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Exact(9)
Since EYFP is a spectral variant derived from EGFP by a few point mutations we could use an anti-EGFP antibody to detect EYFP.
Besides confirming all previously detected mutations we could detect 5 new mutations.
Since the availability of genetic testing for hMSH2, hMLH1 and hMSH6 gene mutations, we could identify 32 HNPCC families with germline alterations in one of these genes.
Sourcing from the global repository of cancer-associated somatic mutations we could predict a large set of putative NAMs leading to downstream rewiring (Experimental Procedures; Table S1).
Among patients with all wild type of these mutations, we could separately evaluate the clinical significance of the predictive and prognostic roles of serum ligands.
Based on these mutations, we could infer both the primary limiting stress that the pathway placed on its host as well as the biochemical mechanisms that the cells used to overcome this stress.
Similar(51)
However, by mutation, we could destabilize the β-finger further and change the rate-limiting step such that an initial conformational change becomes rate limiting.
In order to support our hypothesis that the candidate loci were involved in TPE, and not the result of a second site mutation, we could have recombinationally mapped the Su TPE) phenotype in an attempt to confirm it co-localized with the mapping of the candidate gene.
In skin fibroblasts of 3 patientstients with homozygosity for the G309D-PINK1 mutation, we could demonstrate an impaired activity of the respiratory complex I, an induction of antioxidant defence enzymes and enhanced lipid peroxidation [4], as well as altered α-synuclein mRNA levels [5].
For the KRAS mutation, we could not confirm nor completely disprove its prognostic value.
Since the simulations were performed using the real genotype data at the IGF2-intron3-G3072A mutation, we could not estimate the influence of the percentage of heterogeneous dams.
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