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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Nck1tm1Paw
targeted mutation 1, Tony Pawson
MGI:2667151
Summary 5 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Nck1tm1Paw/Nck1tm1Paw involves: 129/Ola * ICR MGI:2674260
cn2
Apoetm1Unc/Apoetm1Unc
Nck1tm1Paw/Nck1tm1Paw
Nck2tm3Paw/Nck2tm3Paw
Tg(Cdh5-cre/ERT2)1Rha/0
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 MGI:7316557
cn3
Nck1tm1Paw/Nck1tm1Paw
Nck2tm3Paw/Nck2tm3Paw
Tg(Nphs2-cre)1Seq/0
involves: 129S1/Sv * 129X1/SvJ MGI:3624130
cn4
Nck1tm1Paw/Nck1tm1Paw
Nck2tm1Paw/Nck2tm3Paw
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * SJL MGI:3769794
cx5
Nck1tm1Paw/Nck1tm1Paw
Nck2tm1Paw/Nck2tm1Paw
involves: 129/Ola * ICR MGI:2674277


Genotype
MGI:2674260
hm1
Allelic
Composition
Nck1tm1Paw/Nck1tm1Paw
Genetic
Background
involves: 129/Ola * ICR
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nck1tm1Paw mutation (2 available); any Nck1 mutation (40 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype




Genotype
MGI:7316557
cn2
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Nck1tm1Paw/Nck1tm1Paw
Nck2tm3Paw/Nck2tm3Paw
Tg(Cdh5-cre/ERT2)1Rha/0
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (145 available)
Nck1tm1Paw mutation (2 available); any Nck1 mutation (40 available)
Nck2tm3Paw mutation (0 available); any Nck2 mutation (29 available)
Tg(Cdh5-cre/ERT2)1Rha mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Assessment of atherosclerosis initiation and progression in tamoxifen-treated, high-fat diet fed Apoetm1Unc/Apoetm1Unc Tg(Cdh5-cre/ERT2)1Rha/0 Nck1tm1Paw/Nck1tm1Paw Nck2tm3Paw/Nck2tm3Paw mice.

cardiovascular system
• severity of lesions, atherosclerosis progression, and macrophage recruitment are reduced in male, but not female, following 16 weeks of a high-fat diet in tamoxifen-treated mice
• however, serum lipoprotein levels are normal

immune system
• severity of lesions, atherosclerosis progression, and macrophage recruitment are reduced in male, but not female, following 16 weeks of a high-fat diet in tamoxifen-treated mice




Genotype
MGI:3624130
cn3
Allelic
Composition
Nck1tm1Paw/Nck1tm1Paw
Nck2tm3Paw/Nck2tm3Paw
Tg(Nphs2-cre)1Seq/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nck1tm1Paw mutation (2 available); any Nck1 mutation (40 available)
Nck2tm3Paw mutation (0 available); any Nck2 mutation (29 available)
Tg(Nphs2-cre)1Seq mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• by 4 days of age, mutants are smaller than wild-type littermates; this is more apparent by 3 weeks of age

homeostasis/metabolism
• at 3.5 and 4.5 weeks of age, mutants show excessive amounts of albumin in their urine, indicating damage to the filtration barrier

renal/urinary system
• at 3.5 and 4.5 weeks of age, mutants show excessive amounts of albumin in their urine, indicating damage to the filtration barrier
• by 3.5 weeks of age, loss of podocytes is observed
• at E16.5, differentiated foot processes are absent in mutant embryos
• in 4-day old mutants, there is complete fusion of foot processes around the capillary loops of the glomeruli
• by 3.5 weeks of age, focal sclerosis and other defects are observed in the glomeruli
• by 3.5 weeks of age, focal sclerosis is observed in the glomeruli
• mutants have a buildup of proteinaceous material in the kidney tubules
• damaged glomerular filtration barrier




Genotype
MGI:3769794
cn4
Allelic
Composition
Nck1tm1Paw/Nck1tm1Paw
Nck2tm1Paw/Nck2tm3Paw
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nck1tm1Paw mutation (2 available); any Nck1 mutation (40 available)
Nck2tm1Paw mutation (1 available); any Nck2 mutation (29 available)
Nck2tm3Paw mutation (0 available); any Nck2 mutation (29 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice die within a few days of birth with empty stomachs likely due to suckling defects
• one mouse survived to P12 and was small, severely ataxic, and its hindlimbs respond to stimulation with rhythmic extension/flexion seizure-like activity

nervous system
• axons aberrantly re-cross the midline of the grey matter of the spinal cord
• interneurons aberrantly re-cross the midline of the spinal cord
• reduced development of the posterior commissure noted at 12 weeks of age
• axons aberrantly re-cross the midline of the grey matter of the spinal cord
• mice exhibit a shallow dorsal funiculus and does not widen in adulthood compared to controls
• mice exhibit synchronous firing of bilateral ventral motor neurons

behavior/neurological
• one mouse survived to P12 and was small, severely ataxic, and its hindlimbs respond to stimulation with rhythmic extension/flexion seizure-like activity
• mice exhibit a hoping gait that is maintained to adulthood

growth/size/body
• one mouse survived to P12 and was small, severely ataxic, and its hindlimbs respond to stimulation with rhythmic extension/flexion seizure-like activity

cellular
• axons aberrantly re-cross the midline of the grey matter of the spinal cord
• interneurons aberrantly re-cross the midline of the spinal cord




Genotype
MGI:2674277
cx5
Allelic
Composition
Nck1tm1Paw/Nck1tm1Paw
Nck2tm1Paw/Nck2tm1Paw
Genetic
Background
involves: 129/Ola * ICR
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nck1tm1Paw mutation (2 available); any Nck1 mutation (40 available)
Nck2tm1Paw mutation (1 available); any Nck2 mutation (29 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• no double homozygous mutant mice born
• double homozygotes present at Mendelian ratios at E8.5
• by E10.5 double homozygotes reduced to one third of expected
• no double homozygous mutant embryos by E12.5

cellular
• decreased fibroblast mobility
• actin fiber abnormalities

embryo
• deficient axial rotation
• neural tube closure to level of otic vesicles but no further anteriorly
• initial development is normal at the 2 to 4 somite stage
• degenerates rapidly after initial formation
• growing toward headfold structures
• allantois misshapen and balloon like
• lack of chorioallantoic fusion
• due to misshapen allantois
• failure to develop definitive embryonic circulation

nervous system
• neural tube closure to level of otic vesicles but no further anteriorly





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last database update
04/23/2024
MGI 6.23
The Jackson Laboratory