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1 enes such as peripheral myelin protein 2 and oligodendrocyte myelin glycoprotein.
2 n-associated glycoprotein (MAG), Nogo-A, and oligodendrocyte-myelin glycoprotein.
3 itol-specific phospholipase C, which cleaves oligodendrocyte-myelin glycoprotein and Nogo receptors,
4 (myelin-associated glycoprotein), and OMgp (oligodendrocyte myelin glycoprotein), and is important f
5 ffects of three myelin proteins, Nogo, OMgp (oligodendrocyte-myelin glycoprotein), and MAG (myelin-as
6 s, Nogo, myelin-associated glycoprotein, and oligodendrocyte myelin glycoprotein, and mediates their
7 nclude myelin-associated glycoprotein, Nogo, oligodendrocyte-myelin glycoprotein, and chondroitin sul
8 elin-derived axon outgrowth inhibitors Nogo, oligodendrocyte-myelin glycoprotein, and myelin-associat
10 p75 and LINGO-1 conferred responsiveness to oligodendrocyte myelin glycoprotein, as measured by RhoA
11 (myelin-associated glycoprotein), and OMgp (oligodendrocyte myelin glycoprotein), bind to the Nogo-6
12 ks Nogo, myelin-associated glycoprotein, and oligodendrocyte myelin glycoprotein binding to NgR1 with
14 s, Nogo, myelin-associated glycoprotein, and oligodendrocyte myelin glycoprotein, have been implicate
15 he extracellular domain of Nogo-A (Nogo-66), oligodendrocyte myelin glycoprotein (OMgp) and myelin-as
17 CNS regeneration inhibitors include Nogo-A, oligodendrocyte myelin glycoprotein (OMgp), and chondroi
18 eptor for the myelin-derived ligands Nogo-A, oligodendrocyte myelin glycoprotein (OMgp), and myelin-a
21 e adult mammalian CNS, the growth inhibitors oligodendrocyte-myelin glycoprotein (OMgp) and the retic
22 present in myelin, including Nogo, MAG, and oligodendrocyte-myelin glycoprotein (OMgp), have been id
23 linositol (GPI)-anchored CNS myelin protein, oligodendrocyte-myelin glycoprotein (OMgp), is a potent
24 y (Nogo, myelin-associated glycoprotein, and oligodendrocyte myelin glycoprotein) were isolated based