ライフサイエンスコーパス: Nogo receptor

1 a soluble extracellular domain of the human Nogo receptor.

2 nd that the plasticity inhibitors Nogo-A and Nogo receptor 1 (NgR1) are differentially expressed in t

3 We examined whether Nogo Receptor 1 (NgR1) regulates the plasticity associat

4 white matter stroke is in part mediated via Nogo receptor 1 (NgR1) signaling.

5 -GFP, we reevaluated the CST in mice lacking nogo receptor 1 (NgR1), a protein implicated in limiting

6 in the somatosensory cortex of mice lacking Nogo Receptor 1 (NgR1).

7 ) to express a truncated soluble fragment of Nogo receptor 1 (NgSR).

8 axonal regeneration through interaction with Nogo receptor 1, but the function of Nogo-A in neurons i

9 -type and plasticity-sensitized mice lacking Nogo receptor 1.

10 ukocyte common antigen-related (LAR) and the nogo receptors 1 and 3 (NgR), have recently been identif

11 ors for myelin-associated growth inhibitors, Nogo receptors 1 and 3.

12 tyrosine phosphatase sigma (RPTPsigma), and Nogo receptors 1-3 (NgR1-3).

13 lex with the neuronal cell surface receptors Nogo receptor-1 (NgR1) and paired Ig-like receptor-B (Pi

14 LOT usher substance (LOTUS) as an endogenous Nogo receptor-1 (NgR1) antagonist and demonstrated that

15 functions including the gene coding for the Nogo receptor, a key transducer of myelin inhibition.

16 Nogo receptor adopts a leucine-rich repeat (LRR) module

17 mily of neuronal receptors that includes the NOGO receptor, an inhibitor of neuronal regeneration and

18 indicate that increased interaction between Nogo receptor and APP reduces surface expression of APP

19 tein found in CNS myelin, interacts with the Nogo receptor and has been proposed to mediate inhibitio

20 utgrowth inhibition by signaling through the Nogo receptor and paired Ig-like receptor B (PirB).

21 The NEP1-40 peptide competitively binds the Nogo receptor and partially blocks inhibition from MAIs,

22 motor area, inosine combined with NEP1-40, a Nogo receptor antagonist, doubled the number of axon bra

23 we examined the role of LOTUS, an endogenous Nogo receptor antagonist, in promoting functional recove

24 data are consistent with the hypotheses that Nogo receptors are membrane-bound growth cone repellent

25 Nogo receptors are sialoglycoproteins comprised of 8.5 c

26 l further with simultaneous application of a Nogo receptor blocking peptide, suggesting this combinat

27 hree inhibitors can interact with either the Nogo receptor complex or paired immunoglobulin-like rece

28 The Nogo receptor complex, composed of the Nogo-66 receptor

29 ons, LINGO-1 is an integral component of the Nogo receptor complex, which inhibits axonal growth via

30 ysis of p75(NTR), and ectodomain shedding of Nogo receptor, correlated with a 30% decrease in activat

31 RhoGEF, binds p75 directly and regulates p75-Nogo receptor-dependent RhoA activation and neurite inhi

32 sitol-anchored cell-surface receptors of the Nogo Receptor family (NgR1, NgR2, and NgR3) restrict exc

33 We demonstrate the Nogo receptor family (NgR1-3) acts as Abeta receptors me

34 interactions between MAG and members of the Nogo receptor family function to coordinate myelin inhib

35 The Nogo receptor family members NgR1 and NgR2 bind to MAIs

36 p75 and the Nogo receptor form a signaling unit for myelin inhibitor

37 ne-rich repeat and Ig-like domain-containing Nogo receptor interacting protein 1 (LINGO-1) is a negat

38 ne-rich repeat and Ig-like domain-containing Nogo receptor interacting protein 1 (LINGO-1) is a negat

39 e, we identify LRR and Ig domain-containing, Nogo receptor-interacting protein (LINGO-1) as a potent

40 Previously, LRR and Ig domain-containing, Nogo receptor-interacting protein (LINGO-1) has been ide

41 ligand-binding subunit of this complex, the Nogo receptor, is absent in oligodendrocytes, the extrac

42 acid or carrying a targeted deletion of the Nogo receptor (NgR(-/-)) unmasked a strong plasticity of

43 ned an expression library and identified the Nogo receptor (NgR) as a high-affinity OMgp-binding prot

44 Neuronal Nogo receptor (NgR) binds to each of the three inhibitor

45 family, is required as a co-receptor for the Nogo receptor (NgR) to mediate the activity of myelin-as

46 es suggest that an axon surface protein, the Nogo receptor (NgR), may play a role in this process thr

47 When associated with the Nogo receptor (NgR), the transmembrane receptor p75NTR s

48 Nogo receptor (NgR)-mediated control of axon growth reli

49 to the glycosylphosphatidylinositol-anchored Nogo receptor (NgR).

50 xpression or suppressing the activity of the Nogo receptor (NgR).

51 (MAG), exert their effects through the same Nogo receptor (NgR).

52 izing the function of several members of the Nogo receptor (NgR)/RhoA pathway improved the capacity o

53 Three of these factors bind to the Nogo receptor, NgR, which is expressed on axons.

54 We demonstrate that reovirus binds Nogo receptor NgR1, a leucine-rich repeat protein expres

55 de of myelin-derived inhibitors with soluble Nogo receptor (NgR1, RTN4R) decoy protein.

56 Nogo receptors (NgR1, NgR2, and NgR3) are growth cone di

57 We report that mice lacking Nogo receptors (NgR123-null mice) display complete CC ag

58 b) and glycosylphosphatidylinositol-anchored Nogo receptors (NgRs) as exclusive axonal receptors for

59 ce their inhibitory signals through the same Nogo receptor/p75 neurotrophin receptor/LINGO-1 (NgR1/p7

60 udy, we show that a family of proteins named Nogo receptor proteins (NgR1 to NgR3) regulates Abeta pr

61 site of APP mediates interaction of APP with Nogo receptor proteins.

62 eveloped a soluble, truncated version of the Nogo receptor that antagonizes outgrowth inhibition on b

63 entricular infusion of a soluble form of the Nogo receptor that blocks the action of several myelin-a

64 2 in neurons permits the accumulation of the Nogo receptor, thereby linking APC/C(Cdh1) activity with

65 Nogo receptor triple mutants (Ngr1(-/-); Ngr2(-/-); Ngr3

66 ue and axon regeneration is repressed by the Nogo receptor using p75NTR as the signal transducer.

67 A chimeric Nogo receptor variant (NgR(OMNI)) in which Cys(309)-Cys(

68 aves oligodendrocyte-myelin glycoprotein and Nogo receptors, was without benefit.

69 t residues (28-58) are available to bind the Nogo receptor, which is entirely consistent with functio