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Each dose of cellular vaccine was from the same, single-transfected source.
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Thus, TIGAR upregulation results in G1-phase cell-cycle arrest in cancer cells suffering from repairable doses of cellular stress.
However, our data show that TIGAR regulates the cellular ATP levels in cancer cells exposed to low doses of cellular stress.
These data suggested crucial role of TIGAR in inducing G1-phase arrest in cancer cells suffering from low doses of cellular stress.
These data suggested that p53 transcriptionally regulates TIGAR gene promoter only in cancer cells subjected to low doses of cellular insult.
These data confirmed the fact that p53 specifically regulated TIGAR gene promoter exclusively in cancer cells subjected to low doses of cellular stress and at high doses p53-mediated regulation of TIGAR gene was abolished.
The p53-mediated transcription at the TIGAR gene promoter was significantly reduced upon increasing the UV dose, suggesting that p53-mediated transcriptional regulation at TIGAR gene promoter is abolished at higher doses of cellular insult.
Thus, we conclude that TIGAR promotes indirect cell-cycle arrest in cancer cell suffering from low and repairable doses of cellular stress by regulating ATP levels and modulation of the RB E2F1 pathway.
Interestingly, p53 gene silencing did not cause any significant change in the UV-50-induced p53 protein level (lane 6), suggesting that p53 might not transcriptionally regulate TIGAR gene at high doses of cellular stress.
The relation between TIGAR-induced G1 arrest and RB phosphorylation was analysed by immunoprecipitating phosphorylated RB in KB cells subjected to low doses of cellular stress, using phospho-RB antibody.
Using of multifunctional gene vectors improve the loading dose of DNA cellular uptake, controlling the release of DNA and target delivery [25, 73].
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