Overview

Also Known As:Smo^c

Removal of this mouse colony is imminent. If live mice are needed for your studies, it is advised that they be ordered immediately. After removal, the mice will be available from a cryorecovery.

Smo^c mice have loxP sites flanking exon 1 of the smoothened homolog (Drosophila) gene. Exposure to Cre recombinase removes the floxed sequence - creating a null allele. These Smo^c mice may be useful in studying hedgehog signaling and cell proliferation in the dental epithelium, craniofacial development, astrocyte populations, cardiovascular development, and of cardiac neural crest cells.

Donating Investigator

Andrew P McMahon, University of Southern California

Genetic overview

Genetic Background	Generation
	?+F1pF7 (2021-01-06 00:00:00)

Smo^tm2Amc

Allele Type	Gene Symbol	Gene Name
Targeted (Conditional ready (e.g. floxed), Reporter, No functional change)	Smo	smoothened, frizzled class receptor

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Research Applications

Research Tools
Developmental Biology Research

View All Research Applications

Base Price

Starting at:

$278.00 Domestic price for female 4-week

$2,854.50 Domestic price Cryo Recovery

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Details

Detailed Description

These mice possess loxP sites on either side of exon 1 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities.

When bred to a strain with the targeted null allele (Stock No. 004288) and a strain expressing Cre recombinase in the skin (Stock No. 004782), this mutant mouse strain may be useful in studies of hedgehog signalling and cell proliferation in the dental epithelium.

When bred to a strain with the targeted null allele (Stock No. 004288) and a strain expressing Cre recombinase in the nervous system (Stock No. 003771), this mutant mouse strain may be useful in studies of hedgehog signalling and cerebellar foliation. It has been the experience of The Jackson Laboratory Repository that homozygous mice exhibit small eyes.

When bred to a strain with the targeted null allele (Stock No. 004288) and a strain expressing Cre recombinase in the midbrain/dorsal spinal cord (Stock No. 007807), this mutant mouse strain may be useful in studies of craniofacial development.

When bred to a strain expressing Cre recombinase in astrocytes and neural stem cells (see Stock No. 012886 for example), this mutant mouse strain may be useful in studies of specific populations of astrocytes.

When bred to a strain expressing Cre recombinase in endothelial cells (see Stock No. 004128 for example), this mutant mouse strain may be useful in studies of cardiovascular development.

When bred to a strain expressing Cre recombinase in the neural tube/midbrain/dorsal spinal cord (see Stock No. 009107 for example), this mutant mouse strain may be useful in studies of cardiac neural crest cells.

Development

A loxP site flanked targeting vector containing a 400bp fragment of exon 1 and an FRT-flanked neomycin resistance gene was utilized in the construction of this mutant. This construct, with a downstream tau-lacZ, was electroporated into 129X1/SvJ derived AV3 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6J blastocysts. The resulting male chimeric animals were crossed to Swiss Webster females. The strain was then maintained as a homozygote prior to sending to the Jackson Laboratory in 2002.

Expression Data

Expressed Gene	lacZ, beta-galactosidase, E. coli
Site of Expression	When bred with mice containing Cre recombinase, lacZ will be expressed in Cre-expressing cells of the offspring.

Control Suggestions

None Available

Additional Information

Considerations for Choosing Controls

Selected References

Long F; Zhang XM; Karp S; Yang Y; McMahon AP. 2001. Genetic manipulation of hedgehog signaling in the endochondral skeleton reveals a direct role in the regulation of chondrocyte proliferation. Development 128(24):5099-108PubMed: 11748145 MGI: J:73071

View All References

Genetics

Smo^tm2Amc

Allele Symbol: Smo^tm2Amc

Allele Name	targeted mutation 2, Andrew P McMahon
Allele Type	Targeted (Conditional ready (e.g. floxed), Reporter, No functional change)
Allele Synonym(s)	Smo^c; Smo^f; Smo^fl; Smo^flox
Gene Symbol and Name	Smo, smoothened, frizzled class receptor
Gene Synonym(s)
Expressed Gene	lacZ, beta-galactosidase, E. coli
Site of Expression	When bred with mice containing Cre recombinase, lacZ will be expressed in Cre-expressing cells of the offspring.
Strain of Origin	129X1/SvJ
Chromosome	6
Molecular Note	Two loxP sites and an frt-flanked neomycin resistance cassette were inserted flanking ~400 bp of the first coding exon 1 from 44 bp upstream through 358 bp downstream of the translation initiation codon. A tau-LacZ gene was also inserted 3' to the neomycin resistance gene.
Mutations Made By	Joe Vaughan, Harvard University

Disease/Phenotype

Disease Terms

Research Areas By Phenotype

This mouse can be used to support research in many areas including:

Research Tools
- Cre-lox System
  - loxP-flanked Sequences

Genotype: Smo^tm2Amc related

Developmental Biology Research
- Embryonic Lethality (Homozygous)
- Neural Tube Defects
- Internal/Organ Defects
  - heart

Mammalian Phenotype Terms by Genotype

The following phenotype information is associated with a similar, but not exact match to this JAX^® Mice strain

Genotype: Smo^tm2Amc/Smo^tm2Amc Tg(Gfap-cre)73.12Mvs/0
involves: 129X1/SvJ * BALB/c * C57BL/6NHsd

mammalian phenotype

nervous system phenotype
- Normal - mice exhibit normal forebrain morphology and cytoarchitecture
- Normal - the number of astrocytes in the cortex is normal

nervous system phenotype

astrocytosis
- mild in the cortex

Genotype: Smo^tm1Amc/Smo^tm2Amc H2az2^{Tg(Wnt1-cre)11Rth}/?
involves: C57BL/6J * CBA/J

craniofacial phenotype

abnormal craniofacial development

abnormal basisphenoid bone morphology
- rostral half is missing

abnormal mandible morphology
- at E10.5, mandibles are 9% shorter than the wild-type and only undergoes a 1.5-fold along the dorsal-ventral axis compared to a 4-fold expansion in wild-type
- the dentate is reduced in length but the lamina is thicker
- at E10.5, apoptotic cells are observed along the midline and laterally
- at E9.5, there is an increase in apoptotic cells along the midline
- at E11.5, cell proliferation is decreased

absent gonial bone

absent palatine bone

absent styloid process

small temporal bone squamous part
- reduced

absent lower incisors

abnormal mandibular condyloid process morphology
- mice have an extra condylar process

abnormal tooth morphology
- teeth are malformed and arrested

absent lacrimal bone
- absent or appears as a tiny fragment

absent middle ear ossicles

small alisphenoid bone
- reduced

small zygomatic bone
- reduced

abnormal sphenoid bone morphology

abnormal temporal bone morphology

absent orbitosphenoid bone
- missing

absent pterygoid process

absent tongue

abnormal cranium morphology

abnormal ethmoid bone morphology
- mesethmoid bone is missing

absent malleus

absent vomer bone

absent incus

Meckel's cartilage hypoplasia
- hypoplastic and short

nasal bone hypoplasia
- nasal bone is hypoplastic

nasal septum hypoplasia
- the nasal septum is incomplete

absent presphenoid bone

abnormal maxilla morphology
- premaxilla and maxilla retain their lateral-most parts only

absent Reichert cartilage
- the basi- cerato- and thyro hyoid elements are missing

absent stapes

short Meckel's cartilage

digestive/alimentary phenotype

absent tongue

growth/size/body region phenotype

absent lower incisors

abnormal tooth morphology
- teeth are malformed and arrested

nasal septum hypoplasia
- the nasal septum is incomplete

absent tongue

hearing/vestibular/ear phenotype

absent middle ear ossicles

absent malleus

absent gonial bone

absent incus

absent tympanic ring

absent stapes

respiratory system phenotype

abnormal thyroid cartilage morphology

nasal septum hypoplasia
- the nasal septum is incomplete

skeleton phenotype

abnormal basisphenoid bone morphology
- rostral half is missing

absent orbitosphenoid bone
- missing

small zygomatic bone
- reduced

absent gonial bone

abnormal cranium morphology

abnormal ethmoid bone morphology
- mesethmoid bone is missing

abnormal mandible morphology
- the dentate is reduced in length but the lamina is thicker
- at E10.5, apoptotic cells are observed along the midline and laterally
- at E11.5, cell proliferation is decreased
- at E9.5, there is an increase in apoptotic cells along the midline
- at E10.5, mandibles are 9% shorter than the wild-type and only undergoes a 1.5-fold along the dorsal-ventral axis compared to a 4-fold expansion in wild-type

abnormal temporal bone morphology

absent presphenoid bone

absent pterygoid process

small temporal bone squamous part
- reduced

abnormal sphenoid bone morphology

absent Reichert cartilage
- the basi- cerato- and thyro hyoid elements are missing

absent stapes

Meckel's cartilage hypoplasia
- hypoplastic and short

nasal bone hypoplasia
- nasal bone is hypoplastic

abnormal thyroid cartilage morphology

absent palatine bone

absent styloid process

absent vomer bone

short Meckel's cartilage

abnormal maxilla morphology
- premaxilla and maxilla retain their lateral-most parts only

absent lower incisors

absent malleus

abnormal mandibular condyloid process morphology
- mice have an extra condylar process

absent incus

small alisphenoid bone
- reduced

abnormal tooth morphology
- teeth are malformed and arrested

absent lacrimal bone
- absent or appears as a tiny fragment

absent middle ear ossicles

vision/eye phenotype

absent orbitosphenoid bone
- missing

Genotype: Smo^tm1Amc/Smo^tm2Amc Tg(KRT14-cre)1Amc/0
involves: 129X1/SvJ * C57BL/6 * CBA

growth/size/body region phenotype

abnormal incisor morphology
- incisors are smaller in diameter and exhibit abnormal folding of the inner dental epithelium
- incisors show an absence of the papillary layer

absent enamel cord
- molars develop close to the oral surface, indicating virtual absence of a dental cord

fused molars
- first and second molars of both the maxilla and mandible are abnormally fused, forming a single gigantic anlage

abnormal ameloblast morphology
- mitochondria, RER, and Golgi are sparse and evenly distributed in the cytoplasm of incisor ameloblasts and Tomes' processes and the terminal webs do not develop
- amelolasts exhibit premature withdrawal from the cell cylce
- exhibit abnonormally short ameloblasts in the most advanced cusps of first molar region that are overlaid by a scarce, squamous stratum intermedium
- in incisors, the cuboidal ameloblasts are only 15% of the apical-basal height and contain centrally located round nuclei

abnormal enamel organ morphology
- the epithelial enamel organ appears disorganized at the late bell stage in the principal cusps of the first molars

abnormal inner dental epithelium morphology
- incisors exhibit abnormal folding of the inner dental epithelium

abnormal stellate reticulum morphology
- in molars, the stellate reticulum is hypocellular and shows absence of early vascular loops in the coronal aspect

abnormal molar morphology
- the outer dental epithelium forms a continuous layer without the gaps seen in controls
- first and second molars of both the maxilla and mandible are abnormally fused, forming a single gigantic anlage
- the stellate reticulum is hypocellular and shows absence of early vascular loops in the coronal aspect
- dental cord is virtually absent

absent Tomes' process
- Tomes' processes do not develop

abnormal molar cusp morphology
- cusps of first molars are shallow, broad, underdeveloped and misshapen

abnormal outer dental epithelium morphology
- in molars, the outer dental epithelium forms a continuous layer without the gaps observed in controls

mortality/aging

neonatal lethality, complete penetrance
- pups die within 1 day after birth

craniofacial phenotype

abnormal ameloblast morphology
- mitochondria, RER, and Golgi are sparse and evenly distributed in the cytoplasm of incisor ameloblasts and Tomes' processes and the terminal webs do not develop
- exhibit abnonormally short ameloblasts in the most advanced cusps of first molar region that are overlaid by a scarce, squamous stratum intermedium
- amelolasts exhibit premature withdrawal from the cell cylce
- in incisors, the cuboidal ameloblasts are only 15% of the apical-basal height and contain centrally located round nuclei

abnormal enamel organ morphology
- the epithelial enamel organ appears disorganized at the late bell stage in the principal cusps of the first molars

abnormal incisor morphology
- incisors are smaller in diameter and exhibit abnormal folding of the inner dental epithelium
- incisors show an absence of the papillary layer

fused molars
- first and second molars of both the maxilla and mandible are abnormally fused, forming a single gigantic anlage

abnormal inner dental epithelium morphology
- incisors exhibit abnormal folding of the inner dental epithelium

abnormal molar morphology
- the outer dental epithelium forms a continuous layer without the gaps seen in controls
- dental cord is virtually absent
- first and second molars of both the maxilla and mandible are abnormally fused, forming a single gigantic anlage
- the stellate reticulum is hypocellular and shows absence of early vascular loops in the coronal aspect

abnormal stellate reticulum morphology
- in molars, the stellate reticulum is hypocellular and shows absence of early vascular loops in the coronal aspect

abnormal outer dental epithelium morphology
- in molars, the outer dental epithelium forms a continuous layer without the gaps observed in controls

abnormal molar cusp morphology
- cusps of first molars are shallow, broad, underdeveloped and misshapen

absent enamel cord
- molars develop close to the oral surface, indicating virtual absence of a dental cord

absent Tomes' process
- Tomes' processes do not develop

skeleton phenotype

abnormal molar morphology
- dental cord is virtually absent
- the stellate reticulum is hypocellular and shows absence of early vascular loops in the coronal aspect
- first and second molars of both the maxilla and mandible are abnormally fused, forming a single gigantic anlage
- the outer dental epithelium forms a continuous layer without the gaps seen in controls

abnormal molar cusp morphology
- cusps of first molars are shallow, broad, underdeveloped and misshapen

abnormal outer dental epithelium morphology
- in molars, the outer dental epithelium forms a continuous layer without the gaps observed in controls

abnormal enamel organ morphology
- the epithelial enamel organ appears disorganized at the late bell stage in the principal cusps of the first molars

abnormal incisor morphology
- incisors are smaller in diameter and exhibit abnormal folding of the inner dental epithelium
- incisors show an absence of the papillary layer

abnormal ameloblast morphology
- exhibit abnonormally short ameloblasts in the most advanced cusps of first molar region that are overlaid by a scarce, squamous stratum intermedium
- mitochondria, RER, and Golgi are sparse and evenly distributed in the cytoplasm of incisor ameloblasts and Tomes' processes and the terminal webs do not develop
- amelolasts exhibit premature withdrawal from the cell cylce
- in incisors, the cuboidal ameloblasts are only 15% of the apical-basal height and contain centrally located round nuclei

abnormal stellate reticulum morphology
- in molars, the stellate reticulum is hypocellular and shows absence of early vascular loops in the coronal aspect

fused molars
- first and second molars of both the maxilla and mandible are abnormally fused, forming a single gigantic anlage

absent Tomes' process
- Tomes' processes do not develop

abnormal inner dental epithelium morphology
- incisors exhibit abnormal folding of the inner dental epithelium

absent enamel cord
- molars develop close to the oral surface, indicating virtual absence of a dental cord

Genotype: Smo^tm1Amc/Smo^tm2Amc Tg(Nes-cre)1Kln/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL * Swiss Webster

mortality/aging

postnatal lethality, incomplete penetrance
- about 10% of mice survive to 3 weeks of age

nervous system phenotype

decreased brain size
- overall size of mutant brains is smaller than wild-type

small cerebellum
- at P21, cerebella shows more pronounced reduction in size vs wild-type
- AP axis is more dramatically reduced than ML axis
- at E16.5, cerebella appear grossly normal, but reduced in size

abnormal cerebellar foliation
- in lateral regions, foliation is limited to slight indentations only in central and posterior regions

abnormal cerebellum morphology
- four principal fissures are very shallow

Genotype: Smo^tm2Amc/Smo^tm2Amc Tg(Nes-cre)1Kln/0
involves: 129X1/SvJ * C57BL/6 * SJL

nervous system phenotype

abnormal thalamus morphology

Genotype: Smo^tm2Amc/Smo^tm2.1Amc H2az2^{Tg(Wnt1-cre)11Rth}/0 Gt(ROSA)26Sor^tm1Sor/Gt(ROSA)26Sor⁺
involves: 129S4/SvJaeSor * 129X1/SvJ * C57BL/6J * CBA/J

cardiovascular system phenotype

decreased cardiac neural crest cell number
- the number of cardiac neural crest cells reaching the outflow tract is moderately reduced compared to in wild-type mice

impaired cardiac neural crest cell differentiation
- mice exhibit abnormal patterning of cardiac neural crest cells compared to in wild-type mice

cellular phenotype

impaired cardiac neural crest cell differentiation
- mice exhibit abnormal patterning of cardiac neural crest cells compared to in wild-type mice

embryo phenotype

impaired cardiac neural crest cell differentiation
- mice exhibit abnormal patterning of cardiac neural crest cells compared to in wild-type mice

decreased cardiac neural crest cell number
- the number of cardiac neural crest cells reaching the outflow tract is moderately reduced compared to in wild-type mice

nervous system phenotype

impaired cardiac neural crest cell differentiation
- mice exhibit abnormal patterning of cardiac neural crest cells compared to in wild-type mice

decreased cardiac neural crest cell number
- the number of cardiac neural crest cells reaching the outflow tract is moderately reduced compared to in wild-type mice

Genotype: Smo^tm2Amc/Smo^tm2Amc Slc6a3^tm1(cre)Xz/Slc6a3⁺
involves: 129S1/Sv * 129X1/SvJ

mammalian phenotype

nervous system phenotype
- Normal - mice do not exhibit any dopaminergic neuron loss the substantia nigra pars compacta and ventral tegmental area

Genotype: Smo^tm2Amc/Smo^tm2.1Amc H2az2^{Tg(Wnt1-cre)11Rth}/0
involves: 129X1/SvJ * C57BL/6J * CBA/J

cardiovascular system phenotype

transposition of great arteries
- 2 of 23 mice exhibit complete separation of a transposed aorta and hypoplastic pulmonary artery unlike in wild-type mice

abnormal artery morphology
- at E10.5 and E18.5, mice exhibit arch-artery defects compared with wild-type mice

abnormal cardiac outflow tract development
- mice exhibit partial septation of the outflow tract unlike wild-type mice

persistent truncus arteriosis
- in 17 of 23 mice

pulmonary artery hypoplasia
- in 4 of 23 mice

cellular phenotype

abnormal neural crest cell apoptosis
- mice exhibit cell death in neural crest cells unlike in wild-type mice

embryo phenotype

abnormal neural crest cell apoptosis
- mice exhibit cell death in neural crest cells unlike in wild-type mice

Genotype: Smo^tm2Amc/Smo^tm2Amc Tg(Tek-cre)12Flv/0
involves: 129X1/SvJ * C3H * C57BL/6

mammalian phenotype

cardiovascular system phenotype
- Normal - cardiopulmonary development is not disrupted

Genotype: Smo^tm2Amc/Smo^tm2.1Amc Tg(Tek-cre)12Flv/0
involves: 129X1/SvJ * C57BL/6

mammalian phenotype

cardiovascular system phenotype
- Normal - mice exhibit normal outflow tract development

References

Long F; Zhang XM; Karp S; Yang Y; McMahon AP. 2001. Genetic manipulation of hedgehog signaling in the endochondral skeleton reveals a direct role in the regulation of chondrocyte proliferation. Development 128(24):5099-108PubMed: 11748145 MGI: J:73071

Additional - Smo^tm2Amc related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Standard PCR:Smoalternate2
- Genotyping resources and troubleshooting
Dietary Information
- LabDiet® 5K52 formulation (6% fat)
Breeding Considerations

When maintaining a live colony, these mice can be bred as homozygotes. [2020]

The original coat color expected from breeding was Agouti (colony may be still segregating for albino). [2002]
- Additional Breeding and Husbandry Support
Mating System
- Homozygote x Homozygote
Citation
When using the Smo^c mouse strain in a publication, please cite the originating article(s) and include JAX stock #004526 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

AX11 (Maximum)

Pricing & Availability

Available

Domestic
International

Live Mouse

Age

Genotype

Price

weeks

Cryorecovery - Pricing

Service/Product	Description	Price
> >	Homozygous for Smo<tm2Amc>, 1 pair minimum

Payment Terms and Conditions

Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.

The Jackson Laboratory's Genotype Promise

The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.

Terms Of Use

General Terms and Conditions

Questions about Terms of Use

Licensing Information

Phone: 207-288-6470

Email: TechTran@jax.org

Also Known As:Smoc

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Expression Data

Control Suggestions

Additional Information

Selected References

Smotm2Amc

Allele Symbol: Smotm2Amc

Disease Terms

Research Areas By Phenotype

This mouse can be used to support research in many areas including:

Genotype: Smotm2Amc related

Mammalian Phenotype Terms by Genotype

Genotype: Smotm2Amc/Smotm2Amc Tg(Gfap-cre)73.12Mvs/0involves: 129X1/SvJ * BALB/c * C57BL/6NHsd

mammalian phenotype

nervous system phenotype

Genotype: Smotm1Amc/Smotm2Amc H2az2Tg(Wnt1-cre)11Rth/?involves: C57BL/6J * CBA/J

craniofacial phenotype

digestive/alimentary phenotype

growth/size/body region phenotype

hearing/vestibular/ear phenotype

respiratory system phenotype

skeleton phenotype

vision/eye phenotype

Genotype: Smotm1Amc/Smotm2Amc Tg(KRT14-cre)1Amc/0involves: 129X1/SvJ * C57BL/6 * CBA

growth/size/body region phenotype

mortality/aging

craniofacial phenotype

skeleton phenotype

Genotype: Smotm1Amc/Smotm2Amc Tg(Nes-cre)1Kln/0involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL * Swiss Webster

mortality/aging

nervous system phenotype

Genotype: Smotm2Amc/Smotm2Amc Tg(Nes-cre)1Kln/0involves: 129X1/SvJ * C57BL/6 * SJL

nervous system phenotype

Genotype: Smotm2Amc/Smotm2.1Amc H2az2Tg(Wnt1-cre)11Rth/0 Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sor+involves: 129S4/SvJaeSor * 129X1/SvJ * C57BL/6J * CBA/J

cardiovascular system phenotype

cellular phenotype

embryo phenotype

nervous system phenotype

Genotype: Smotm2Amc/Smotm2Amc Slc6a3tm1(cre)Xz/Slc6a3+involves: 129S1/Sv * 129X1/SvJ

mammalian phenotype

Genotype: Smotm2Amc/Smotm2.1Amc H2az2Tg(Wnt1-cre)11Rth/0involves: 129X1/SvJ * C57BL/6J * CBA/J

cardiovascular system phenotype

cellular phenotype

embryo phenotype

Genotype: Smotm2Amc/Smotm2Amc Tg(Tek-cre)12Flv/0involves: 129X1/SvJ * C3H * C57BL/6

mammalian phenotype

Genotype: Smotm2Amc/Smotm2.1Amc Tg(Tek-cre)12Flv/0involves: 129X1/SvJ * C57BL/6

mammalian phenotype

References

Additional - Smotm2Amc related

Genotyping Protocols

Dietary Information

Breeding Considerations

Mating System

Citation

Animal Health Reports

Live Mouse

Cryorecovery - Pricing

Payment Terms and Conditions

The Jackson Laboratory's Genotype Promise

Terms Of Use

Licensing Information

Also Known As:Smo^c

Smo^tm2Amc

Allele Symbol: Smo^tm2Amc

Genotype: Smo^tm2Amc related

Genotype: Smo^tm2Amc/Smo^tm2Amc Tg(Gfap-cre)73.12Mvs/0
involves: 129X1/SvJ * BALB/c * C57BL/6NHsd

Genotype: Smo^tm1Amc/Smo^tm2Amc H2az2^{Tg(Wnt1-cre)11Rth}/?
involves: C57BL/6J * CBA/J

Genotype: Smo^tm1Amc/Smo^tm2Amc Tg(KRT14-cre)1Amc/0
involves: 129X1/SvJ * C57BL/6 * CBA

Genotype: Smo^tm1Amc/Smo^tm2Amc Tg(Nes-cre)1Kln/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL * Swiss Webster

Genotype: Smo^tm2Amc/Smo^tm2Amc Tg(Nes-cre)1Kln/0
involves: 129X1/SvJ * C57BL/6 * SJL

Genotype: Smo^tm2Amc/Smo^tm2.1Amc H2az2^{Tg(Wnt1-cre)11Rth}/0 Gt(ROSA)26Sor^tm1Sor/Gt(ROSA)26Sor⁺
involves: 129S4/SvJaeSor * 129X1/SvJ * C57BL/6J * CBA/J

Genotype: Smo^tm2Amc/Smo^tm2Amc Slc6a3^tm1(cre)Xz/Slc6a3⁺
involves: 129S1/Sv * 129X1/SvJ

Genotype: Smo^tm2Amc/Smo^tm2.1Amc H2az2^{Tg(Wnt1-cre)11Rth}/0
involves: 129X1/SvJ * C57BL/6J * CBA/J

Genotype: Smo^tm2Amc/Smo^tm2Amc Tg(Tek-cre)12Flv/0
involves: 129X1/SvJ * C3H * C57BL/6

Genotype: Smo^tm2Amc/Smo^tm2.1Amc Tg(Tek-cre)12Flv/0
involves: 129X1/SvJ * C57BL/6

Additional - Smo^tm2Amc related