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Qaagi - Book of Why

Causes

Effects

by targeted disruption of the mouse thioredoxin gene(passive) caused byEarly embryonic lethality

targeted disruption of the mouse thioredoxin gene(passive) caused byEarly embryonic lethality

by targeted disruption of the mouse thioredoxin gene [ J(passive) caused byEarly embryonic lethality

Phenotype Homozygous disruption of this genecausesearly embryonic lethality

deletion of the Hdac3 gene in micecausesearly embryonic lethality

by targeted disruption of the mouse(passive) caused byEarly embryonic lethality

The complete ablation of the Stx4 gene in micecausesearly embryonic lethality

Targeted disruption of STAT3causesearly embryonic lethality

by targeted disruption of the mouse thioredoxin(passive) caused byEarly embryonic lethality

by targeted disruption of the TRAF - interacting protein ( TRIP ) gene(passive) caused byEarly embryonic lethality

Knockout of this genecausesearly embryonic lethality

genetic inactivation of CycK in micecausesearly embryonic lethality

a result of many mutationscauseearly embryonic lethality

direct - targeted gene deletion of Klf5causedearly embryonic lethality

2 genecausesearly embryonic lethality

complete loss of function of some of these genescausesearly embryonic lethality

many mutationscauseearly embryonic lethality

by disruption of the gene for choline kinase(passive) caused byEarly embryonic lethality ...

loss - of - function mutationsoften causeearly embryonic lethality

A second site mutationcausingearly embryonic lethality

genecausesearly embryonic lethality

Deletion of Hdac3 in the germ linecausedearly embryonic lethality

the deletion of whichcausesearly embryonic lethality

whose absencecausesearly embryonic lethality

Targeted disruption of the synovial sarcoma - associated SS18 genecausesearly embryonic lethality

the double knockoutcausedearly embryonic lethality

by global Shp2 deficiency(passive) caused byearly embryonic lethality

by impaired mesoderm development(passive) caused byearly embryonic lethality

by targeted disruption of the 3-hydroxy-3-methylglutaryl - CoA reductase gene(passive) caused byEarly embryonic lethality

targeted disruption of the 3-hydroxy-3-methylglutaryl - CoA reductase gene(passive) caused byEarly embryonic lethality

by constitutive loss of function(passive) caused byearly embryonic lethality

constitutive loss of function(passive) caused byearly embryonic lethality

Inherited defectsmay causeearly embryonic lethality

mouse knockoutscauseearly embryonic lethality

Bub1 losscausesearly embryonic lethality

by disruption of the gene for choline kinase , the first enzyme in phosphatidylcholine biosynthesis(passive) caused byEarly embryonic lethality

the genes ... when disruptedmay causehuman embryonic lethality

in turncan ... causeearly embryonic lethality

by disruption of the gene for choline kinase alpha , the first enzyme in phosphatidylcholine biosynthesis(passive) caused byEarly embryonic lethality

disruption of the gene for choline kinase alpha , the first enzyme in phosphatidylcholine biosynthesis(passive) caused byEarly embryonic lethality

from defective cell divisionmight resultfrom defective cell division

one anotherinfluenceone another

the most extreme and therefore fatal casescausesthe most extreme and therefore fatal cases

from its complete ablation ( Yang et al . , 2012resultingfrom its complete ablation ( Yang et al . , 2012

in good pregnancy ratesresultsin good pregnancy rates

in in vitro transformation andresultsin in vitro transformation and

in cell cycle arrestresultedin cell cycle arrest

to cell deathleadingto cell death

the terminal differentiation of both embryonic and adult epitheliainfluencesthe terminal differentiation of both embryonic and adult epithelia

to MEL-28 functionmust contributeto MEL-28 function

certainlywould ... originatecertainly

from defects in the vascular systemresultingfrom defects in the vascular system

from the disruption of important genesresultingfrom the disruption of important genes

from placental defectsresultingfrom placental defects

from Mdm4 lossresultingfrom Mdm4 loss

in partmay ... be resultingin part

from RNAiresultingfrom RNAi

the assumption of TRD(passive) caused exclusively bythe assumption of TRD

from ubiquitous silencing of CG6672 ( Figure 4Aresultingfrom ubiquitous silencing of CG6672 ( Figure 4A

to hybrid male inviabilityleadsto hybrid male inviability

from a severe chondrodysplasiaresultingfrom a severe chondrodysplasia

from RNAi depletion of asymmetrically abundant transcripts in wild type ( N2 ) andresultingfrom RNAi depletion of asymmetrically abundant transcripts in wild type ( N2 ) and

in these independently uncommon conditions and that the course of PTA was medial and distant from the trigeminal nerve based on 3D - CT angiographymight have resultedin these independently uncommon conditions and that the course of PTA was medial and distant from the trigeminal nerve based on 3D - CT angiography

from overexpression of Rasresultingfrom overexpression of Ras

howevermay causehowever

from MKK manipulations under SPCH or FAMA promotersresultingfrom MKK manipulations under SPCH or FAMA promoters

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