Overview

Also Known As: ages with stiffened joints

This spontaneous mutation, which causes diminished inorganic pyrophosphate in the plasma and consequently extensive ectopic mineralization of the joints, arterial vasculature, the dermal sheath of vibrissae, and multiple internal organs, provides a model for generalized arterial calcification of infancy, otitis media with effusion, and tympanosclerotic otitis.

Genetic overview

Genetic Background	Generation

Enpp1^asj

Allele Type	Gene Symbol	Gene Name
Chemically induced (ENU)	Enpp1	ectonucleotide pyrophosphatase/phosphodiesterase 1

View Genetics

Research Applications

Internal/Organ Research
Endocrine Deficiency Research
Developmental Biology Research

View All Research Applications

Base Price

Starting at:

$2,854.50 Domestic price Cryo Recovery

View Price List

Details

Detailed Description

Homozygotes have a diminished ability to hydrolyze ATP into AMP and inorganic phosphate, resulting in diminished inorganic pyrophosphate in the plasma and consequently extensive ectopic mineralization, particularly in the arterial blood vessels and heart, joints, kidneys, dermal sheath of vibrissae, the blood vessels but not parenchyma of the liver, as well as in the retina. Homozygotes initially appear normal but by 2 months of age they hold their forepaws closer to the body and develop a slow hobbling gait due to joint calcification. Kingman et al. (2017) found that on a diet rich in phosphorus and low in magnesium these homozygotes show accelerated stiffening of the joints and hobbling gait, but to a lesser degree than do mice homozygous for the allelic mutation ages with stiffened joints 2 Jackson (see stock 019107). Li et al (2013) showed that the lifespan of homozygotes on this high phosphorous/low magnesium diet is significantly reduced to an average of 6.4 weeks, but with no increase in embryonic lethality when pregnant dams are fed this diet. Although initially defined as a recessive allele, heterozygotes have approximately half the normal level of ENPP1 enzymatic activity in liver, lower than normal plasma PP_i, and when fed the diet rich in phosphorus/low in magnesium there is significant mineralization of the kidney medullary tubules and arcuate and renal arteries. Homozygotes also develop a distinct pathology in the middle ears that includes a thickened stapedial artery wall, fusion of the malleus and incus, and white patch on the tympanic membrane that may be calcification and are all typical symptoms of typanosclerosis. They also have a thickened round window membrane, a significant increase in mucin-secreting goblet cells, and severe otitis media resulting in moderate to severe conductive hearing loss by 3 months, which advances with age. Homozygotes may breed, but the ability to breed and maintain a litter is curtailed by progressive physical disability. Elevated dietary magnesium is one of several treatments shown to ameliorate the phenotype (Kingman et al., 2017; Li et al, 2015; Albright et al., 2015).

Development

The ages with stiffened joints mutation was discovered in the progeny of an ENU mutagenized C57BL/6J male that had been bred with a C57BL/6J female. This mutation has been maintained on the pure C57BL/6J background by backcross-intercross using either female or male homozygotes in the backcrosses to C57BL/6J. In 2011 this strain reached generation N11.

Control Suggestions

000664 C57BL/6J

Additional Information

Considerations for Choosing Controls

Selected References

Harris BS; Ward-Bailey PF; Yu H; Bergstrom DE; Bronson RT; Donahue LR. 2011. Ages with stiffened joints, A new mutation in Enpp1 MGI Direct Data SubmissionMGI: J:174912
Li Q; Guo H; Chou DW; Berndt A; Sundberg JP; Uitto J. 2013. Mutant Enpp1asj mice as a model for generalized arterial calcification of infancy. Dis Model Mech 6(5):1227-35PubMed: 23798568 MGI: J:201689
Tian C; Harris BS; Johnson KR. 2016. Ectopic Mineralization and Conductive Hearing Loss in Enpp1asj Mutant Mice, a New Model for Otitis Media and Tympanosclerosis. PLoS One 11(12):e0168159PubMed: 27959908 MGI: J:251638

View All References

Genetics

Enpp1^asj

Allele Symbol: Enpp1^asj

Allele Name	ages with stiffened joints
Allele Type	Chemically induced (ENU)
Allele Synonym(s)	ages with stiffened joints; Enpp1^asj
Gene Symbol and Name	Enpp1, ectonucleotide pyrophosphatase/phosphodiesterase 1
Gene Synonym(s)	ARHR2; Pca-1; Pdnp1; COLED; NPPS; phosphodiesterase I/nucleotide pyrophosphatase 1; tiptoe walking; Pca-1; expressed sequence C76301; RIKEN cDNA 4833416E15 gene; twy; 4833416E15Rik; Npps; PDNP1; E-NPP1; PC-1; Pca; PCA1; lymphocyte antigen 41; CD203c; ttw; twy; Pca; AI428932; expressed sequence AI428932; Ly-41; tiptoe walking-Yoshimura; NPP1; Ly-41; M6S1; C76301; nucleotide pyrophosphatase; 4833416E15Rik; plasma cell alloantigen; plasma cell alloantigen 1; Pc1; Npps; Pdnp1
Strain of Origin	C57BL/6J
Chromosome	10
Molecular Note	This ENU induced mutation was found to be an exon 7 T to A point mutation at position 737, predicted to change a valine to an aspartic acid.

Disease/Phenotype

Disease Terms

Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).

arterial calcification of infancy

Model with phenotypic similarity to human disease where etiologies are distinct. Human genes are associated with this disease. Orthologs of these genes do not appear in the mouse genotype(s).

otitis media

Models with phenotypic similarity to human diseases where etiology is unknown or involving genes where ortholog is unknown.

tympanosclerosis

Research Areas By Genotype

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

Genotype: Enpp1^asj related

Internal/Organ Research
- Skeleton
Endocrine Deficiency Research
- Bone/Bone Marrow Defects
Developmental Biology Research
- Skeletal Defects

Mammalian Phenotype Terms by Genotype

The following phenotype relates to a compound genotype created using this strain

Genotype: Enpp1^asj/Enpp1^asj
C57BL/6J-Enpp1/GrsrJ

behavior/neurological phenotype

abnormal gait
- on an 'acceleration diet'rich in phosphorus and low in magnesium, mutants show accelerated stiffening of the joints and hobbling gait
- slow, hobbling gait beginning at around 2 months of age due to joint disease

abnormal resting posture
- by 2 months of age homozygotes have a stiff posture with the front legs held in toward the body

cellular phenotype

increased middle ear goblet cell number
- by 2 weeks of age homozygotes have an excess of goblet cells around the opening of the Eustachian tubes and in the Eustachian tube ducts, this is still seen at 2 months of age, and excessive mucin secretion interferes with ciliary function

craniofacial phenotype

abnormal malleus morphology

abnormal round window morphology
- the round window membrane is thicker than normal and there is overossification of the reound window ridge

abnormal snout skin morphology

abnormal stapedial artery morphology
- the wall of the stapedial artery is thicker than normal with excessive calcium deposition

incudomalleolar fusion
- fusion of the malleus and incus

growth/size/body region phenotype

abnormal snout skin morphology

hearing/vestibular/ear phenotype

abnormal auditory tube morphology
- amorphous tissue is found in the Eustachian tubes

abnormal malleus morphology

abnormal middle ear morphology
- although abnormalities are not found in the inner ear, all ears with elevated ABR thresholds have middle ear defects such as retracted tympanic membrane, effusion in the middle ear, thickened epithelium with fibrous polyps, and in older mice the excessive accumulation of discharge in the external ear canal

abnormal round window morphology
- the round window membrane is thicker than normal and there is overossification of the reound window ridge

abnormal stapedial artery morphology
- the wall of the stapedial artery is thicker than normal with excessive calcium deposition

abnormal tympanic membrane morphology
- white patch at pars tensa and retracted tempanic membrane by 6 months of age

conductive hearing loss

impaired hearing
- auditory brainstem response shows moderate to severe hearing loss by 3 months of age

increased middle ear goblet cell number
- by 2 weeks of age homozygotes have an excess of goblet cells around the opening of the Eustachian tubes and in the Eustachian tube ducts, this is still seen at 2 months of age, and excessive mucin secretion interferes with ciliary function

increased or absent threshold for auditory brainstem response
- although no indication of vestibular impairment is found, hearing is impaired with normal hearing at 3 weeks of age, 20-25 db elevations in thresholds occurs by 6 weeks of age, a stable period of little increase in thresholds between 6 and 12 weeks, then a loss of 20-15 db between 12 and 18 weeks of age
- only one of eleven homozygotes have normal ABR thresholds in both ears at 12 weeks of age

increased susceptibility to otitis media

incudomalleolar fusion
- fusion of the malleus and incus

middle ear effusion
- at 8 weeks the middle ear cavity is filled with an aqueous effusion containing amorphous tissue masses, and at 12 weeks it is filled with pus-like secretions and an amorphous tissue mass

middle ear polyps

tympanic membrane retraction

homeostasis/metabolism phenotype

abnormal mineral level
- at 7 weeks of age, mice on the acceleration diet show severe mineralization in the muzzle area, showing calcium and phosphorus in a 2:1 ratio, similar to that in endochondral bone and the presence of hydroxyapatite
- g vibrissae
- mice from mothers on the acceleration diet during pregnancy exhibit extensive mineralization in the aorta, the coronary and carotid arteries, the retina, the blood vessels of the liver, and in the kidneys
- mice from mothers on the acceleration diet during pregnancy exhibit extensive mineralization in the dermal sheath of vibrissae as early as 4 weeks of age and progresses with age, showing a 17.7-fold increase in mineral content of the muzzle skin containing vibrissae
- on a normal diet, mutants exhibit less mineralization in the dermal sheath of vibrissae
- on a normal diet, vascular mineralization is not seen until around 5 months of age compared to 4 weeks of age on the acceleration diet

calcinosis
- treatment in mice homozygous for the ages with stiffened joints 2 Jackson allele, which was assessed on the BALB/cJ backgroud
- feeding a high phosphorous/low magnesium diet from 4 weeks of age until assessment at 12 weeks of age increases the calcium deposits throughout all of the affected tissues and additionally in the liver but this is less severe than the response to the same treatment in mice homozygous for the ages with stiffened joints 2 Jackson allele, which was assessed on the BALB/cJ backgroud

decreased circulating phosphate level
- homozygotes have approximately 20% of normal plasma concentrations of PPi, with concomitant PPi:Pi ratio reduction

middle ear effusion
- at 8 weeks the middle ear cavity is filled with an aqueous effusion containing amorphous tissue masses, and at 12 weeks it is filled with pus-like secretions and an amorphous tissue mass

cardiovascular system phenotype

abnormal aorta morphology
- mice from mothers on the acceleration diet during pregnancy and also fed this diet exhibit extensive mineralization in the aorta

abnormal carotid artery morphology
- mice from mothers on the acceleration diet during pregnancy and also fed this diet exhibit extensive mineralization in the carotid arteries

abnormal coronary artery morphology
- mice from mothers on the acceleration diet during pregnancy and also fed this diet exhibit extensive mineralization in the coronary arteries

abnormal kidney arcuate artery morphology

abnormal liver vasculature morphology
- mice from mothers on the acceleration diet during pregnancy and also fed this diet exhibit mineralized blood vessels in the liver, but no mineralization in the liver parenchyma

abnormal stapedial artery morphology
- the wall of the stapedial artery is thicker than normal with excessive calcium deposition

calcified aorta
- seen in mice from mothers on the acceleration diet during pregnancy and also fed this diet

calcified artery
- mice from mothers on the acceleration diet during pregnancy and also fed this diet show calcification of the carotid and coronary arteries

immune system phenotype

increased susceptibility to otitis media

joint inflammation

osteoarthritis
- arthritis found in the spine at 12 weeks of age
- osteoarthritis found in many joints and joints are very stiff and unbendable at 7 months of age

osteomyelitis
- severe osteomyelitis of the joints and unusual synovial cysts found at 13 weeks of age

integument phenotype

abnormal skin adnexa morphology
- mice from mothers on the acceleration diet during pregnancy exhibit extensive mineralization in the dermal sheath of vibrissae as early as 4 weeks of age and shows progression with age, showing a 17.7-fold increase in mineral content of the muzzle skin containing vibrissae
- ntaining vibrissae
- on a normal diet, mutants exhibit less mineralization in the dermal sheath of vibrissae

abnormal snout skin morphology

abnormal vibrissa follicle morphology
- mineralization of the capsule of the follicles of the vibrissae is found at 7 months of age

calcified skin
- mice from mothers on the acceleration diet during pregnancy and fed the same diet exhibit extensive mineralization in the dermal sheath of vibrissae as early as 4 weeks of age which progresses with age
- severe calcification of the fibrous capsule surrounding the muzzle vibrissae by 15 weeks of age

limbs/digits/tail phenotype

abnormal elbow joint morphology
- dilated joint spaces and hyperplastic synovium in the elbows found at 11 weeks of age

abnormal knee joint morphology
- dilated joint spaces and hyperplastic synovium in the knees found at 11 weeks of age

liver/biliary system phenotype

abnormal liver vasculature morphology
- mice from mothers on the acceleration diet during pregnancy and also fed this diet exhibit mineralized blood vessels in the liver, but no mineralization in the liver parenchyma

mortality/aging

increased sensitivity to induced morbidity/mortality
- Normal - however, mice show normal lifespan on a normal diet
- pups from mothers on the acceleration diet during pregnancy and the placed on the same diet at weaning exhibit reduced lifespan, with more than 50% of mice dying spontaneously before the age of 6 weeks and only 4 of 28 mice surviving to 12 weeks of age

renal/urinary system phenotype

abnormal kidney arcuate artery morphology

abnormal kidney morphology
- mice from mothers on the acceleration diet during pregnancy and also fed this diet exhibit extensive mineralization in the kidneys, affecting primarily the medullary tubules and arcuate and renal arteries

skeleton phenotype

abnormal elbow joint morphology
- dilated joint spaces and hyperplastic synovium in the elbows found at 11 weeks of age

abnormal knee joint morphology
- dilated joint spaces and hyperplastic synovium in the knees found at 11 weeks of age

abnormal malleus morphology

abnormal round window morphology
- the round window membrane is thicker than normal and there is overossification of the reound window ridge

abnormal stapedial artery morphology
- the wall of the stapedial artery is thicker than normal with excessive calcium deposition

decreased joint mobility
- on an 'acceleration diet' rich in phosphorus and low in magnesium, mutants show accelerated stiffening of the joints and hobbling gait
- stiffening of the joints is seen by around 2 months of age, particularly the forepaws

incudomalleolar fusion
- fusion of the malleus and incus

joint inflammation

osteoarthritis
- arthritis found in the spine at 12 weeks of age
- osteoarthritis found in many joints and joints are very stiff and unbendable at 7 months of age

osteomyelitis
- severe osteomyelitis of the joints and unusual synovial cysts found at 13 weeks of age

vision/eye phenotype

abnormal retina morphology
- mice from mothers on the acceleration diet during pregnancy and also fed this diet exhibit extensive mineralization in the retina

calcified retina
- seen in mice from mothers on the acceleration diet during pregnancy and also fed this diet

Genotype: Enpp1^asj/Enpp1⁺
C57BL/6J-Enpp1/GrsrJ

cardiovascular system phenotype

abnormal renal artery morphology
- mineralization of the medulary tubules and arcuate and renal arteries is found in heterozygotes, not just homozygotes, when fed a diet rich in phosphorus and low in magnesium

homeostasis/metabolism phenotype

decreased circulating phosphate level
- heterozygotes have reduced levels of plasma PPi, approximately 60% of normal levels

renal/urinary system phenotype

abnormal renal artery morphology
- mineralization of the medulary tubules and arcuate and renal arteries is found in heterozygotes, not just homozygotes, when fed a diet rich in phosphorus and low in magnesium

References

Harris BS; Ward-Bailey PF; Yu H; Bergstrom DE; Bronson RT; Donahue LR. 2011. Ages with stiffened joints, A new mutation in Enpp1 MGI Direct Data SubmissionMGI: J:174912
Li Q; Guo H; Chou DW; Berndt A; Sundberg JP; Uitto J. 2013. Mutant Enpp1asj mice as a model for generalized arterial calcification of infancy. Dis Model Mech 6(5):1227-35PubMed: 23798568 MGI: J:201689
Tian C; Harris BS; Johnson KR. 2016. Ectopic Mineralization and Conductive Hearing Loss in Enpp1asj Mutant Mice, a New Model for Otitis Media and Tympanosclerosis. PLoS One 11(12):e0168159PubMed: 27959908 MGI: J:251638

Additional - Enpp1^asj related

Technical Support

Contact Technical Support

Genotyping Protocols
- Restriction Enzyme Digest:Enpp1^asj
- Pyrosequencing:Enpp1^asj
- End Point Analysis:Enpp1^asj-EP
- Sanger sequencing:Enpp1^asj
- Genotyping resources and troubleshooting
Citation
When using the ages with stiffened joints mouse strain in a publication, please cite the originating article(s) and include JAX stock #012810 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200

Pricing & Availability

Cryo Recovery

Domestic
International

Live Mouse

Age

Genotype

Price

weeks

Cryorecovery - Pricing

Service	Genotype	Price
	Heterozygous for Enpp1<asj>

We will fulfill your order by providing at least two carriers for each strain ordered. The total number, sex, and genotypes provided will vary, although typically 8 or more animals are provided. Please check genotypes which will be recovered. While the genotypes of all animals produced will be communicated to you prior to scheduling shipment, the genotypes of animals provided may not reflect the mating scheme and genotypes described in the strain description. Animals are typically ready to ship in 11-14 weeks. If a second recovery is required to produce the minimum number of animals, then delivery time would increase to approximately 25 weeks. If we fail to produce animals of the correct genotype, you will not be charged. We cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation.

Related Products and Services

Frozen Mouse Embryo	C57BL/6J-Enpp1<asj>/GrsrJ Frozen Embryos	$2595.00
Frozen Mouse Embryo	C57BL/6J-Enpp1<asj>/GrsrJ Frozen Embryos	$2595.00
Frozen Mouse Embryo	C57BL/6J-Enpp1<asj>/GrsrJ Frozen Embryos	$3373.50
Frozen Mouse Embryo	C57BL/6J-Enpp1<asj>/GrsrJ Frozen Embryos	$3373.50

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.

Terms Of Use

Terms of Use

General Terms and Conditions

Questions about Terms of Use

Licensing Information

Phone: 207-288-6470

Email: TechTran@jax.org

JAX® Mice, Products & Services Conditions of Use

"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCT(S)" means biological materials supplied by JACKSON, and their derivatives. "SERVICES" means projects conducted by JACKSON for other parties that may include but are not limited to the use of MICE or PRODUCTS. "RECIPIENT" means each recipient of MICE, PRODUCTS, or SERVICES provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE, PRODUCTS or SERVICES from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON’s prior written authorization.

No Warranty

MICE, PRODUCTS AND SERVICES ARE PROVIDED "AS IS". JACKSON EXTENDS NO WARRANTIES OF ANY KIND, EITHER EXPRESS, IMPLIED, OR STATUTORY, WITH RESPECT TO MICE, PRODUCTS OR SERVICES, INCLUDING ANY IMPLIED WARRANTY OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE, OR ANY WARRANTY OF NON-INFRINGEMENT OF ANY PATENT, TRADEMARK, OR OTHER INTELLECTUAL PROPERTY RIGHTS.

Credit for PRODUCTS or SERVICES

In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of, PRODUCTS or SERVICES, JACKSON will, at its option, provide credit or replacement for the PRODUCT received or the SERVICES provided; JACKSON makes no other representations and this shall be the exclusive remedy of the purchaser. Please note specific policy for live mice.

Animal Care and Use for SERVICES

Consistent with the requirement for a written understanding regarding animal care and use, the JACKSON Animal Care and Use Committee will review the animal care and use protocol(s) associated with any SERVICES to be performed at JACKSON, and JACKSON shall have ultimate responsibility and authority for the care of animals while on site or in JACKSON custody.

No Liability

In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS, or SERVICES, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. Unless prohibited by law, in purchasing or receiving MICE, PRODUCTS, or SERVICES from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.

MICE, PRODUCTS or SERVICES are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.

The foregoing represents the General Terms and Conditions applicable to JACKSON’s MICE, PRODUCTS or SERVICES. In addition, special terms and conditions of sale of certain MICE, PRODUCTS, or SERVICES may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and SERVICES by JACKSON, and by its licensees and distributors.

Acceptance of delivery of MICE, PRODUCTS or SERVICES shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or SERVICES by JACKSON.

Also Known As: ages with stiffened joints

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Additional Information

Selected References

Enpp1asj

Allele Symbol: Enpp1asj

Disease Terms

Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).

Model with phenotypic similarity to human disease where etiologies are distinct. Human genes are associated with this disease. Orthologs of these genes do not appear in the mouse genotype(s).

Models with phenotypic similarity to human diseases where etiology is unknown or involving genes where ortholog is unknown.

Research Areas By Genotype

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

Genotype: Enpp1asj related

Mammalian Phenotype Terms by Genotype

Genotype: Enpp1asj/Enpp1asjC57BL/6J-Enpp1/GrsrJ

behavior/neurological phenotype

cellular phenotype

craniofacial phenotype

growth/size/body region phenotype

hearing/vestibular/ear phenotype

homeostasis/metabolism phenotype

cardiovascular system phenotype

immune system phenotype

integument phenotype

limbs/digits/tail phenotype

liver/biliary system phenotype

mortality/aging

renal/urinary system phenotype

skeleton phenotype

vision/eye phenotype

Genotype: Enpp1asj/Enpp1+C57BL/6J-Enpp1/GrsrJ

cardiovascular system phenotype

homeostasis/metabolism phenotype

renal/urinary system phenotype

References

Additional - Enpp1asj related

Genotyping Protocols

Citation

Animal Health Reports

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200

Live Mouse

Cryorecovery - Pricing

Related Products and Services

Payment Terms and Conditions

The Jackson Laboratory's Genotype Promise

Terms of Use

Licensing Information

JAX® Mice, Products & Services Conditions of Use

No Warranty

Credit for PRODUCTS or SERVICES

Animal Care and Use for SERVICES

No Liability

Enpp1^asj

Allele Symbol: Enpp1^asj

Genotype: Enpp1^asj related

Genotype: Enpp1^asj/Enpp1^asj
C57BL/6J-Enpp1/GrsrJ

Genotype: Enpp1^asj/Enpp1⁺
C57BL/6J-Enpp1/GrsrJ

Additional - Enpp1^asj related