Exact(4)
As cirrhosis progresses, expression of the ileal bile acid transporter increases, resulting in less bile acids reaching the large bowel, likely due to decreased concentration of bile salts.
Interestingly, impairment in the function of VMAT-2, which accumulates cytoplasmic DA into synaptic vesicles as seen in mice heterozygous for this transporter, increases the MA neurotoxicity [ 48].
From a pharmacological point of view, inhibition of the NE reuptake transporter increases synaptic NE disposal directly by stimulating glycogenolysis and gluconeogenesis, resulting in raised blood glucose levels [ 22].
The expression of the A. nidulans AtrC (ANIG_03608) transporter increases in the presence of cycloheximide, but the corresponding gene deletion mutant had no obvious phenotype or sensitivity towards cycloheximide [ 30, 59].
Similar(56)
Although expression of both the Gxf1 and the Sut1 transporter increased the xylose transport performance, the effect of the Gxf1 transporter was significantly more pronounced.
In particular, the Gxf1 transporter increased the overall xylose transport performance by three times with respect to the control strain, which is comparable with results from previous studies [ 9, 23].
The RMSD value for the whole transporter increased in the first 50 ns, reaching a plateau at ~4 Å that was maintained until the end of the simulation time.
In particular, ABC2 transporter increased the tolerance limit of S. cerevisiae about 80-fold against decane.
ii) Among these highly expressed SLCs, Slc25a5 (an ATP/ADP transporter) increased by 3.2 folds and was the most noticeable perturbation in SLC expression.
This protection was not due to decreased expression of dopamine transporter, increased expression of vesicular monoamine transporter, or interference with the acute effects of MPP+ on mitochondrial respiration (Supplementary Figures S3A and B).
Correspondingly, the major resistance mechanisms that limit the extent of DNA damage include reduced drug uptake by the ABC transporter, increased drug inactivation by cellular detoxification, increased DNA adduct repair by DNA repair systems, etc. [ 18].
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