ライフサイエンスコーパス: collagen V

1 to immobilized fibronectin, collagen I, and collagen V.

2 prospect of blocking Klebsiella adhesion to collagen V.

3 he extracellular matrix proteins laminin and collagen V.

4 novo Abs to self-Ags, K-alpha1 tubulin, and collagen V.

5 that caused 50% reduction in col5a1 mRNA and collagen V.

6 in regulating tissue-specific production of collagen V.

7 The sequence of this THP was derived from collagen V, a component of collagen I fibrils.

8 During development (E18-P10) both collagen V and XI were comparably expressed; however, co

9 Tendons with altered collagen V and/or XI expression (Col5a1(+/-); Col11a1(+/

10 identified two main ligands for NG2, namely, collagens V and VI.

11 Collagens V and XI comprise a single regulatory type of

12 The data demonstrate coordinate roles for collagens V and XI in the regulation of fibril nucleatio

13 of this study was to determine the roles of collagens V and XI in the regulation of tendon fibrillog

14 nts: keratocan, keratan sulfate, collagen I, collagen V, and collagen VI.

15 a2(V) and alpha1(V) chains, respectively, of collagen V, and is most often caused by COL5A1 null alle

16 including procollagen I, procollagen III, pN-collagen V, and prolysyl oxidase.

17 dies to self-antigens (K-alpha 1 tubulin and collagen V) before and after antibody-directed therapy a

18 Analysis of collagen V binding of different MrkD1P mutants revealed

19 Collagen V, broadly expressed as alpha1(V)2 alpha2(V) he

20 igens such as vimentin, cardiac myosin (CM), collagen V (Col V), agrin, and angiotensin II receptor t

21 We have shown previously that collagen V (col(V)) autoimmunity is a consistent feature

22 T cell-mediated autoimmunity to collagen V (col-V), a sequestered yet immunogenic self-p

23 (DSA) and antibodies (Abs) to self-antigens, collagen-V (Col-V), and K-alpha1-Tubulin (KAT) in pathog

24 ) and decorin, and upregulation of biglycan, collagen V, collagen XII, PAI-1, Scleraxis, and Mohawk b

25 The ACL also had a higher collagen V content than did the flexor digitorum longus

26 ments, as well as the role of alterations in collagen V expression in the pathobiology in classic Ehl

27 ibril assembly and abnormal fibrils, lacking collagen V, generated by unregulated sequestration of ty

28 e critical differential regulatory roles for collagen V in tendon and ligament structure and function

29 We define the function of collagen V in tendons and ligaments, as well as the role

30 suggest that alpha1(V)3 homotrimers, a rare collagen V isoform that occurs in the absence of suffici

31 ially compensate for loss of the most common collagen V isoform.

32 associated self-antigens Kalpha1-tubulin and Collagen-V leading to the development of obliterative ai

33 s suggest that collagen V overexpression and collagen V-mediated immune response play roles in the pa

34 magnetic NMR that positions a triple-helical collagen V mimic (synthesized with nitroxide spin labels

35 uted by the trailing strand of the synthetic collagen V mimic, which also appears to ligate the catal

36 rum longus tendons from a haplo-insufficient collagen V mouse model of classic Ehlers Danlos syndrome

37 Collagen V mutations underlie classic Ehlers-Danlos synd

38 The collagen V-null ACL and flexor digitorum longus tendon b

39 Targeting was specific, resulting in collagen V-null tendons and ligaments.

40 Rotary shadowing of mixtures of NG2 and collagen V or VI confirms a direct interaction between t

41 antigens and autoantigens such as vimentin, collagen V, or alpha-tubulin and it has been postulated

42 cked transforming growth factor-beta-induced collagen V overexpression and alleviated transforming gr

43 Previous studies suggest that collagen V overexpression and collagen V-mediated immune

44 f miR-185 and miR-186 may be responsible for collagen V overexpression during idiopathic pulmonary fi

45 aimed to identify dysregulated miRNA-related collagen V overexpression during idiopathic pulmonary fi

46 V and XI were comparably expressed; however, collagen V predominated in mature (P30) tendons.

47 ment structure and function and suggest that collagen V regulatory dysfunction is associated with an

48 S hallmarks to arise separately from loss of collagen V roles in control of collagen fibril growth an

49 e absence of collagen XI with a reduction in collagen V was associated with the most severe fibril ph

50 l fibrils with periodic immunoreactivity for collagen V where type I/V interactions regulate nucleati

51 We propose an evolving role for collagen V/XI isoforms as an adaptable polymeric templat