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We found that overexpression of either miR-10a or miR-10b led to a robust downregulation of both WNT1 and MSX1 (Fig. 7E), which are both expressed in the midbrain/hindbrain boundary and are involved in the patterning of mouse midbrain neurons (Arenas et al., 2015).
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PGC-1α controls the expression of the GTPases dynamin-related protein 1 (Drp1) and mitofusin 2 (Mfn2) in human skeletal muscle and mouse ventral midbrain neurons [ 19, 49].
Expression of a similar murine splicing form of TCF7L2 (designated as a form with exons 12-13-14-17-18) was recently located to postmitotic neurons of mouse midbrain [ 8].
Thus, loss of Nurr1 function early during development in mice leads to the absence of midbrain neurons, while reduction of Nurr1 function in adulthood leads to a slowly progressive loss of striatal dopamine and markers of DAn.
Altogether, these results suggest that Smarca1 promotes the differentiation from immature to mature mDA neurons in the developing mouse midbrain.
It has been demonstrated that knockdown of Cul1 in primary mouse midbrain, as well as cortical culture, renders neurons susceptible to death, suggesting that Cul1 may have a role in maintaining the integrity of post-mitotic neurons.
In contrast to the situation in mice, there is a more diffuse infection of cortical and midbrain neurons as well as choroid and ependymal epithelial cells.
Mixed cultures of cortical or midbrain neurons and glial cells were prepared as described (Vaarmann et al., 2010), from mouse pups 1 3 days postpartum.
DA midbrain neurons are first generated near the midbrain-hindbrain junction and migrate radially to their final position in the ventral midbrain [27], [28].
For immunocytochemistry primary midbrain neurons were plated on cover slips.
Dopamine midbrain neurons are first generated near the midbrain-hindbrain junction and migrate radially to their final position in the ventral midbrain.
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