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1 LTBP and the LAP propeptides of TGF-beta (isoforms 1 and
2 LTBP-1 expression increased during the first 12 d in cul
3 LTBP-1 mRNA expression was reduced in slow-track (0.99 +
4 LTBP-1 was not detected in extracted beaded-string micro
5 LTBP-2 colocalized with tropoelastin within the perichon
6 LTBP-2 expression was not detected by in situ hybridizat
7 LTBPs and fibrillins are highly homologous molecules, an
8 orming growth factor beta-binding protein 1 (LTBP-1) targets latent complexes of transforming growth
9 identify latent TGF-beta binding protein 1 (LTBP-1), an extracellular matrix protein and key regulat
11 orming growth factor-beta-binding protein-1 (LTBP-1) belongs to a family of extracellular glycoprotei
13 s such as latent TGF-beta binding protein-1 (LTBP-1), decorin, biglycan, and fibromodulin can bind an
14 ibulin-4 (Fbln4) null cultures, fibrillin-1, LTBP-1, and LTBP-4 are incorporated into microfibrils.
15 ression reduced left atrial dimension (19%), LTBP-1 hydrolysis (40%), and collagen content (32%) when
16 th factor beta (TGF-beta) binding protein 2 (LTBP-2) is an integral component of elastin-containing m
18 orming growth factor-beta-binding protein-3 (LTBP-3) sequesters pro-myostatin in the extracellular ma
20 aVbeta6-mediated latent TGF-beta activation; LTBP-3 is unable to substitute for LTBP-1 in this assay.
23 trates that the binding sites for LTBP-1 and LTBP-4 are different and suggests that EGF3 may also con
26 d two TGF-beta1-binding proteins, LTBP-1 and LTBP-4; expression of the latter is necessary for secret
32 3; type I, II, and III receptors; as well as LTBP-1, decorin, and biglycan were up-regulated during a
33 rillins and their associated ligands such as LTBPs, fibulins, and EMILINs are of particular interest
34 e show that the covalent association between LTBP-1 and the extracellular matrix is transglutaminase
35 pite these differences, interactions between LTBP-1 and fibrillin-1 compete for interactions between
40 ll as by CARASIL mutations and disrupts both LTBP-1 binding to fibronectin and its incorporation into
41 1 knockout mice had increased levels of both LTBP-4 expression and TGF-beta activation, as well as en
42 gest that during differentiation of ES cells LTBP-1 facilitates endothelial cell organization via a T
45 fibrillin-1 (Fbn1) null fibroblast cultures, LTBP-1 and LTBP-4 are not incorporated into microfibrils
47 erved that a two-residue insertion in 8-Cys3(LTBP-1) increased the potential for disulfide exchange o
51 cated that enhanced binding of LAP to 8-Cys3(LTBP-4) is achieved if the residues A, S, and R are chan
52 sfected CHO cultures revealed that deltaN293 LTBP-1S was matrix associated via a transglutaminase-dep
57 In tissues where LTBP-1 is not expressed, LTBP-4 may substitute for LTBP-1, because the C-terminal
59 The results reveal a functional role for LTBP-1 in latent TGF-beta activation and suggest that ac
60 her, these data identify a critical role for LTBP-4 in the regulation of latent TGF-beta1 activation
62 ated demonstrates that the binding sites for LTBP-1 and LTBP-4 are different and suggests that EGF3 m
64 is not expressed, LTBP-4 may substitute for LTBP-1, because the C-terminal end of LTBP-4 binds equal
65 Modelling of a homologous TB domain from LTBP-1 (residues 1018-1080) suggests that hydrophobic co
73 f TGF-beta by PSCs in vitro by investigating LTBP-1 organisation with fibrillar fibronectin and show
74 ins that includes three additional isoforms (LTBP-2, -3, and -4) and the matrix proteins fibrillin-1
75 e, we present evidence that MFS mice lacking LTBP-3 have improved survival, essentially no aneurysms,
76 though alphavbeta6 recognizes an RGD on LAP, LTBP-1 is required for alphaVbeta6-mediated latent TGF-b
77 rix is transglutaminase dependent, as little LTBP-1 is recovered from matrix digests prepared from cu
79 signaling caused by a lack of HtrA1-mediated LTBP-1 processing as mechanism underlying CARASIL pathog
80 odeling), a 60% increase in MT1-MMP-mediated LTBP-1 hydrolysis and a 190% increase in collagen conten
83 activate latent TGF-beta1 in the absence of LTBP, these mechanisms are not as efficient as those tha
86 These data suggest that the association of LTBP with the latent TGF-beta complex is important for p
88 tion of latent TGFbeta complexes composed of LTBP-3 and TGFbeta contributes to aortic disease progres
91 ression system, we have mapped the domain of LTBP-1 mediating covalent association with small latent
92 of LTBP-1S were used to identify domains of LTBP-1 involved in cross-linking and formation of TGF-be
95 ponse to bleomycin, but expression either of LTBP-4 lacking the TGF-beta-binding site or only the TGF
99 rylation of Smad2, and ectopic expression of LTBP-3 in mature mouse skeletal muscle increases fiber a
107 ll latent TGF-beta1 with deletion mutants of LTBP-1 showed that the third eight-cysteine repeat of LT
108 amino-terminal region of LTBP-1S, mutants of LTBP-1S with deletions of either the amino-terminal 293
111 y antibodies to the amino-terminal region of LTBP-1 block transglutaminase-dependent cross-linking of
112 domains within the amino-terminal region of LTBP-1S, mutants of LTBP-1S with deletions of either the
113 ibodies to the amino and carboxyl regions of LTBP-1S abrogate TGF-beta generation by vascular cell co
114 aining amino, middle, or carboxyl regions of LTBP-1S were used to identify domains of LTBP-1 involved
115 owed that the third eight-cysteine repeat of LTBP-1 is necessary and sufficient for covalent interact
119 To gain insight into the potential roles of LTBP in early development, we isolated the Xenopus LTBP-
120 We reported that a specific sequence of LTBP-1 is required for latent TGF-beta activation by the
122 fibulins may affect matrix sequestration of LTBPs, because in vitro interactions between these prote
124 antibody, a TGF-beta receptor antagonist, or LTBP gene silencing results in the reversal of TGF-beta-
126 owth factors interact with fibrillins and/or LTBPs and are also targeted to the extracellular matrix.
128 the ability of PSCs to mechanically organise LTBP-1 and activate TGF-beta through a mechanism involvi
130 een LAP and latent TGF-beta-binding protein (LTBP) produces the most common form of latent TGF-beta,
132 sforming growth factor-beta binding protein (LTBP), which plays roles in targeting and activation, a
142 transforming growth factor-binding protein (LTBP-1) and activation of transforming growth factor-dep
143 ransforming growth factor-1 binding protein (LTBP-1), and MT1-MMP-specific LTBP-1 proteolytic activit
144 lly described as a TGF-beta-masking protein, LTBP-1 is involved both in the sequestration of latent T
146 forming growth factor-beta-binding proteins (LTBPs) are extracellular matrix (ECM) glycoproteins that
147 forming growth factor-beta-binding proteins (LTBPs) are extracellular matrix (ECM) glycoproteins that
149 g growth factor (TGF)-beta binding proteins (LTBPs) modulate the secretion and activation of latent T
150 illins and latent TGF-beta-binding proteins (LTBPs) which are localized to fibrillar structures in th
151 he role of latent TGF-beta-binding proteins (LTBPs), key regulators of TGF-beta bioavailability and a
155 GF-beta1 and two TGF-beta1-binding proteins, LTBP-1 and LTBP-4; expression of the latter is necessary
158 t of fibroblasts with bleomycin up-regulated LTBP-4 mRNA, protein, and soluble LTBP-4-bound large lat
159 omycin-induced TGF-beta1 activation required LTBP-4, since lung fibroblasts deficient in LTBP-4 did n
160 -regulated LTBP-4 mRNA, protein, and soluble LTBP-4-bound large latent TGF-beta1 complexes in Thy-1 (
161 nding protein (LTBP-1), and MT1-MMP-specific LTBP-1 proteolytic activity was increased by 4-fold in t
164 ata were consistent with the hypothesis that LTBP-1 is a fibrillin-associated protein present in cert
166 other elastic fiber proteins, implying that LTBP-2 performs a yet undiscovered function in early dev
168 observations give support to the notion that LTBP-3 is important for the control of TGF-beta action.
169 The findings of this study suggest that LTBP-2 is an essential component for the formation of mi
170 beaded-string microfibrils, suggesting that LTBP-1 is not an integral structural component of microf
171 enotype related to glaucoma, suggesting that LTBP-2 deficiency primarily causes lens dislocation but
172 y determined DN protection and suggests that LTBP-1 may be involved in the pathogenesis of DN through
174 nct mechanisms that may be determined by the LTBP isoform and its potential interaction with the matr
176 binding site was within three domains of the LTBP-1 C terminus, and in fibrillin-1 the site was defin
179 Previous studies have revealed that the LTBP-LAP interaction is mediated by intracellular exchan
180 xons and shows a similar organization to the LTBP-2 gene, suggesting that these genes originated from
182 We previously generated mice in which the LTBP-binding cysteine residues in LAP TGF-beta1 were mut
184 d that inclusion of a polyclonal antibody to LTBP-1 during EB differentiation suppressed the expressi
186 ch the cysteines that link the propeptide to LTBP were mutated to serines, thereby blocking covalent
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