Sentence examples for proficient human from inspiring English sources

Portions of exon 3 of TGFBR2 and exon 10 of AVCR2 (shown in Fig. 1) were amplified by PCR from the MMR proficient human colon carcinoma cell line FET (kind gift of Michael Brattain, Ph.D. Roswell Park Cancer Inst; Buffalo, NY).

These data further support the notion that the radiosensitivity of DSB repair proficient human tumour cell lines may be partly determined by the predisposition of these cell lines to activate non-conservative DSB rejoining pathways.

Recently, we have found for the first time that RUNX2 attenuates p53/TAp73-dependent p53/TAp73-dependentesproperin p53-proficient human osteosarcoma-DNAivedamage cells.

TH-302 cytotoxicity is greatly enhanced by Chk1 inhibition in p53-deficient but not in p53-proficient human cancer cell lines.

To examine the expression pattern of RUNX2 following DNA damage, p53-proficient human osteosarcoma-derived U2OS cells were exposed to ADR, which leads to DNA double-strand breaks.

These data raise the possibility that the radiosensitivity of DSB repair-proficient human tumour cell lines may be partly determined by the predisposition of these cell lines to activate non-conservative DSB rejoining pathways.

These observations were then extended to MMR-proficient human cell lines that were demonstrated to be 100-fold more sensitive to treatment with MNNG than MMR-deficient cells (Karran, 2001).

Similar results were also obtained in p53-proficient human colon carcinoma-derived HCT116 cells (Supplementary Figure S3), indicating that ADR-dependent induction of RUNX2 is not restricted to U2OS cells.

SaOS2 cells (p53-deficient human osteosarcoma cell line) and U2OS cells (p53-proficient human osteosarcoma cell line) were cultured in Dulbecco's modified Eagle's medium and RPMI 1640 medium, respectively.

A cell-free plasmid reactivation assay was used to determine the fidelity of DNA double-strand break (DSB) repair in a panel of eight DSB repair-proficient human tumour cell lines.

These results suggest that during the time available for repair of potentially mutagenic lesions, repair-proficient human cells excise 1-NOP adducts more rapidly than they excise BPDE adducts.