ライフサイエンスコーパス: nidogen

1 nteraction with the beta-propeller domain of nidogen.

2 these cellular processes observed on laminin-nidogen.

3 We identified the nidogen 1 (NID1) gene on 1q42 associated with nevus coun

4 he novel candidate lung metastasis proteins, Nidogen 1 (NID1) was confirmed to promote lung metastasi

5 tion, although BMI-1 promotes ESFT adhesion, nidogen 1 inhibits cellular adhesion in vitro.

6 hment of laminin subunits alpha4 and alpha2, nidogen 1, and decorin (FDR-adjusted P value < 10(-7)) a

7 dhesion-associated basement membrane protein nidogen 1.

8 Nidogens 1 and 2 occurred in both networks but did not f

9 ads to specific induction of fibronectin and nidogen-1 (ie, matrix-bridging proteins that link togeth

10 enhanced degradation of extracellular matrix nidogen-1 and laminin beta1 in tumor xenografts.

11 heir ability to self-assemble, interact with nidogen-1 and type IV collagen, and form extracellular m

12 IG superfamily and binds to the wall of the nidogen-1 G2 beta-barrel using beta-strands C, D and F.

13 l structure at 2.0 A resolution of the mouse nidogen-1 G2-perlecan IG3 complex.

14 Homozygous knockout of nidogen-1 in the mouse showed only mild pathological cha

15 d electron microscopy were used to study the nidogen-1 knockout animals.

16 For that purpose, eyes of C57BL/6 and nidogen-1 knockout mice were stained immunohistochemical

17 Nidogen-1 residues participating in the extensive interf

18 In summary, the knockout of nidogen-1 showed mild but significant morphological chan

19 In normal mice, nidogen-1 was present in many basement membranes, but sh

20 novel LacdiNAc-positive species ECM1, AMACO, nidogen-1, alpha-dystroglycan, and neurofascin.

21 mice were stained immunohistochemically for nidogen-1, and intraocular pressure measurements and lig

22 ing from the presence of laminin LN domains, nidogen-1, and the nidogen-binding site in laminin.

23 n type Ialpha, fatty-acid-binding-protein 5, nidogen-1, cartilage oligomeric matrix protein, and insu

24 teins from chick embryos, such as laminin-1, nidogen-1, collagens IV and XVIII, perlecan, and agrin.

25 It binds collagen IV, laminin-1, entactin/nidogen-1, fibronectin and vitronectin, but not collagen

26 IV collagen alpha1-alpha6 chains, perlecan, nidogen-1, nidogen-2, and netrin-4 were found on both fa

27 Distribution and lack of nidogen-1, part of numerous basement membranes, were stu

28 e data suggest that alterations of laminins, nidogen-1/entactin, and epithelial integrin in DR cornea

29 he alpha1, alpha5, and beta1 laminin chains; nidogen-1/entactin; integrin alpha3 and beta1 chains in

30 iously described decreased immunostaining of nidogen-1/entactin; laminin chains alpha1, alpha5, beta1

31 ) constituents, laminin 10, collagen IV, and nidogen-2 (but not perlecan) are considerably lower (<60

32 Our novel findings that laminins and nidogen-2 drive CPCs toward chondrogenesis may help in t

33 was to investigate the role of laminins and nidogen-2 in osteoarthritis (OA) and their potential to

34 evels of laminin-alpha1, laminin-alpha5, and nidogen-2 in their pericellular matrix, and laminin-alph

35 Nidogen-2 increased SOX9 gene expression.

36 ed from patients with late-stage knee OA and nidogen-2 knockout mice.

37 Knockdown of nidogen-2 reduced SOX9 expression, whereas it up-regulat

38 n alpha1-alpha6 chains, perlecan, nidogen-1, nidogen-2, and netrin-4 were found on both faces, but th

39 The distribution of laminin gamma3 chain, nidogen-2, netrin-4, matrilin-2, and matrilin-4 is descr

40 of laminins appear in OA cartilage and that nidogen-2-null mice exhibit typical osteoarthritic featu

41 in part, but not completely; be replaced by nidogen-2.

42 Laminin, nidogen, agrin, collagen IV, and XVIII are major constit

43 Here, we show that the presence of nidogens (also known as entactins) at the NMJ is the mai

44 cell surfaces, polymerizing, and binding to nidogen and collagen IV.

45 laminin-1 (alpha 1 beta 1 gamma 1), entactin/nidogen and fibronectin; accumulation of fibronectin and

46 several new extracellular molecules, such as nidogen and heparan sulfate proteoglycans, in axonal tra

47 nal extracellular matrix proteins, including nidogen and perlecan (Figure 1, bottom).

48 Nidogen and perlecan are large multifunctional basement

49 ion, is mediated by the central G2 domain in nidogen and the third immunoglobulin (IG)-like domain in

50 ement membrane components, laminin, entactin/nidogen, and collagen IV, was similar in the different t

51 to bind calcium, fibronectin (FN), laminin, nidogen, and fibrinogen.

52 Laminin, entactin/nidogen, and fibronectin immunoreactivities were similar

53 roteinase-3 and degradation of fibrin(ogen), nidogen, and perlecan in the adventitia of descending ao

54 the lens epithelium, whereas collagen XVIII, nidogen, and the laminin gamma 1 and beta1 chains are sy

55 nin, collagen IV, collagen XVIII, agrin, and nidogen are major protein constituents of the chick reti

56 ne components type IV collagen, laminin, and nidogen, as well as the large tenascin-C isoform, fibron

57 ting that the G2 domain is not necessary for nidogen assembly.

58 a short arm terminus to laminin through the nidogen binding locus was generated and compared with th

59 Thus, LAR-laminin-nidogen binding may play a role in regulating cell signa

60 LAR- laminin-nidogen binding was regulated by alternative splicing of

61 quence resulted in disruption of the laminin-nidogen-binding activity.

62 ce of laminin LN domains, nidogen-1, and the nidogen-binding site in laminin.

63 Mice with a targeted deletion of the nidogen-binding site of laminin gamma1 were used to stud

64 consensus glycosylation sites and a putative nidogen-binding site.

65 -Trp-Thr-Asp (YWTD) beta-propeller domain in nidogen bound to laminin epidermal-growth-factor-like (L

66 ar matrices appears to be mediated through a nidogen bridge with a lesser contribution arising from a

67 erved when HeLa cells were plated on laminin-nidogen, but not when plated on a fibronectin surface.

68 ce in C. elegans and that collagen XVIII and nidogen can have important roles in synapse organization

69 -specific expression of alphaLNNd, a laminin/nidogen chimeric protein that provides a missing polymer

70 The extracellular matrix laminin-nidogen complex was identified as a ligand for the LAR-F

71 inding affinity to neurite-promoting laminin-nidogen complexes.

72 the TeNT-nidogen interaction by using small nidogen-derived peptides or genetic ablation of nidogens

73 Nidogen (entactin) can form a ternary complex with type

74 Although members of the nidogen (entactin) protein family are structural compone

75 egans basement membrane-associated molecules nidogen/entactin (NID-1) and type XVIII collagen (CLE-1)

76 r including laminins, fibronectins, elastin, nidogen/entactin, proteoglycans, and matrix-bound cytoki

77 agen, perlecan, bamacan, laminin-1, entactin-nidogen, fibronectin) in SEF areas and in PCL.

78 on of B. burgdorferi quantities to the mouse nidogen gene allowed comparison of B. burgdorferi number

79 We show that the Caenorhabditis elegans nidogen homologue nid-1 generates three isoforms that di

80 etween the MUC4-NIDO domain and fibulin-2, a nidogen-interacting protein.

81 Inhibition of the TeNT-nidogen interaction by using small nidogen-derived pepti

82 The interaction between laminin and nidogen is crucial to the assembly of basement membranes

83 Nidogen is localized to body wall basement membranes and

84 letely wild-type pattern, demonstrating that nidogen is not essential for type IV collagen assembly i

85 mponents of basement membranes, we find that nidogen is not required for basement membrane assembly i

86 ation of a single axon in vivo, we show that nidogen is required for the axon to switch from circumfe

87 and alpha(1)beta(1), which bind fibronectin, nidogens, laminin isoforms, and collagen type IV, occurs

88 Here we showed that the nidogen-like (NIDO) domain of MUC4, which is similar to

89 e show that the expression of the Drosophila Nidogen (Ndg) gene at different embryonic stages and in

90 e created a physical map of the region using Nidogen (Nid) as a molecular starting point for cloning

91 ting with the extracellular matrix component nidogen, nid-1, and the intracellular adaptor alpha-lipr

92 h is similar to the G1-domain present in the nidogen or entactin (an extracellular matrix protein), c

93 t a second, as yet unidentified, activity of nidogen overlaps with perlecan binding and accounts for

94 ogen-derived peptides or genetic ablation of nidogens prevented the binding of TeNT to neurons and pr

95 iaPaCa PC cells, lacking endogenous MUC4 and nidogen protein.

96 regulating cell signaling induced by laminin-nidogen, resulting in cell morphological changes.

97 In the extracellular matrix component nidogen, the YWTD domain functions to bind laminin.

98 , laminin-2, fibronectin, various collagens, nidogen, thrombospondin, or complement factors C3 and C3

99 Entactin (nidogen) was a specific target for stromelysin-1 in the