ライフサイエンスコーパス: collagen II

1 chains sequentially, at Gly(775)-Leu(776) in collagen II.

2 acellular matrix macromolecules aggrecan and collagen II.

3 GAG synthesis and expression of AGGRECAN and COLLAGEN II.

4 ed with the R992C (p.R1192C) substitution in collagen II.

5 binding site on the triple-helical region of collagen II.

6 onectin, laminin, and collagen IV but not to collagen II.

7 model is proposed for the DR4 recognition of collagen II (261-273), an antigen immunodominant in huma

8 Immunization with collagen II, a collagen-induced arthritis (CIA) model, r

9 Mutations in collagen II, a main structural protein of cartilage, are

10 nd significantly reduced IgG1 and IgG2a anti-collagen II Ab levels in PKC-theta-deficient mice.

11 ted both collagen-induced arthritis and anti-collagen II Ab-mediated arthritis.

12 Serum titers of anti-collagen-II Abs were reduced especially during the late

13 se, bone sialoprotein, bone Gla protein, and collagen II, all indicators of osteogenesis/chondrogenes

14 n I fibrils and established that the tips of collagen II also had a near paraboloidal shape.

15 vious experiments with the gene (Col2a1) for collagen II, an early and abundant marker of chondrocyte

16 The knockdown increased collagen II and aggrecan deposition in the cell layers.

17 roS/g of scaffold) showed significantly more collagen II and aggrecan in the intermediate zone than a

18 puter analysis of the surface of the mutated collagen II and binding assays showed that a Cys substit

19 e results indicate that interactions between collagen II and collagen IX are site specific and that s

20 amined molecular interactions between normal collagen II and collagen IX, and the effect of a Cys sub

21 modulin-collagen interaction sites using the collagen II and III Toolkit peptide libraries.

22 ntrast, transgenic mice expressing wild-type collagen II and mice in which the expression of the tran

23 d an enhanced proliferative response against collagen II and produced higher levels of IFN-gamma but

24 The enzyme recognises five sites on collagen II and three sites on collagen III.

25 Collagen-II and Mycobacterium-specific T cell responses

26 s that embrace the entire helical domains of collagens II and III, to map MMP-3 interaction sites.

27 r matrix (ECM) genes including aggrecan, and collagens II and VI, along with elevated transforming gr

28 issue-specific expression of opticin, PRELP, collagen II, and collagen IX mRNAs was investigated by i

29 in SOX9 activity would inhibit production of collagen II, and eventually other cartilage matrix prote

30 teady state mRNA levels coding for aggrecan, collagen II, and link protein in chondrocytes exposed to

31 BHP treatment and CA MEK inhibited aggrecan, collagen II, and Sox9 mRNA expression.

32 ated with a reduced titer of pathogenic anti-collagen II antibodies.

33 d that the nontriple helical telopeptides of collagen II are not essential for the specific binding o

34 for cartilage-specific aggrecan and type II collagen II, as assessed by determination of messenger R

35 Gene expression of aggrecan and collagen II, as well as glycosaminoglycan production, we

36 We used hyaluronic/collagen II-based (HA/Col) hydrogel that incorporates li

37 rix proteins such as Lubricin, Aggrecan, and Collagen II, but additionally expressed Collagen X, indi

38 skeletal tissues and the presence of mutant collagen II, but also identifies cellular and matrix ele

39 ed in a recombinant system and cleaved to pC-collagen II by procollagen N-proteinase.

40 Single amino acid substitutions in collagen II cause heterogeneous cartilage disorders incl

41 Citrullinated collagen II (CII) is a well-known autoantigen in rheumat

42 eport experiments in another disease system, collagen II (CII)-induced arthritis (CIA) in DBA/1LacJ (

43 Collagen II (CII)-induced arthritis in DBA/1j mice is me

44 an unusual phenotype characterized by strong collagen II (Col2a1) gene expression but barely detectab

45 cellular matrix proteins, including NCAM and collagen II (Col2a1) in the limb bud.

46 ar matrix and cell adhesion genes, including collagen II (Col2a1), were markedly upregulated, accompa

47 , Runx2, and Osterix was low, as was that of collagen II, collagen I, and aggrecan, thus altering the

48 lage formation and plays a role in the early collagen II-dependent developmental events.

49 iofacial cartilage, most prominently loss of collagen II deposition.

50 ch growth plate and were flanked by immature collagen II-expressing chondrocytes facing perichondrial

51 Finally, collagen II expression predicts poor prognosis in high-g

52 High collagen II expression was associated with significantly

53 Once disrupted, the ILM and the collagen II fibrillar network failed to regenerate despi

54 the molecular events in the self-assembly of collagen II fibrils are apparently similar to those in s

55 II was then used as a substrate to generate collagen II fibrils by cleavage with procollagen C-prote

56 ed by N- and C-telopeptide domains) found in collagen II fibrils processed normally.

57 ly and at equilibrium were comparable to the collagen II fibrils seen in embryonic tissues and probab

58 ing of collagen IX on the surface of nascent collagen II fibrils.

59 ation site, increases the affinity of mutant collagen II for collagen IX, and possibly alters the spe

60 In addition to the major aggrecan/collagen II framework, the interacting complex of collag

61 er with a RT-PCR detection of collagen I and collagen II gene expression to show that chondrocytes is

62 e in mice using regulatory elements from the collagen II gene.

63 pression of SOX9 and downstream aggrecan and collagen II genes.

64 of a site-specific interaction of DDR2 with collagen II gives novel insight into the nature of the i

65 ylation, demonstrating that the D2 period of collagen II harbours a specific DDR2 recognition site.

66 racellular matrix showed strong aggrecan and collagen II immunostaining in undamaged DDH cartilage, w

67 acterized the role of consecutive domains of collagen II in stabilizing the triple helix.

68 proteins (e.g., Aggrecan, MMP-13, ADAMTS-5, collagen II) in human knee joint chondrocytes and regula

69 the mutated monomer in mixtures with normal collagen II increased the lag time for fibril assembly a

70 sis-inducing ligand (TRAIL) in vivo in which collagen II-induced (CII-induced) arthritis-susceptible

71 ociation equilibrium constant of collagen IX-collagen II interaction is 15 x 10(6) M(-1).

72 llagen II was further defined by recombinant collagen II-like proteins consisting predominantly of ta

73 ted glycosaminoglycan and cartilage-specific collagen II matrix, but show very low or no expression o

74 and that single amino acid substitutions in collagen II may change the molecular interactions with c

75 tes expressing the thermolabile R992C mutant collagen II molecules endured endoplasmic reticulum stre

76 deposits in mice expressing the R992C mutant collagen II molecules indicated their poor formation and

77 Our studies demonstrated that mutant collagen II molecules were characterized by altered elec

78 rocesses activated by the presence of mutant collagen II molecules.

79 ural information contained in collagen I and collagen II monomers.

80 rmostabilities of the Arg75Cys and Arg789Cys collagen II mutants suggest that, in contrast to the the

81 ice with conditional expression of the R992C collagen II mutation.

82 ccur efficiently prior to the removal of the collagen II N-propeptides.

83 ied the effects of the presence of the R992C collagen II on the biological processes taking place in

84 of a Cys substitution for Arg-alpha1-519 in collagen II on these interactions.

85 collagenase with a substrate preference for collagen II over collagens I and III.

86 Here, we employed a collagen II peptide library to characterize high-affinit

87 fusion protein, containing an immunodominant collagen II peptide, significantly delayed the onset and

88 age to RA (DRB1*0401) complexed with a human collagen II peptide.

89 ng of tandem repeats of the D1, D2, D3 or D4 collagen II periods revealed the presence of a gradient

90 nteraction between collagen IX molecules and collagen II polymers.

91 Receptor expressed under the control of the Collagen II promoter (PTHrPR*).

92 expression of PTHrP under the control of the collagen II promoter in transgenic mice resulted in mark

93 ression of a reporter construct containing a collagen II promoter/enhancer insert; however, this nega

94 Increased collagen II protein accumulation did not associate with

95 ibrous (Collagen-I rich), and cartilaginous (Collagen-II, proteoglycan-rich) matrix components are re

96 Collagen II served as a potent stimulator of DDR2 autoph

97 F-beta by CD4(+) T cells, and suppression of collagen II-specific CD4(+) T cell proliferation.

98 stimulated Tregs suppressing proinflammatory collagen II-specific Th cells.

99 a second binding site near the N terminus of collagen II (starting at helix residue 127) in Toolkit p

100 hat polycystin 2 deficiency causes increased collagen II synthesis with upregulation of secretory pat

101 Mice treated with AAV-8 containing collagen II T-cell epitopes demonstrated a significant r

102 Here, we evaluated the ability of collagen II T-cell epitopes packaged in adeno-associated

103 for four epitopes derived from complement 3, collagen II, thymosin beta4, and gelsolin.

104 by the binding of collagen IX to recombinant collagen II variants lacking fragments of 234 amino acid

105 site(s) on collagen II, we used recombinant collagen II variants with specific deletions of one of t

106 that excessive accumulation of thermolabile collagen II was associated with the activation of an "un

107 As expected, DDR2 binding to collagen II was dependent on triple-helical collagen and

108 We found that the D2 period of collagen II was essential for DDR2 binding and receptor

109 Collagen II was found to be a much better ligand for DDR

110 The DDR2 binding site on collagen II was further defined by recombinant collagen

111 In addition, the broad deposition of collagen II was largely abolished.

112 pression of the transgene encoding the R992C collagen II was switched off were characterized by norma

113 The pC-collagen II was then used as a substrate to generate col

114 To map the DDR2 binding site(s) on collagen II, we used recombinant collagen II variants wi

115 the amount of 4-hydroxyproline and the Tm of collagen II were reduced, and the extracellular matrix w

116 esults indicated that the C-terminal half of collagen II, which includes the D3 and D4 periods, has a

117 nsight into the nature of the interaction of collagen II with matrix receptors.