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1 growth factor, insulin-like growth factor 2, thrombospondin 1.
2 ive expression of angiogenic inhibitors like thrombospondin-1.
3 ain, but they do not hetero-oligomerize with thrombospondin-1.
4 r soluble P-selectin, platelet factor 4, and thrombospondin-1.
5 responses to the matricellular glycoprotein thrombospondin-1.
6 IF-1alpha) and VEGF and a down-regulation of thrombospondin-1.
7 DL (oxLDL), cell-derived microparticles, and thrombospondin-1.
8 of both transforming growth factor-beta and thrombospondin-1.
9 o dependent and might have been regulated by thrombospondin-1.
10 rivative of the natural angiogenic inhibitor thrombospondin-1.
11 le guanylyl cyclase-cGMP signaling inhibitor thrombospondin-1.
12 the production of the angiogenesis inhibitor thrombospondin-1.
13 d its receptor on T cells, but also by Ab to thrombospondin-1.
14 the production of the angiogenesis inhibitor thrombospondin-1.
15 otably plasminogen activator inhibitor-1 and thrombospondin-1.
16 CD47 is a receptor for the secreted protein thrombospondin-1.
17 ding activity and structural similarities to thrombospondin-1.
18 tivities of recombinant signature domains of thrombospondin-1, -2, and -4 to interact with CD47 and m
19 ant protein containing functional domains of thrombospondin-1, 3TSR, have been shown to be necessary
20 l fibroblasts through the down-regulation of thrombospondin 1, a latent transforming growth factor-be
22 activity of nitric oxide (NO) is blocked by thrombospondin-1, a potent antagonist of NO/cGMP signali
23 ucose-responsive fragment of the promoter of thrombospondin-1, a potent antiangiogenic and proatherog
25 and downregulates the angiogenesis inhibitor thrombospondin-1, along with other members of the thromb
26 AME, the guanylyl cyclase inhibitors ODQ and thrombospondin-1 also abated IR-induced IL10 expression
32 responsible for binding to LRP1, whereas the thrombospondin 1 and spacer domains are responsible in A
33 hough very similar, the signature domains of thrombospondin-1 and -2 differ in several potentially im
37 dostatin (an angiogenesis inhibitor), or for thrombospondin-1 and basic fibroblast growth factor, con
38 ncreased expression levels of antiangiogenic thrombospondin-1 and inhibited S1177 phosphorylation of
39 responses by the matricellular glycoprotein thrombospondin-1 and is therefore assumed to be the rece
42 evels of two potent angiogenesis inhibitors, thrombospondin-1 and maspin, were lower compared to cont
43 at least in part through down-regulation of thrombospondin-1 and plasminogen activator inhibitor typ
44 Here, we report a novel interaction between thrombospondin-1 and SIRP-alpha on nonphagocytic cells.
45 treatment, rescued the induced expression of thrombospondin-1 and the defect in endothelial cell prol
48 that exogenous decorin induced expression of thrombospondin-1 and TIMP3, two powerful angiostatic age
50 progeny, platelets, are important sources of thrombospondins 1 and 2 and that these thrombopoietic ce
54 entified vascular endothelial growth factor, thrombospondins 1 and 2, and slit as mediators partially
55 al growth factor165, ADAMTS9 neither cleaved thrombospondins 1 and 2, nor bound vascular endothelial
56 vior such as CD44, CCNE2 (cyclin E2), THBS1 (thrombospondin 1), and CSPG2 (chondroitin sulfate proteo
57 nsforming growth factor-beta induced factor, thrombospondin 1, and platelet derived growth factor-C w
58 essel maturation, including PDGFb, TGF-beta, thrombospondin-1, and CXCL10; consistently, they were ch
60 crovascular endothelial cells interacts with thrombospondin-1, and this interaction is involved in mo
61 ocrine cancer, administration of endostatin, thrombospondin-1, and tumstatin peptides, as well as del
62 DEB fibroblasts decreased type XII collagen, thrombospondin-1, and Wnt-5A expression, reduced tumor c
63 roblasts led to increased type XII collagen, thrombospondin-1, and Wnt-5A, while reexpression of wild
66 he annexin A6/LDL receptor-related protein 1/thrombospondin 1 (ANXA6/LRP1/TSP1) complex in tumor cell
68 ve to wild-type mice, implicating endogenous thrombospondin-1 as a physiologic antagonist of NO-media
76 for proapoptotic proteins including p53 and thrombospondin-1, but p53 was unchanged, and thrombospon
78 ery of the endogenous angiogenesis inhibitor thrombospondin-1 by platelets may be a critical host res
79 and (3) a stimulatory role for thrombin, the thrombospondin-1/CD36 axis and cyclooxygenase 1 in subse
80 mia-reperfusion injury is exacerbated by the thrombospondin-1-CD47 system through inhibition of nitri
82 on injury (IRI), which is exacerbated by the thrombospondin-1/CD47 pathway through inhibition of nitr
84 ncluding vascular endothelial growth factor, thrombospondin 1, connective tissue growth factor, hepat
85 ADAMTS13 constructs, we show that the first thrombospondin-1, Cys-rich, and spacer domains of ADAMTS
86 on of ancillary C-terminal disintegrin-like, thrombospondin-1, cysteine-rich, and spacer domains to b
87 The results demonstrate that noncatalytic thrombospondin-1/cysteine-rich/spacer domains are princi
89 nvolved in the angiogenic process, including thrombospondin 1, delta-like 4, BclII modifying factor,
90 The role of CD47 was determined using the thrombospondin-1-derived agonist peptide 4N1K and the CD
95 c EPCs have phenotypic differences involving thrombospondin-1 expression compared with nondiabetic EP
96 loproteinase-1, matrix metalloproteinase-10, thrombospondin-1, extracellular matrix matricryptic frag
97 ondin-2 and -4 were less active than that of thrombospondin-1 for inhibiting binding of radiolabeled
111 istic relation between NO/cGMP signaling and thrombospondin-1 in vascular smooth muscle cells to regu
112 enuated in vitro antiangiogenic responses to thrombospondin-1, including blockade of migration, tube
114 ion of the powerful angiostatic glycoprotein Thrombospondin 1 independently of Beclin 1 transcription
115 CD47, CD36, and integrin-binding domains of thrombospondin-1 independently enhance the inflammasome-
116 nsplantations, we show that platelet-derived thrombospondin-1 is a critical negative regulator during
121 , inhibition of T cell receptor signaling by thrombospondin-1 is mediated by CD47 and requires its mo
125 of the most potent angiogenesis inhibitors, thrombospondin-1, is up-regulated in the platelets of tu
126 and retina from enucleated eyes of C57BL/6, thrombospondin-1 knockout (TSP-1KO), and TGF-beta2 recep
127 rotein containing the CD36 binding domain of thrombospondin-1 (known as the TSR domain) induced assoc
128 Finally, crossing the KrP transgene onto a thrombospondin-1 KO background reversed the vascular cha
129 -and-actin bundling when clustered either by thrombospondin-1, laminin, or antibody to the syndecan-1
130 nal tubular epithelial cells, treatment with thrombospondin-1 led to phosphorylation of SIRP-alpha an
132 Further, this work implicates the use of thrombospondin-1 levels in platelets as an indicator of
135 is study, we investigate the function of the thrombospondin-1-like glycoprotein, Nel (neural epiderma
137 s demonstrated by showing that LPA abrogated thrombospondin-1-mediated inhibition of neovascularizati
138 DAMTS-13 mutant lacking the second to eighth thrombospondin-1 motifs and the complement components C1
139 Disintegrin-like and Metalloproteinase with Thrombospondin-1 motifs) protein family, cleaves large p
141 is a consequence of both increased levels of thrombospondin-1 mRNA in megakaryocytes, as well as incr
143 lasma levels of von Willebrand factor (VWF), thrombospondin-1, myeloperoxidase, ADAMTS-13, and active
147 y of oxygen levels in the ischemic tissue of thrombospondin-1-null mice as measured by electron param
148 elve hours after 25-Gy hindlimb irradiation, thrombospondin-1-null mice showed significantly less cel
152 tions of the NO synthase substrate arginine, thrombospondin-1-null platelets have elevated basal cGMP
153 in skeletal muscle perfusion was enhanced in thrombospondin-1-null relative to wild-type mice, implic
157 marrow-derived macrophages that lack either thrombospondin-1 or CD47 exhibit diminished induction of
159 binding of radiolabeled signature domain of thrombospondin-1 or SIRPalpha (signal-regulatory protein
160 M organization, we find that accumulation of thrombospondin-1 or thrombospondin-5 puncta within cell-
161 pression levels of either tubulointerstitial thrombospondin-1 or transforming growth factor-beta desp
162 by antibodies, recombinant type 1 repeats of thrombospondin-1, or CD36-binding peptides was sufficien
164 nant C-terminal regions of thrombospondin-1, thrombospondin-1 peptides, or CD47 antibodies was also s
165 d messenger RNA expression of interleukin-6, thrombospondin-1, plasminogen activator inhibitor-1, and
167 sferase 2 (POFUT2) was described for TSRs of thrombospondin-1, properdin, and F-spondin within the se
172 of CD47 (an alphavbeta3 integrin coreceptor/thrombospondin-1 receptor) and integrins alphavbeta3 and
175 evels of another key antiangiogenic protein, thrombospondin-1, reinforcing its antitumor and antiangi
179 ng in ischemic soft tissues, suggesting that thrombospondin-1 signaling via its receptor CD47 could c
180 le cells, picomolar concentrations of native thrombospondin-1 similarly inhibited NO signaling in vas
182 -898 mimics the antiangiogenic properties of thrombospondin-1, so we hypothesized that ABT-898 will p
183 ugh some fragments and peptides derived from thrombospondin-1 stimulate or inhibit platelet aggregati
184 l metalloprotease (M), disintegrin-like (D), thrombospondin-1 (T), Cys-rich (C), and spacer (S) domai
185 ARID domain-dependent, BAF-A associations at THROMBOSPONDIN 1 (THBS1) led to the concomitant upregula
187 on of the TGF-beta-regulated biomarker genes thrombospondin-1 (THBS1) and cartilage oligomeric protei
190 -regulated the potent angiogenesis inhibitor thrombospondin-1, thereby triggering a negative feedback
191 or CD47 by recombinant C-terminal regions of thrombospondin-1, thrombospondin-1 peptides, or CD47 ant
192 nhibition can be explained by the ability of thrombospondin-1 to disrupt the interaction between CD47
193 jury, possibly due to the stimulation of the thrombospondin-1-transforming growth factor-beta pathway
194 rtilage oligomeric matrix protein (COMP) and thrombospondin 1 (TSP-1) correlated moderately well with
196 aneous somatic Ca2+ transients, synaptogenic thrombospondin 1 (TSP-1) release, and synapse formation.
198 ial growth factor (VEGF), but high levels of thrombospondin 1 (TSP-1), predicted liver dysfunction af
202 sis through binding to the type 1 repeats of thrombospondin-1 (TSP-1) and activating Fyn tyrosine kin
203 grins) and ECM noncellular components [i.e., thrombospondin-1 (TSP-1) and fibronectin (FN)] seem to t
204 uced angiogenesis and elevated expression of thrombospondin-1 (TSP-1) and its receptor CD36, anti-ang
205 he capacity to bind the CD47-binding partner thrombospondin-1 (TSP-1) and that treatment of aged eryt
206 tion, the loss of p53 led to a deficiency in thrombospondin-1 (TSP-1) expression, a potent antiangiog
207 nteractions with proteins and proteoglycans, thrombospondin-1 (TSP-1) functions at the interface of t
210 ine fashion by stimulating the expression of thrombospondin-1 (Tsp-1) in fibroblasts present in both
218 cular permeability and angiogenesis, whereas thrombospondin-1 (TSP-1) is a potent angiogenic inhibito
222 he expression of an anti-angiogenic protein, thrombospondin-1 (TSP-1) is down-regulated in the prosta
225 d decrease in p53 expression, thus enhancing thrombospondin-1 (TSP-1) release from EC and reducing FG
226 of atherogenesis, we considered the role of thrombospondin-1 (TSP-1), a matricellular protein releas
229 ntiangiogenic factors, including endostatin, thrombospondin-1 (TSP-1), and pigment epithelium-derived
230 nd re-expression of a synaptogenic molecule, thrombospondin-1 (TSP-1), apart from supporting neuronal
231 xtensive in vitro and in vivo validations on thrombospondin-1 (TSP-1), because it has been previously
232 ent derived from the second type-1 repeat of thrombospondin-1 (TSP-1), is known to possess antiangiog
234 mice deficient in tumstatin, endostatin, or thrombospondin-1 (TSP-1), to address the role that these
235 iptionally down-regulating the production of thrombospondin-1 (TSP-1)--known earlier for both its ant
247 tein expression of anti-angiogenic peptides (thrombospondin-1, TSP-1; and endostatin) as well as pro-
248 le expressed significantly reduced levels of thrombospondin 1 (TSP1) (P = 0.042) and increased levels
249 onic opiate treatment of rats down-regulates thrombospondin 1 (TSP1) expression in the nucleus accumb
254 e levels of an extracellular matrix protein, thrombospondin 1 (TSP1), an angiogenesis inhibitor.
259 lated with downregulation of anti-angiogenic thrombospondin-1 (Tsp1) and related proteins, such as co
260 -regulated STAT3 phosphorylation, astrocytic thrombospondin-1 (TSP1) and synaptic low-density lipopro
261 njury via a mechanism mediated by astrocytic thrombospondin-1 (TSP1) and synaptic low-density lipopro
268 from mice lacking the angiogenesis inhibitor thrombospondin-1 (TSP1) exhibit exaggerated angiogenic r
271 s calcineurin/NFATc1-dependent expression of thrombospondin-1 (Tsp1) in lung endothelial cells to dri
276 nvolved in the regulation of angiogenesis is thrombospondin-1 (TSP1), a matricellular glycoprotein kn
277 that, upon CREB activation, HDAC2 represses thrombospondin-1 (TSP1), a potent angiogenesis inhibitor
278 ntiation 1 (Id1), which negatively regulates thrombospondin-1 (TSP1), an inhibitor of angiogenesis.
279 ited tumor angiogenesis via the induction of Thrombospondin-1 (TSP1), and consequently suppressed tum
280 in the levels of the angiogenesis inhibitor thrombospondin-1 (TSP1), but the mechanisms underlying t
281 by JHDM1D-mediated epigenetic regulation of thrombospondin-1 (TSP1), forming a JHDM1D/TSP1/TGF-beta/
282 d to be an inhibitory signaling receptor for thrombospondin-1 (TSP1), the molecular mechanism for tra
283 he hypothesis that the matricellular protein thrombospondin-1 (TSP1), through binding to and activati
284 ently, we reported that the secreted protein thrombospondin-1 (TSP1), through its cell surface recept
290 EOC cells with a recombinant version of the thrombospondin-1 type I repeats (3TSR) induced more apop
291 TS (A Disintegrin and metalloproteinase with thrombospondin-1 type repeats) family of enzymes have be
293 The KD value of the aptamer M55 binding to thrombospondin-1 was determined as 0.5 +/- 0.2 muM with
294 Inhibition of T cell receptor signaling by thrombospondin-1 was lost in CD47-deficient T cells that
295 binding selectivity, the signature domain of thrombospondin-1 was more potent than those of thrombosp
298 ty group box-1 protein, chemokine CXCL4, and thrombospondin-1 were significantly higher in patients w
299 Here, we found that both CD47 and its ligand thrombospondin-1 were upregulated after renal IRI in mic
300 telet-derived growth factor, collagen I, and thrombospondin-1) were higher in PEDF-null mice at basel
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