the primary mutation(passive) was created bya nonsense codon
The mutation found in MH5887createda nonsense codon
depletion of eRF1 [ 14(passive) caused bynonsense codon readthrough
a base substitutionresultinga nonsense codon
and EcoRI , Klenow filling in the resulting 5′ overhangs , and circularizationto createa nonsense codon
transcriptional errorscreatingnonsense codons
mutations and ... as a result(passive) are ... caused byNonsense codons
multicopy ITT1(passive) caused bynonsense codons
these omnipotent suppressors(passive) caused bynonsense codon readthrough
a primary unusual change in a gene occurring spontaneously or by induction(passive) created bya nonsense codon
to be the substitution of T for C at position 3185creatinga nonsense codon
about one third of all known disease - causing mutationsoriginatea nonsense codon
point mutationscreatinga nonsense codon
either from a point mutation or a frameshiftresultingeither from a point mutation or a frameshift
to a truncation at residue 437 andledto a truncation at residue 437 and
to the production of truncated N - terminal APC fragmentsleadingto the production of truncated N - terminal APC fragments
in the expression of a truncated polypeptide [ 3resultsin the expression of a truncated polypeptide [ 3
the variant is reportable , STOP Step 4cresultsthe variant is reportable , STOP Step 4c
NMD and the 3′-most exoncausingNMD and the 3′-most exon
termination of a polypeptide chain E. Genetic codecausetermination of a polypeptide chain E. Genetic code
translation to stop prematurelycausestranslation to stop prematurely
an RNA partitioning shifttriggeran RNA partitioning shift
in a stop codon that would not make sense in the reading of the sequencewould resultin a stop codon that would not make sense in the reading of the sequence
termination of a polypeptide chain UAA ( ocher ) , UAG ( amber ) , and UGA ( opalcausetermination of a polypeptide chain UAA ( ocher ) , UAG ( amber ) , and UGA ( opal
normal translationpreventnormal translation
a decay pathway distinct from that seen for Fed-1 mRNA in the darktriggera decay pathway distinct from that seen for Fed-1 mRNA in the dark
termination of a polypeptide chain – UAA ( ochre ) , UAG ( ambercausetermination of a polypeptide chain – UAA ( ochre ) , UAG ( amber
premature stop sitescreatepremature stop sites
from point mutations that result in stop codons , which prematurely terminate the translation processresultfrom point mutations that result in stop codons , which prematurely terminate the translation process
in the production of truncated proteins that have the potential to increase disease severitywould ... resultin the production of truncated proteins that have the potential to increase disease severity
deadenylation - independent decapping in mammalian cellsmight triggerdeadenylation - independent decapping in mammalian cells
the protein from being synthesizedpreventsthe protein from being synthesized
nuclear eventscould influencenuclear events
from an introduced upstream reading frameresultingfrom an introduced upstream reading frame
in truncated inferred proteins ( Table 7 , which is published as supporting information on the PNAS web sitealso resultingin truncated inferred proteins ( Table 7 , which is published as supporting information on the PNAS web site
the CYBB gene to be non - functional ( Figure 2causedthe CYBB gene to be non - functional ( Figure 2
in lack of detectable functional protein ( 53resultingin lack of detectable functional protein ( 53
in polarityresultin polarity
in a null phenotyperesultsin a null phenotype
in truncation of the protein , a splicing errorresultingin truncation of the protein , a splicing error
pre - mRNA splicing ( reviewed in references 32can influencepre - mRNA splicing ( reviewed in references 32
the termination of translation ( i.e. the end of the polypeptide chaincausesthe termination of translation ( i.e. the end of the polypeptide chain
at the filled EcoRI sitewas createdat the filled EcoRI site
premature termination of translaВ tioncausingpremature termination of translaВ tion
alt - mRNA up - regulationcausealt - mRNA up - regulation
at position 79 ( TGA ) by a frameshift and nonsense mutations at codons 209createdat position 79 ( TGA ) by a frameshift and nonsense mutations at codons 209
in a complete loss of enzyme activityresultsin a complete loss of enzyme activity
in termination of the protein sequence with amino acid 252resultingin termination of the protein sequence with amino acid 252
to a truncated proteinleadingto a truncated protein
the expression a Pretty element of contentresultsthe expression a Pretty element of content