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The level of excision repair cross-complementing 1 (ERCC1) gene expression, which is important in the repair of the cisplatin DNA adducts, is reported to be related to the level of cisplatin resistance in tumor cells.
A low level of excision was also noted in cells without TM treatment; we attributed this to the previously reported <0.1% spontaneous Cre activity that was reported for this line [37] (Figure 4B, lanes 2 and 3).
This low level of excision in P. berghei blood stages mediated by FLP or FLPL was comparable to that what we have observed with FLP-based excision of FRTed sequences in P. falciparum blood stages.
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The Southern blots showed essentially complete excision of the p53 alleles in spleen and liver and moderate levels of excision of kidney and lung, and low levels of excision in brain, heart, and eye; similar to what had been reported previously in the Rosa26-CreERT2 line [20].
From a panel of eight integrase mutants (collectively referred to as "Int*"), we identified several that exhibited high levels of excision and promiscuous recombination.
In this study, we show that prostasin is decreased in an ovarian cancer drug-resistant cell line and in ovarian cancer patients with high levels of excision repair cross-complementing 1, a marker for chemoresistance.
Gene expression levels of excision repair cross-complementing group 1 (ERCC1), DPD, and topoisomerase-1 (TOP1) were determined using TaqMan real-time PCR Life Technologiess, Foster City, CA, USA) as described previously (Kuramochi et al, 2006).
However, there was no statistically significant difference between group 1 and group 2 animals (Student's t-test; P=0.5356), suggesting that the level of PEX13 excision did not influence lifespan for the mutant population.
A comparison of the level of DNA excision repair (repair replication and unscheduled DNA synthesis) confirms that some forms of alkylating-agent damage (probably mono-filar DNA adducts) are less completely removed by both normal and malignant rodent cells than by their human counterparts, rendering rodent cells more susceptible to the toxic potential of unexcised lesions.
Further elevated levels of nucleotide excision repair (NER) genes show a novel mechanism by which drinking GTPs prevents UV-induced immunosuppression [ 81].
4 During the same time period, an increasing number of correlative biomarker analyses demonstrated that the efficacy of platinum agents was associated with intratumoral levels of the excision repair cross-complementing group 1 (ERCC1) gene, with high levels indicating resistance.
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