Strain Name:

B6(Cg)-Cys1cpk/J

Stock Number:

000152

Availability:

Repository-Cryopreserved

Description

Strain Information

Former Names C57BL/6J-Cys1cpk/J    (Changed: 05-JUL-05 )
C57BL/6J-cpk    (Changed: 15-DEC-04 )
Type Mutant Strain; Spontaneous Mutation;
Additional information on Genetically Engineered Mutant Mice.
Specieslaboratory mouse
GenerationN36

Appearance
black
Related Genotype: a/a

Control Information

  Control
   Untyped from the colony
 
  Considerations for Choosing Controls

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms
Polycystic Kidney Disease, Autosomal Recessive; ARPKD - Models with phenotypic similarity to human disease where etiologies are distinct.2
2 Human genes are associated with this disease. Orthologs of those genes do not appear in the mouse genotype(s).
View Mammalian Phenotype Terms

Mammalian Phenotype Terms
      assigned by genotype

Cys1cpk/Cys1+

        B6(Cg)-Cys1cpk/J
  • hearing/vestibular/ear phenotype
  • abnormal Reissner membrane morphology (MGI Ref ID J:1001)
    • the perilymphatic side of Reissner's membrane is transparent but the endolymphatic side is normal
  • abnormal organ of Corti (MGI Ref ID J:1001)
    • the organ of Corti is absent from the first cochlear turn but present in the second cochlear turn
    • in the second cochlear turn the inner and outer hair cells are normal but debris is seen in Nuel's space and the outer pillar cells
    • abnormal cochlear inner hair cell morphology (MGI Ref ID J:1001)
      • in the upper portion of the first turn of the cochlea, vesicle formation is seen in the inner hair cells
    • abnormal pillar cell morphology (MGI Ref ID J:1001)
      • some inner pillar cells show a cystic formation at the base of the cell
    • absent cochlear outer hair cells (MGI Ref ID J:1001)
      • in the upper portion of the first turn of the cochlea outer hair cells are absent
  • decreased brainstem auditory evoked potential (MGI Ref ID J:1001)
    • hearing is impaired with auditory evoked potential indicating some hearing loss at 90 db
  • nervous system phenotype
  • abnormal cochlear inner hair cell morphology (MGI Ref ID J:1001)
    • in the upper portion of the first turn of the cochlea, vesicle formation is seen in the inner hair cells
  • absent cochlear outer hair cells (MGI Ref ID J:1001)
    • in the upper portion of the first turn of the cochlea outer hair cells are absent
  • cochlear ganglion hypoplasia (MGI Ref ID J:1001)
    • few spiral ganglia are seen in the first cochlear turn

Cys1cpk/Cys1cpk

        B6(Cg)-Cys1cpk/J
  • lethality-postnatal
  • postnatal lethality (MGI Ref ID J:31533)
    • die around 19 days of age
    • die by 20-23 days of age
  • renal/urinary system phenotype
  • abnormal urine color (MGI Ref ID J:6718)
    • urine is colorless in grossly affected mice
  • enlarged kidney (MGI Ref ID J:9290)
    • increase in kidney size is the result of both increased cystic fluid and increased cell mass
    • at 23 days of age, kidneys occupy almost the entire abdominal cavity
    • at 17-24 days of age, average kidneys size was 16 mm x 11 mm compared to 6 mm x 3 mm in wild-type mice
    • increased kidney weight (MGI Ref ID J:9290)
      • kidney weight is increased in newborns and a progressive increase in kidney wet and dry weight as well as size is seen with age
  • kidney cysts (MGI Ref ID J:9290)
    • initially presents as dilation of the proximal tubule in fetal and newborn mice, then shifts to dilation of the cortical and medullary collecting ducts after the first week of life
    • epithelial hyperplasia but not polypoid hyperplasia is seen in the cysts
    • large cysts occupy the entire kidney, distort the corticomedullary junction, involve collecting ducts and other portions of the kidney, and are lined with flattened epithelium the is frequently squamous
    • polycystic kidney (MGI Ref ID J:31533)
      • bilateral polycystic kidneys become apparent by 8 - 9 days of age
  • homeostasis/metabolism phenotype
  • abnormal urine color (MGI Ref ID J:6718)
    • urine is colorless in grossly affected mice
  • increased blood urea nitrogen level (MGI Ref ID J:9290)
    • progressive azotemia seen starting at 1 week of age
    • mean BUN was 120mg% compared to 0.2mg% in wild-type mice
  • growth/size phenotype
  • distended abdomen (MGI Ref ID J:31533)
    • apparent by 8 - 9 days of age
    • seen at 10-13 days of age
  • hematopoietic system phenotype
  • decreased hematocrit (MGI Ref ID J:9290)
    • seen at 2 - 3 weeks of age
  • behavior/neurological phenotype
  • lethargy (MGI Ref ID J:6718)
    • become progressively lethargic

Cys1cpk/Cys1cpk

        B6(Cg)-Cys1cpk/JUnc
  • life span-post-weaning/aging
  • premature death (MGI Ref ID J:7202)
    • most die by 4 weeks of age with a few rare survivors reaching 5 weeks of age
  • renal/urinary system phenotype
  • abnormal urine color (MGI Ref ID J:7202)
    • at around 4 weeks of age urine becomes colorless
  • enlarged kidney (MGI Ref ID J:7202)
    • at 3 weeks of age the kidney occupies almost the entire abdominal cavity and constitutes about 25% of body weight
  • kidney cysts (MGI Ref ID J:7202)
    • cysts are grossly visible on cut surfaces of kidneys at 3 weeks of age with mild cystic changes already visible at E17
    • progressive dilation of the proximal convoluted tubules and collecting ducts associated with intracellular vacuoles in proximal convoluted tubule cells
  • homeostasis/metabolism phenotype
  • abnormal urine color (MGI Ref ID J:7202)
    • at around 4 weeks of age urine becomes colorless
  • increased blood urea nitrogen level (MGI Ref ID J:7202)
  • increased circulating creatinine level (MGI Ref ID J:7202)
  • growth/size phenotype
  • distended abdomen (MGI Ref ID J:7202)
    • seen at 3 weeks of age
  • behavior/neurological phenotype
  • lethargy (MGI Ref ID J:7202)
    • seen at around 4 weeks of age
  • tremors (MGI Ref ID J:7202)
    • seen at around 4 weeks of age

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

Cys1cpk/Cys1+

        involves: C57BL/6J * CD-1
  • renal/urinary system phenotype
  • kidney cysts (MGI Ref ID J:33739)
    • proximal tubular cysts seen in 1 year old heterozygotes
  • liver/biliary system phenotype
  • liver cysts (MGI Ref ID J:33739)
    • heptatic cysts lined with biliary epithelium are seen in 1 year old heterozygotes
  • liver fibrosis (MGI Ref ID J:33739)
    • seen in 1 year old heterozygotes, associated with hepatic cysts

Cys1cpk/Cys1+

        C.B6(Cg)-Cys1cpk
  • liver/biliary system phenotype
  • liver cysts (MGI Ref ID J:99616)
    • massive hepatic biliary ductal cysts are seen in 1 year old heterozygotes
  • liver fibrosis (MGI Ref ID J:99616)
    • associated with liver cysts

Cys1cpk/Cys1cpk

        involves: C57BL/6J * CD-1
  • lethality-postnatal
  • postnatal lethality (MGI Ref ID J:33739)
    • uremic mortality is seen in less than 10% of homozygotes at 14-20 days of age
  • renal/urinary system phenotype
  • enlarged kidney (MGI Ref ID J:33739)
    • seen at 4 days of age
  • kidney cysts (MGI Ref ID J:33739)
    • at 4 days of age proximal tubule cysts are seen with focal collecting duct dilations in the cortex and outer medulla and by 8-20 days of age collecting duct cysts expand to replace almost all the normal kidney tissue
    • cells lining the proximal tubule cysts and later the collecting duct cysts appear immature
  • homeostasis/metabolism phenotype
  • increased blood urea nitrogen level (MGI Ref ID J:33739)
    • azotemia seen at 12 days of age
  • endocrine/exocrine gland phenotype
  • pancreatic cysts (MGI Ref ID J:33739)
    • all pancreatic ducts have cysts
  • liver/biliary system phenotype
  • biliary cyst (MGI Ref ID J:33739)
    • all common bile ducts have cysts
  • liver cysts (MGI Ref ID J:33739)
    • intrahepatic bile duct cysts consisting of focal dilations in the triad region through to the terminal intrahepatic branches without signs of significant periductal proliferation
  • immune system phenotype
  • spleen hypoplasia (MGI Ref ID J:33739)
  • thymus hypoplasia (MGI Ref ID J:33739)
  • hematopoietic system phenotype
  • spleen hypoplasia (MGI Ref ID J:33739)
  • thymus hypoplasia (MGI Ref ID J:33739)
  • digestive/alimentary phenotype
  • pancreatic cysts (MGI Ref ID J:33739)
    • all pancreatic ducts have cysts

Cys1cpk/Cys1cpk

        C.B6(Cg)-Cys1cpk
  • renal/urinary system phenotype
  • enlarged kidney (MGI Ref ID J:99616)
    • rapid kidney enlargement after birth associated with development of cysts in the collecting ducts
    • EGF treatment reduced kidney size but did not improve kidney function
  • kidney cysts (MGI Ref ID J:99616)
    • after birth cysts shift to the collecting ducts and cysts are lined with a single layer of epithelial cells with polygonal principal-like cell appearance
    • EGF treatment reduces the severity of kidney cysts
    • kidney cortex cysts (MGI Ref ID J:99616)
      • newborns have cysts in the inner cortical proximal tubules
  • homeostasis/metabolism phenotype
  • increased blood urea nitrogen level (MGI Ref ID J:99616)
    • significant by 10 days of age
  • endocrine/exocrine gland phenotype
  • abnormal islet of Langerhans morphology (MGI Ref ID J:99616)
    • almost no islets of Langerhans seen
  • pancreatic cysts (MGI Ref ID J:99616)
    • dilation of the pancreatic ducts present in newborns
  • pancreatic fibrosis (MGI Ref ID J:99616)
    • periductal fibrosis
  • liver/biliary system phenotype
  • bile duct dilation (MGI Ref ID J:99616)
    • common bile duct dilation
    • EGF treatment reduces bile duct dilation
  • biliary cyst (MGI Ref ID J:99616)
    • intrahepatic biliary duct cysts associated with peridcuctal hyperplasia and fibrosis
  • liver fibrosis (MGI Ref ID J:99616)
    • peridcuctal fibrosis associated with intrahepatic biliary duct cysts
  • growth/size phenotype
  • decreased body size (MGI Ref ID J:99616)
    • seen at 5 and 15 days of age
  • digestive/alimentary phenotype
  • abnormal islet of Langerhans morphology (MGI Ref ID J:99616)
    • almost no islets of Langerhans seen
  • pancreatic cysts (MGI Ref ID J:99616)
    • dilation of the pancreatic ducts present in newborns
  • pancreatic fibrosis (MGI Ref ID J:99616)
    • periductal fibrosis

Cys1cpk/Cys1cpk

        D2J.B6(Cg)-Cys1cpk
  • renal/urinary system phenotype
  • enlarged kidney (MGI Ref ID J:99620)
    • kidneys are grossly enlarged
    • increased kidney weight (MGI Ref ID J:99620)
      • kidney wet weight is increased to 1.96g - 2.12g compared to 0.16g - 0.19g in wild-type mice
  • kidney cysts (MGI Ref ID J:99620)
    • multiple cysts of varying size that obscure the demarcation between the cortex and medulla
    • cysts become larger with age and are initially found in the proximal tubules epithelial intercellular spaces are often focally ballooned
  • homeostasis/metabolism phenotype
  • increased blood urea nitrogen level (MGI Ref ID J:99620)
    • mean BUN is 143mg% compared to 21mg% in wild-type mice
  • increased circulating creatinine level (MGI Ref ID J:99620)
    • mean creatinine is 0.66mg% compared to 0.23mg% in wild-type mice
  • endocrine/exocrine gland phenotype
  • abnormal exocrine pancreas morphology (MGI Ref ID J:99620)
    • poorly-formed acini are connected to enlarged, dilated ducts
    • exocrine cells containing zygomen granules are seen in clusters unassociated with well-formed acini
  • abnormal islet of Langerhans morphology (MGI Ref ID J:99620)
    • few if any well-formed islets are found
  • pancreatic fibrosis (MGI Ref ID J:99620)
    • normal architecture is replaced by sheets of fibrous tissue
  • liver/biliary system phenotype
  • abnormal bile duct morphology (MGI Ref ID J:99620)
    • bile ductules are somewhat enlarged
  • liver fibrosis (MGI Ref ID J:99620)
    • some portal areas have increased fibrous tissue
  • behavior/neurological phenotype
  • abnormal suckling behavior (MGI Ref ID J:99620)
    • feed poorly during the first few hours of life and generally fail to thrive
  • lethargy (MGI Ref ID J:99620)
  • digestive/alimentary phenotype
  • abnormal exocrine pancreas morphology (MGI Ref ID J:99620)
    • poorly-formed acini are connected to enlarged, dilated ducts
    • exocrine cells containing zygomen granules are seen in clusters unassociated with well-formed acini
  • abnormal islet of Langerhans morphology (MGI Ref ID J:99620)
    • few if any well-formed islets are found
  • pancreatic fibrosis (MGI Ref ID J:99620)
    • normal architecture is replaced by sheets of fibrous tissue

Cys1cpk/Cys1cpk

        129.B6-Cys1cpk
  • renal/urinary system phenotype
  • increased kidney weight (MGI Ref ID J:116210)
  • kidney cysts (MGI Ref ID J:116210)
  • liver/biliary system phenotype
  • liver inflammation (MGI Ref ID J:116210)
  • endocrine/exocrine gland phenotype
  • pancreatic cysts (MGI Ref ID J:116210)
  • immune system phenotype
  • liver inflammation (MGI Ref ID J:116210)
  • digestive/alimentary phenotype
  • pancreatic cysts (MGI Ref ID J:116210)
View Research Applications

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

Cys1cpk related

Developmental Biology Research
Internal/Organ Defects (kidney)

Internal/Organ Research
Kidney Defects (polycystic kidney disease)

Genes & Alleles

Gene & Allele Information

Allele Symbol Cys1cpk
Allele Name congenital polycystic kidneys
Allele Type Spontaneous
Common Name(s) ck; cpk;
Strain of OriginB6.Cg-Pldn
Gene Symbol and Name Cys1, cystin 1
Chromosome 12
Gene Common Name(s) 2900006B19Rik; AV218859; RIKEN cDNA 2900006B19 gene; ck; congenital polycystic kidneys; cpk; cystic kidneys; expressed sequence AV218859;
Molecular Note The underlying mutation responsible for the phenotype in the cpk mouse consists of a tandem deletion of 12 bp and 19 bp. The result is a frame-shift within exon 1 that truncates the protein. Northern analysis from kidney and liver revealed the presenceof transcript in homozygous mutant animals at reduced levels compared to wild-type. [MGI Ref ID J:74701]

Genotyping

Genotyping Information

Genotyping Protocols

Cys1cpk, STD PCR, vers. 1

Helpful Links

Optimizing PCR Protocols

References

References

Additional References

Woo D; Lee GY; Anderson E; Aziz N. 2001. Immature ovaries and polycystic kidneys in the congenital polycystic kidney mouse may be due to abnormal sex steroid metabolism. Mol Cell Endocrinol 176(1-2):155-62. [PubMed: 11369455]  [MGI Ref ID J:82596]

Cys1cpk related

Ali SM; Wong VY; Kikly K; Fredrickson TA; Keller PM; DeWolf WE Jr; Lee D; Brooks DP. 2000. Apoptosis in polycystic kidney disease: involvement of caspases. Am J Physiol Regul Integr Comp Physiol 278(3):R763-9. [PubMed: 10712299]  [MGI Ref ID J:114279]

Atencio IA; Villarreal LP. 1994. Polyomavirus replicates in differentiating but not in proliferating tubules of adult mouse polycystic kidneys. Virology 201(1):26-35. [PubMed: 8178487]  [MGI Ref ID J:17871]

Avner ED. 1993. Epithelial polarity and differentiation in polycystic kidney disease. J Cell Sci Suppl 17:217-22. [PubMed: 8144700]  [MGI Ref ID J:18532]

Aziz N; Anderson E; Lee GY; Woo DD. 2001. Arrested testis development in the cpk mouse may be the result of abnormal steroid metabolism. Mol Cell Endocrinol 171(1-2):83-8. [PubMed: 11165015]  [MGI Ref ID J:67183]

Aziz N; Brown D; Lee WS; Naray-Fejes-Toth A. 1996. Aberrant 11beta-hydroxysteroid dehydrogenase-1 activity in the cpk mouse: implications for regulation by the Ke 6 gene. Endocrinology 137(12):5581-8. [PubMed: 8940387]  [MGI Ref ID J:37226]

Aziz N; Maxwell MM; Brenner BM. 1994. Coordinate regulation of 11 beta-HSD and Ke 6 genes in cpk mouse: implications for steroid metabolic defect in PKD. Am J Physiol 267(5 Pt 2):F791-7. [PubMed: 7977782]  [MGI Ref ID J:21186]

Chiu MG; Johnson TM; Woolf AS; Dahm-Vicker EM; Long DA; Guay-Woodford L; Hillman KA; Bawumia S; Venner K; Hughes RC; Poirier F; Winyard PJ. 2006. Galectin-3 associates with the primary cilium and modulates cyst growth in congenital polycystic kidney disease. Am J Pathol 169(6):1925-38. [PubMed: 17148658]  [MGI Ref ID J:116210]

Cho H; Buchanan J; Strong D; Yamada Y; Yoo TJ. 1991. The molecular and structural basis of hearing impairment in mice with the cpk mutant gene. Ann N Y Acad Sci 630:262-4. [PubMed: 1952600]  [MGI Ref ID J:1001]

Davisson MT; Guay-Woodford LM; Harris HW; D'Eustachio P. 1991. The mouse polycystic kidney disease mutation (cpk) is located on proximal chromosome 12. Genomics 9(4):778-81. [PubMed: 2037305]  [MGI Ref ID J:11200]

Doctor RB; Johnson S; Brodsky KS; Amura CR; Gattone V; Fitz JG. 2007. Regulated ion transport in mouse liver cyst epithelial cells. Biochim Biophys Acta 1772(3):345-54. [PubMed: 17208416]  [MGI Ref ID J:121384]

Fry JL Jr; Koch WE; Jennette JC; McFarland E; Fried FA; Mandell J. 1985. A genetically determined murine model of infantile polycystic kidney disease. J Urol 134(4):828-33. [PubMed: 4032601]  [MGI Ref ID J:99620]

Gattone VH 2d; Andrews GK; Niu FW; Chadwick LJ; Klein RM; Calvet JP. 1990. Defective epidermal growth factor gene expression in mice with polycystic kidney disease. Dev Biol 138(1):225-30. [PubMed: 1968405]  [MGI Ref ID J:10330]

Gattone VH 2d; Calvet JP; Cowley BD Jr; Evan AP; Shaver TS; Helmstadter K; Grantham JJ. 1988. Autosomal recessive polycystic kidney disease in a murine model. A gross and microscopic description. Lab Invest 59(2):231-8. [PubMed: 3404974]  [MGI Ref ID J:9290]

Gattone VH 2nd; Lowden DA; Cowley BD Jr. 1995. Epidermal growth factor ameliorates autosomal recessive polycystic kidney disease in mice. Dev Biol 169(2):504-10. [PubMed: 7781894]  [MGI Ref ID J:26131]

Gattone VH 2nd; MacNaughton KA; Kraybill AL. 1996. Murine autosomal recessive polycystic kidney disease with multiorgan involvement induced by the cpk gene. Anat Rec 245(3):488-99. [PubMed: 8800407]  [MGI Ref ID J:33739]

Gattone VH 2nd; Maser RL; Tian C; Rosenberg JM; Branden MG. 1999. Developmental expression of urine concentration-associated genes and their altered expression in murine infantile-type polycystic kidney disease. Dev Genet 24(3-4):309-18. [PubMed: 10322639]  [MGI Ref ID J:54490]

Gattone VH; Ricker JL; Trambaugh CM; Klein RM. 2002. Multiorgan mRNA misexpression in murine autosomal recessive polycystic kidney disease. Kidney Int 62(5):1560-9. [PubMed: 12371956]  [MGI Ref ID J:104014]

Guay-Woodford LM. 2003. Murine models of polycystic kidney disease: molecular and therapeutic insights. Am J Physiol Renal Physiol 285(6):F1034-49. [PubMed: 14600027]  [MGI Ref ID J:87130]

Guay-Woodford LM; Green WJ; Lindsey JR; Beier DR. 2000. Germline and somatic loss of function of the mouse cpk gene causes biliary ductal pathology that is genetically modulated. Hum Mol Genet 9(5):769-78. [PubMed: 10749984]  [MGI Ref ID J:61399]

Harding MA; Chadwick LJ; Gattone VH 2d; Calvet JP. 1991. The SGP-2 gene is developmentally regulated in the mouse kidney and abnormally expressed in collecting duct cysts in polycystic kidney disease. Dev Biol 146(2):483-90. [PubMed: 1864465]  [MGI Ref ID J:11365]

Harding MA; Gattone VH 2d; Grantham JJ; Calvet JP. 1992. Localization of overexpressed c-myc mRNA in polycystic kidneys of the cpk mouse. Kidney Int 41(2):317-25. [PubMed: 1552705]  [MGI Ref ID J:543]

Hou X; Mrug M; Yoder BK; Lefkowitz EJ; Kremmidiotis G; D'Eustachio P; Beier DR; Guay-Woodford LM. 2002. Cystin, a novel cilia-associated protein, is disrupted in the cpk mouse model of polycystic kidney disease. J Clin Invest 109(4):533-40. [PubMed: 11854326]  [MGI Ref ID J:74701]

Lakshmanan J; Fisher DA. 1993. An inborn error in epidermal growth factor prohormone metabolism in a mouse model of autosomal recessive polycystic kidney disease. Biochem Biophys Res Commun 196(2):892-901. [PubMed: 8240367]  [MGI Ref ID J:15417]

Mandell J; Koch WK; Nidess R; Preminger GM; McFarland E. 1983. Congenital polycystic kidney disease. Genetically transmitted infantile polycystic kidney disease in C57BL/6J mice. Am J Pathol 113(1):112-4. [PubMed: 6624875]  [MGI Ref ID J:7202]

Mrug M; Zhou J; Woo Y; Cui X; Szalai AJ; Novak J; Churchill GA; Guay-Woodford LM. 2008. Overexpression of innate immune response genes in a model of recessive polycystic kidney disease. Kidney Int 73(1):63-76. [PubMed: 17960140]  [MGI Ref ID J:135367]

Nakamura T; Ebihara I; Fukui M; Osada S; Tomino Y; Masaki T; Goto K; Furuichi Y; Koide H. 1993. Increased endothelin and endothelin receptor mRNA expression in polycystic kidneys of cpk mice. J Am Soc Nephrol 4(4):1064-72. [PubMed: 7904485]  [MGI Ref ID J:18219]

Ogborn MR; Sareen S; Tomobe K; Takahashi H; Crocker JF. 1995. Renal tubule Na,K-ATPase polarity in different animal models of polycystic kidney disease. J Histochem Cytochem 43(8):785-90. [PubMed: 7622841]  [MGI Ref ID J:27468]

Ojeda JL. 1999. Abnormal tenascin expression in murine autosomal recessive polycystic kidneys. Nephron 82(3):261-9. [PubMed: 10395999]  [MGI Ref ID J:57379]

Orellana SA; Sweeney WE; Neff CD; Avner ED. 1995. Epidermal growth factor receptor expression is abnormal in murine polycystic kidney. Kidney Int 47(2):490-9. [PubMed: 7723235]  [MGI Ref ID J:23046]

Ostrom L; Tang MJ; Gruss P; Dressler GR. 2000. Reduced Pax2 gene dosage increases apoptosis and slows the progression of renal cystic disease. Dev Biol 219(2):250-8. [PubMed: 10694420]  [MGI Ref ID J:61157]

Preminger GM; Koch WE; Fried FA; McFarland E; Murphy ED; Mandell J. 1982. Murine congenital polycystic kidney disease: a model for studying development of cystic disease. J Urol 127(3):556-60. [PubMed: 7062441]  [MGI Ref ID J:6718]

Ribacchi R. 1975. [Congenital polycystic kidney in PM/Se mice] Lav Ist Anat Istol Patol Univ Studi Perugia 35(3):81-8. [PubMed: 1232513]  [MGI Ref ID J:15028]

Ricker JL; Gattone VH 2nd; Calvet JP; Rankin CA. 2000. Development of autosomal recessive polycystic kidney disease in BALB/c-cpk/cpk mice. J Am Soc Nephrol 11(10):1837-47. [PubMed: 11004214]  [MGI Ref ID J:99616]

Rocco MV; Neilson EG; Hoyer JR; Ziyadeh FN. 1992. Attenuated expression of epithelial cell adhesion molecules in murine polycystic kidney disease. Am J Physiol 262(4 Pt 2):F679-86. [PubMed: 1566881]  [MGI Ref ID J:574]

Russell ES; McFarland EC. 1977. Cystic kidneys, ck Mouse News Lett 56:40.  [MGI Ref ID J:31533]

Takahashi H; Calvet JP; Dittemore-Hoover D; Yoshida K; Grantham JJ; Gattone VH 2d. 1991. A hereditary model of slowly progressive polycystic kidney disease in the mouse. J Am Soc Nephrol 1(7):980-9. [PubMed: 1883968]  [MGI Ref ID J:11399]

Woo D; Lee GY; Anderson E; Aziz N. 2001. Immature ovaries and polycystic kidneys in the congenital polycystic kidney mouse may be due to abnormal sex steroid metabolism. Mol Cell Endocrinol 176(1-2):155-62. [PubMed: 11369455]  [MGI Ref ID J:82596]

Health & husbandry

Health & Colony Maintenance Information

Currently there no information available for this strain. This may be due to the supply level of this strain.

Purchasing information

Pricing, Supply Level & Notes, Controls, General Terms & Conditions

Pricing

Pricing for USA, Canada and Mexico shipping destinations View International pricing
Weeks of AgePrice*Gender
Cryorecovery Fee $1900.00
*Price(s) in US dollars ($)

Additional Supply Details

Pricing for International shipping destinations View USA Canada and Mexico pricing
Weeks of AgePrice*Gender
Cryorecovery Fee $2470.00
*Price(s) in US dollars ($)

Additional Supply Details

Supply Details

Standard SupplyRepository-Cryopreserved. Must Be Recovered. Please refer to pricing and supply notes for further information.
Supply Notes
  • Cryorecovery of Strains Needing Progeny Testing.
    The recovery process begins when a signed agreement form is returned to the Customer Service Department after order placement. Although results vary by strain, at least two untested males and two untested females (two pairs) will be recovered, typically within 15 weeks of our receipt of the signed agreement form. If the first recovery attempt is unsuccessful or only one pair is recovered, a second recovery will be done, extending the overall recovery time to approximately 25 weeks. However, all pups recovered will be sent.

    Progeny testing is required to identify the genotype of mice of this strain, as a genotyping assay is not available. This type of testing involves breeding the recovered animals and assessing the phenotype of the offspring in order to identify animals carrying the mutation of interest. We can perform the progeny testing for you as a service or we can ship all recovered animals (at least two untested pairs) to you for progeny testing at your facility. If you perform the progeny testing, there is NO guarantee that a carrier will be identified. If we perform progeny testing as a service, additional breeding time will be required. In this case, when a male and female (one pair) are identified that carry the mutation, they and their offspring will be shipped. Delivery time for strains requiring progeny testing often exceeds 25 weeks and may take 12 months or more due to the difficulties in breeding some strains. The progeny testing cost is in addition to the recovery cost and is based on the number of boxes used and the time taken to produce the mice identified as carrying the mutation. Please note that identified pairs may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation of the strain. Mating schemes are sometimes modified for successful cryopreservation. Please contact Customer Service for more information on the cost of progeny testing for a strain: Tel: 1-800-422-6423 or 1-207-288-5845.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice
    One to two pairs will be recovered to establish a Dedicated Supply of mice. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 or 1-207-288-5845.

  • 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
   Untyped from the colony
 
  Considerations for Choosing Controls
  USA, Canada and Mexico - Control Pricing Information for Genetically Engineered Mutant Strains.
  International - Control Pricing Information for Genetically Engineered Mutant Strains.

General Terms and Conditions


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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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Tel: 800.422.6423 or 207.288.5845
Fax: 207.288.6150
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Terms of Use

Terms of Use


General Terms and Conditions


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General inquiries

Contracts Administration

phone:207-288-6470
fax:207-288-6655

JAX® Mice & Services Conditions of Use

“Each recipient institution, including its employees and other researchers under its control (RECIPIENT), of mice or services using mice from The Jackson Laboratory (TJL) agrees that such mice, descendants of those mice derived by inbreeding or crossbreeding, including unmodified derivatives of those mice or their descendants (“MICE”) shall not be: (i) used for any purpose other than the internal research of the RECIPIENT, (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 with respect to MICE. Acceptance of MICE from TJL shall be deemed agreement by RECIPIENT to these conditions, and departure from these conditions requires The Jackson Laboratory’s prior written authorization.”

No Warranty

MICE, PRODUCTS AND SERVICES ARE PROVIDED “AS IS”. THE LABORATORY 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.

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, The Jackson Laboratory will, at its option, provide credit or replacement for the MICE or product received or the services provided.

No Liability

In no event shall The Jackson Laboratory, 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 The Jackson Laboratory, its agents or employees. In purchasing or receiving MICE, products or services from The Jackson Laboratory, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges The Jackson Laboratory from all such causes of action or damages, and further agrees to defend and indemnify The Jackson Laboratory from any costs or damages arising out of any third party claims.

MICE and biological materials 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 The Jackson Laboratory’s MICE, products and services. In addition, special terms and conditions of sale of certain MICE, products and services may be set forth separately in The Jackson Laboratory 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 The Jackson Laboratory, 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 The Jackson Laboratory, 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 services by The Jackson Laboratory.


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