Sentence examples for enhanced efflux from inspiring English sources

enhanced efflux pump activity to excrete the solvent present in the cytoplasm [19].

Given that SR load is unchanged, this is the result of reduced [Ca2+]i in the vicinity of the RyR2 (due to enhanced efflux via NCX), which reduces the open probability of the channel.

Among the various molecular mechanisms associated with MDR in experimental tumour models, one of the most extensively studied involves decreased drug accumulation due to enhanced efflux by ATP-dependent transporter proteins such as P-glycoprotein (Pgp), the human multidrug resistance-associated protein 1 (MRP1), and the recently described breast cancer resistance protein (BCRP).

Acquired or intrinsic drug resistance mechanisms extensively studied in anticancer treatment are enhanced efflux through activation of transmembrane proteins, increased detoxification (e.g., via activation of glutathione transferases) and activation of anti-apoptosis or cell cycle arrest through survival signals such as Bcl-2 or p53.

This strategy of employing a toxic substrate surrogate for competitive growth enrichment is particularly beneficial for engineering efflux pumps to accelerate extrusion of biofuel with low toxicity, such as n-octane and higher alkanes [ 8], since mildly toxic compounds could not select for AcrB mutants effectively for enhanced efflux.

Enhanced efflux of drug was not observed between the 41M and 41McisR6 cells.

This phenomenon, called multidrug resistance, can result from limitation of cellular drug accumulation by limiting uptake, enhancing efflux or affecting membrane lipids such as ceramid [5].

16 Polymorphisms in transport proteins can mediate resistance to many agents active against cancer and infectious diseases via enhancing efflux of the drugs from cells.

This includes genes that may: decrease uptake of doxorubicin (SLC22A15), enhance efflux of doxorubicin (ABCC1, ABCG2, ABCD3, ABCA1), enhance conversion of doxorubicin to doxorubicinol (AKR1B10, AKR1B1), doxorubicin deoxyaglycone or doxorubicin semiquinone (NQO1), and inhibit the ability of doxorubicin to damage tumour cells through the generation of reactive oxygen species (CAT).

The rate of α-pinene release was assayed (Table  1) and interestingly, the mutants that improved efflux of n-octane also enhanced the efflux rate of α-pinene (Table  1) despite the structural dissimilarity of the substrates.

The results showed that Al concentrations ≥ 200 μM induced the efflux of citrate, while Al concentrations ≥ 500 μM enhanced the efflux of oxalate.