a T1796A transversionresultsin the substitution mutation
the MluI mutagenesis(passive) created bysubstitution mutations
means of a range of sources directly about the reading and storage of DNA(passive) may be caused byA substitution mutation
means of a variety of sources directly regarding the reading and storage of DNA(passive) may be caused byA substitution mutation
a number of sources directly related to the reading and storage of DNA(passive) can be caused byA substitution mutation
in the papA gene(passive) was createdThe C44S substitution mutation
The blood disease Sickle - cell anemia(passive) is caused byThe blood disease Sickle - cell anemia
17 beta - hydroxysteroid dehydrogenase 3 deficiency " ( Free full textcauses17 beta - hydroxysteroid dehydrogenase 3 deficiency " ( Free full text
in an alternate codon , altering the amino acid at this position onlyresultingin an alternate codon , altering the amino acid at this position only
a difference in the protein ... but a mutation can completely change the entire codemay causea difference in the protein ... but a mutation can completely change the entire code
in a novel methionine 47 residues further downstream in the S8 hippocampus transcript ( Figure 6bresultingin a novel methionine 47 residues further downstream in the S8 hippocampus transcript ( Figure 6b
one base to be replaced with a different onecauseone base to be replaced with a different one
a frame shiftcan causea frame shift
in a different amino acid being placed at a specific position in a protein , causing small changesresultin a different amino acid being placed at a specific position in a protein , causing small changes
a different amino acid to be placed at a specific location , causing small changes in the proteinmay causea different amino acid to be placed at a specific location , causing small changes in the protein
a different amino acid to be placed at a specific location , resulting in major changes to the protein and leading to radically different characteristics in the offspringmay causea different amino acid to be placed at a specific location , resulting in major changes to the protein and leading to radically different characteristics in the offspring
a significant decrease in receptor functioncauseda significant decrease in receptor function
the type 2A diseasecausingthe type 2A disease
to double amino acid substitutions Tyr45Ser and Pro47Leu changesleadingto double amino acid substitutions Tyr45Ser and Pro47Leu changes
the following : Change in the coding of amino acids codon to a particular stop codon resulting in an incomplete protein , which is usually non - functionalcan causethe following : Change in the coding of amino acids codon to a particular stop codon resulting in an incomplete protein , which is usually non - functional
in mepA overexpressionmay resultin mepA overexpression
to amino acid change affecting enzyme functionleadingto amino acid change affecting enzyme function
to disturbed left - right patterning and axial truncation in 59459 - 2 mutants A mutant characterized by a short tail as well as heart defects including situs inversus ( Figure 3Aleadsto disturbed left - right patterning and axial truncation in 59459 - 2 mutants A mutant characterized by a short tail as well as heart defects including situs inversus ( Figure 3A
in an in - frame stop codonresultingin an in - frame stop codon
the TATA , the YY1 + 60 , and the USF elements allresultedthe TATA , the YY1 + 60 , and the USF elements all
in a termination codonresultingin a termination codon
in codon changeresultedin codon change
in constitutive activation of c - KIT that confer constitutive activationresultin constitutive activation of c - KIT that confer constitutive activation
its ubiquitin - dependent degradationpreventsits ubiquitin - dependent degradation
the terminator codon 5-UAG-3 to occur at an interior position in a particular type of mRNAcausingthe terminator codon 5-UAG-3 to occur at an interior position in a particular type of mRNA
a new splice variant which had lost 55 nucleotides , and gained a human - specific C - terminal domain ( Florio et al . , 2016createda new splice variant which had lost 55 nucleotides , and gained a human - specific C - terminal domain ( Florio et al . , 2016
to specifically disrupt these putative zinc fingersdesignedto specifically disrupt these putative zinc fingers
to a missense mutationleadingto a missense mutation
in a stop codon in the open reading frame of exon 5resultsin a stop codon in the open reading frame of exon 5
to the incorporation of any known natural or synthetic amino acid ... subject to the following provisosmay leadto the incorporation of any known natural or synthetic amino acid ... subject to the following provisos
recessive allele le(passive) caused byrecessive allele le
to situs inversus and posterior truncation.(Aleadsto situs inversus and posterior truncation.(A
in the change of the conserved arginine 43 to tryptophan in the PX domainresultsin the change of the conserved arginine 43 to tryptophan in the PX domain
a new hydrogen bond between Q2481 and the conserved tyrosine ( TYRcould createa new hydrogen bond between Q2481 and the conserved tyrosine ( TYR
E349 K in TMS2resultedE349 K in TMS2
a genetic disorder(passive) caused bya genetic disorder
in the switching of a valine for a glutamine within the catalytic domainresultsin the switching of a valine for a glutamine within the catalytic domain
a benefit to an organismcausesa benefit to an organism
AfeI sitescreatingAfeI sites
steric interference with the binding of EGFR TKIs to the ATP binding sitecausessteric interference with the binding of EGFR TKIs to the ATP binding site