD105) and activated glial cells (anti-gl
66 of action of TRC105, an anti-angiogenic anti-Endoglin antibody currently evaluated in clinical trials
67           These data show that both Alk5 and endoglin are directly involved in the process of EMT, th
68                         Our results identify endoglin as a critical component of TGFbeta1 signaling i
69      Taken together, these results establish endoglin as a critical mediator of autophagy and demonst
70 h factor, placenta growth factor, or soluble endoglin as assessed by ELISA.
71 luble fms-like tyrosine kinase-1 and soluble endoglin, as assessed by enzyme-linked immunosorbent ass
72          It does so by activating ALK2-Smad1 endoglin-associated signaling.
73 ng platform detects as few as 1000 copies of endoglin at concentrations as low as 83 fM with high det
74 e cardiac fibroblast and show that targeting endoglin attenuates cardiac fibrosis, thereby providing
75                                          The endoglin/beta-arrestin2 interaction results in endoglin
76                                     Alk5 and endoglin both mediate endothelial cell proliferation in
77 mapping analysis of the different domains of endoglin by examining their contributions to the selecti
78  have shown that the extracellular domain of endoglin can be cleaved and released into the circulatio
79 profiles demonstrated that low expression of endoglin (CD105) correlated with a subgroup of adipose-d
80                                              Endoglin (CD105) is an endothelial-specific transforming
81                Our array data suggested that endoglin (CD105) mRNA is significantly upregulated in HC
82                                              Endoglin (CD105), a receptor of the transforming growth
83                                              Endoglin (CD105), a transmembrane protein of the transfo
84 ing is modulated by the TGF-beta co-receptor endoglin (CD105).
85 nvolved in inflammation, strongly adhered to endoglin-coated plates and to endoglin-expressing endoth
86  was localized to the orphan domain of human endoglin composed of the amino acid sequence 26-359.
87 ese findings provide the first evidence that endoglin decreases PCa cell motility through activation
88              Moreover, the data suggest that endoglin deficiency impaired SDF1 expression in endothel
89 cient to restore a low-motility phenotype in endoglin deficient cells.
90 , genistein was shown to induce reversion of endoglin-deficient cells to a low motility, endoglin-rep
91                                  Tumors from endoglin-deficient mice adapted to the weakened angiogen
92 during the response to hindlimb ischemia, in endoglin-deficient mice.
93 on to a low-motility phenotype in aggressive endoglin-deficient PCa cells.
94 teins (IGFBP) in the conditioned medium from endoglin-deficient PrSCs and that endoglin-dependent reg
95                                         This endoglin-dependent adhesion was abolished by soluble end
96 nalling to focal adhesion kinase (FAK) in an endoglin-dependent manner.
97 d increased endothelial cell migration in an endoglin-dependent manner.
98  addressed this question by investigation of endoglin-dependent prostate cancer progression in a TRAM
99 edium from endoglin-deficient PrSCs and that endoglin-dependent regulation of IGFBP-4 secretion was c
100                                      Whereas endoglin did not have a direct impact on either Smad 2/3
101 ymerizing ZP proteins such as betaglycan and endoglin do not contain this cleavage site.
102    Other ZP proteins (namely, betaglycan and endoglin) do not polymerize but serve as important membr
103                    Unlike endothelial cells, endoglin does not modulate Smad-mediated TGF-beta signal
104  in physiology and disease, the mechanism of endoglin down-regulation remains unknown.
105 ontrast, in the presence of activated ErbB2, endoglin downregulation in MCF10A cells leads to enhance
106                                              Endoglin downregulation in non-tumorigenic MCF10A breast
107                                     Although endoglin dysfunction contributes to numerous vascular co
108 ndings indicate an important role of soluble endoglin ECD in the regulation of angiogenesis and highl
109                              Finally, murine endoglin ECD-Fc acted as an anti-angiogenic factor that
110 ane assay, the mouse and the truncated human endoglin ECD-Fc both significantly reduced VEGF-induced
111                We found that mouse and human endoglin ECD-Fc bound directly, specifically, and with h
112                                  A number of endoglin ectodomain-targeting antibodies (Abs) can effec
113 lts show, for the first time, that targeting endoglin, either with neutralizing antibodies or a ligan
114 determine vesicle size, purity and Flt-1 and endoglin (Eng) expression.
115 d specific promoter/enhancer combinations of Endoglin (ENG) have been shown to target blood and endot
116                                              Endoglin (ENG), a co-receptor for several TGFbeta-family
117                           Here, we show that endoglin (Eng), a receptor for the TGFbeta superfamily,
118                                              Endoglin (Eng), an accessory receptor for the transformi
119                                              Endoglin (ENG), an ancillary receptor for several member
120  matrix metalloproteinase-2 (MMP-2), MMP-14, endoglin (ENG), and superoxide dismutase 3 in ascending
121 amily, activin-like kinase-type 1 (ALK1) and endoglin (ENG), which are associated with hereditary hem
122 Wnt signalling pathways are integrated in an endoglin (Eng)-dependent manner in cardiac and haematopo
123 strate that the TGFbeta auxiliary coreceptor endoglin (eng, CD105) is expressed in a subset of neural
124 h the RGD-containing extracellular domain of endoglin, enhanced leukocyte transmigration, and this in
125                                              Endoglin enhances ALK1-SMAD1/5 signaling in different ce
126             Nevertheless, tumors deprived of endoglin exhibited a delayed onset of resistance to anti
127 gly adhered to endoglin-coated plates and to endoglin-expressing endothelial cells.
128 support the notion that individuals with low endoglin-expressing PCa will benefit from genistein trea
129           We further identified that reduced endoglin expression attenuates cardiac fibrosis, preserv
130 omal cells (PrSC) confirmed that suppressing endoglin expression decreased cell proliferation, the ab
131 e cohort of invasive breast cancers, lack of endoglin expression in the tumor cell compartment correl
132                         We first report that endoglin expression is increased in the left ventricle o
133                 We hypothesized that reduced endoglin expression may limit cardiac fibrosis in heart
134                    We here show that loss of endoglin expression mediated by either antisense DNA or
135    In this study, we have observed increased endoglin expression on the cell surface of an HCV core-e
136                             We have observed endoglin expression on the HCV core-expressing cell surf
137                                We identified endoglin expression on the majority of blasts from patie
138 emonstrated significantly (P </= .04) higher endoglin expression than both alpha(v)beta(3) integrin a
139  and tumor induced angiogenesis (by means of Endoglin expression).
140 nfirm these data, we assessed the effects of endoglin-Fc (an endoglin ligand trap) on metastasis form
141 on of angiogenesis and highlight efficacy of endoglin-Fc as a potential anti-angiogenesis therapeutic
142 reatment with TRC105 in the resection model, endoglin-Fc-expressing tumors showed strong inhibition o
143 ressed on endothelial cells were identified: endoglin, Fms-like tyrosine kinase-3 ligand, EGF-like re
144                     alpha5beta1 integrin and endoglin form a complex on the cell surface and co-inter
145 al-specific TGF-beta superfamily coreceptor, endoglin, form a heteromeric complex and bind similar TG
146 er photobleaching (FRAP) to demonstrate that endoglin forms stable homodimers that function as a scaf
147 trasensitive detection and quantification of endoglin from unprocessed human urine samples using a gi
148 le-1 (PECAM-1), CD144/VE-cadherin, and CD106/Endoglin, from vascular endothelial cells.
149  Several agents that interfere with ALK1 and endoglin function are currently in clinical trials for a
150 nstrate that GIPC is a critical component of endoglin function during developmental angiogenesis in v
151               However the mechanism by which endoglin functions at this early developmental stage is
152 xtracellular domain (ECD) of mouse and human endoglin fused to an immunoglobulin Fc domain.
153 ereas bone morphogenetic protein-9 enhances, endoglin/GIPC-mediated membrane scaffolding of PI3K and
154                                              Endoglin has been identified as an important suppressor
155                  This function was tested in endoglin heterozygous mice (Eng(+/-)) and their wild-typ
156 enetic protein receptor genes, ENG, encoding endoglin (HHT1), or ACVRL1 encoding ALK1 (HHT2), and con
157 aryocytic maturation, and the CD150(+)CD9(lo)endoglin(hi) fraction, which contains erythroid lineage-
158    Additionally, we observed upregulation of endoglin/ID1 mRNA expression in chronic HCV patient live
159 , an increase in alphaV integrins present in endoglin immunoprecipitates, and enhanced alphaV integri
160 s and point to a role for BMP9 signaling via endoglin in a switch from an SDF1-responsive autocrine p
161 together, these findings point to a role for endoglin in both hemangioblast specification and hematop
162 a activity and identify a novel function for endoglin in controlling pericyte behavior.
163 time points, further supports a function for endoglin in early hematopoiesis.
164  pericyte migration, aberrant association of endoglin in focal complexes, an increase in alphaV integ
165 used recruitment of ALK1 into a complex with endoglin in human umbilical vein endothelial cells (HUVE
166 stent with these data, ectopic expression of endoglin in MDA-MB-231 cells blocks TGF-beta-enhanced ce
167                                Expression of endoglin in NCSCs declined with age, coinciding with a r
168 stablish the pathophysiologic involvement of endoglin in prostate cancer progression; furthermore, th
169 dings demonstrate a cell autonomous role for endoglin in smooth muscle cell specification contributin
170                            Overexpression of endoglin in the neural crest caused pericardial hemorrha
171 at MMP-14 is the likely cleavage protease of endoglin in the setting of preeclampsia.
172 ine CXCL12, suggesting a regulatory role for endoglin in transendothelial leukocyte trafficking.
173                       The mechanism by which endoglin inhibits PCa cell motility is unknown.
174  transforming growth factor-beta co-receptor Endoglin inhibits the migration of prostate and breast c
175 nteracted directly with endoglin and reduced endoglin interaction with alphaV integrin.
176 onstrate for the first time that endothelial endoglin interacts with leukocyte integrin alpha5beta1 v
177                          We demonstrate that endoglin interacts with the PI3K subunits p110alpha and
178 doglin/beta-arrestin2 interaction results in endoglin internalization and co-accumulation of endoglin
179 directly phosphorylates this motif to induce endoglin internalization and degradation via the lysosom
180 ed BMP9-dependent recruitment of co-receptor endoglin into this angiogenesis-mediating signaling comp
181                                              Endoglin is a co-receptor predominantly expressed in end
182                          Membrane-associated endoglin is a coreceptor for TGFbeta1 signaling and has
183                                              Endoglin is a transforming growth factor beta (TGF-beta)
184                                              Endoglin is a transforming growth factor beta (TGF-beta)
185                                              Endoglin is a transforming growth factor beta (TGFbeta)
186                                              Endoglin is an accessory receptor for TGF-beta that has
187                                              Endoglin is an accessory receptor for TGFbeta and can as
188                                      Soluble endoglin is an anti-angiogenic protein that is released
189                                        Human endoglin is an RGD-containing transmembrane glycoprotein
190                         Therefore, targeting endoglin is currently being explored in clinical trials
191                                     Although endoglin is essential for angiogenesis and its expressio
192                     Here we demonstrate that endoglin is expressed in a subset of invasive breast can
193          However, the mechanism of action of endoglin is not well defined.
194                                              Endoglin is part of the TGF-beta receptor complex and ha
195          The mechanism through which soluble endoglin is released from the placenta is currently unkn
196 jects with heart failure and determined that endoglin is required for TGFbeta1 signaling in human car
197                           Furthermore, the S-endoglin/L-endoglin mRNA expression ratio was significan
198  and eng(+/+) ES cells revealed that lack of endoglin leads to profound reductions in the levels of k
199 luble fms-like tyrosine kinase-1 and soluble endoglin levels and restored fetal growth in mice that w
200 ts with GM6001 decreased circulating soluble endoglin levels in mouse serum (P </= 0.05).
201                      The results reveal that endoglin levels in urine have the potential to predict f
202 weeks through 20 weeks of gestation, soluble endoglin levels were significantly higher in women in wh
203 , we assessed the effects of endoglin-Fc (an endoglin ligand trap) on metastasis formation.
204              We now demonstrate that soluble endoglin limits TGFbeta1 signaling and type I collagen s
205 -megakaryocyte progenitor and CD150(+)CD9(hi)endoglin(lo) cells are TPO-responsive and that the latte
206 te progenitor population, the CD150(+)CD9(lo)endoglin(lo) fraction of Lin(-)cKit(+)IL7 receptor alpha
207 fraction is distinct from the CD150(+)CD9(hi)endoglin(lo) fraction, which contains bipotential precur
208  is therefore important to determine whether endoglin loss affects genistein's efficacy and, if so, b
209 luble fms-like tyrosine kinase 1 and soluble endoglin, markers thought to be related to the disease.
210 more, cell-sorting experiments revealed that endoglin marks the hemangioblast on day 3 of EB differen
211 hree types of targeted MBs (MB(Integrin), MB(Endoglin), MB(VEGFR2)) was tested in cell culture under
212                 SPARC deficiency resulted in endoglin-mediated blockade of pericyte migration, aberra
213 of ALK2, but not TGFbetaRI (ALK5), abrogated endoglin-mediated decreases in cell motility and constit
214                                Functionally, endoglin-mediated fibronectin/alpha5beta1 integrin and T
215 at both BMPRII and ActRIIA are necessary for endoglin-mediated suppression of human PCa cell invasion
216                                              Endoglin-mediated suppression of invasion was also shown
217 o type II TGFbeta receptors are required for endoglin-mediated suppression of invasion: activin A rec
218              However, the mechanism by which endoglin mediates TGF-beta signaling through ALK-1 and A
219                                              Endoglin modulates the crucial balance between pro- and
220                Furthermore, the S-endoglin/L-endoglin mRNA expression ratio was significantly lower i
221 ut not a threonine phosphorylation-defective endoglin mutant blocked cell detachment and the antiprol
222 ted that only NCSC expressing high levels of endoglin (NCSC(CD105+)) had myogenic differentiation pot
223                          In vitro TRC105, an endoglin-neutralizing antibody, increased VEGF signaling
224 n younger explants but, by stage 16, loss of endoglin no longer alters proliferation rates.
225 tential was deficient in NCSCs obtained from endoglin null embryos.
226 tors, TbetaRII preferentially phosphorylated endoglin on cytosolic domain serine residues Ser(634) an
227 ive (ca)ALK1, but not caALK5, phosphorylated endoglin on cytosolic domain threonine residues.
228 ase 1 (ALK1), type II receptors, co-receptor endoglin, or to mature BMP9 domain targeting antibodies
229                Moreover, we demonstrate that Endoglin overexpression abrogates the increased migratio
230 th treatments produced a decrease in soluble endoglin (P </= 0.05).
231 d lower serum PlGF (P=0.003), higher soluble endoglin (P=0.006), and higher sFlt-1:PlGF ratio (P=0.00
232                            Evaluation of the endoglin pathway suggested that enhanced osteogenesis am
233                Finally, administration of an endoglin peptide containing the consensus matrix metallo
234 horylation in HUVECs and indicate a role for endoglin phosphorylation in the regulation of endothelia
235 lation, suggesting a sequential mechanism of endoglin phosphorylation.
236 ic expression of HCV core protein.IMPORTANCE Endoglin plays a crucial role in fibrogenesis and angiog
237                                              Endoglin plays a key role in angiogenesis by modulating
238        Here we show that PRH can bind to the Endoglin promoter in immortalised prostate and breast ce
239                                     Overall, endoglin promotes autophagy by impeding Smad2 transcript
240 EMT) in the heart, the expression pattern of endoglin prompted a re-examination.
241 pression in these cells results in increased Endoglin protein expression, whereas PRH knockdown resul
242 , whereas PRH knockdown results in decreased Endoglin protein expression.
243 19, P=0.02); at 18 to 25 weeks, with soluble endoglin (r=0.18, P=0.02); and at 26 to 33 weeks, with s
244 satility index correlated with serum soluble endoglin (r=0.19, P=0.02) and sFlt-1 levels (r=0.17, P=0
245 llular distribution studies demonstrate that endoglin recruits GIPC to the plasma membrane and co-loc
246                              We propose that endoglin regulates primitive hematopoiesis by modulating
247 tion of BrdU incorporation shows that, while endoglin regulates proliferation at an early stage, redu
248 s also the mechanism responsible for soluble endoglin release in preeclampsia, we investigated the ex
249 and the effects of its inhibition on soluble endoglin release.
250  endoglin-deficient cells to a low motility, endoglin-replete phenotype.
251                                 Mutations in endoglin result in the vascular defect known as heredita
252 odels of cancer revealed that deficiency for endoglin resulted in a tumor vasculature that displayed
253 -dependent adhesion was abolished by soluble endoglin, RGD peptides, the anti-integrin alpha5beta1 in
254 wn of Smad1 increased motility and abrogated endoglin's effects.
255                     Soluble Flt1 and soluble endoglin, secreted by the placenta, are increased in the
256 wth factor receptor-1 [VEGFR-1]) and soluble endoglin (sEng) are elevated in preeclampsia, and their
257                            A soluble form of endoglin (sEng) has been shown to cause endothelial dysf
258 pregnancy-specific syndrome in which soluble endoglin (sEng) is a prognostic marker and plays a patho
259  of this study was to compare plasma soluble endoglin (sEng) levels with standard clinical evaluation
260 e circulating antiangiogenic factor, soluble endoglin (sEng), is elevated in the blood circulation of
261 o release the antiangiogenic factor, soluble endoglin (sEng).
262              Collectively, our study defines endoglin shedding and deregulated TGF-beta signaling dur
263        In addition to this coupling process, endoglin shedding is further amplified by increased MMP-
264 h several other endoglin Abs tested, enhance endoglin shedding through direct coupling of endoglin an
265                In patient samples, increased endoglin signaling after VEGF inhibition was observed.
266 fine a novel mechanism for the regulation of endoglin signaling and function in endothelial cells and
267 ion by HCV core protein was dependent on the endoglin signaling pathway using activin receptor-like k
268 c response, and refractoriness to diminished endoglin signaling was accompanied by increased metastat
269 oding activin receptor-like kinase 1 (ALK1), endoglin, Smad4, and bone morphogenetic protein 9 (BMP9)
270 like kinase 1 (ALK1) Fc blocking peptide and endoglin small interfering RNA (siRNA).
271                                              Endoglin specifically enhanced TGF-beta1-induced phospho
272 angiogenic mitogens as critical mediators of endoglin stability and function.
273                                      Because endoglin suppresses PCa cell motility in an activin-like
274 on Smad activation, but were associated with endoglin suppression and accentuated expression of bone
275 or down-regulation by TRACON105 (TRC105), an endoglin-targeting antibody currently in clinical trials
276 1 is a preferred TGFbeta receptor kinase for endoglin threonine phosphorylation in HUVECs and indicat
277 of cell surface markers, including CD105 (or endoglin), Thy1 [or CD90 (cluster of differentiation 90)
278 loy the first transgenic zebrafish model for endoglin to demonstrate that GIPC is a critical componen
279 tion in a manner dependent on the ability of endoglin to interact with beta-arrestin2.
280 tion in a manner dependent on the ability of endoglin to interact with GIPC.
281 dothelial phenotype (Cx40(+), VEGFR2(+), and endoglin(-)) to the surrounding endocardium (Cx40(-), VE
282 te transmigration through cell monolayers of endoglin transfectants was clearly enhanced in the prese
283 ac fibroblasts and further show that soluble endoglin treatment attenuates cardiac fibrosis in an in
284  factor (VEGF) as Src-activators that induce endoglin turnover following (612)YIY(614) phosphorylatio
285 ogical activity of STBM associated Flt-1 and endoglin was assessed by the ability of VEGF, PlGF and T
286 ocarcinoma mouse prostate) mouse model where endoglin was genetically deleted.
287                               In this model, endoglin was haploinsufficient such that its allelic del
288 ation and Smad-responsive promoter activity, endoglin was shown to constitutively activate Smad1, wit
289                                      Soluble endoglin was strongly correlated with sFlt1 and PlGF lev
290                          The soluble form of endoglin was suggested to contribute to the pathogenesis
291                An increased level of soluble endoglin was usually accompanied by an increased ratio o
292 trate that this interaction produces soluble endoglin, we treated trophoblastic BeWo cells with eithe
293                       As Alk5 interacts with endoglin, we utilized siRNA and a specific inhibitor, HT
294 like tyrosine kinase 1 (sFlt-1), and soluble endoglin were prospectively measured in 159 women from 1
295 NFalpha) and myeloid differentiation factor (Endoglin) were increased in myeloid cells from p65 KO tu
296 and released into the circulation as soluble endoglin, which disrupts TGFbeta1 signaling in endotheli
297  directly to the TGF-beta accessory receptor endoglin, which, in the presence of TGF-beta1, results i
298                        ALK1 and ALK5 bind to endoglin with differential dependence on TbetaRII, which
299 owever, the pathophysiologic significance of endoglin with respect to prostate tumorigenesis has yet
300 n interactions between endogenous MMP-14 and endoglin within the preeclamptic placenta.

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