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1 nlos syndrome (COL3A1 encoding the chains of Type III collagen).
2 itope recognized by a monoclonal antibody to type III collagen.
3 vascular smooth muscle cell adhesiveness to type III collagen.
4 ease is caused by a point mutation of Gly in type III collagen.
5 ivity and acted as a molecular chaperone for type III collagen.
6 ) results from mutations in the formation of type III collagen.
7 e recovered cross-linked to helical sites in type III collagen.
8 agens, GFOGER and GLOGER, are not present in type III collagen.
9 r-beta, connective tissue growth factor, and type III collagen.
10 wth factor (TGF)-beta1, type I collagen, and type III collagen.
11 ncentration due to elevated transcription of type III collagen.
12 an alternative transcript that cannot encode type III collagen.
13 L3A1 gene, which encodes the polypeptides in type III collagen.
14 nsile strength, and a higher ratio of type I:type III collagen.
15 this alternative transcript does not encode type III collagen.
16 RNA expression of fibronectin and type I and type III collagens.
17 e, which is composed primarily of type I and type III collagens.
18 ith differences in adhesiveness to type-I or type-III collagens.
19 s-Danlos syndrome without the characteristic type III collagen abnormalities or the craniofacial feat
22 peptides derived from the sequence of human type III collagen and 9 peptides derived from the cyanog
23 genetic disorder characterized by defective type III collagen and a high risk of arterial morbidity
24 II collagen-coated Petri dishes nor inhibits type III collagen and ADP-induced platelet aggregation,
25 ine profile, an extracellular matrix rich in type III collagen and hyaluronan, attenuated biomechanic
27 we show that FKBP22 catalyzes the folding of type III collagen and interacts with type III collagen,
28 MEFs) is associated with increased levels of type III collagen and pigment epithelium-derived factor,
29 opeptides (N propeptide of type I [PINP] and type III collagen), and tissue levels of messenger RNA f
30 eoepitope-specific N-terminal pro-peptide of type III collagen, and liver stiffness favored aldefermi
31 ression, attenuated deposition of type I and type III collagen, and normalized total hydroxyproline c
32 agen, the unhydroxylated quarter fragment of type III collagen, and synthetic peptides as substrates.
33 yaluronic acid, amino-terminal propeptide of type III collagen, and tissue inhibitor of matrix metall
35 , varying numbers of GXY triplets from human type III collagen around the collagenase cleavage site w
36 is revealed greater deposition of type I and type III collagen as well as increased collagen type I:I
40 without the carboxyl-terminal propeptide (pN type III collagen), but binding to triple helical collag
41 ombinant protein binds to type I, but not to type III collagen by affinity column chromatography.
42 y an important role in specific functions of type III collagen by modulating the local triple-helical
43 otease (MMP)-degraded type I collagen (C1M), type III collagen (C3M), type IV collagen (C4M) and a pr
44 perfusion of human and murine blood through type III collagen-coated capillaries at arterial shear r
45 he binding of the recombinant protein to the type III collagen-coated micro titer wells in a dose-dep
53 and lymphocytic inflammation, and increased type III collagen deposition below the bronchial epithel
54 development of interstitial fibrosis, whilst type III collagen deposition was observed in areas of F4
55 low temperature triggers the folding of the type III collagen domain in a zipper-like fashion that r
56 ooth muscle actin, cellular fibronectin, and type III collagen expression all appeared to increase.
57 of c-Jun amino-terminal kinase (JNK) blocked type III collagen expression in LRP-1-deficient MEFs, su
58 s of a statistically significant increase in type III collagen expression or a decrease in type I col
60 actin, fibronectin, vimentin, and type I and type III collagen expression; and reduced total tissue c
62 her dermal or wound matrix proteins, such as type III collagen, fibrin, and fibronectin, and a mixtur
63 degradation (C3M) and formation (PRO-C3) of type III collagen further, higher PRO-C3 was associated
65 differences in genetic polymorphisms in the type III collagen gene between donor and recipient tissu
67 we quantitatively determined origin-specific type III collagen gene expression in fibrotic areas cont
68 ful, dose-dependent inhibition of type I and type III collagen gene expression in normal and SSc cell
69 rocytes contain an unusual transcript of the type III collagen gene in which exons 1-23 are replaced
71 ressed in chondrocytes, transcription of the type III collagen gene may continue from an alternative
74 f a series of homotrimer peptides that model type III collagen have been performed to correlate confo
75 to understand better the structural role of type III collagen in cartilage, we find that type III co
77 f PGs was increased to 200 nM, the amount of type III collagen in the cell layer extracts was reduced
78 effect by increasing the amount of refolded type III collagen in vitro and FKBP19 seems to interact
79 of collagen mimetic peptides for type I and type III collagens in four different systems, including
80 membranes, the recombinant protein inhibits type III collagen-induced platelet aggregation also in a
81 The peptide inhibits the type I, but not the type III, collagen-induced platelet aggregation and the
85 is of tissues from mutant mice revealed that type III collagen is essential for normal collagen I fib
89 sition of extracellular matrix, particularly type III collagen, is linked to poor outcomes in patient
90 the imino acid-poor 785-796 region of human type III collagen just C-terminal to the matrix metallop
91 racellular matrix biomaterials (hyaluronans, type III collagen, laminin) found in stem cell niches.
92 In the articular cartilages of adult joints, type III collagen makes an appearance in varying amounts
93 type III collagen in cartilage, we find that type III collagen molecules with unprocessed N-propeptid
94 ation suggested that, although production of type III collagen mRNA is repressed in chondrocytes, tra
98 type IV collagen (C4M) and a pro-peptide of type III collagen (PRO-C3) were measured by ELISA in pre
99 lagen biomarkers of type I collagen (reC1M), type III collagen (PRO-C3), type IV collagen (C4G), type
100 neoepitope-specific N-terminal propeptide of type III collagen (Pro-C3; -22% and -33%) and enhanced l
102 ormation was enhanced by 19%, and the type I/type III collagen ratio was shifted toward higher abunda
103 fied a high affinity binding region in human type III collagen recognized by alpha(1)I and alpha(2)I.
104 ive binding site of the platelet receptor to type III collagen resides in these portions of the prote
105 let repeating peptide containing the natural type III collagen sequence from residues 991 to 1032 inc
106 chondrocytes, indicating that repression of type III collagen synthesis during chondrogenesis is tra
107 rophages, and measurement of origin-specific type III collagen synthesis identified cells of intracar
109 preferences of these PPIases in vitro using type III collagen, the unhydroxylated quarter fragment o
110 showed that FKBP22 catalyzed the folding of type III collagen through its prolyl isomerase activity
111 roblasts, producing predominantly type I and type III collagen, transform into myofibroblasts (a smoo
112 ructural properties exhibited by the natural type III collagen triple helix, we synthesized, crystall
115 ding of type III collagen and interacts with type III collagen, type VI collagen, and type X collagen
116 quarter, 252 residues, of the natural human type III collagen was attached to (GPP)7 with the type X
117 ydrolyzed all the tested substrates in which type III collagen was the favorite substrate with 2.16 m
118 at telopeptides from both N and C termini of type III collagen were linked in the tissue to helical c
119 ntrol, increased accumulations of type I and type III collagens were detected by immunohistochemistry
120 ns located near the C terminus of type I and type III collagens, where trimerization occurs and tripl
121 hermal stable triple helices and thus favors type III collagen, which has a relatively flexible cleav
122 The present findings emphasize the role of type III collagen, which is synthesized in mature articu
123 ima of both group 1 and 2 stents was rich in type III collagen, with reduced staining in group 3.