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Oppositely, angiotensin II treatment induced significant decreases in PDE4D variant expressions (−19% for 76 kDa and −26% for 52 kDa, Fig. 4B) and PDE4D transcript (−54%, Fig. 3B).
Results were analysed at the Ct level and references for the genes analysed are summarised in Table 2. Survivin, caspase-3, and their splice variant expressions were determined by design primers and probes labelled at the 5′ end with FAM and at the 3′ end with TAMRA.
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The prediction of our theoretical model that alternative splicing is favored by a strong tissue specificity in splicing variant expression fits well with the observation that PS genes are expressed in more tissues than MS genes (Figure 2B).
Therefore, m-spinesin variants may have distinct biological functions arising from organ-specific variant expression.
Instead, from whatever cause, CIN is directed towards solutions to environmental stresses when it arises, which would then account for the conditional variant expression of aneuploidy in cellular contexts.
Elevated growth hormone (GH) levels lead to increased circulating insulin-like growth factor-I (IGF-I), but the effects on localised muscle IGF-I splice variant expression is not known.
This suggests a possible interaction between the genetic variant, expression and the group phenotype.
These data suggest that as in mice, human splice variant expression varies between organs.
For this, we induced CPY* and variant expression in wild type cells.
It suggests that if splicing variant expression is free to evolve in different tissues, selection should promote tissue specific expression.
In our study we found highly variant expression levels in the layers of the cerebellar cortex and different expression dynamics between Purkinje and granule cells.
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