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Recent studies demonstrated that ApoER2 interacts with the NMDA receptor, thereby mediating a Reelin-dependent function in learning and memory in the adult brain [40].
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We previously showed that Lis1 binds Dab1 in a Reelin-dependent manner and that Lis1 and Reelin functionally interact [23].
We show that a reelin-dependent ApoER2 downregulation mechanism uncouples newborn neurons from NPCs, thereby enabling neurons to migrate.
Together, our results provide foundation for the highly orchestrated clearance of neocortical projection neurons from their birth site, indicating that a reelin-dependent ApoER2 downregulation mechanism uncouples newborn neurons from NPCs, thereby enabling neurons to migrate (Fig. 4G).
Our study provides groundwork for the highly orchestrated clearance of neocortical neurons from their birth site, suggesting that a reelin-dependent ApoER2 downregulation mechanism uncouples newborn neurons from progenitor cells, thereby enabling neurons to migrate.
We suggest that insulin resistance mediates a shift from muscle dependent to brain dependent strategies of making a livelihood.
The deleterious effects of toxic concentrations of oligomeric amyloid-β on synaptic strength are partly counteracted by Reelin-dependent activation of Src family kinases, which is mediated by lipoprotein receptors and modulated in an apolipoprotein E isoform-dependent manner.
Our data suggest that (1) reelin stimulates migration toward the CP via activation of ApoER2, in a Dab1- and Pi3K-dependent but VLDLR- and GSK3β-independent manner and (2) reelin-dependent signaling as well as reelin-independent but Pi3K-dependent signaling facilitate neuronal migration from lower IZ toward the CP (see Figure S1 and also Figure 8).
It is possible that this Reelin-dependent receptor crosstalk also influences signaling from heterooligomeric EphA/EphB clusters, which could be relevant for the proposed function of Reelin as a tumor suppressor.
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These effects were mediated by a pH-dependent mechanism rather than via CO2 per se.
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