JAX
Mouse Strain Datasheet - 000200
C3FeB6 A/Aw-J-Ankank/J
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...
Read More +Genetic overview
| Genetic Background | Generation |
|---|---|
|
C3FeB6 |
|
A
| Allele Type | Gene Symbol | Gene Name |
|---|---|---|
| Spontaneous | a | nonagouti |
Aw-J
| Allele Type | Gene Symbol | Gene Name |
|---|---|---|
| Spontaneous | a | nonagouti |
Ankank
| Allele Type | Gene Symbol | Gene Name |
|---|---|---|
| Spontaneous | Ank | progressive ankylosis |
Research Applications
- Dermatology Research
- Developmental Biology Research
- Immunology, Inflammation and Autoimmunity Research
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/Aw-J-ank was frozen in 1987 by breeding N32 homozygotes to C3FeB6-A/Aw-J to get heterozygous N33 embryos.
Control Suggestions
Selected References
- 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.. In: . . MGI: J:109949
- 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.. In: . . MGI: J:7672
- Ho AM; Johnson MD; Kingsley DM. 2000. Role of the mouse ank gene in control of tissue calcification and arthritis [see comments]. In: . . MGI: J:63420
- Krug HE. 1998. Fibroblasts from mice with progessive ankylosis proliferate excessively in response to transforming growth factor-beta 1.. In: . . MGI: J:109902
- 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.. In: . . MGI: J:109935
- Krug HE; Taurog JD. 2000. HLA-B27 has no effect on the phenotypic expression of progressive ankylosis in ank/ank mice. In: . . MGI: J:62431
- Krug HE; Wietgrefe MM; Ytterberg SR; Taurog JD; Mahowald ML. 1997. Murine progressive ankylosis is not immunologically mediated.. In: . . MGI: J:109905
- Mahowald ML; Krug H; Halverson P. 1989. Progressive ankylosis (ank/ank) in mice: an animal model of spondyloarthropathy. II. Light and electron microscopic findings.. In: . . MGI: J:23576
- 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.. In: . . MGI: J:69128
- 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.. In: . . MGI: J:109879
- Sampson HW. 1988. Ultrastructure of the mineralizing metacarpophalangeal joint of progressive ankylosis (ank/ank) mice.. In: . . MGI: J:109941
- Sampson HW. 1988. Spondyloarthropathy in progressive ankylosis (ank/ank) mice: morphological features.. In: . . MGI: J:109942
- Sampson HW; Davis RW; Dufner DC. 1991. Spondyloarthropathy in progressive ankylosis mice: ultrastructural features of the intervertebral disk.. In: . . MGI: J:751
- Sweet HO; Green MC. 1981. Progressive ankylosis, a new skeletal mutation in the mouse.. In: . . MGI: J:6580
A
Allele Symbol: A
| Allele Name | wild-type agouti |
|---|---|
| Allele Type | Spontaneous |
| Allele Synonym(s) | dark-bellied agouti |
| Gene Symbol and Name | a, nonagouti |
| Gene Synonym(s) | AGSW; AGTI; AGTIL; ASP; As; As; SHEP9; agouti; agouti signal protein; agouti suppressor |
| 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. |
Ankank
Allele Symbol: Ankank
| Allele Name | progressive ankylosis |
|---|---|
| Allele Type | Spontaneous |
| Allele Synonym(s) | ank |
| Gene Symbol and Name | Ank, progressive ankylosis |
| Gene Synonym(s) | ANK; CCAL2; CMDJ; CPPDD; D15Ertd221e; D15Ertd221e; DNA segment, Chr 15, ERATO Doi 221, expressed; HANK; MANK; SLC61A1; ank; mKIAA1581 |
| 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 Terms
Research Areas By Genotype
This mouse can be used to support research in many areas including:
Genotype: Ankank related
- Dermatology Research
- Skin and Hair Texture Defects
- Developmental Biology Research
- Growth Defects
- Growth Defects (homozygous)
- Skeletal Defects
- Growth Defects
- Immunology, Inflammation and Autoimmunity Research
- Immunodeficiency Associated with Other Defects
- Inflammation
Mammalian Phenotype Terms by Genotype
The following phenotype information is associated with a similar, but not exact match to this JAX® Mice strain
Genotype: Ankank/Ankank
Not Specified
skeleton phenotype
- abnormal chondrocyte morphology
- 6-8 week old affected mice have chondrocytes with numerous large vacuoles and abnormal condensations of glycogen (MGI Ref ID J:751)
- 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 (MGI Ref ID J:751)
- in some disk regions cartilage is so heavily mineralized that mineral deposists extend beyond the extracellular matrix over cell cytoplasm (MGI Ref ID J:751)
- ossification of intervertebral disk space is common (MGI Ref ID J:751)
- calcified intervertebral disk
- crystals are in the form of calcium hydroxyapatite (MGI Ref ID J:751)
Genotype: Ankank/Ankank
involves: BALB/c * C3H * C57BL/6 * JGBF/Le
skeleton phenotype
- abnormal osteoblast physiology
cardiovascular system phenotype
- calcified aorta
- aortic media exhibit calcification and chondrogenic differentiation unlike wild-type aortas (MGI Ref ID J:110028)
Genotype: Ankank/Ankank
involves: C3HeB/FeJ * C57BL/6J * JGBF/LeJ
mortality/aging
- premature death
- few mutants survive beyond 5 months of age (MGI Ref ID J:6580)
immune system phenotype
- arthritis
- histology of the digit joints shows narrowing of the joint spaces, erosion of cartilage, accumulation of debris, and ectopic calcification (MGI Ref ID J:63420)
growth/size/body region phenotype
- abnormal cementum morphology
- at 12 weeks, enlargement of the cementum (MGI Ref ID J:122727)
- abnormal tooth hard tissue morphology
- decreased body weight
- lower body weight, first noticeable between 10 and 20 days of age (MGI Ref ID J:6580)
reproductive system phenotype
- reduced female fertility
- do not produce more than two litters (MGI Ref ID J:6580)
- reduced male fertility
- do not produce more than two litters (MGI Ref ID J:6580)
skeleton phenotype
- abnormal cartilage morphology
- abnormal cementum morphology
- at 12 weeks, enlargement of the cementum (MGI Ref ID J:122727)
- abnormal femur morphology
- metaphyseal trabeculae reduced in both thickness and number (MGI Ref ID J:168526)
- abnormal joint capsule morphology
- abnormal joint mobility
- joint mobility is decreased at 6 weeks and is more severe at 12 weeks similar to in Anktm1.1Kng homozygotes (MGI Ref ID J:122727)
- 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 (MGI Ref ID J:6580)
- 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 (MGI Ref ID J:122727)
- stiffness of joints observed at 4-5 weeks of age (MGI Ref ID J:168526)
- wean age homozygotes are unable to grasp a wire cage tope due to stiffness in the digits (MGI Ref ID J:63420)
- 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 (MGI Ref ID J:6580)
- abnormal joint morphology
- bone volume in joints is significantly increased and increases in severity with time (MGI Ref ID J:122727)
- joint space narrowing, accumulation of debris in the joint space, and ectopic calcification in and around the affected joints (MGI Ref ID J:63420)
- mutants develop a noninflammatory degenerative joint disease, with stiffness of joints starting in forefeet and toes, quickly spreading to other joints (MGI Ref ID J:6580)
- 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 (MGI Ref ID J:6580)
- necrosis in the fibrous tissue of the joints, including the ligaments and cartilage (MGI Ref ID J:6580)
- synovial lining in most places, except over articular cartilage or ligament, has a thickened surface layer (MGI Ref ID J:6580)
- abnormal ligament morphology
- abnormal sesamoid bone of gastrocnemius morphology
- some of the sesamoid bones are enlarged and appear to be fused with the nearest long bone (MGI Ref ID J:6580)
- abnormal skeleton morphology
- progressive ankylosis (MGI Ref ID J:6580)
- abnormal tendon morphology
- degeneration in many, although not all, tendons associated with affected joints (MGI Ref ID J:6580)
- abnormal tooth hard tissue morphology
- arthritis
- histology of the digit joints shows narrowing of the joint spaces, erosion of cartilage, accumulation of debris, and ectopic calcification (MGI Ref ID J:63420)
- 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 (MGI Ref ID J:6580)
- ectopic calcification in and around the affected joints (MGI Ref ID J:63420)
- excessive bony deposits in joints (MGI Ref ID J:168526)
- 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 (MGI Ref ID J:6580)
- 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 (MGI Ref ID J:6580)
- kyphosis
- adults exhibit thoracic kyphosis and prominent haunches (MGI Ref ID J:6580)
muscle phenotype
- abnormal tendon morphology
- degeneration in many, although not all, tendons associated with affected joints (MGI Ref ID J:6580)
craniofacial phenotype
- abnormal cementum morphology
- at 12 weeks, enlargement of the cementum (MGI Ref ID J:122727)
- abnormal tooth hard tissue morphology
behavior/neurological phenotype
- abnormal gait
- slow halting gait, with all feet flat against the surface (MGI Ref ID J:6580)
- abnormal posture
- adults exhibit a rigid posture (MGI Ref ID J:6580)
- decreased grip strength
- unable to grab cage bars at 4-5 weeks of age (MGI Ref ID J:168526)
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) (MGI Ref ID J:6580)
- abnormal femur morphology
- metaphyseal trabeculae reduced in both thickness and number (MGI Ref ID J:168526)
- abnormal limb morphology
- in the limbs, abnormalities are more severe in the distal than proximal joints and in the forelimbs than in the hindlimbs (MGI Ref ID J:6580)
- abnormal sesamoid bone of gastrocnemius morphology
- some of the sesamoid bones are enlarged and appear to be fused with the nearest long bone (MGI Ref ID J:6580)
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 (MGI Ref ID J:63420)
References
- 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.. In: . . MGI: J:109949
- 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.. In: . . MGI: J:7672
- Ho AM; Johnson MD; Kingsley DM. 2000. Role of the mouse ank gene in control of tissue calcification and arthritis [see comments]. In: . . MGI: J:63420
- Krug HE. 1998. Fibroblasts from mice with progessive ankylosis proliferate excessively in response to transforming growth factor-beta 1.. In: . . MGI: J:109902
- 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.. In: . . MGI: J:109935
- Krug HE; Taurog JD. 2000. HLA-B27 has no effect on the phenotypic expression of progressive ankylosis in ank/ank mice. In: . . MGI: J:62431
- Krug HE; Wietgrefe MM; Ytterberg SR; Taurog JD; Mahowald ML. 1997. Murine progressive ankylosis is not immunologically mediated.. In: . . MGI: J:109905
- Mahowald ML; Krug H; Halverson P. 1989. Progressive ankylosis (ank/ank) in mice: an animal model of spondyloarthropathy. II. Light and electron microscopic findings.. In: . . MGI: J:23576
- 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.. In: . . MGI: J:69128
- 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.. In: . . MGI: J:109879
- Sampson HW. 1988. Ultrastructure of the mineralizing metacarpophalangeal joint of progressive ankylosis (ank/ank) mice.. In: . . MGI: J:109941
- Sampson HW. 1988. Spondyloarthropathy in progressive ankylosis (ank/ank) mice: morphological features.. In: . . MGI: J:109942
- Sampson HW; Davis RW; Dufner DC. 1991. Spondyloarthropathy in progressive ankylosis mice: ultrastructural features of the intervertebral disk.. In: . . MGI: J:751
- Sweet HO; Green MC. 1981. Progressive ankylosis, a new skeletal mutation in the mouse.. In: . . MGI: J:6580
Additional - A related
- Blewitt ME; Vickaryous NK; Hemley SJ; Ashe A; Bruxner TJ; Preis JI; Arkell R; Whitelaw E. 2005. An N-ethyl-N-nitrosourea screen for genes involved in variegation in the mouse.. In: . . MGI: J:99816
- Bultman SJ; Michaud EJ; Woychik RP. 1992. Molecular characterization of the mouse agouti locus.. In: . . MGI: J:3523
- Bundschuh VG; Madry M. 1988. [atwp mutation in an albino mouse substrain (AB/Hum-1)]. In: . . MGI: J:16568
- Cota CD; Liu RR; Sumberac TM; Jung S; Vencato D; Millet YH; Gunn TM. 2008. Genetic and phenotypic studies of the dark-like mutant mouse.. In: . . MGI: J:143333
- Czyzyk TA; Sikorski MA; Yang L; McKnight GS. 2008. Disruption of the RIIbeta subunit of PKA reverses the obesity syndrome of Agouti lethal yellow mice.. In: . . MGI: J:131039
- Dickie MM. 1969. Mutations at the agouti locus in the mouse.. In: . . MGI: J:30922
- Dry FW. 1928. The agouti coloration of the mouse (Mus Musculus) and the rat (Mus Norvegicus).. In: . . MGI: J:46318
- Dunn LC. 1945. A New Eye Color Mutant in the Mouse with Asymmetrical Expression.. In: . . MGI: J:13122
- Galbraith DB; Wolff GL; Brewer NL. 1979. Tissue microenvironment and the genetic control of hair pigment patterns in mice. In: . . MGI: J:156092
- Green EL. 1968. . In: Handbook on Genetically Standardized Jax Mice. The Jackson Laboratory, Bar Harbor, ME. MGI: J:36414
- Guido V; and The Mouse Mutant Resource (MMR) at The Jackson Laboratory. 2002. Two new mutations of white bellied agouti, w-46J and w-47J. In: . . MGI: J:77218
- Jackson IJ; Budd PS; Keighren M; McKie L. 2007. Humanized MC1R transgenic mice reveal human specific receptor function.. In: . . MGI: J:129904
- Kelly EM. 1957. Beige, bg. In: . . MGI: J:29744
- Mather K; North SB. 1940. Umbrous: a case of dominance modification in mice.. In: . . MGI: J:280
- MouseBookTM. 2005. Information obtained from MouseBook<sup>TM</sup>, Medical Research Council Mammalian Genetics Unit, Harwell, UK.. In: . . MGI: J:169366
- Mutant Mouse Regional Resource Centers. 2004. Information obtained from the Mutant Mouse Regional Resource Centers (MMRRC). In: . . MGI: J:94077
- Perry WL; Copeland NG; Jenkins NA. 1994. The molecular basis for dominant yellow agouti coat color mutations.. In: . . MGI: J:21244
- Phillips RJS. 1966. A cis-trans position effect at the A locus of the house mouse.. In: . . MGI: J:5027
- Quevedo WC Jr.; Chase HB. 1958. An analysis of the light mutation of coat color in mice.. In: . . MGI: J:13094
- Silvers WK. 1979. The Coat Colors of Mice; A Model for Mammalian Gene Action and Interaction. In: The Coat Colors of Mice. Springer-Verlag, New York. MGI: J:78801
- Siracusa LD; Washburn LL; Swing DA; Argeson AC; Jenkins NA; Copeland NG. 1995. Hypervariable yellow (Ahvy), a new murine agouti mutation: Ahvy displays the largest variation in coat color phenotypes of all known agouti alleles.. In: . . MGI: J:24247
- Zheng B; Sage M; Cai WW; Thompson DM; Tavsanli BC; Cheah YC; Bradley A. 1999. Engineering a mouse balancer chromosome.. In: . . MGI: J:56548
- von Lehmann E. 1973. Coat colour genetics of the tobacco-mouse (Mus poschiavinus Fatio). In: . . MGI: J:22593
Additional - Aw-J related
- Aberg T; Wang XP; Kim JH; Yamashiro T; Bei M; Rice R; Ryoo HM; Thesleff I. 2004. Runx2 mediates FGF signaling from epithelium to mesenchyme during tooth morphogenesis.. In: . . MGI: J:92174
- Banerjee H; Das A; Srivastava S; Mattoo HR; Thyagarajan K; Khalsa JK; Tanwar S; Das DS; Majumdar SS; George A; Bal V; Durdik JM; Rath S. 2012. A role for apoptosis-inducing factor in T cell development.. In: . . MGI: J:191446
- Barsh GS; Epstein CJ. 1989. Physical and genetic characterization of a 75-kilobase deletion associated with al, a recessive lethal allele at the mouse agouti locus.. In: . . MGI: J:9799
- Baurle J; Vogten H; Grusser-Cornehls U. 1998. Course and targets of the calbindin D-28k subpopulation of primary vestibular afferents.. In: . . MGI: J:118430
- Boran T; Lesot H; Peterka M; Peterkova R. 2005. Increased apoptosis during morphogenesis of the lower cheek teeth in tabby/EDA mice.. In: . . MGI: J:112546
- Chinta SJ; Rane A; Yadava N; Andersen JK; Nicholls DG; Polster BM. 2009. Reactive oxygen species regulation by AIF- and complex I-depleted brain mitochondria.. In: . . MGI: J:145908
- Cui CY; Hashimoto T; Grivennikov SI; Piao Y; Nedospasov SA; Schlessinger D. 2006. Ectodysplasin regulates the lymphotoxin-beta pathway for hair differentiation.. In: . . MGI: J:111051
- Cui CY; Kunisada M; Esibizione D; Grivennikov SI; Piao Y; Nedospasov SA; Schlessinger D. 2007. Lymphotoxin-beta regulates periderm differentiation during embryonic skin development.. In: . . MGI: J:129949
- Cui CY; Yin M; Sima J; Childress V; Michel M; Piao Y; Schlessinger D. 2014. Involvement of Wnt, Eda and Shh at defined stages of sweat gland development.. In: . . MGI: J:217500
- Cunningham D; Spychala K; McLarren KW; Garza LA; Boerkoel CF; Herman GE. 2009. Developmental expression pattern of the cholesterogenic enzyme NSDHL and negative selection of NSDHL-deficient cells in the heterozygous Bpa(1H)/+ mouse.. In: . . MGI: J:155028
- Dickie MM. 1969. Mutations at the agouti locus in the mouse.. In: . . MGI: J:30922
- Esibizione D; Cui CY; Schlessinger D. 2008. Candidate EDA targets revealed by expression profiling of primary keratinocytes from Tabby mutant mice.. In: . . MGI: J:143603
- Granholm DE; Reese RN; Granholm NH. 1996. Agouti alleles alter cysteine and glutathione concentrations in hair follicles and serum of mice (A y/a, A wJ/A wJ, and a/a).. In: . . MGI: J:32132
- Granholm DE; Reese RN; Granholm NH. 1995. Agouti alleles influence thiol concentrations in hair follicles and extrafollicular tissues of mice (Ay/a, AwJ/AwJ, a/a).. In: . . MGI: J:31403
- Hisatomi T; Nakao S; Murakami Y; Noda K; Nakazawa T; Notomi S; Connolly E; She H; Almulki L; Ito Y; Vavvas DG; Ishibashi T; Miller JW. 2012. The regulatory roles of apoptosis-inducing factor in the formation and regression processes of ocular neovascularization.. In: . . MGI: J:185543
- Jones JM; Huang JD; Mermall V; Hamilton BA; Mooseker MS; Escayg A; Copeland NG; Jenkins NA; Meisler MH. 2000. The mouse neurological mutant flailer expresses a novel hybrid gene derived by exon shuffling between Gnb5 and Myo5a.. In: . . MGI: J:61324
- Kappenman KE; Dvoracek MA; Harvison GA; Fuller BB; Granholm NH. 1992. Tyrosinase abundance and activity in murine hairbulb melanocytes of agouti mutants (C57BL/6J-a/a, Ay/a, and AwJ/AwJ).. In: . . MGI: J:1295
- Katoh A; Yoshida T; Himeshima Y; Mishina M; Hirano T. 2005. Defective control and adaptation of reflex eye movements in mutant mice deficient in either the glutamate receptor delta2 subunit or Purkinje cells.. In: . . MGI: J:101081
- Knapp PE; Adjan VV; Hauser KF. 2009. Cell-specific loss of kappa-opioid receptors in oligodendrocytes of the dysmyelinating jimpy mouse.. In: . . MGI: J:146365
- Leblond F; Poirier S; Yu C; Duquette N; Mayer G; Thorin E. 2014. The anti-hypercholesterolemic effect of low p53 expression protects vascular endothelial function in mice.. In: . . MGI: J:215071
- Lee M; Kim A; Chua SC Jr; Obici S; Wardlaw SL. 2007. Transgenic MSH overexpression attenuates the metabolic effects of a high-fat diet.. In: . . MGI: J:126508
- Lorivel T; Roy V; Hilber P. 2014. Fear-related behaviors in Lurcher mutant mice exposed to a predator.. In: . . MGI: J:226730
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Additional - Ankank related
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