Description

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Strain Information

Former Names Hairless    (Changed: 15-DEC-04 ) Type Mutant Strain; Spontaneous Mutation; Additional information on Genetically Engineered and Mutant Mice. Type Inbred Strain; Additional information on Inbred Strains. Visit our online Nomenclature tutorial. Species laboratory mouse H2 Haplotype k

Appearance
unpigmented, without hair
Related Genotype: Tyrp1^b/Tyrp1^b Tyr^c/Tyr^c Myo5a^d/Myo5a^d Hr^hr/Hr^hr

albino, unaffected
Related Genotype: Tyrp1^b/Tyrp1^b Tyr^c/Tyr^c Myo5a^d/Myo5a^d Hr^hr/+

Description
Mice homozygous for the hr spontaneous mutation have a higher incidence and earlier onset of leukemia, reducible by virus-specific antibody. Deficiency of splenic T helper cells (Ly-1+) may account for low cellular immune response of homozygous mutant mice. The coat is normal on hr/hr mice up to 10 days but then hair is lost from the follicle. Waves of hair growth with few thin fuzzy hairs ocur at monthly intervals for some time but homozygotes eventually become continuously hairless. Vibrissae are repeatedly regrown and shed, becoming more abnormal with age. Toenails are long and curved. There is hyperkeratosis of stratified epithelium and the upper part of hair canals beginning at 14 days. Hair club formation is abnormal. Cysts form from the hyperkeratotic upper part of hair canals and sheaths of abnormal follicles stranded in dermis. Some cysts also form from sebaceous glands. All cysts undergo sebaceous transformation and later keratinization. HRS/J mice, fed an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat), fail to develop atherosclerotic aortic lesions in contrast to several highly susceptible strains of mice (e.g. C57BL/6J, Stock No. 000664; C57L/J, Stock No. 000668, C57BR/cdJ, Stock No. 000667, and SM/J, Stock No. 000687).

Development
The hairless mutation (Hr^hr) was found in a mouse caught in an aviary in London in 1924. It was brought to The Jackson Laboratory in 1956 by Dr. E. L. Green who had received it from Dr. H. Chase at Brown University in 1952. Dr. Green crossed it to a BALB/c female and the stock was sibling mated. The genotype was fixed homozygous for brown (Tyrp1^b), albino (Tyr^c), dilute (Myo5a^d) and kept segregating for hairless. Since the hairless females do not nurse their litters it was bred hairless males x haired females. In 1964 at generation F24 the strain was named HRS/J. Embryos were cryopreserved in 1992 from haired females mated to hairless males at F90.

Control Information

	Control
	Heterozygote from the colony
Considerations for Choosing Controls

Related Strains

Strains carrying   Ahr^b-2 allele

000645	A/HeJ
000646	A/J
000130	B6.C-H17c/(HW14)ByJ
000370	B6.C-H38c/(HW119)ByJ
001026	BALB/cByJ
000653	BUB/BnJ
000659	C3H/HeJ
000656	CBA/J
000657	CE/J
000352	CXB2/ByJ
000353	CXB3/ByJ
000354	CXB4/ByJ
000355	CXB5/ByJ
000357	CXB7/ByJ
000679	P/J
000930	PERA/EiJ
000644	SEA/GnJ
000280	SF/CamEiJ

View Strains carrying   Ahr^b-2     (18 strains)

Strains carrying   Hr^hr allele

001737	B6.Cg-Hrhr H2-T18a/J
002922	D2.HRS-Hrhr/J
001103	HRS/J-Hrhr Esdb/+ Esdb/J
002335	SKH2/J
000147	WLHR/LeJ

View Strains carrying   Hr^hr     (5 strains)

Strains carrying   Myo5a^d allele

001005	AKXD1/TyJ
001003	AKXD11/TyJ
000765	AKXD13/TyJ
000779	AKXD14/TyJ
000954	AKXD15/TyJ
001093	AKXD18/TyJ
000776	AKXD2/TyJ
001062	AKXD21/TyJ
000947	AKXD22/TyJ
000949	AKXD25/TyJ
000764	AKXD27/TyJ
000959	AKXD3/TyJ
000285	B6.Cg-Rorasg + +/+ Myo5ad Bmp5se/J
012889	B6N;TKDU-Myo5ad Cacna2d2du/J
000652	BDP/J
000036	BXD1/TyJ
000013	BXD16/TyJ
000015	BXD18/TyJ
000010	BXD19/TyJ
000077	BXD21/TyJ
000043	BXD22/TyJ
000081	BXD25/TyJ
000029	BXD29-Tlr4lps-2J/J
010981	BXD29/Ty
000037	BXD5/TyJ
000007	BXD6/TyJ
000084	BXD8/TyJ
000105	BXD9/TyJ
000284	CWD/LeJ
000670	DBA/1J
000671	DBA/2J
000963	DBA/2J-Myo5ad+17J/Myo5ad/J
000964	DBA/2J-Myo5ad+18J/Myo5ad/J
000067	DBA/2J-Myo5ad+2J/Myo5ad/J
000674	I/LnJ
001850	MEV-Q/TyJ
001855	MEV-V/TyJ
003345	MEV/2Ty-Emv64/J
000679	P/J
000644	SEA/GnJ
000390	STOCK Myo5ad Ds/J
000994	STOCK a Myo5ad Mregdsu/J
000286	STOCK a/a Myo5ad fd/+ +/J

View Strains carrying   Myo5a^d     (43 strains)

Strains carrying other alleles of Ahr

000690	129P3/J
000645	A/HeJ
000646	A/J
000648	AKR/J
002920	B6(D2N).Spretus-Ahrb-3/J
006203	B6.129(FVB)-Ahrtm3.1Bra/J
002831	B6.129-Ahrtm1Bra/J
000130	B6.C-H17c/(HW14)ByJ
000136	B6.C-H34c/(HW22)ByJ
000370	B6.C-H38c/(HW119)ByJ
008599	B6.Cg-Cyp1a2/Cyp1a1tm2Dwn Ahrd Tg(CYP1A1,CYP1A2)1Dwn/DwnJ
002921	B6.D2N-Ahrd/J
002727	B6;129-Ahrtm1Bra/J
001026	BALB/cByJ
000652	BDP/J
000653	BUB/BnJ
000659	C3H/HeJ
000663	C57BL/6By
001139	C57BL/6ByJ
000664	C57BL/6J
000662	C57BLKS/J
000667	C57BR/cdJ
000668	C57L/J
000669	C58/J
000926	CAROLI/EiJ
000928	CAST/EiJ
000656	CBA/J
000657	CE/J
000351	CXB1/ByJ
000352	CXB2/ByJ
000353	CXB3/ByJ
000354	CXB4/ByJ
000355	CXB5/ByJ
000356	CXB6/ByJ
000357	CXB7/ByJ
002937	D2.B6-Ahrb-1/J
000671	DBA/2J
000674	I/LnJ
000675	LG/J
000676	LP/J
000677	MA/MyJ
000550	MOLF/EiJ
000684	NZB/BlNJ
000679	P/J
000930	PERA/EiJ
000726	RBF/DnJ
000682	RF/J
000644	SEA/GnJ
000280	SF/CamEiJ
000686	SJL/J
001146	SPRET/EiJ
000688	ST/bJ
000689	SWR/J
000693	WC/ReJ KitlSl/J
000933	YBR/EiJ

View Strains carrying other alleles of Ahr     (55 strains)

Strains carrying other alleles of Hr

007621	B6.129S6-Hrtm1Cct/J
001737	B6.Cg-Hrhr H2-T18a/J
000758	C57BL/6J-Hbbp Hrrh-7J/J
002922	D2.HRS-Hrhr/J
001103	HRS/J-Hrhr Esdb/+ Esdb/J
000266	RHJ/Le
001591	RHJ/LeJ
002335	SKH2/J
000147	WLHR/LeJ

View Strains carrying other alleles of Hr     (9 strains)

Strains carrying other alleles of Myo5a

005012	A.B6 Tyr+-Myo5ad-l31J/J
001005	AKXD1/TyJ
001003	AKXD11/TyJ
000765	AKXD13/TyJ
000779	AKXD14/TyJ
000954	AKXD15/TyJ
001093	AKXD18/TyJ
000776	AKXD2/TyJ
001062	AKXD21/TyJ
000947	AKXD22/TyJ
000949	AKXD25/TyJ
000764	AKXD27/TyJ
000959	AKXD3/TyJ
001013	B10.D2/nSnJ-Myo5ad-n/J
000502	B6 x B6CBCa Aw-J/A-Myo5aflr Gnb5flr/J
000285	B6.Cg-Rorasg + +/+ Myo5ad Bmp5se/J
012889	B6N;TKDU-Myo5ad Cacna2d2du/J
000652	BDP/J
000036	BXD1/TyJ
000013	BXD16/TyJ
000015	BXD18/TyJ
000010	BXD19/TyJ
000077	BXD21/TyJ
000043	BXD22/TyJ
000081	BXD25/TyJ
000029	BXD29-Tlr4lps-2J/J
010981	BXD29/Ty
000037	BXD5/TyJ
000007	BXD6/TyJ
000084	BXD8/TyJ
000105	BXD9/TyJ
000284	CWD/LeJ
000670	DBA/1J
000671	DBA/2J
000963	DBA/2J-Myo5ad+17J/Myo5ad/J
000964	DBA/2J-Myo5ad+18J/Myo5ad/J
000067	DBA/2J-Myo5ad+2J/Myo5ad/J
000253	DLS/LeJ
000674	I/LnJ
001850	MEV-Q/TyJ
001855	MEV-V/TyJ
003345	MEV/2Ty-Emv64/J
000679	P/J
000644	SEA/GnJ
000390	STOCK Myo5ad Ds/J
000994	STOCK a Myo5ad Mregdsu/J
000286	STOCK a/a Myo5ad fd/+ +/J

View Strains carrying other alleles of Myo5a     (47 strains)

Additional Web Information

Genetic Quality Control Annual Report
JAX^® NOTES, January 1989; 436. Phenotypic abnormalities in hr-locus mutants.
JAX^® NOTES, October 1988; 435. Introduction of Rhino (hr^rh) into Jackson Laboratory Production Colonies.
JAX^® NOTES, Spring 1990; 441. Imperforate Vagina and Mucometra in Mice.

Phenotype

Phenotype Information

View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI

      assigned by genotype

Hr^hr/Hr^hr

        HRS/J

• hearing/vestibular/ear phenotype
• absent linear vestibular evoked potential
  • VESPs are absent at the maximum stimulus intensity used   (MGI Ref ID J:116914)
• tumorigenesis
• leukemia
  • increased incidence   (MGI Ref ID J:5726)
  • increased incidence   (MGI Ref ID J:5908)
  • at 8 to 10 months of age 45% of homozygotes have lymphoid leukemia, compared with only 1% in heterozygotes, and approximately 72% of these homozygotes develop myeloid leukemia later in life up to 18 months of age   (MGI Ref ID J:24786)
• hematopoietic system phenotype
• decreased T cell number
  • of CD5+ T cells   (MGI Ref ID J:6087)
• decreased T cell proliferation
  • to alloantigens by T helper cells   (MGI Ref ID J:6375)
• increased macrophage cell number
  • although heterozygotes and homozygotes have the same total number of peritoneal cells, the percentage expressing Mac-1 is an average of 30% in homozygotes versus an average of 14% in heterozygotes   (MGI Ref ID J:150402)
• immune system phenotype
• decreased T cell number
  • of CD5+ T cells   (MGI Ref ID J:6087)
• decreased T cell proliferation
  • to alloantigens by T helper cells   (MGI Ref ID J:6375)
• increased macrophage cell number
  • although heterozygotes and homozygotes have the same total number of peritoneal cells, the percentage expressing Mac-1 is an average of 30% in homozygotes versus an average of 14% in heterozygotes   (MGI Ref ID J:150402)
• cellular phenotype
• decreased T cell proliferation
  • to alloantigens by T helper cells   (MGI Ref ID J:6375)

The following phenotype information may relate to a genetic background differing from this JAX^® Mice strain.

Hr^hr/Hr^hr

        Background Not Specified

• endocrine/exocrine gland phenotype
• abnormal mammary gland morphology
  • small   (MGI Ref ID J:2409)
  • nipple at bottom of cup-shaped depression in skin   (MGI Ref ID J:2409)
  • no ducts   (MGI Ref ID J:2409)
• sebaceous gland atrophy   (MGI Ref ID J:2409)
• reproductive system phenotype
• abnormal mammary gland morphology
  • small   (MGI Ref ID J:2409)
  • nipple at bottom of cup-shaped depression in skin   (MGI Ref ID J:2409)
  • no ducts   (MGI Ref ID J:2409)
• behavior/neurological phenotype
• abnormal nursing
  • failure   (MGI Ref ID J:2409)
• integument phenotype
• abnormal mammary gland morphology
  • small   (MGI Ref ID J:2409)
  • nipple at bottom of cup-shaped depression in skin   (MGI Ref ID J:2409)
  • no ducts   (MGI Ref ID J:2409)
• abnormal skin morphology
  • thickened cutis   (MGI Ref ID J:2409)
• • abnormal dermis reticular layer morphology
    • cystic   (MGI Ref ID J:2409)
  • dermal cysts   (MGI Ref ID J:14889)
  • epidermal hyperplasia   (MGI Ref ID J:14940)
  • hyperkeratosis   (MGI Ref ID J:14940)
• alopecia   (MGI Ref ID J:2409)
  • beginning ~15 days of age and progressing from nose back   (MGI Ref ID J:2405)
• deformed nails
  • curved   (MGI Ref ID J:2409)
• sebaceous gland atrophy   (MGI Ref ID J:2409)

View Research Applications

Research Applications

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

Hr^hr related

Cancer Research
Increased Tumor Incidence
      Leukemia
      Leukemia: lymphocytic
      Lymphomas
      Lymphomas: thymic
      Skin Cancers
      Skin Cancers: Induced
Toxicology

Cardiovascular Research
Diet-Induced Atherosclerosis
      Relatively Resistant

Dermatology Research
Skin and Hair Texture Defects

Immunology and Inflammation Research
Immunodeficiency Associated with Other Defects

Research Tools
Toxicology Research
      drug/compound testing

Myo5a^d related

Dermatology Research
Color and White Spotting Defects

Mouse/Human Gene Homologs
Griscelli Syndrome

Genes & Alleles

Gene & Allele Information provided by MGI

Allele Symbol		Ahrb-2
Allele Name		b-2 variant
Allele Type		Not Applicable
Common Name(s)		Ahb-2; Ahh;
Strain of Origin		BALB/cBy
Gene Symbol and Name		Ahr, aryl-hydrocarbon receptor
Chromosome		12
Gene Common Name(s)		Ah; Ahh; Ahre; In; aromatic hydrocarbon responsiveness; aryl hydrocarbon hydroxylase; bHLHe76; dioxin receptor; inflammatory reactivity;
General Note		C57BL/6 carries the responsive Ahrb allele; DBA/2 carries nonresponsive Ahrd. Heterozygotes (Ahrb/Ahrd) are responsive (J:5282). Later work identified a second (J:8895) and later a third (J:22144) allele conferring response. Thus the allele in C57, C58, and MA/My strains is now Ahrb-1; Ahrb-2 is carried by BALB/cBy, A, and C3H; and Ahrb-3 by Mus spretus, M. caroli, and MOLF/Ei. The nonresponsive strains AKR, DBA/2, and 129 carry Ahrd (J:22144). Nucleotide and amino acid sequence differences between Ahrb-1 and Ahrd have been determined (J:17460). Strain of origin - this allele was found in BALB/cByJ, A/J, C3H/HeJ, CBA strains
Molecular Note		This allele encodes a high affinity, heat labile, 104 kDa receptor containing 848 amino acids. Sequencing studies of cDNA from C57BL/6J congenic mice homozygous for this allele identified nucleotide substitutions in the ORF that would cause 5 amino acid differences between the C57BL/6J and BALB/cBy peptides, and 2 amino acid differences between the BALB/cBy and DBA/2J peptides. A T to C transition in exon 11 replaces the opal termination codon in the C57BL/6J allele with an arginine codon in the BALB/cByallele. This change would extend translation of the BALB/cBy mRNA by 43 amino acids, accounting for the larger size of the peptide produced by this allele (104 kDa, vs 95 kDa for the C57BL/6J allele). [MGI Ref ID J:15153] [MGI Ref ID J:22144]
Allele Symbol		Hrhr
Allele Name		hairless
Allele Type		Spontaneous
Common Name(s)		hr;
Gene Symbol and Name		Hr, hairless
Chromosome		14
Gene Common Name(s)		ALUNC; AU; HSA277165; MUHH; MUHH1; N; ba; baldy; bldy; rh; rh-bmh; rhino-bald Mill Hill;
Molecular Note		The hr allele is the result of a retroviral integration. Insertion of murine leukemia proviral sequences into intron 6 results in aberrant splicing of the gene. [MGI Ref ID J:19624] [MGI Ref ID J:92053] [MGI Ref ID J:9252]
Allele Symbol		Myo5ad
Allele Name		dilute
Allele Type		Spontaneous
Common Name(s)		d; dv; maltese dilution;
Strain of Origin		old mutant of the mouse fancy
Gene Symbol and Name		Myo5a, myosin VA
Chromosome		9
Gene Common Name(s)		9630007J19Rik; AI413174; AI661011; D; Dbv; Dop; GS1; MVa; MYH12; MYO5; MYR12; Myo5; MyoVA; RIKEN cDNA 9630007J19 gene; d; dilute; expressed sequence AI413174; expressed sequence AI661011; flail; flailer; flr; myosin V; nmf244;
General Note		Mutations at the Myo5a locus lighten coat color through an abnormal morphology of melanocytes that causes uneven pigmentation of the hair shaft (J:11005). Most of these mutations also cause severe neurological defects; in some mutant forms, these defectslead to early death (J:12978), while in others life span is normal, but convulsions and loss of equilibrium occur after about four months of age (J:16915). Maltese dilution, as this mutation was originally called, is an old mutation of the mouse fancy. The blue-gray color of the hair produced by this mutation in nonagouti (a/a) mice is caused by clumping of the melanin pigment into a few large masses (J:12958). The melanocytes are misshapen, with fewer and thinner dendritic processes than wild-type melanocytes, and melanin granules are largely clumped around the nucleus (J:12970). Incorporation of tyrosine into melanin proceeds at a normal rate (J:12173), and the fine structure of the melanin granules is normal (J:5346). Cultured primary melanocytesfrom dilute homozygotes are normal in morphology but display clustering of melanosomes (J:37976). Griscelli disease (Chediak-Higashi-like syndrome, OMIM 214450) is a human autosomal recessive disorder whose symptoms include pigment dilution, immunodeficiency, and acute lethal lymphocyte and macrophage activation. Melanocyte malformation is characteristic of the pigment abnormality. The immunological abnormality includes absence of cutaneous hypersensitivity and impaired function of natural-killer cells. Griscelli disease resembles the dilute-lethal mouse mutant, except for the neurological disorder in the mouse. The locus for Griscelli disease colocalizes with the locus for myosin Va, which is mutated in at least some Griscelli patients. Griscelli disease is thus the homolog of mouse Maltese dilution (J:41253). The original Myo5ad mutation which identified the locuswas caused by insertion of an ecotropic murine leukemia virus (see Emv3) (J:6844, J:6587). All other mutations examined lack the virus. Reversions of Myo5ad to wild-type, which have been reported frequently, are caused by excision of the virusleaving exactly one long terminal repeat in place (J:7092). The virus is integrated into a noncoding region of the DNA (J:7751).
Molecular Note		This mutation is the result of the integration of the ecotropic murine leukemia virus Emv-3 into the normal Myo5ad gene. [MGI Ref ID J:6587]

Genotyping

Genotyping Information

Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Additional References

Cachon-Gonzalez MB; Fenner S; Coffin JM; Moran C; Best S; Stoye JP. 1994. Structure and expression of the hairless gene of mice. Proc Natl Acad Sci U S A 91(16):7717-21. [PubMed: 8052649]  [MGI Ref ID J:19624]

Morrissey PJ; Parkinson DR; Schwartz RS; Waksal SD. 1980. Immunologic abnormalities in HRS/J mice. I. Specific deficit in T lymphocyte helper function in a mutant mouse. J Immunol 125(4):1558-62. [PubMed: 6447727]  [MGI Ref ID J:6375]

Poland A; Glover E. 1990. Characterization and strain distribution pattern of the murine Ah receptor specified by the Ahd and Ahb-3 alleles. Mol Pharmacol 38(3):306-12. [PubMed: 2169579]  [MGI Ref ID J:34840]

Reske-Kunz AB; Scheid MP; Boyse EA. 1979. Disproportion in T-cell subpopulations in immunodeficient mutant hr/hr mice. J Exp Med 149(1):228-33. [PubMed: 310859]  [MGI Ref ID J:6087]

Ahr^b-2 related

Nebert DW; Considine N; Owens IS. 1973. Genetic expression of aryl hydrocarbon hydroxylase induction. VI. Control of other aromatic hydrocarbon-inducible mono-oxygenase activities at or near the same genetic locus. Arch Biochem Biophys 157(1):148-59. [PubMed: 4716952]  [MGI Ref ID J:84313]

Nebert DW; Gielen JE. 1972. Genetic regulation of aryl hydrocarbon hydroxylase induction in the mouse. Fed Proc 31(4):1315-25. [PubMed: 4114109]  [MGI Ref ID J:5282]

Nebert DW; Jensen NM; Shinozuka H; Kunz HW; Gill TJ 3rd. 1982. The Ah phenotype. Survey of forty-eight rat strains and twenty inbred mouse strains. Genetics 100(1):79-87. [PubMed: 7095422]  [MGI Ref ID J:6809]

Nebert DW; Robinson JR; Niwa A; Kumaki K; Poland AP. 1975. Genetic expression of aryl hydrocarbon hydroxylase activity in the mouse. J Cell Physiol 85(2 Pt 2 Suppl 1):393-414. [PubMed: 1091656]  [MGI Ref ID J:84317]

Niwa A; Kumaki K; Nebert DW; Poland AP. 1975. Genetic expression of aryl hydrocarbon hydroxylase activity in the mouse. Distinction between the 'responsive' homozygote and heterozygote at the Ah locus. Arch Biochem Biophys 166(2):559-64. [PubMed: 1119809]  [MGI Ref ID J:84316]

Poland A; Glover E. 1990. Characterization and strain distribution pattern of the murine Ah receptor specified by the Ahd and Ahb-3 alleles. Mol Pharmacol 38(3):306-12. [PubMed: 2169579]  [MGI Ref ID J:34840]

Poland A; Glover E; Taylor BA. 1987. The murine Ah locus: a new allele and mapping to chromosome 12. Mol Pharmacol 32(4):471-8. [PubMed: 2823093]  [MGI Ref ID J:8895]

Poland A; Palen D; Glover E. 1994. Analysis of the four alleles of the murine aryl hydrocarbon receptor. Mol Pharmacol 46(5):915-21. [PubMed: 7969080]  [MGI Ref ID J:22144]

Robinson JR; Considine N; Nebert DW. 1974. Genetic expression of aryl hydrocarbon hydroxylase induction. Evidence for the involvement of other genetic loci. J Biol Chem 249(18):5851-9. [PubMed: 4413562]  [MGI Ref ID J:84315]

Schmid FA; Pena RC; Robinson W; Tarnowski GS. 1967. Toxicity of intraperitoneal injections of 7, 12-dimethylbenz[a]anthracene in inbred mice. Cancer Res 27(3):558-62. [PubMed: 6021513]  [MGI Ref ID J:26440]

Schmidt JV; Carver LA; Bradfield CA. 1993. Molecular characterization of the murine Ahr gene. Organization, promoter analysis, and chromosomal assignment. J Biol Chem 268(29):22203-9. [PubMed: 8408082]  [MGI Ref ID J:15153]

Smith AG; Clothier B; Robinson S; Scullion MJ; Carthew P; Edwards R; Luo J; Lim CK; Toledano M. 1998. Interaction between iron metabolism and 2,3,7,8-tetrachlorodibenzo-p-dioxin in mice with variants of the Ahr gene: a hepatic oxidative mechanism. Mol Pharmacol 53(1):52-61. [PubMed: 9443932]  [MGI Ref ID J:45850]

Thomas PE; Hutton JJ; Taylor BA. 1973. Genetic relationship between aryl hydrocarbon hydroxylase inducibility and chemical carcinogen induced skin ulceration in mice. Genetics 74(4):655-9. [PubMed: 4750810]  [MGI Ref ID J:5387]

Hr^hr related

Aberg KM; Man MQ; Gallo RL; Ganz T; Crumrine D; Brown BE; Choi EH; Kim DK; Schroder JM; Feingold KR; Elias PM. 2008. Co-regulation and interdependence of the mammalian epidermal permeability and antimicrobial barriers. J Invest Dermatol 128(4):917-25. [PubMed: 17943185]  [MGI Ref ID J:135506]

Ahmad W; Panteleyev AA; Christiano AM. 1999. The molecular basis of congenital atrichia in humans and mice: mutations in the hairless gene. J Investig Dermatol Symp Proc 4(3):240-3. [PubMed: 10674375]  [MGI Ref ID J:59939]

Astner S; Wu A; Chen J; Philips N; Rius-Diaz F; Parrado C; Mihm MC; Goukassian DA; Pathak MA; Gonzalez S. 2007. Dietary lutein/zeaxanthin partially reduces photoaging and photocarcinogenesis in chronically UVB-irradiated Skh-1 hairless mice. Skin Pharmacol Physiol 20(6):283-91. [PubMed: 17717424]  [MGI Ref ID J:128747]

Balansky RM; Izzotti A; D'Agostini F; Camoirano A; Bagnasco M; Lubet RA; De Flora S. 2003. Systemic genotoxic effects produced by light, and synergism with cigarette smoke in the respiratory tract of hairless mice. Carcinogenesis 24(9):1525-32. [PubMed: 12844483]  [MGI Ref ID J:85507]

Brooke HC. 1926. Hairless mice J Hered 17:173-74.  [MGI Ref ID J:2405]

Brouxhon S; Konger RL; VanBuskirk J; Sheu TJ; Ryan J; Erdle B; Almudevar A; Breyer RM; Scott G; Pentland AP. 2007. Deletion of prostaglandin E2 EP2 receptor protects against ultraviolet-induced carcinogenesis, but increases tumor aggressiveness. J Invest Dermatol 127(2):439-46. [PubMed: 16977324]  [MGI Ref ID J:117581]

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Sweet HO. 1983. Dilute suppressor, a new suppressor gene in the house mouse. J Hered 74(4):305-6. [PubMed: 6886377]  [MGI Ref ID J:7171]

Yoshimura A; Fujii R; Watanabe Y; Okabe S; Fukui K; Takumi T. 2006. Myosin-Va facilitates the accumulation of mRNA/protein complex in dendritic spines. Curr Biol 16(23):2345-51. [PubMed: 17141617]  [MGI Ref ID J:117928]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, RG10/RG30.

Colony Maintenance

Diet Information	LabDiet® 5K52/5K67

Purchasing information

Pricing, Supply Level & Notes, Controls

General Supply Notes

• This strain is included in the Mouse Mutant Resource collection.
• Genomic DNA is available for this strain from the Mouse DNA Resource.

Control Information

	Control
	Heterozygote from the colony
Considerations for Choosing Controls
Control Pricing Information for Genetically Engineered Mutant Strains.

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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.

See Terms of Use tab for General Terms and Conditions

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.

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Ordering Information
JAX^® Mice
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phone:	207-288-6470
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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"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "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 the 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 or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.

In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.

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 and PRODUCTS 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.