Overview

Also Known As: progressive ankylosis

The progressive ankylosis allele (ank) is a spontaneous recessive mutation that causes a severe phenotype of joint calcification and degeneration. Few homozygotes survive beyond 5 months of age, although the adults can breed. Generally no more than 2 litters are produced by homozygotes of either sex. At 4 or 5 weeks of age, homozygotes can be identified by their inability to grasp a wire cage lid with their front paws when suspended above it. The joints swell with a milky fluid, and undergo a process proceeding through mononuclear inflammatory infiltration, hydroxyapatite deposition and increased calcification, hyperplasia, and fibrous and bony ankylosis. (for details see Mahowald et al., 1989; Hakim et al., 1984; Sweet and Green, 1981.) The front feet are affected before the hind feet and the phenotype is more severe in the most distal joints of the limbs. Hyperplasia and degeneration of the joint tissues, and ankylosis occur progressively, decreasing mobility and resulting i...

Genetic overview

Genetic Background	Generation

A^w-J

Allele Type	Gene Symbol	Gene Name
Spontaneous	a	nonagouti

A

Allele Type	Gene Symbol	Gene Name
Spontaneous	a	nonagouti

Ank^ank

Allele Type	Gene Symbol	Gene Name
Spontaneous	Ank	progressive ankylosis

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Research Applications

Dermatology Research
Developmental Biology Research
Immunology, Inflammation and Autoimmunity Research
Mouse/Human Gene Homologs

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Base Price

Starting at:

$2,854.50 Domestic price Cryo Recovery

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Details

Detailed Description

The progressive ankylosis allele (ank) is a spontaneous recessive mutation that causes a severe phenotype of joint calcification and degeneration. Few homozygotes survive beyond 5 months of age, although the adults can breed. Generally no more than 2 litters are produced by homozygotes of either sex. At 4 or 5 weeks of age, homozygotes can be identified by their inability to grasp a wire cage lid with their front paws when suspended above it. The joints swell with a milky fluid, and undergo a process proceeding through mononuclear inflammatory infiltration, hydroxyapatite deposition and increased calcification, hyperplasia, and fibrous and bony ankylosis. (for details see Mahowald et al., 1989; Hakim et al., 1984; Sweet and Green, 1981.) The front feet are affected before the hind feet and the phenotype is more severe in the most distal joints of the limbs. Hyperplasia and degeneration of the joint tissues, and ankylosis occur progressively, decreasing mobility and resulting in a rigid, crouched posture in the adult. Their gate becomes slow, halting, and flatfooted. The morphological changes underlying the stiffening of the vertebral column and resulting thoracic kyphosis are detailed by Sampson, 1988a and 1988b, and Sampson et al., 1991.

There is an immune cell involvement in the joints secondary to the central defect. Treatment of ank/ank mice with hydrocortisone beginning at 5 weeks of age resulted in reduced synovial and subsynovial hyperplasia, reduced growth of cartilaginous and bony bridges, and increased accumulation of intra-articular apatite possibly due to the reduction in macrophage activity (Hakim et al., 1986.). Reconstitution of wild type mice with bone marrow or spleen cells from ank/ank mice does not transfer disease and reconstitution of ank/ank mice with wild type bone marrow or spleen cells does not prevent disease (Krug et al., 1997). Additionally, there is an immune cell defect. There is a reduction in the response of spleen cells to phytohaemagglutinin or concanavalin A although the response to LPS appears normal. Spleen cells or macrophages from ank/ank mice do not suppress normal spleen cell responses to phytohaemagglutinin and wild type spleen cells or macrophages do not restore phytohaemagglutinin responsiveness to spleen cells from ank/ank mice (Krug et al., 1989). Fibroblasts from ank/ank mice are Hyperproliferative in response to transforming growth factor beta 1 (Krug, 1998). No impact was found on the phenotype of ank/+ or ank/ank mice when transgenic HLA-B27 was co-expressed (Krug and Taurog, 2000).

In addition to progressive ankylosis and calcification of the peripheral joints and axial skeleton, homozygotes have a smaller overall body size, and some develop balanitis, priapism, and scaling skin lesions on the plantar surface of the paws. The hypermineralization phenotype is associated with abnormal inorganic pyrophophate levels and the downregulation of osteopontin (Harmey et al., 2004).

Development

The progressive ankylosis mutation arose spontaneously in the strain JGBF/Le (Stock No. 000260), a balanced stock for jagged tail (jg) and buff (bf). An affected female displaying a flat-footed gait with rigid toes was the founder for the ank strain. This female's progeny were bred onto a C3FeB6 background via an outcross-intercross breeding scheme. Thus homozygotes were bred to C3FeB6F1 then their obligate heterozygous offspring were sibling mated to produce homozygous breeders for the next generation. The initial characterization was done on N5F1 mice. In June 1976 this strain was at N6, in early 1979 it was at N11, and in November 1983 it reached N24. Neither jg nor bf have been found in this strain since N2. C3FeB6-A/A^w-J-ank was frozen in 1987 by breeding N32 homozygotes to C3FeB6-A/A^w-J to get heterozygous N33 embryos.

Control Suggestions

+/? sibling
001203 C3FeB6F1/J A/A^w-J

Additional Information

Considerations for Choosing Controls

Selected References

Reichenberger E; Tiziani V; Watanabe S; Park L; Ueki Y; Santanna C; Baur ST; Shiang R; Grange DK; Beighton P; Gardner J; Hamersma H; Sellars S; Ramesar R; Lidral AC; Sommer A; Raposo do Amaral CM; Gorlin RJ; Mulliken JB; Olsen BR. 2001. Autosomal dominant craniometaphyseal dysplasia is caused by mutations in the transmembrane protein ANK. Am J Hum Genet 68(6):1321-6PubMed: 11326338 MGI: J:109879
Krug HE. 1998. Fibroblasts from mice with progessive ankylosis proliferate excessively in response to transforming growth factor-beta 1. J Investig Med 46(4):134-9PubMed: 9635372 MGI: J:109902
Krug HE; Wietgrefe MM; Ytterberg SR; Taurog JD; Mahowald ML. 1997. Murine progressive ankylosis is not immunologically mediated. J Rheumatol 24(1):115-22PubMed: 9002021 MGI: J:109905
Krug HE; Mahowald ML; Clark C. 1989. Progressive ankylosis (ank/ank) in mice: an animal model of spondyloarthropathy. III. Proliferative spleen cell response to T cell mitogens. Clin Exp Immunol 78(1):97-101PubMed: 2805429 MGI: J:109935
Sampson HW. 1988. Ultrastructure of the mineralizing metacarpophalangeal joint of progressive ankylosis (ank/ank) mice. Am J Anat 182(3):257-69PubMed: 3213824 MGI: J:109941
Sampson HW. 1988. Spondyloarthropathy in progressive ankylosis (ank/ank) mice: morphological features. Spine 13(6):645-9PubMed: 3175755 MGI: J:109942
Hakim FT; Brown KS; Oppenheim JJ. 1986. Hereditary joint disorder in progressive ankylosis (ank/ank) mice. II. Effect of high-dose hydrocortisone treatment on inflammation and intraarticular calcium hydroxyapatite deposits. Arthritis Rheum 29(1):114-23PubMed: 3004514 MGI: J:109949
Mahowald ML; Krug H; Halverson P. 1989. Progressive ankylosis (ank/ank) in mice: an animal model of spondyloarthropathy. II. Light and electron microscopic findings. J Rheumatol 16(1):60-6PubMed: 2541245 MGI: J:23576
Krug HE; Taurog JD. 2000. HLA-B27 has no effect on the phenotypic expression of progressive ankylosis in ank/ank mice J Rheumatol 27(5):1257-9PubMed: 10813297 MGI: J:62431
Ho AM; Johnson MD; Kingsley DM. 2000. Role of the mouse ank gene in control of tissue calcification and arthritis [see comments] Science 289(5477):265-70PubMed: 10894769 MGI: J:63420
Sweet HO; Green MC. 1981. Progressive ankylosis, a new skeletal mutation in the mouse. J Hered 72(2):87-93PubMed: 7276519 MGI: J:6580
Nurnberg P; Thiele H; Chandler D; Hohne W; Cunningham ML; Ritter H; Leschik G; Uhlmann K; Mischung C; Harrop K; Goldblatt J; Borochowitz ZU; Kotzot D; Westermann F; Mundlos S; Braun HS; Laing N; Tinschert S. 2001. Heterozygous mutations in ANKH, the human ortholog of the mouse progressive ankylosis gene, result in craniometaphyseal dysplasia. Nat Genet 28(1):37-41PubMed: 11326272 MGI: J:69128
Sampson HW; Davis RW; Dufner DC. 1991. Spondyloarthropathy in progressive ankylosis mice: ultrastructural features of the intervertebral disk. Acta Anat (Basel) 141(1):36-41PubMed: 1659102 MGI: J:751
Hakim FT; Cranley R; Brown KS; Eanes ED; Harne L; Oppenheim JJ. 1984. Hereditary joint disorder in progressive ankylosis (ank/ank) mice. I. Association of calcium hydroxyapatite deposition with inflammatory arthropathy. Arthritis Rheum 27(12):1411-20PubMed: 6095872 MGI: J:7672

View All References

Genetics

A^w-J

Allele Symbol: A^w-J

Allele Name	white bellied agouti Jackson
Allele Type	Spontaneous
Allele Synonym(s)	white bellied agouti Jackson; A^w-J
Gene Symbol and Name	a, nonagouti
Gene Synonym(s)	agouti signal protein; As; ASP; As; agouti; agouti suppressor; AGTI; SHEP9; AGSW; AGTIL
Strain of Origin	C57BL/6J
Chromosome	2

A

Allele Symbol: A

Allele Name	wild-type agouti
Allele Type	Spontaneous
Allele Synonym(s)	A; wild-type agouti
Gene Symbol and Name	a, nonagouti
Gene Synonym(s)	agouti signal protein; As; ASP; As; agouti; agouti suppressor; AGTI; SHEP9; AGSW; AGTIL
Strain of Origin	various
Chromosome	2
General Note	The A allele is usually regarded as a wild-type allele. For example,the C3H and CBA mouse sublines are homozygous for agouti. Hairs are black with a subapical yellow band. This black-yellow-black pattern is referred to as agouti. The general appearance is yellowish brown, slightly lighter on the belly than on the back.
Molecular Note	This allele, often referred to as wild-type, comprises a novel 131 amino acid protein encoded in a gene comprising four exons, three coding, spanning 18kb. Unique changes in this gene account for all other alleles that have been molecularly characterized. The expression of this allele is almost always dominant to other alleles of this gene.

Ank^ank

Allele Symbol: Ank^ank

Allele Name	progressive ankylosis
Allele Type	Spontaneous
Allele Synonym(s)	progressive ankylosis; Ank^ank
Gene Symbol and Name	Ank, progressive ankylosis
Gene Synonym(s)	D15Ertd221e; CMDJ; DNA segment, Chr 15, ERATO Doi 221, expressed; D15Ertd221e; mKIAA1581; CPPDD; HANK; MANK; CCAL2; ank; ANK; SLC61A1; SLC62A1
Strain of Origin	JGBF/LeJ
Chromosome	15
Molecular Note	A single nucleotide G to T substitution is predicted to result in a substitution at codon 440 from Glu to a stop codon in the encoded protein.

Disease/Phenotype

Disease Terms

Research Areas By Genotype

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

Genotype: Ank^ank related

Dermatology Research
- Skin and Hair Texture Defects
Developmental Biology Research
- Skeletal Defects
- Growth Defects
  - Growth Defects (homozygous)
Immunology, Inflammation and Autoimmunity Research
- Immunodeficiency Associated with Other Defects
- Inflammation
Mouse/Human Gene Homologs
- craniometaphyseal dysplasia, autosomal dominant

Mammalian Phenotype Terms by Genotype

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

Genotype: Ank^ank/Ank^ank
involves: C3HeB/FeJ * C57BL/6J * JGBF/LeJ

behavior/neurological phenotype

abnormal gait
- slow halting gait, with all feet flat against the surface

abnormal posture
- adults exhibit a rigid posture

decreased grip strength
- unable to grab cage bars at 4-5 weeks of age

homeostasis/metabolism phenotype

abnormal ion homeostasis
- primary skin fibroblast cultures show an increase in intracellular and a decrease in extracellular pyrophosphate indicative of defective phosphate homeostatis, and this defect is corrected by transfection with wildtype Ank

immune system phenotype

arthritis
- histology of the digit joints shows narrowing of the joint spaces, erosion of cartilage, accumulation of debris, and ectopic calcification

limbs/digits/tail phenotype

abnormal digit morphology
- toes of the forefeet are stiff and flattened at 33 and 35 days of age, while these abnormalities occur later in the hindfeet (11-17 weeks of age)

abnormal femur morphology
- metaphyseal trabeculae reduced in both thickness and number

abnormal limb morphology
- in the limbs, abnormalities are more severe in the distal than proximal joints and in the forelimbs than in the hindlimbs

abnormal sesamoid bone of gastrocnemius morphology
- some of the sesamoid bones are enlarged and appear to be fused with the nearest long bone

abnormal transverse acetabular ligament morphology
- calcification of the transverse acetabular ligament, which bridges the acetabular notch of the hip, is seen at 17 weeks of age

mortality/aging

premature death
- few mutants survive beyond 5 months of age

muscle phenotype

abnormal tendon morphology
- degeneration in many, although not all, tendons associated with affected joints

calcified tendon
- some calcification in the tendons around the shoulder joint at 11 weeks of age

reproductive system phenotype

reduced female fertility
- do not produce more than two litters

reduced male fertility
- do not produce more than two litters

skeleton phenotype

abnormal cartilage morphology
- cartilage erosion
- degeneration and increase in calcification in the cartilage

abnormal cementum morphology
- at 12 weeks, enlargement of the cementum

abnormal femur morphology
- metaphyseal trabeculae reduced in both thickness and number

abnormal joint morphology
- bone volume in joints is significantly increased and increases in severity with time
- joint space narrowing, accumulation of debris in the joint space, and ectopic calcification in and around the affected joints
- mutants develop a noninflammatory degenerative joint disease, with stiffness of joints starting in forefeet and toes, quickly spreading to other joints
- mutants show increased numbers of osteoblast-like cells in the synovial membrane of joints and excessive amount of fibrous tissue, cartilage, and bone in joints at later stages, with many areas of cystic necrosis
- necrosis in the fibrous tissue of the joints, including the ligaments and cartilage
- synovial lining in most places, except over articular cartilage or ligament, has a thickened surface layer

abnormal ligament morphology
- calcification of the transverse acetabular ligament, which bridges the acetabular notch of the hip, is seen at 17 weeks of age
- degeneration in many, although not all, ligaments associated with affected joints

abnormal sesamoid bone of gastrocnemius morphology
- some of the sesamoid bones are enlarged and appear to be fused with the nearest long bone

abnormal skeleton morphology
- progressive ankylosis

abnormal synovial joint cavity morphology
- reduction in the size of the joint cavities in the forefoot at 33 days of age, with excessive osteoblasts
- the joint cavity of the shoulder appears shrunken and opaque, with some calcification in the tendons around the joint at 11 weeks of age

abnormal tendon morphology
- degeneration in many, although not all, tendons associated with affected joints

abnormal tooth hard tissue morphology
- the calcified materials surrounding the neck and tooth of all 12 molars is increased
- the neck thickness relative to the enamel cap width is increased

abnormal transverse acetabular ligament morphology
- calcification of the transverse acetabular ligament, which bridges the acetabular notch of the hip, is seen at 17 weeks of age

arthritis
- histology of the digit joints shows narrowing of the joint spaces, erosion of cartilage, accumulation of debris, and ectopic calcification

calcified joint
- abnormal and increased calcification within some of the joints (knee, elbow, vertebral column) and joint cavities, resulting in calcified masses at various places near joints
- ectopic calcification in and around the affected joints
- excessive bony deposits in joints

calcified tendon
- some calcification in the tendons around the shoulder joint at 11 weeks of age

decreased joint mobility
- joint mobility is decreased at 6 weeks and is more severe at 12 weeks similar to in Ank^tm1.1Kng homozygotes
- progressive loss of mobility of the joints occurs with age; stiffening of the joints is first apparent at 4-5 weeks of age in the forefeet and eventually involves all the joints of the limbs and vertebral column
- reduction in joint mobility in the forelimb joints are more severe than in the hindlimbs and distal joint in the hindlimbs are more severely affected than proximal joints
- stiffness of joints observed at 4-5 weeks of age
- wean age homozygotes are unable to grasp a wire cage tope due to stiffness in the digits
- when lifted by the tail from a wire grid, 4.5-5 week old mutants are unable to cling to the grid as the toes are very rigid

fused joints
- fore and hind feet at 31 weeks of age have toe bones that show bony and cartilaginous fusions across the joints, usually including the sesamoid bones
- progressive akylosis, such that by 17 weeks of age, the joints of the foot, including the wrist, and of the ribs with adjacent sternebrae are completely ankylosed

kyphosis
- adults exhibit thoracic kyphosis and prominent haunches

craniofacial phenotype

abnormal cementum morphology
- at 12 weeks, enlargement of the cementum

abnormal tooth hard tissue morphology
- the calcified materials surrounding the neck and tooth of all 12 molars is increased
- the neck thickness relative to the enamel cap width is increased

growth/size/body region phenotype

abnormal cementum morphology
- at 12 weeks, enlargement of the cementum

abnormal tooth hard tissue morphology
- the calcified materials surrounding the neck and tooth of all 12 molars is increased
- the neck thickness relative to the enamel cap width is increased

decreased body weight
- lower body weight, first noticeable between 10 and 20 days of age

Genotype: Ank^ank/Ank^ank
involves: BALB/c * C3H * C57BL/6 * JGBF/Le

cardiovascular system phenotype

calcified aorta
- aortic media exhibit calcification and chondrogenic differentiation unlike wild-type aortas

cellular phenotype

abnormal osteoblast physiology
- Normal - however, hypercalcification in osteoblasts can be reversed by soluble Enpp1 and Spp1
- osteoblasts exhibit hypercalcification compared with wild-type cell

skeleton phenotype

abnormal osteoblast physiology
- Normal - however, hypercalcification in osteoblasts can be reversed by soluble Enpp1 and Spp1
- osteoblasts exhibit hypercalcification compared with wild-type cell

Genotype: Ank^ank/Ank^ank
Not Specified

skeleton phenotype

abnormal chondrocyte morphology
- 6-8 week old affected mice have chondrocytes with numerous large vacuoles and abnormal condensations of glycogen

abnormal intervertebral disk morphology
- EM analysis shows accumulation of electron-dense crystals aligned along collagen fibers; mitochondria of some cells have a high affinity for calcium phosphate crystals
- in some disk regions cartilage is so heavily mineralized that mineral deposists extend beyond the extracellular matrix over cell cytoplasm
- ossification of intervertebral disk space is common

calcified intervertebral disk
- crystals are in the form of calcium hydroxyapatite

References

Reichenberger E; Tiziani V; Watanabe S; Park L; Ueki Y; Santanna C; Baur ST; Shiang R; Grange DK; Beighton P; Gardner J; Hamersma H; Sellars S; Ramesar R; Lidral AC; Sommer A; Raposo do Amaral CM; Gorlin RJ; Mulliken JB; Olsen BR. 2001. Autosomal dominant craniometaphyseal dysplasia is caused by mutations in the transmembrane protein ANK. Am J Hum Genet 68(6):1321-6PubMed: 11326338 MGI: J:109879
Krug HE. 1998. Fibroblasts from mice with progessive ankylosis proliferate excessively in response to transforming growth factor-beta 1. J Investig Med 46(4):134-9PubMed: 9635372 MGI: J:109902
Krug HE; Wietgrefe MM; Ytterberg SR; Taurog JD; Mahowald ML. 1997. Murine progressive ankylosis is not immunologically mediated. J Rheumatol 24(1):115-22PubMed: 9002021 MGI: J:109905
Krug HE; Mahowald ML; Clark C. 1989. Progressive ankylosis (ank/ank) in mice: an animal model of spondyloarthropathy. III. Proliferative spleen cell response to T cell mitogens. Clin Exp Immunol 78(1):97-101PubMed: 2805429 MGI: J:109935
Sampson HW. 1988. Ultrastructure of the mineralizing metacarpophalangeal joint of progressive ankylosis (ank/ank) mice. Am J Anat 182(3):257-69PubMed: 3213824 MGI: J:109941
Sampson HW. 1988. Spondyloarthropathy in progressive ankylosis (ank/ank) mice: morphological features. Spine 13(6):645-9PubMed: 3175755 MGI: J:109942
Hakim FT; Brown KS; Oppenheim JJ. 1986. Hereditary joint disorder in progressive ankylosis (ank/ank) mice. II. Effect of high-dose hydrocortisone treatment on inflammation and intraarticular calcium hydroxyapatite deposits. Arthritis Rheum 29(1):114-23PubMed: 3004514 MGI: J:109949
Mahowald ML; Krug H; Halverson P. 1989. Progressive ankylosis (ank/ank) in mice: an animal model of spondyloarthropathy. II. Light and electron microscopic findings. J Rheumatol 16(1):60-6PubMed: 2541245 MGI: J:23576
Krug HE; Taurog JD. 2000. HLA-B27 has no effect on the phenotypic expression of progressive ankylosis in ank/ank mice J Rheumatol 27(5):1257-9PubMed: 10813297 MGI: J:62431
Ho AM; Johnson MD; Kingsley DM. 2000. Role of the mouse ank gene in control of tissue calcification and arthritis [see comments] Science 289(5477):265-70PubMed: 10894769 MGI: J:63420
Sweet HO; Green MC. 1981. Progressive ankylosis, a new skeletal mutation in the mouse. J Hered 72(2):87-93PubMed: 7276519 MGI: J:6580
Nurnberg P; Thiele H; Chandler D; Hohne W; Cunningham ML; Ritter H; Leschik G; Uhlmann K; Mischung C; Harrop K; Goldblatt J; Borochowitz ZU; Kotzot D; Westermann F; Mundlos S; Braun HS; Laing N; Tinschert S. 2001. Heterozygous mutations in ANKH, the human ortholog of the mouse progressive ankylosis gene, result in craniometaphyseal dysplasia. Nat Genet 28(1):37-41PubMed: 11326272 MGI: J:69128
Sampson HW; Davis RW; Dufner DC. 1991. Spondyloarthropathy in progressive ankylosis mice: ultrastructural features of the intervertebral disk. Acta Anat (Basel) 141(1):36-41PubMed: 1659102 MGI: J:751
Hakim FT; Cranley R; Brown KS; Eanes ED; Harne L; Oppenheim JJ. 1984. Hereditary joint disorder in progressive ankylosis (ank/ank) mice. I. Association of calcium hydroxyapatite deposition with inflammatory arthropathy. Arthritis Rheum 27(12):1411-20PubMed: 6095872 MGI: J:7672

Additional - A related

Additional - A^w-J related

Additional - Ank^ank related

Technical Support

Contact Technical Support

Genotyping Protocols
- Sanger sequencing:Ank^ank
- Separated PCR:A^w-J
- Genotyping resources and troubleshooting
Appearance
- agouti with stiff feet
  Related Genotype: A/A Ank^ank/Ank^ank
  
  white-bellied agouti with stiff feet
  Related Genotype: A/A^w-J Ank^ank/Ank^ank
  
  agouti, unaffected
  Related Genotype: A/A +/?
  
  white-bellied agouti, unaffected
  Related Genotype: A/A^w-J +/? or A^w-J/A^w-J +/?
Citation
When using the progressive ankylosis mouse strain in a publication, please cite the originating article(s) and include JAX stock #000200 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

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Live Mouse

Age

Genotype

Price

weeks

Cryorecovery - Pricing

Service	Genotype	Price
	ÊHeterozygous for ank, Compound Heterozygous for allele A and allele A<w-J> or Homozygous for A

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.

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Also Known As: progressive ankylosis

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Additional Information

Selected References

Aw-J

Allele Symbol: Aw-J

A

Allele Symbol: A

Ankank

Allele Symbol: Ankank

Disease Terms

Research Areas By Genotype

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

Genotype: Ankank related

Mammalian Phenotype Terms by Genotype

Genotype: Ankank/Ankankinvolves: C3HeB/FeJ * C57BL/6J * JGBF/LeJ

behavior/neurological phenotype

homeostasis/metabolism phenotype

immune system phenotype

limbs/digits/tail phenotype

mortality/aging

muscle phenotype

reproductive system phenotype

skeleton phenotype

craniofacial phenotype

growth/size/body region phenotype

Genotype: Ankank/Ankankinvolves: BALB/c * C3H * C57BL/6 * JGBF/Le

cardiovascular system phenotype

cellular phenotype

skeleton phenotype

Genotype: Ankank/AnkankNot Specified

skeleton phenotype

References

Additional - A related

Additional - Aw-J related

Additional - Ankank related

Genotyping Protocols

Appearance

Citation

Animal Health Reports

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

Live Mouse

Cryorecovery - Pricing

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

A^w-J

Allele Symbol: A^w-J

Ank^ank

Allele Symbol: Ank^ank

Genotype: Ank^ank related

Genotype: Ank^ank/Ank^ank
involves: C3HeB/FeJ * C57BL/6J * JGBF/LeJ

Genotype: Ank^ank/Ank^ank
involves: BALB/c * C3H * C57BL/6 * JGBF/Le

Genotype: Ank^ank/Ank^ank
Not Specified

Additional - A^w-J related

Additional - Ank^ank related