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