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1 nlos syndrome (COL3A1 encoding the chains of Type III collagen).
2  vascular smooth muscle cell adhesiveness to type III collagen.
3 ease is caused by a point mutation of Gly in type III collagen.
4 ) results from mutations in the formation of type III collagen.
5 e recovered cross-linked to helical sites in type III collagen.
6 agens, GFOGER and GLOGER, are not present in type III collagen.
7 r-beta, connective tissue growth factor, and type III collagen.
8 wth factor (TGF)-beta1, type I collagen, and type III collagen.
9 ncentration due to elevated transcription of type III collagen.
10 an alternative transcript that cannot encode type III collagen.
11 L3A1 gene, which encodes the polypeptides in type III collagen.
12  this alternative transcript does not encode type III collagen.
13 itope recognized by a monoclonal antibody to type III collagen.
14 RNA expression of fibronectin and type I and type III collagens.
15 e, which is composed primarily of type I and type III collagens.
16 ith differences in adhesiveness to type-I or type-III collagens.
17 s-Danlos syndrome without the characteristic type III collagen abnormalities or the craniofacial feat
18  the proper oxidation of the cystine knot of type III collagen after the short triple helix.
19 from the cyanogen bromide fragment of bovine type III collagen, alpha1(III)CB4.
20  peptides derived from the sequence of human type III collagen and 9 peptides derived from the cyanog
21 II collagen-coated Petri dishes nor inhibits type III collagen and ADP-induced platelet aggregation,
22 ine profile, an extracellular matrix rich in type III collagen and hyaluronan, attenuated biomechanic
23 we show that FKBP22 catalyzes the folding of type III collagen and interacts with type III collagen,
24 MEFs) is associated with increased levels of type III collagen and pigment epithelium-derived factor,
25 opeptides (N propeptide of type I [PINP] and type III collagen), and tissue levels of messenger RNA f
26 ression, attenuated deposition of type I and type III collagen, and normalized total hydroxyproline c
27 agen, the unhydroxylated quarter fragment of type III collagen, and synthetic peptides as substrates.
28 yaluronic acid, amino-terminal propeptide of type III collagen, and tissue inhibitor of matrix metall
29                  The preference of MMP-1 for type III collagen appears to be primarily based on the f
30 , varying numbers of GXY triplets from human type III collagen around the collagenase cleavage site w
31      Collagenases cleave all three chains of type III collagen at specific sites characterized by a G
32 IC may arise from defects in both type I and type III collagen biosynthesis.
33 gnificant increase in the relative amount of type III collagen but no mutant alpha1(I) chain.
34 without the carboxyl-terminal propeptide (pN type III collagen), but binding to triple helical collag
35 ombinant protein binds to type I, but not to type III collagen by affinity column chromatography.
36 y an important role in specific functions of type III collagen by modulating the local triple-helical
37  perfusion of human and murine blood through type III collagen-coated capillaries at arterial shear r
38 he binding of the recombinant protein to the type III collagen-coated micro titer wells in a dose-dep
39       The labeled peptide-1 does not bind to type III collagen-coated microtiter wells.
40     The recombinant protein neither binds to type III collagen-coated Petri dishes nor inhibits type
41                           We have shown that type III collagen (Col3), a component of tumor stroma, r
42 on the flexibility of the hydrolysis site of type III collagen compared with types I and II.
43                In contrast, human and bovine type III collagen contained no 3Hyp at any site, despite
44 cell-associated proteins and upregulation of type III collagen degradation marker.
45  and lymphocytic inflammation, and increased type III collagen deposition below the bronchial epithel
46 development of interstitial fibrosis, whilst type III collagen deposition was observed in areas of F4
47  low temperature triggers the folding of the type III collagen domain in a zipper-like fashion that r
48 ooth muscle actin, cellular fibronectin, and type III collagen expression all appeared to increase.
49 of c-Jun amino-terminal kinase (JNK) blocked type III collagen expression in LRP-1-deficient MEFs, su
50 s of a statistically significant increase in type III collagen expression or a decrease in type I col
51                                              Type III collagen expression was increased in the midlea
52 actin, fibronectin, vimentin, and type I and type III collagen expression; and reduced total tissue c
53 her dermal or wound matrix proteins, such as type III collagen, fibrin, and fibronectin, and a mixtur
54                              Analysis of the type III collagen gene (COL3A1) revealed a polymorphic A
55  differences in genetic polymorphisms in the type III collagen gene between donor and recipient tissu
56                                    The chick type III collagen gene contains an internal promoter in
57 we quantitatively determined origin-specific type III collagen gene expression in fibrotic areas cont
58 ful, dose-dependent inhibition of type I and type III collagen gene expression in normal and SSc cell
59 rocytes contain an unusual transcript of the type III collagen gene in which exons 1-23 are replaced
60          Thus transcriptional control of the type III collagen gene is highly complex, with two promo
61 ressed in chondrocytes, transcription of the type III collagen gene may continue from an alternative
62                             Mutations in the type III collagen gene, COL3A1, are associated with the
63                Binding of HSP47 to bovine pN type III collagen has only minor effects on the thermal
64 f a series of homotrimer peptides that model type III collagen have been performed to correlate confo
65  to understand better the structural role of type III collagen in cartilage, we find that type III co
66 little is known about the rate of folding of type III collagen in patients with EDS.
67 f PGs was increased to 200 nM, the amount of type III collagen in the cell layer extracts was reduced
68  effect by increasing the amount of refolded type III collagen in vitro and FKBP19 seems to interact
69  membranes, the recombinant protein inhibits type III collagen-induced platelet aggregation also in a
70 The peptide inhibits the type I, but not the type III, collagen-induced platelet aggregation and the
71                                              Type III collagen is a critical collagen that comprises
72                                              Type III collagen is a fibrillar forming collagen compri
73                                In the adult, type III collagen is a major component of the extracellu
74 is of tissues from mutant mice revealed that type III collagen is essential for normal collagen I fib
75                                              Type III collagen is known to be prominent at sites of h
76                                              Type III collagen is present in prechondrogenic mesenchy
77                  A characteristic feature of type III collagen is the presence of a stabilizing C-ter
78  the imino acid-poor 785-796 region of human type III collagen just C-terminal to the matrix metallop
79 racellular matrix biomaterials (hyaluronans, type III collagen, laminin) found in stem cell niches.
80 In the articular cartilages of adult joints, type III collagen makes an appearance in varying amounts
81 type III collagen in cartilage, we find that type III collagen molecules with unprocessed N-propeptid
82 ation suggested that, although production of type III collagen mRNA is repressed in chondrocytes, tra
83        Biochemical analysis of the amount of type III collagen produced by dermal fibroblasts has pro
84 fied a high affinity binding region in human type III collagen recognized by alpha(1)I and alpha(2)I.
85 ive binding site of the platelet receptor to type III collagen resides in these portions of the prote
86 let repeating peptide containing the natural type III collagen sequence from residues 991 to 1032 inc
87  chondrocytes, indicating that repression of type III collagen synthesis during chondrogenesis is tra
88 rophages, and measurement of origin-specific type III collagen synthesis identified cells of intracar
89 ve tissue disorder that leads to a defect in type III collagen synthesis.
90  preferences of these PPIases in vitro using type III collagen, the unhydroxylated quarter fragment o
91 ructural properties exhibited by the natural type III collagen triple helix, we synthesized, crystall
92 en found at the carboxyl-terminal end of the type III collagen triple helix.
93 on and interstitial accumulation of collagen type III, collagen type IV and fibronectin.
94 ding of type III collagen and interacts with type III collagen, type VI collagen, and type X collagen
95  quarter, 252 residues, of the natural human type III collagen was attached to (GPP)7 with the type X
96 ydrolyzed all the tested substrates in which type III collagen was the favorite substrate with 2.16 m
97 at telopeptides from both N and C termini of type III collagen were linked in the tissue to helical c
98 ntrol, increased accumulations of type I and type III collagens were detected by immunohistochemistry
99 ns located near the C terminus of type I and type III collagens, where trimerization occurs and tripl
100 hermal stable triple helices and thus favors type III collagen, which has a relatively flexible cleav
101   The present findings emphasize the role of type III collagen, which is synthesized in mature articu
102 ima of both group 1 and 2 stents was rich in type III collagen, with reduced staining in group 3.
103 llagen mRNA and interstitial accumulation of type III collagen within the renal cortex.

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