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Because of this terminology, stop codons have also been referred to as nonsense codons.
Usually a nonsense codon (stop codon) or a four-base codon are used.
Thus, nonsense codons lie more than 50-54 nucleotides upstream from the last exon boundary whereas natural stop codons are located within terminal exons.
This may be particularly beneficial in genetic disorders where the mRNA contains a mutation causing premature stop codon or nonsense codon.
When this happens, no tRNA can recognize it, but releasing factor can recognize nonsense codons and causes the release of the polypeptide chain.
This gene contains several nonsense codons compared to other family members that render the transcript a candidate for nonsense-mediated mRNA decay (NMD).
It has been observed that the ability of a nonsense codon to cause mRNA degradation depends on its relative location to the downstream sequence element and associated proteins.
Eukaryotic messages are subject to surveillance by nonsense mediated decay (NMD), which checks for the presence of premature stop codons (nonsense codons) in the message.
The organism which expresses such a synthetase can then be genetically programmed to incorporate the unnatural amino acid into a desired protein in the usual way, with the nonsense codon now coding for the unnatural amino acid.
Additionally, researchers have built upon an established technique in which one can insert an unnatural amino acid into a peptide sequence by charging synthetic tRNA that recognizes a nonsense codon with an unnatural amino acid.
This model proposes not only that the sequences excised contained random clusters of in-frame nonsense codons but also that the splice junction signal sequences and the branchpoint sequence originate from nonsense codons.
A nonsense mutation is a point mutation in a sequence of DNA that results in a premature stop codon, or a nonsense codon in the transcribed mRNA, and possibly a truncated, and often nonfunctional protein product.
This lack of a stop codon results a significant issue for cells.
Genes with different or multiple stop codons will be unaffected.
Unlike stop codons, the codon alone is not sufficient to begin the process.
Based on their frequency in the non-selected library, stop codons were expected at a rate of 27%.
In the standard genetic code, there are several stop codons:
The stop codon is found after residue 1463 of the amino acid sequence.
In this, start and stop codon positions are colored green and red respectively.
Later, it was demonstrated that different release factors recognize different stop codons.
It is an open reading frame, meaning that it does not contain a stop codon.
The 3' region downstream from the stop codon is separated into two parts:
There is no termination after the stop codon.
An adenosine present at the polymorphic site represents the third position in a stop codon.
These contrasted results imply that complex interactions are taking place downstream of the stop codon.
AddDecorations is used to draw any additional characteristics, for example the sites of start and stop codons within the feature.
The editing creates an early stop codon, which, upon translation, produces a shorter protein.
This variation would lie beyond stop codons, which show a high rate of in-frame loss in yeast.
As a result, the rate of errors in which translation continues beyond a stop codon increases from about 0.3% to about 1%.
When stop codons, tryptophan and methionine are all excluded, R 2increases by only 0.046 on average.
This causes the protein to be shortened because of the stop codon interrupting its normal code.
Only the first exon was sequenced for stop codon mutations, but none were found.
It fixes defective protein as an alternative to Stop codon suppression treatment.
This leads to a premature stop codon, shortening the protein that is supposed to be transcribed.
This causes a longer version of exon 2 to be included in the processed transcript, including an early stop codon.
The stop codon is not an amino acid, but is included for completeness.
This means that the stop codon in the cDNA is no longer an issue.