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To characterize the effects of the R100W mutation in cell signaling in vivo, a set of mutants, in which the residue R100 was substituted with different amino acids, were expressed in E. coli as hproNGF precursor proteins, and purified to 99% purity, after refolding from inclusion bodies (Table S1), as mature hNGFor unprocessed hproNGF proteins.

In contrast to this finding, other reports using this same mutation in cell lines and in transgenic mice demonstrated a tight correlation between the anti-apoptotic and anti-proliferative functions of Bcl-2 and demonstrated these two functions could not be separated [28], [29].

The first, a Y93C missense mutation in cell line NMB, was not detected in 135 unrelated healthy individuals.

The in vitro selection of cells exhibiting a hemizygous mutation "hidden" within cells with a heterozygous mutation and the generation of 17p LOH or of a new point mutation in the other allele (initially/ in vivo wild-type allele) may be vital in elucidating the lack of a single TP53 heterozygous mutation in cell lines.

Since the function of BRCA1 in SCE following replication fork collapse is more profound when ATR is depleted, this could be another molecular mechanism explaining why a second mutation in cell cycle checkpoint genes is important for BRCA1 associated cancer development in addition to permitting survival of the cells with BRCA1 mutations.

Analysis at the genomic level of 67 tumour samples and 37 cell lines revealed at least 2 bona-fide mutations in cell lines without allelic loss at 11q23: a 4bp-deletion causing skip of exon 3 resulting in a premature stop codon in cell line N206, and a Y93C mutation in cell line NMB located in a region affected by germline SDHD mutations causing hereditary paraganglioma.

Similar(54)

Again, this contrasted with the marked shift to point mutation in cells lacking Xrcc2.

Defects conferred by the single dinG mutation in cells that carry an oppositely oriented rrn are suppressed by RNase H over-expression and by the rpoC* mutation.

Apc mutation in cells from the MMTV-PyMT mouse model also results in increased expression of MDR1 and a greater population of TICs.

The unbalanced loss of these important biosynthetic precursors might explain the detrimental fitness effect of becoming Cit+ via the citT mutation in cells lacking gltA1.

Here we describe the acquisition of a hotspot PIK3CA mutation in cells selected for resistance to the HER2 tyrosine kinase inhibitor lapatinib.

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