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1 TSP-1 also inhibited VASP phosphorylation stimulated by
2 TSP-1 and the CD36 binding peptide induced phosphorylati
3 TSP-1 binds to matrix components, proteases, cytokines,
4 TSP-1 blockade also prevents the PH in a second model, c
5 TSP-1 converts latent transforming growth factor-beta1 (
6 TSP-1 deficiency resulted in significantly reduced TGF-b
7 TSP-1 disruption abrogated age-associated capillary rare
8 TSP-1 disruption did not affect inflammatory gene expres
9 TSP-1 disruption did not significantly affect weight gai
10 TSP-1 expression was induced in endothelial cells (ECs)
11 TSP-1 functioned in a positive feedback loop to stabiliz
12 TSP-1 has been shown to reduce von Willebrand factor (VW
13 TSP-1 induced in ECs by reactive oxygen species (ROS) mo
14 TSP-1 is a potent antiangiogenic and proatherogenic prot
15 TSP-1 is reported to be a p53-target gene and p53 is a k
16 TSP-1 plays no direct role in the regulation of its own
17 TSP-1 prevented PGE-stimulated cAMP accrual and phosphor
18 TSP-1 supports an anti-inflammatory phenotype of microgl
19 TSP-1 tethering of ERK in the cytoplasm promoted a level
20 TSP-1 upregulation in the diabetic heart prevents chambe
21 TSP-1-/- animals had more extensive postinfarction remod
22 TSP-1/CD36 interactions were shown to regulate angiogene
23 matrix protein (COMP) and thrombospondin 1 (TSP-1) correlated moderately well with the MRSS, but the
25 Basal muscle expression of thrombospondin 1 (TSP-1) was approximately 900% greater in 14d- and 28d-tr
26 (VEGF), but high levels of thrombospondin 1 (TSP-1), predicted liver dysfunction after resection.
30 g to the type 1 repeats of thrombospondin-1 (TSP-1) and activating Fyn tyrosine kinase and MAPK pathw
31 cellular components [i.e., thrombospondin-1 (TSP-1) and fibronectin (FN)] seem to trigger different p
32 and elevated expression of thrombospondin-1 (TSP-1) and its receptor CD36, anti-angiogenic factors.
33 d the CD47-binding partner thrombospondin-1 (TSP-1) and that treatment of aged erythrocytes with a TS
34 p53 led to a deficiency in thrombospondin-1 (TSP-1) expression, a potent antiangiogenic protein, and
35 roteins and proteoglycans, thrombospondin-1 (TSP-1) functions at the interface of the cell membrane a
36 The N700S polymorphism of thrombospondin-1 (TSP-1) has been identified as a potential genetic risk f
47 how TGF-beta activation by thrombospondin-1 (TSP-1) is both required and sufficient for the developme
48 n anti-angiogenic protein, thrombospondin-1 (TSP-1) is down-regulated in the prostate and liver of U1
52 creasing evidence suggests thrombospondin-1 (TSP-1), a potent proatherogenic matricellular protein, a
53 ors, including endostatin, thrombospondin-1 (TSP-1), and pigment epithelium-derived factor (PEDF), as
55 and in vivo validations on thrombospondin-1 (TSP-1), because it has been previously shown to be impor
56 he second type-1 repeat of thrombospondin-1 (TSP-1), is known to possess antiangiogenic activity.
57 The matricellular protein, thrombospondin-1 (TSP-1), is prominently expressed during tissue repair.
58 tumstatin, endostatin, or thrombospondin-1 (TSP-1), to address the role that these endogenous angiog
59 gulating the production of thrombospondin-1 (TSP-1)--known earlier for both its anti-angiogenic and p
68 anti-angiogenic peptides (thrombospondin-1, TSP-1; and endostatin) as well as pro-angiogenic factors
71 ed TSP-1 transcription and the activity of a TSP-1 promoter-reporter construct stimulated by high glu
72 d that treatment of aged erythrocytes with a TSP-1-derived peptide enabled their phagocytosis by huma
73 We examined thrombospondin-1 (THBS1, alias TSP-1) expression in human synovial tissue (ST) during t
75 a demonstrate that NOL7 significantly alters TSP-1 expression and may be a master regulator that coor
76 a demonstrate that NOL7 significantly alters TSP-1 expression and may be a master regulator that coor
79 I44) and sialoadhesin (Siglec-1) to COMP and TSP-1 in multiple regression analyses significantly impr
80 r the aberrant angiogenesis in diabetics and TSP-1 involvement in development of various vascular dia
89 r therapy, a reciprocal relationship between TSP-1 and NR4A2 expression levels was measured in patien
91 kinase inhibitor, SB203580, instead blocked TSP-1 expression and a p38 activator, MKK6, increased TS
92 Moreover, inhibition of Src kinases blocked TSP-1-mediated regulation of cAMP concentrations and the
97 identified three potential biomarkers CD163, TSP-1 and IL-1RII whose response to steroids was signifi
98 iated antiangiogenic pathway induced by CD36-TSP-1 interaction that inhibits VEGFR2 signaling and the
115 riptional networks, suggesting that enhanced TSP-1 expression may help restore tissue homeostasis dur
119 l of a partial hepatectomy (PH) and explored TSP-1 induction, progression of liver regeneration, and
123 tudies introduce a new signaling pathway for TSP-1, CD36, and Syk, and address the role of these prot
130 perative alpha-granule release profile (high TSP-1/low VEGF) showed substantially worse postoperative
131 ecipitation confirmed that recombinant human TSP-1 can bind BMP-2 and -4 and antagonize their effects
132 1 in diabetic atherosclerosis, hyperglycemic TSP-1(-/-)/ApoE(-/-) double knockout mice were compared
139 hanced migration of microglia is detected in TSP-1 null retina, and these microglia express markers a
140 c kidney injury was demonstrated directly in TSP-1 null mice, which showed significant protection aga
141 rgic signaling may be an important factor in TSP-1-mediated cell-matrix and cell-cell interactions su
142 with extracellular ATP caused an increase in TSP-1 expression in a time- and concentration-dependent
145 ated region, and its elimination resulted in TSP-1 reactivation, impaired angiogenesis in Matrigel pl
147 the production of BrM components, including TSP-1, PEDF, and tropoelastin in vitro and increased the
149 ased VEGF and IL-8 expression, but increased TSP-1 expression in BT474 breast cancer cells that expre
152 proliferation and VEGF production, increased TSP-1 and endostatin, and inhibited corneal neovasculari
153 ied with inhibition of hyperglycemia-induced TSP-1 expression and reduced protein O-glycosylation fol
157 protein glycosylation efficiently inhibited TSP-1 transcription and the activity of a TSP-1 promoter
159 g-standing cardiovascular benefits, inhibits TSP-1 expression in glucose-stimulated human aortic smoo
161 monoclonal antibodies to human TSP-2 and its TSP-1 homolog have given insights into the structure of
162 nes raise this threshold which leads to less TSP-1 production, while signals that promote the generat
163 n uveitis, in the presence of TLR-4 ligands, TSP-1 is initially produced by recruited macrophages but
164 cytometry analysis revealed that, in males, TSP-1 knockout reduced macrophage infiltration and phago
165 t-like synoviocytes (FLSs) expressed minimal TSP-1 mRNA levels with high transcript levels of NR4A2,
166 therapeutic strategies designed to modulate TSP-1 synthesis in conditions that simulate tumor and pe
168 betic db/db mice exhibited marked myocardial TSP-1 upregulation in the interstitial and perivascular
169 how that in cultured rat spinal cord neurons TSP-1 decreased neuronal excitability by reducing the ac
170 s of heparin further enhances the ability of TSP-1 to participate in high affinity binding to glycosa
172 glucose, we demonstrated that activation of TSP-1 transcription is mediated by the hexosamine pathwa
173 whether the altered VWF-reducing activity of TSP-1 underlies the observed prothrombotic phenotype.
174 angiogenesis in this model as application of TSP-1 inhibited angiogenesis and blockade of both TSP-1
180 ogical assessment indicated that deletion of TSP-1 reduced inflammatory cell infiltration of muscle f
182 ort that the von Willebrand type C domain of TSP-1 is likely responsible for this BMP-2/4-binding act
183 agent based on the antiangiogenic domain of TSP-1, designated 3TSR (for three TSP-1 type 1 repeats),
184 the high affinity heparin-binding domain of TSP-1, designated TSPN-1, in association with the synthe
189 unding C-terminal and N-terminal elements of TSP-1 and interact with other extracellular molecules.
190 es as the predominant sites of expression of TSP-1 in IR injury and showed colocalization of TSP-1 wi
192 st that U19/EAF2 regulates the expression of TSP-1 via blocking p53 repression of the TSP-1 promoter.
201 In this context, physiological levels of TSP-1 appear to support VEGFR2 function on both the cell
204 T2 MRI parameters revealed that loss of TSP-1 modestly inhibited inflammation only in gluteal mu
205 Rotary shadowing electron microscopy of TSP-1 has shown elongation of the stalk and diminution o
208 that together make up the complex network of TSP-1 regulation both at the transcriptional and post-tr
213 RPE is controlled by untranslated regions of TSP-1 mRNA that regulate coupling of TSP-1 mRNA to polys
216 istance, and identify txr1 as a regulator of TSP-1 production and an agent for its chemotherapeutic m
218 es unique regions of three type-I-repeats of TSP-1 and used engineered human neural stem cells (hNSC)
226 eptide possessing a CD36 binding sequence of TSP-1, while the effects of TSP-1 were prevented by a CD
230 -specific posttranscriptional suppression of TSP-1 production in response to high glucose in microvas
235 , as well as those in the periphery of older TSP-1 null mice, secrete interleukin-17A, a cytokine ass
237 Decrease of Txr1 or treatment with TSP-1 or TSP-1 mimetic peptide sensitized cells to taxane cytotox
239 the in vitro studies, suppression of CD47 or TSP-1 expression in newborn mice by a novel in vivo smal
240 b or knocking down the expression of CD47 or TSP-1, but not signal regulatory protein alpha by small
242 V600E) cells in which either B-Raf(V600E) or TSP-1 were knocked down were implanted orthotopically in
243 me PCR analysis of retina derived from WT or TSP-1 null mice at various time intervals after light- o
244 in part, through activation of the HER2-p38-TSP-1 pathway and inhibition of the HER2-PI3K-AKT-VEGF/I
245 ardiac fibroblasts populating collagen pads, TSP-1 incorporation into the matrix did not activate tra
246 demonstrate that, through this new pathway, TSP-1 is responsible for the remote AC-mediated recovery
249 increased vascularity is mediated by reduced TSP-1 and TSP-2 levels and causes delayed tumor growth r
250 Ectopic NR4A2 expression led to reduced TSP-1 mRNA and protein levels with concomitant increases
251 herefore plays a dominant role in regulating TSP-1 production in the target organ during acute inflam
254 led to the design of the first serum stable TSP-1 mimetic agonist peptide able to trigger selective
261 hat stimulates release of ATP, we found that TSP-1 expression increased after mechanical strain and w
263 d healthy controls, supporting the idea that TSP-1 levels are correlated with disease progression.
266 the phosphorylation of VASP, indicating that TSP-1 modulated the cAMP/PKA signaling events through a
269 use model of lung cancer, we have shown that TSP-1 plays a critical and cell-autonomous role in suppr
270 assertion based on sequence similarity that TSP-1 shares with the von Willebrand type C domain of Cr
271 within the developing CNS, and suggest that TSP-1 and -2 act as a permissive switch that times CNS s
277 letion studies identified a 5' region of the TSP-1 promoter repressed by NR4A2 and proangiogenic tran
281 orter assay, p53 transfection suppressed the TSP-1 promoter activity and U19/EAF2 co-transfection blo
282 -positive blood vessels, suggesting that the TSP-1 down-regulation can contribute to increased angiog
286 GF in the synovium, after treatment with the TSP-1-derived peptide were studied in the peptidoglycan-
290 investigate the therapeutic benefit of this TSP-1-derived peptide sequence and its effect on connect
291 domain of TSP-1, designated 3TSR (for three TSP-1 type 1 repeats), has significant antiangiogenic an
292 In summary, we identified for the first time TSP-1 as a BMP-2/-4 antagonist and presented a structura
293 al role of CD47 in the cellular responses to TSP-1 was demonstrated further using inhibitory antibodi
294 revealed by comparing wild-type (WT) versus TSP-1 null allografts in corneal transplantation, as the
296 recruitment of circulating monocytes, while TSP-1 inhibition or knockout bone marrow prevents TGF-be
297 hagocytic activity, which is consistent with TSP-1-enhanced phagocytosis and pro-inflammatory cytokin
299 then crossed dysferlinopathic BlaJ mice with TSP-1 knockout mice and assessed disease progression lon
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