ライフサイエンスコーパス: OMgp

1 OMgp immunoreactivity decorated the surface of mature my

2 OMgp inhibits LTP in part through PirB but independently

3 OMgp was also reported to be an extracellular matrix (EC

4 cluster of NgR1 supports binding of Nogo-66, OMgp, and MAG.

5 Like Nogo-A, OMgp contributes significantly to the inhibitory activit

6 d the Nogo receptor (NgR) as a high-affinity OMgp-binding protein.

7 echanistic studies revealed that Nogo-66 and OMgp suppress LTP in an NgR1-dependent manner.

8 ippocampal slices of adult mice, Nogo-66 and OMgp suppress NMDA receptor-dependent long-term potentia

9 ively increases its affinity for Nogo-66 and OMgp.

10 When applied acutely, however, MAG-Fc and OMgp-Fc induce a modest degree of growth cone collapse t

11 A, MAG (myelin-associated glycoprotein), and OMgp (oligodendrocyte myelin glycoprotein), and is impor

12 o, MAG (myelin-associated glycoprotein), and OMgp (oligodendrocyte myelin glycoprotein), bind to the

13 Nogo, MAG and OMgp are three prototypical myelin inhibitors that signa

14 m wild-type mice, but myelin lacking MAG and OMgp is indistinguishable from control.

15 The myelin-derived proteins Nogo, MAG and OMgp limit axonal regeneration after injury of the spina

16 In contrast, deletion of MAG and OMgp stimulates neither axonal growth nor enhanced locom

17 r Nogo-A and synergistic actions for MAG and OMgp, presumably through shared receptors.

18 Nogo, MAG, and OMgp are myelin-associated proteins that bind to a neuro

19 signaling from myelin-derived Nogo, MAG, and OMgp consolidates the neural circuitry established durin

20 Our data indicate that while Nogo, MAG, and OMgp may modulate axon sprouting, they do not play a cen

21 ee proteins in mature myelin (Nogo, MAG, and OMgp) have been purported to be critical in causing both

22 and the myelin inhibitors (Nogo-A, MAG, and OMgp).

23 Three molecules, Nogo-A, MAG, and OMgp, are produced by oligodendrocytes and share neurona

24 hree major myelin inhibitors, Nogo, MAG, and OMgp, in injury-induced axonal growth, including compens

25 ee different myelin proteins, Nogo, MAG, and OMgp, inhibit regenerating axons after CNS injury.

26 ree proteins found in myelin--Nogo, MAG, and OMgp--inhibit axon regeneration in vitro and bind to the

27 associated inhibitors such as Nogo, MAG, and OMgp.

28 a high-affinity receptor for Nogo, MAG, and OMgp.

29 ory proteins in CNS myelin: Nogo-A, MAG, and OMgp.

30 Nogo and OMgp complex with the neuronal cell surface receptors No

31 Here, we examine whether Nogo and OMgp influence functional synaptic plasticity, the effic

32 generation present in myelin--MAG, Nogo, and OMgp--all interact with the same receptor complex to eff

33 ccessfully identified a highly specific anti-OMgp antibody and observed OMgp staining in white matter

34 However, we show here that the anti-OMgp antiserum used in previous studies to define the fu

35 Similarly, substrate-bound OMgp strongly inhibits neurite outgrowth of NgR1 wild-ty

36 Introduction of exogenous NgR confers OMgp responsiveness to otherwise insensitive neurons.

37 In rat spinal cord, OMgp was not localized to compact myelin, as previously

38 ata also raise the possibility of a role for OMgp in disorders of cell proliferation such as NF1.

39 he Oligodendrocyte-Myelin glycoprotein gene (OMgp) is placed within an intron of the NF1 gene.

40 go-66), oligodendrocyte myelin glycoprotein (OMgp) and myelin-associated glycoprotein (MAG), exert th

41 ibitors oligodendrocyte-myelin glycoprotein (OMgp) and the reticulon RTN4 (Nogo) are broadly expresse

42 Oligodendrocyte myelin glycoprotein (OMgp) is expressed by both neurons and oligodendrocytes

43 Nogo-A, oligodendrocyte myelin glycoprotein (OMgp), and chondroitin sulfate proteoglycans (CSPGs), an

44 Nogo-A, oligodendrocyte myelin glycoprotein (OMgp), and myelin-associated glycoprotein (MAG) to media

45 AG, and oligodendrocyte-myelin glycoprotein (OMgp), have been identified as myelin-associated inhibit

46 rotein, oligodendrocyte-myelin glycoprotein (OMgp), is a potent inhibitor of neurite outgrowth in cul

47 ing the oligodendrocyte myelin glycoprotein (OMgp).

48 G), and oligodendrocyte myelin glycoprotein (OMgp).

49 In OMgp-null mice, CNS nodes were abnormally wide and colla

50 Analysis of CNS nodes in OMgp-null mice failed to reveal any nodal or paranodal d

51 Furthermore, the OMgp antiserum labeled OMgp-null nodes, but not nodes from versican V2-deficien

52 h we have identified, do not bind Nogo, MAG, OMgp or NgR.

53 y rescues neurite inhibition by Nogo66, MAG, OMgp, and myelin in cultured neurons.

54 ynamics after acute exposure to soluble MAG, OMgp, or Nogo-66, but is not required for these ligands

55 ting effects of three myelin proteins, Nogo, OMgp (oligodendrocyte-myelin glycoprotein), and MAG (mye

56 -1 (NgR1) binds the myelin inhibitors NogoA, OMgp, and myelin-associated glycoprotein (MAG) and has b

57 Neither Nogo-66 nor OMgp influences basal synaptic transmission or paired-pu

58 hly specific anti-OMgp antibody and observed OMgp staining in white matter only after initiation of m

59 sms that mediate this inhibitory activity of OMgp, we screened an expression library and identified t

60 of the NgR2 stalk, shows superior binding of OMgp, Nogo-66, and MAG compared with wild-type NgR1 or N

61 previous studies to define the functions of OMgp at nodes is not specific.

62 ngly argue against the nodal localization of OMgp and its proposed functions at nodes, and reveal OMg

63 Overexpression of OMgp alters mitogenic signaling in NIH3T3 fibroblasts.

64 Overexpression of OMgp alters PDGF signaling in fibroblasts which results

65 Cells overexpressing OMgp grow more slowly in serum compared to controls and

66 its proposed functions at nodes, and reveal OMgp's authentic localization relative to nodes and myel

67 Unexpectedly, we found that OMgp interacts with MAG with a higher affinity compared

68 nodal collateral sprouting, indicating that OMgp does not participate in CNS node of Ranvier assembl

69 We report that OMgp also has growth suppressive effects and downregulat

70 Furthermore, the OMgp antiserum labeled OMgp-null nodes, but not nodes fr

71 V2-deficient mice, and preadsorption of the OMgp antiserum with recombinant versican V2 blocked noda

72 Interfering with the OMgp/NgR pathway may allow lesioned axons to regenerate

73 Thus, OMgp is an important inhibitor of neurite outgrowth that

74 axons of dorsal root ganglia insensitive to OMgp.