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induced mutation(passive) created bynull alleles
the targeted mutationcreateda null allele
the wpk mutationmay causea null allele
The majority of the mutationscausednull alleles
splicing mutations(passive) caused bynull alleles
NHEJ mutationsto createnull alleles
that mutations predictedto createnull alleles
Subsequent mutationscreatedthe null allele
The two most common mutationscreatenull alleles
a T - DNA insertion that cosegregates with the mutation(passive) caused bya null allele
Removal of the floxed sequencecreatesa null allele
a targeted homologous recombination event in which the entire sano ORF was replaced with white+(passive) created bynull alleles
GSTM1 Deletioncausingnull genotype
gene deletion(passive) caused bya null allele
stop - gain mutations ( QOMattawa and QOBrescia(passive) caused byNull alleles
a possible mutation in the highly conserved primer areas(passive) caused bynull alleles
a frameshift mutation ( green lettering ) were subsequently introducedto createa null allele , dnc-6(−
mutations at the primer regions which hinder primer hybridization(passive) caused bynull alleles
mutations at locus - specific primer annealing sites(passive) caused bynull alleles
that the transgene integrated into an intron of Commd10 ( COMM domain containing 10 ) on chromosome 18creatinga Commd10 null allele
Mice harbouring this allele were then crossed with a Cre - deleter strainto createthe null allele
Because frameshift mutations lead to premature termination codons , they are usually assumedto createnull alleles
mutations in the primer binding sites which stops the primers from annealing(passive) are usually caused byNull alleles
Roughly one out of 10 mutations in a given gene is expectedto causea null allele
deletion of an RNaseIII domain(passive) created bya Dicer - null allele
a nonsense mutation at aa180 truncating the protein before its actin binding domain [ 43(passive) caused bya null allele
transposon insertionscan createnull alleles
care ... the interpretation of results obtained in mice that have been generated fibromialiga genetic manipulation such as transgenesis or site - directed mutation , especially muta- tionscausethe null allele
a deletion within the dpp gene(passive) caused bya null allele
introducing a frameshift mutation into the aac(2')-Ia coding region by allelic replacement [ 78(passive) was created bya null allele
Altering the genetic sequence in reverse genetics typically involves directed deletions and point mutations ( site - directed mutagenesis )to createnull alleles
the deletion of the entire At5g01075 coding region(passive) caused bya null allele
gene trap insertionscreatenull alleles
Exonic T - DNA insertionsmay createnull - alleles
the retrotransposon insertionhad createda null allele
Exons 2 and 3 ... are excised by Cre recombinaseto createa null allele
variants expectedto causenull alleles
variants predictedto causea null allele
Cre - mediated deletion of exon 2 results in a frame shift and premature termination within the CAR leader sequencecreatinga null allele
deletion of the common C - terminal zinc fingers(passive) created byan Ikaros null allele
to embryonic lethality in homozygous mutant animalsleadingto embryonic lethality in homozygous mutant animals
early embryonic lethality and apoptosis of the inner cell mass ( ICM ) with reported mitotic chromosome condensation and segregation defects ... Nacerddine et al . , 2005causesearly embryonic lethality and apoptosis of the inner cell mass ( ICM ) with reported mitotic chromosome condensation and segregation defects ... Nacerddine et al . , 2005
to haploinsufficiency ( i.e. through cytoplasmic degradationpotentially leadingto haploinsufficiency ( i.e. through cytoplasmic degradation
from different molecular mechanisms , including large gene deletions , intron mutations , nonsense mutations , frameshift mutations due to small insertions or deletions , and missense mutations associated with amino acid substitutions in potentially critical structural elements [ 23resultfrom different molecular mechanisms , including large gene deletions , intron mutations , nonsense mutations , frameshift mutations due to small insertions or deletions , and missense mutations associated with amino acid substitutions in potentially critical structural elements [ 23
to a gene product not containing the active site of the enzymeleadingto a gene product not containing the active site of the enzyme
severe growth delay and sterility only at 25 ° C butcausessevere growth delay and sterility only at 25 ° C but
a ` no ASEL / R ' phenotype ( class III phenotype ) , rather than a ` 2 ASER ' ( class II ) phenotype ( Chang et al . , 2003causea ` no ASEL / R ' phenotype ( class III phenotype ) , rather than a ` 2 ASER ' ( class II ) phenotype ( Chang et al . , 2003
in the loss of some Siglecs ( e.g. , Siglec-12 , -14 , andresultingin the loss of some Siglecs ( e.g. , Siglec-12 , -14 , and
to an enhanced lethalityleadsto an enhanced lethality
to coronary heart disease risk : a meta - analysiscontributesto coronary heart disease risk : a meta - analysis
the bias in assignment tests(passive) caused bythe bias in assignment tests
to BPES phenotype due to haploinsufficiency or dominant - negative effect [ 20,23leadingto BPES phenotype due to haploinsufficiency or dominant - negative effect [ 20,23
to BPES phenotype due to haploinsufficiency [ 16 ] or dominant - negative effect [ 26leadingto BPES phenotype due to haploinsufficiency [ 16 ] or dominant - negative effect [ 26
GSTT1 null genotype ... to lung cancer risk in asian populationscontributesGSTT1 null genotype ... to lung cancer risk in asian populations
GSTT1 null genotype ... to coronary heart disease riskcontributesGSTT1 null genotype ... to coronary heart disease risk
to BPES phenotype due to haploinsufficiency [ 4 ] or dominant - negative effect [ 20,23leadingto BPES phenotype due to haploinsufficiency [ 4 ] or dominant - negative effect [ 20,23
to the excess of homozygotes observedwould ... contributeto the excess of homozygotes observed
the levels of AOPPsmight influencethe levels of AOPPs
autosomal recessive retinitis pigmentosa | Stargardt 's disease | STGD1causingautosomal recessive retinitis pigmentosa | Stargardt 's disease | STGD1
to increased risk of male infertility : a meta - analysiscontributesto increased risk of male infertility : a meta - analysis
an overestimation of homozygotes and FST valuescan causean overestimation of homozygotes and FST values
to overestimation of homozygotes Models of EvolutionLeadsto overestimation of homozygotes Models of Evolution
the majority of Usher syndrome ( Usher 1D ) GENERIF , Score=1000 , Pubmed I d : 15891640 , UMLKSK CUIcausethe majority of Usher syndrome ( Usher 1D ) GENERIF , Score=1000 , Pubmed I d : 15891640 , UMLKSK CUI
deviations from Hardy - Weinberg equilibriumcan causedeviations from Hardy - Weinberg equilibrium
Significant deviations from HW equilibrium(passive) could be caused bySignificant deviations from HW equilibrium
to reduced message or protein levelsleadto reduced message or protein levels
to reduced levels of endoglin protein on the surface of endothelial cellsleadto reduced levels of endoglin protein on the surface of endothelial cells
to abnormally low levels of cGMP in the rod and cone cellsleadsto abnormally low levels of cGMP in the rod and cone cells
either in missing data , in the case of homozygous individuals , or heterozygous individuals erroneously scored as homozygotesresulteither in missing data , in the case of homozygous individuals , or heterozygous individuals erroneously scored as homozygotes
different symptoms , which are less severe in heterozygotes ( ie , less severe than antimorphs ) and are lethal in homozygotescausedifferent symptoms , which are less severe in heterozygotes ( ie , less severe than antimorphs ) and are lethal in homozygotes
elevated acetylation levels at histone H3 K14 ( Fig . 5causedelevated acetylation levels at histone H3 K14 ( Fig . 5
in a twofold drop in acetate levels during growth in glucose ... compared to the acetate level for the wild - type strainresultedin a twofold drop in acetate levels during growth in glucose ... compared to the acetate level for the wild - type strain
A lot of the complexity with dealing with Allele objects(passive) are caused byA lot of the complexity with dealing with Allele objects
in complete absence of the LDL receptorresultin complete absence of the LDL receptor
in zero activity of the genehowever resultsin zero activity of the gene
excess relative risk λ = λnull ≥ 0 and have selection coefficient s = snull ≥ 0 , which is assumed to have been constantcauseexcess relative risk λ = λnull ≥ 0 and have selection coefficient s = snull ≥ 0 , which is assumed to have been constant
no visibly abnormal phenotype , presumably as a consequence of the functional redundancy of unc-93causeno visibly abnormal phenotype , presumably as a consequence of the functional redundancy of unc-93
in false genotypingcan resultin false genotyping
in little or no protein seen with staining with anti - plectin antibodiesmay resultin little or no protein seen with staining with anti - plectin antibodies
in little or no protein seen with staining with anti - α6β4 integrin antibodiesmay resultin little or no protein seen with staining with anti - α6β4 integrin antibodies