B6Rcc.Cg-Spp1tm1Rit ApcMin/Cnrm

Status

Available to order

EMMA IDEM:02002
International strain nameB6Rcc.Cg-Spp1tm1Rit ApcMin/Cnrm
Alternative nameC57 BL/6RCC Min/+ OPN-/-
Strain typeTargeted Mutant Strains : Knock-out
Allele/Transgene symbolSpp1tm1Rit,
Gene/Transgene symbolSpp1

Information from provider

ProviderUrsula Günthert
Provider affiliationInstitut für Pathologie, University of Basel
Genetic informationEthylnitrosurea induced mutation. A transversion point mutation in the Apc (adenomatosis polyposis coli) gene that alters nucleotide 2549 from a T to an A and converts codon 850 from one encoding a leucine to a stop codon, generating the mutant allele ApcMin (adenomatosis polyposis coli; multiple intestinal neoplasia). The neomycin cassette from pMC1neo was inserted into the EagI site in exon 6 of the Spp1 (secreted phosphoprotein 1; formerly: Opn, osteopontin) gene (a 4.8 kb fragment from 129 mice), that had been cloned into pBluescript (Rittling et al., 1998).
Phenotypic informationMin/+: development of early stages of colon carcinoma: polyps. Opn (Spp1) -/-: influence on colon carcinoma not known.
References
  • A dominant mutation that predisposes to multiple intestinal neoplasia in the mouse.;Moser A R, Pitot H C, Dove W F, ;1990;Science (New York, N.Y.);247;322-4; 2296722
  • Mice lacking osteopontin show normal development and bone structure but display altered osteoclast formation in vitro.;Rittling S R, Matsumoto H N, McKee M D, Nanci A, An X R, Novick K E, Kowalski A J, Noda M, Denhardt D T, ;1998;Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research;13;1101-11; 9661074

Information from EMMA

Archiving centreCNR, Consiglio Nazionale delle Ricerche, Monterotondo, Italy

Disease and phenotype information

Orphanet associated rare diseases, based on orthologous gene matching

MGI phenotypes (allele matching)
  • abnormal mammary gland development / MGI
  • abnormal ovarian folliculogenesis / MGI
  • abnormal ovarian follicle morphology / MGI
  • absent mature ovarian follicles / MGI
  • absent corpus luteum / MGI
  • abnormal vagina epithelium morphology / MGI
  • decreased body weight / MGI
  • increased incidence of induced tumors / MGI
  • ovary atrophy / MGI
  • uterus atrophy / MGI
  • reproductive system phenotype / MGI
  • adrenal gland hyperplasia / MGI
  • absent nipple / MGI
  • increased mammary gland tumor incidence / MGI
  • mammary gland hyperplasia / MGI
  • anemia / MGI
  • premature death / MGI
  • increased intestinal adenoma incidence / MGI
  • increased intestinal adenocarcinoma incidence / MGI
  • abnormal pregnancy / MGI
  • extended life span / MGI
  • aneuploidy / MGI
  • increased incidence of tumors by chemical induction / MGI
  • decreased intestinal adenoma incidence / MGI
  • decreased hematocrit / MGI
  • hyperlipidemia / MGI
  • melena / MGI
  • rectal prolapse / MGI
  • abnormal intestinal mucosa morphology / MGI
  • increased mammary adenocarcinoma incidence / MGI
  • intestinal obstruction / MGI
  • abnormal intestinal goblet cell morphology / MGI
  • abnormal large intestine crypts of Lieberkuhn morphology / MGI
  • intestine polyps / MGI
  • abnormal enterocyte proliferation / MGI
  • decreased T cell number / MGI
  • decreased NK cell number / MGI
  • decreased splenocyte number / MGI
  • neoplasm / MGI
  • increased circulating triglyceride level / MGI
  • increased circulating free fatty acid level / MGI
  • postnatal growth retardation / MGI
  • increased colonic adenoma incidence / MGI
  • hepatic steatosis / MGI
  • decreased macrophage cell number / MGI
  • increased prostaglandin level / MGI
  • abnormal embryo development / MGI
  • abnormal embryo size / MGI
  • abnormal egg cylinder morphology / MGI
  • abnormal cell physiology / MGI
  • embryonic lethality, complete penetrance / MGI
  • decreased embryo size / MGI
  • embryonic lethality between implantation and placentation / MGI
  • absent mandible / MGI
  • abnormal brain development / MGI
  • acrania / MGI
  • perinatal lethality, complete penetrance / MGI
  • lethality throughout fetal growth and development, incomplete penetrance / MGI
  • absent midbrain / MGI
  • absent forebrain / MGI
  • abnormal liver morphology / MGI
  • decreased acute inflammation / MGI
  • decreased tumor necrosis factor secretion / MGI
  • decreased interferon-gamma secretion / MGI
  • decreased physiological sensitivity to xenobiotic / MGI
  • increased bone mineral density / MGI
  • abnormal osteoclast physiology / MGI
  • abnormal cardiovascular system physiology / MGI
  • abnormal inflammatory response / MGI
  • decreased susceptibility to viral infection / MGI
  • dilated renal tubules / MGI
  • decreased heart weight / MGI
  • delayed wound healing / MGI
  • nervous system phenotype / MGI
  • abnormal physiological neovascularization / MGI
  • renal tubular necrosis / MGI
  • increased osteoclast cell number / MGI
  • decreased osteoclast cell number / MGI
  • decreased bone resorption / MGI
  • abnormal osteoblast physiology / MGI
  • abnormal response to infection / MGI
  • decreased cardiac muscle contractility / MGI
  • increased susceptibility to injury / MGI
  • skeleton phenotype / MGI
  • hyporesponsive to tactile stimuli / MGI
  • increased circulating creatinine level / MGI
  • increased blood urea nitrogen level / MGI
  • decreased susceptibility to type IV hypersensitivity reaction / MGI
  • increased interleukin-10 secretion / MGI
  • decreased interleukin-12 secretion / MGI
  • increased interleukin-4 secretion / MGI
  • decreased sensitivity to induced cell death / MGI
  • increased trabecular bone thickness / MGI
  • mortality/aging / MGI
  • decreased fibroblast chemotaxis / MGI
  • increased bone marrow cell number / MGI
  • abnormal blood cell morphology/development / MGI
  • abnormal bone mineralization / MGI
  • increased hematopoietic stem cell number / MGI
  • increased sensitivity to induced morbidity/mortality / MGI

Literature references

  • A dominant mutation that predisposes to multiple intestinal neoplasia in the mouse.;Moser A R, Pitot H C, Dove W F, ;1990;Science (New York, N.Y.);247;322-4; 2296722
  • Mice lacking osteopontin show normal development and bone structure but display altered osteoclast formation in vitro.;Rittling S R, Matsumoto H N, McKee M D, Nanci A, An X R, Novick K E, Kowalski A J, Noda M, Denhardt D T, ;1998;Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research;13;1101-11; 9661074

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Order

Availabilities

Requesting frozen sperm or embryos is generally advisable wherever possible, in order to minimise the shipment of live mice.

  • Frozen embryos. Delivered in 4 weeks (after paperwork in place). €1740*
  • Rederivation of mice from frozen stock, delivery time available upon request . €3880*

Due to the dynamic nature of our processes strain availability may change at short notice. The local repository manager will advise you in these circumstances.

* In addition users have to cover all the shipping costs (including the cost for returning dry-shippers, where applicable).

More details on pricing and delivery times

Practical information

Example health report
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Material Transfer Agreement (MTA)
For this strain no provider MTA is needed. Distribution is based on the EMMA conditions only.

EMMA conditions
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