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1 lication of a three-state "hopping" model of chain migration.
2 , and blockade of Reelin signaling increased chain migration.
3 r of D-1 that forms nonenzymatically by acyl chain migration.
4 e equivalent to that previously described as chain migration.
5 cell-cell interactions underlying homotypic chain migration.
6 ar protrusions and disrupted directional and chain migration.
7 blockade abrogates their pathology-directed chain migration, a developmentally relevant mode of tang
8 pus, moreover, likely contributes to ectopic chain migration and aberrant integration of newborn DGCs
10 escent NSCs enhances proliferation, promotes chain migration and transmigration, and activates intrac
11 gly, lamellipodia formation and in vivo ENCC chain migration defects are rescued by inhibition of ROC
13 o associated with neurons undergoing ectopic chain migration into the ischemic striatum and cerebral
14 ains under these conditions, suggesting that chain migration is characteristic of SVZ precursors.
19 nsive network of pathways for the tangential chain migration of neuronal precursors throughout the la
20 other cellular functions of NPCs, namely the chain migration of NPCs from neurospheres, perhaps as a
21 the adult human SVZ appears to be devoid of chain migration or large numbers of newly formed young n
22 generate neuroblasts that undergo restricted chain migration over an extended distance of more than 2
23 and initiate the transition from tangential chain migration to individual radial migration outside o
25 confirmed using different markers, neuronal chain migration was not demonstrated, and no serial reco
26 ere morphology (neurosphere number, size and chain migration) were assessed in response to cytotoxic
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