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We are interested in determining whether Ago2 mutants might also exhibit elevated spontaneous vesicle fusion affecting Drosophila learning and memory.
These mutants might also display reduced in vivo fitness because of the high energetic cost associated with Yop effector over-translocation.
We predicted that, like rutabaga2080 and dunce1, some of these olfactory LTM mutants might also be characterized by distinct attention-like defects in our behavioral and electrophysiological paradigms because LTM pathways are likely to modulate attention.
Loss of FGF4 in Oct4 mutants might also be expected to result in failure in PrE segregation.
We next examined whether the PPARγ mutants might also retain the ability to interact with transcriptional coactivators.
This reduced chaperone function might be due to haploinsufficiency but, because DNAJB6 is present in cells as polydispersed complexes, mutants might also exert dominant-negative effects on the wild-type protein.
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The reduced rate of chorismate production in the bradytrophic mutant might also reduce the amount of secondary metabolites derived from aromatic amino acids.
We have recently proposed that the HCF phenotype observed in the adg1-1/tpt-1 double mightt might also be connected to an increased reduction state of QA and the plastoquinone pool (PQ) in the dark [ 20].
The remarkably low ATPase activity of the R444M mutant might also be explained by a cooperativity defect in the hexamer, since its expression in a wild-type Hsp104 background greatly interferes with function.
So we further tested whether these mutants might be also defective in the step that follows DNA binding, i.e., synapsis and DNA cleavage.
Since our morphological analysis revealed a reduction of innervation and vascularization in Nscl-2 well before the mutant mice became obese we wondered whether Nscl-2 mutant WAT might also show an aberrant release of adipokines prior to the abnormal gain of weight.
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