Overview

This LSL-KrasG12D strain carries a point mutation (G12D) in the Kras (v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog) gene whose expression is blocked by the presence of a loxP-flanked stop codon. Homozygotes die in utero. Cre-mediated recombination can excise the stop codon and permit the oncogenic protein to be expressed. Intranasal infection with an adenovirus encoding Cre results in a very high frequency of lung tumors and permits controlled timing of tumor initiation and tumor multiplicity. This strain may be useful in studies of cancer and development.

Donating Investigator

Terry Van Dyke, NIH

Genetic overview

Genetic Background	Generation

Kras^tm4Tyj

Allele Type	Gene Symbol	Gene Name
Targeted (Conditional ready (e.g. floxed), No functional change)	Kras	Kirsten rat sarcoma viral oncogene homolog

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Research Applications

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Details

Detailed Description

This strain carries a point mutation (G12D) whose expression is blocked by the presence of a loxP-flanked stop codon. Homozygotes die in utero. Cre-mediated recombination can excise the stop codon and permit the oncogenic protein to be expressed. Intranasal infection with an adenovirus encoding Cre results in a very high frequency of lung tumors and permits controlled timing of tumor initiation and tumor multiplicity. This strain may be useful in studies of cancer and development.

In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.

Development

A targeting vector was designed to place a G12D point mutation in exon 1 of the gene and a loxP-flanked STOP element upstream of the mutation. The STOP element incorporates a PGK-puromycin selection cassette at the 5' end in an opposite directional orientation. An adenoviral strong splice acceptor, typically used in gene trap vectors, is fused upstream of the his3 stuffer fragment to prevent splicing around the stopper (in the case that transcription isn't completely silenced). A mutant splice donor site is on the 3' end and a tetrameric tandem array of SV40 PolyA. The stopper was designed to fit into genomic Sal1 or Xho1 sites. The stop cassette prevents the expression of mutant Kras until it is removed by Cre mediated recombination of the Loxp sites, thus allowing expression of oncogenic Kras. The construct was electroporated into 129S4/SvJae-derived J1 embryonic stem (ES) cells. The mice were backcrossed to C57BL/6 for approximately 15 generations (NCI) and then backcrossed to C57BL/6NCr for 19 generations. Upon arrival at The Jackson Laboratory, the mice were crossed to C57BL/6NJ (Stock No. 005304) at least once to establish the colony.

Control Suggestions

Wild-type from the colony
005304 C57BL/6NJ

Additional Information

Considerations for Choosing Controls

Selected References

Jackson EL; Willis N; Mercer K; Bronson RT; Crowley D; Montoya R; Jacks T; Tuveson DA. 2001. Analysis of lung tumor initiation and progression using conditional expression of oncogenic K-ras. Genes Dev 15(24):3243-8PubMed: 11751630 MGI: J:73445

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Genetics

Kras^tm4Tyj

Allele Symbol: Kras^tm4Tyj

Allele Name	targeted mutation 4, Tyler Jacks
Allele Type	Targeted (Conditional ready (e.g. floxed), No functional change)
Allele Synonym(s)	targeted mutation 4, Tyler Jacks; Kras^tm4Tyj
Gene Symbol and Name	Kras, Kirsten rat sarcoma viral oncogene homolog
Gene Synonym(s)	C-K-RAS; RASK2; CFC2; NS; KRAS1; AI929937; Kras-2; Kras2; Kras-2; KRAS2; Kirsten rat sarcoma oncogene 2, expressed; KI-RAS; NS3; K-ras; K-RAS2B; K-RAS4A; K-RAS4B; K-RAS2A; expressed sequence AI929937; c-Ki-ras; p21; Kras2; Ki-ras; RALD; c-Ki-ras2; K-Ras; OES
Strain of Origin	129S4/SvJae
Chromosome	6
Molecular Note	By homologous recombination in ES cells, the Kras2 locus was targeted with a cassette containing an oncogenic form of the KRAS2 protein in which the glycine at position 12 had been substituted with a an aspartic acid. A loxP flanked stop codon was included upstream of the inserted Kras2 sequence, such that the mutant transcript would be expressed only after cre-mediated recombination.
Mutations Made By	Dr. Tyler Jacks, Massachusetts Institute of Technology

Disease/Phenotype

Disease Terms

Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).

lung cancer

Model with phenotypic similarity to human disease where etiologies are distinct. Human genes are associated with this disease. Orthologs of these genes do not appear in the mouse genotype(s).

juvenile myelomonocytic leukemia

Characteristics of this human disease are associated with transgenes and other mutation types in the mouse.

Models with phenotypic similarity to human diseases where etiology is unknown or involving genes where ortholog is unknown.

endometriosis

No similarity to the expected human disease phenotype was found. One or more human genes are associated with this human disease. The mouse genotype may involve mutations to orthologs of one or more of these genes, but the phenotype did not resemble the disease.

acute myeloid leukemia

Research Areas By Genotype

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

Mammalian Phenotype Terms by Genotype

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

Genotype: Kras^tm4Tyj/Kras⁺ Tg(Mx1-cre)1Cgn/0
involves: 129S4/SvJae * BALB/c * C57BL/6 * CBA

digestive/alimentary phenotype

increased esophageal papilloma incidence
- 8 of 22 mice injected with pIpC develop squamous papillomas involving the esophageal mucosa

increased oral papilloma incidence
- 2 of 6 non-pIpC treated mice show oral squamous papillomas
- 8 of 25 mice injected with pIpC develop squamous papillomas involving the oral mucosa

immune system phenotype

abnormal myelopoiesis
- 4-7 week old mice injected with pIpC develop a myeloproliferative disorder
- all mice that are not treated with pIpC also develop a hematopoietic disease, however these mice exhibit expression of the mutant Kras, indicating that most likely endogenous IFN expression is sufficient to induce the cre transgene
- bone marrow cells from pIpC injected mice readily form colonies, predominately monocyte colony-forming units (M-CFUs) in a growth factor-independent manner unlike controls
- bone marrow of mice injected with pIpC shows myelomonocytic expansion

enlarged spleen
- mice injected with pIpC develop moderate to severe splenomegaly

increased granulocyte number
- leukocytosis in mice injected with pIpC is mainly due to an increase in granulocyte population

increased leukocyte cell number
- leukocytosis, usually involving increases in granulocytes, in both pIpC and non-pIpC treated mice

increased spleen red pulp amount
- mice injected with pIpC show expansion of the red pulp by varying degrees of granulocytic

lymphoid hyperplasia
- 6 of 17 mice injected with pIpC develop nodal lymphoid hyperplasia

myeloid hyperplasia
- myeloid hyperplasia of bone marrow
- myeloproliferative phenotype

integument phenotype

increased skin papilloma incidence
- 12 of 19 mice injected with pIpC develop squamous papillomas involving the anal and vulvo-vaginal skin and 8 of 22 mice develop squamous papillomas involving the ear
- 2 of 6 non-pIpC treated mice show ear squamous papillomas

ruffled hair
- ruffled fur

liver/biliary system phenotype

abnormal hepatobiliary system morphology
- perivascular and periportal infiltration in liver by myeloid and erythroid cells similar to what is seen in spleen

mortality/aging

premature death
- survival for around 35 days after pI-pC treatment
- survival of around 58 days even without pI-pC treatment

endocrine/exocrine gland phenotype

increased lymphoblastic lymphoma incidence
- 2 of 6 non pIpC treated mice show thymic lymphomas
- 7 of 25 mice injected with pIpC develop thymic T cell lymphoblastic lymphomas

neoplasm

increased esophageal papilloma incidence
- 8 of 22 mice injected with pIpC develop squamous papillomas involving the esophageal mucosa

increased lung adenoma incidence
- 10 of 17 mice injected with pIpC exhibit multiple nodules in the lungs consisting of proliferating type II penumocytes
- 5 of 6 non pIpC treated mice show pulmonary adenomas

increased lymphoblastic lymphoma incidence
- 2 of 6 non pIpC treated mice show thymic lymphomas
- 7 of 25 mice injected with pIpC develop thymic T cell lymphoblastic lymphomas

increased oral papilloma incidence
- 2 of 6 non-pIpC treated mice show oral squamous papillomas
- 8 of 25 mice injected with pIpC develop squamous papillomas involving the oral mucosa

increased papilloma incidence
- squamous papillomas

increased skin papilloma incidence
- 12 of 19 mice injected with pIpC develop squamous papillomas involving the anal and vulvo-vaginal skin and 8 of 22 mice develop squamous papillomas involving the ear
- 2 of 6 non-pIpC treated mice show ear squamous papillomas

respiratory system phenotype

increased lung adenoma incidence
- 10 of 17 mice injected with pIpC exhibit multiple nodules in the lungs consisting of proliferating type II penumocytes
- 5 of 6 non pIpC treated mice show pulmonary adenomas

growth/size/body region phenotype

cachexia
- becoming emaciated

hematopoietic system phenotype

abnormal definitive hematopoiesis
- develop lethal hematopoietic disease

abnormal erythrocyte morphology

abnormal myelopoiesis
- 4-7 week old mice injected with pIpC develop a myeloproliferative disorder
- all mice that are not treated with pIpC also develop a hematopoietic disease, however these mice exhibit expression of the mutant Kras, indicating that most likely endogenous IFN expression is sufficient to induce the cre transgene
- bone marrow cells from pIpC injected mice readily form colonies, predominately monocyte colony-forming units (M-CFUs) in a growth factor-independent manner unlike controls
- bone marrow of mice injected with pIpC shows myelomonocytic expansion

anemia
- mice injected with pIpC become anemic

decreased hematocrit
- mice injected with pIpC have a mean hematocrit of 27% compared with 45% in controls

enlarged spleen
- mice injected with pIpC develop moderate to severe splenomegaly

extramedullary hematopoiesis
- erythroid expansion was seen in red pulp of spleen in 5 of 16 cases
- expansion of red pulp in spleen by granulocyte/monocyte lineages in 11 out of 16 cases
- the liver shows perivascular and periportal infiltration by myeloid and erythroid cell populations

increased granulocyte number
- leukocytosis in mice injected with pIpC is mainly due to an increase in granulocyte population

increased leukocyte cell number
- leukocytosis, usually involving increases in granulocytes, in both pIpC and non-pIpC treated mice

increased spleen red pulp amount
- mice injected with pIpC show expansion of the red pulp by varying degrees of granulocytic

myeloid hyperplasia
- myeloid hyperplasia of bone marrow
- myeloproliferative phenotype

Genotype: Kras^tm4Tyj/Kras⁺ Tg(MMTV-cre)4Mam/0
involves: 129S4/SvJae * FVB

digestive/alimentary phenotype

submandibular gland hyperplasia
- submandibular gland hyperplasia is seen in mutant mice

endocrine/exocrine gland phenotype

submandibular gland hyperplasia
- submandibular gland hyperplasia is seen in mutant mice

Genotype: Kras^tm4Tyj/Kras⁺ Tg(Prm-cre)58Og/0
involves: 129S4/SvJae

cardiovascular system phenotype

abnormal placental labyrinth vasculature morphology
- fetal blood vessels underlying inner labyrinth layer are absent

absent vitelline blood vessels
- at E9.5 vasculature is poorly developed; vasculature has a primitive honeycomb-like network lacking branching vitelline vessels, while large vitelline vessels are absent

mortality/aging

embryonic lethality during organogenesis, complete penetrance
- mutants die between E9.5 and 11.5

cellular phenotype

increased embryonic tissue cell apoptosis
- at death, embryos exhibit widespread apoptosis

embryo phenotype

abnormal placenta labyrinth morphology
- marked defect in inner labyrinth layer is observed at E9.5

abnormal placental labyrinth vasculature morphology
- fetal blood vessels underlying inner labyrinth layer are absent

absent vitelline blood vessels
- at E9.5 vasculature is poorly developed; vasculature has a primitive honeycomb-like network lacking branching vitelline vessels, while large vitelline vessels are absent

embryonic growth arrest
- embryos show developmental arrest

increased embryonic tissue cell apoptosis
- at death, embryos exhibit widespread apoptosis

pale yolk sac
- at E9.5, yolk sacs are pale and roughened

Genotype: Kras^tm4Tyj/Kras⁺ Tg(Tek-cre)12Flv/0
involves: 129S4/SvJae * C3H * C57BL/6

mammalian phenotype

embryo phenotype
- mutants show normal vascularization of the yolk sac and placental labyrinth

Genotype: Kras^tm4Tyj/Kras⁺ Tg(SFTPC-rtTA)5Jaw/0 Tg(tetO-cre)1Jaw/0
involves: 129/Sv * C57BL/6

mortality/aging

postnatal lethality, complete penetrance
- death in the early postnatal period

respiratory system phenotype

abnormal branching involved in lung morphogenesis
- at E16.5, lungs show even more severe defects than in Kras:Meox2-cre embryos, with large epithelial-lined pouches in place of finely branched network of airways seen in wild-type
- branching defect persists through late gestation leading to early postnatal lethality
- with doxycycline treatment beginning at E6.5, a dramatic lung branching defect is observed

abnormal bronchus epithelium morphology
- markers of ciliated and Clara cells in the bronchi are significantly reduced at E18.5 compared to controls, indicating block in differentiation of lung epithelium

abnormal lung epithelium morphology
- branching defect originates in epithelium rather than mesenchyme

Genotype: Kras^tm4Tyj/Kras⁺ Meox2^tm1(cre)Sor/Meox2⁺
involves: 129S4/SvJae * 129S4/SvJaeSor

cardiovascular system phenotype

abnormal atrioventricular valve morphology
- atrioventricular valve malformations

abnormal cardiovascular system physiology
- heart defects lead to heart failure and death in embryos by ~E14.5

conotruncal ridge hyperplasia
- excess cushion tissue often leads to obstructed outflow tract

double outlet right ventricle
- at E13.5, embryos frequently show double outlet right ventricle

hemorrhage
- embryos appear normal at E12.5, but rapidly develop peripheral hemorrhages by E13.5, consistent with heart failure

ventricular septal defect
- all embryonic hearts have prominent septal defects

homeostasis/metabolism phenotype

edema
- embryos appear normal at E12.5, but rapidly develop edema by E13.5, consistent with heart failure

integument phenotype

pallor
- embryos appear normal at E12.5, but rapidly develop pallor by E13.5, consistent with heart failure

liver/biliary system phenotype

increased hepatocyte apoptosis
- at E12.5 fetal livers show large areas of apoptosis

liver hypoplasia
- at E12.5, fetal livers appear hypocellular

mammalian phenotype

embryo phenotype
- mutants show normal vascularization of the yolk sac and placental labyrinth

mortality/aging

embryonic lethality during organogenesis, incomplete penetrance
- embryos are recovered at a lower frequency (15% vs expected 25%) at E13.5

lethality throughout fetal growth and development, complete penetrance
- homozygous embryos die by E14.5

respiratory system phenotype

abnormal branching involved in lung morphogenesis
- decrease in branching is associated with formation of large, fluid-filled sacs rather than normal terminal branches
- defects in lung branching are apparent by E11.5 compared to controls in vivo and in cultured lungs

abnormal bronchus morphology
- at E12.5, lungs exhibit large dilated bronchi; defect is more pronounced at E14.5

dilated respiratory conducting tubes
- at E12.5, lungs exhibit large dilated bronchi; defect is more pronounced at E14.5

impaired branching involved in bronchus morphogenesis
- at E12.5, mutant lungs exhibit large dilated bronchi whereas wild-type lungs show secondary and tertiary bronchi
- at E14.5, mutants lungs display dilated bronchi and only a few terminal bronchi

impaired branching involved in terminal bronchiole morphogenesis
- at E14.5, mutants lungs display only a few terminal bronchioles

cellular phenotype

increased hepatocyte apoptosis
- at E12.5 fetal livers show large areas of apoptosis

embryo phenotype

abnormal embryonic erythropoiesis
- fetal-derived hematopoietic progenitors form larger CFU-E (colony-forming unit-erythroid) and BFU-E (burst-forming unit-erythroid) colonies compared with controls

hematopoietic system phenotype

abnormal embryonic erythrocyte morphology
- red blood cells appear immature compared to wild-type and occasionally highly atypical, consisten with a block in erythroid differentiation

abnormal embryonic erythropoiesis
- fetal-derived hematopoietic progenitors form larger CFU-E (colony-forming unit-erythroid) and BFU-E (burst-forming unit-erythroid) colonies compared with controls

Genotype: Kras^tm4Tyj/Kras⁺
involves: 129S4/SvJae

neoplasm

increased lung adenocarcinoma incidence
- a few adenocarcinomas develop in mice following Ad-Cre administration
- in cre adenovirus-treated mice

increased lung adenoma incidence
- mice develop lung adenomas with a few adenocarcinomas following intratracheal administration of an adenovirus expressing Cre (Ad-Cre)
- treatment with MLN4924, a small molecular inhibitor of NAE, beginning at 13 weeks after Ad-Cre administration reduces tumor burden, with a reduction in both number of hyperplastic areas and adenomas and size of the tumors
- presence of atypical adenomatous hyperplasia after Cre-adenovirus treatment

increased lung tumor incidence
- 20% and 100% of mice develop lung lesions at 6 weeks and 20 weeks, respectively, post intranasal adenoviral cre administration
- treatment with adenoviral Cre to induce oncogenic Kras expression results in lung tumor development, but causes a lower tumor burden and decreased overall tumor area compared to induced mutants on a Spry2-null background
- cre adenovirus-treated mice develop fewer tumors than in Kras^tm4Tyj/Kras⁺ Rb1^tm3Tyj/Rb1^tm3Tyj mice
- cre adenovirus-treated mice develop lung adenocarcinomas, papillary adenomas and bronchiolar hyperplasia and dysplasia
- large tumors easily visible on the surface of the lungs at eight weeks after Cre-adenovirus treatment
- mice treated with adenovirus cre develop lung lesions in 4 to 6 months

abnormal tumor morphology
- tumors from cre adenovirus-treated mice exhibit increased cell proliferation compared to in tumors from Kras^tm4Tyj/Kras⁺ Rbl2^tm2Tyj/Rbl2^tm2Tyj mice

decreased tumor growth/size
- cre adenovirus-treated mice develop smaller tumors than in cre adenovirus-treated Kras^tm4Tyj/Kras⁺ Rbl2^tm2Tyj/Rbl2^tm2Tyj mice

increased lung carcinoma incidence
- the most common lesion is adenocarcinoma after Cre-adenovirus treatment

hematopoietic system phenotype

increased regulatory T cell number
- following injection of a cre adenovirus in the ovarian bursa, mice with endometriosis also exhibit an increase in spleen and regional lymph nodes T regulatory cells compared with un-injected Kras^tm4Tyj Tg(MUC1)79.24Gend mice

reproductive system phenotype

uterus adenomyosis
- following injection of a cre adenovirus in the ovarian bursa, mice develop ovarian lesions consisting of endometrial glandular epithelium unlike un-injected Kras^tm4Tyj micefollowing injection of a cre adenovirus in the ovarian bursa, mice develop ovarian lesions consisting of endometrial glandular epithelium unlike un-injected Kras^tm4Tyj mice
- op ovarian lesions consisting of endometrial glandular epithelium unlike un-injected Kras^tm4Tyj mice

immune system phenotype

increased regulatory T cell number
- following injection of a cre adenovirus in the ovarian bursa, mice with endometriosis also exhibit an increase in spleen and regional lymph nodes T regulatory cells compared with un-injected Kras^tm4Tyj Tg(MUC1)79.24Gend mice

mortality/aging

premature death
- median life span of cre adenovirus-treated mice is 32 weeks

respiratory system phenotype

increased lung adenocarcinoma incidence
- a few adenocarcinomas develop in mice following Ad-Cre administration
- in cre adenovirus-treated mice

increased lung adenoma incidence
- mice develop lung adenomas with a few adenocarcinomas following intratracheal administration of an adenovirus expressing Cre (Ad-Cre)
- treatment with MLN4924, a small molecular inhibitor of NAE, beginning at 13 weeks after Ad-Cre administration reduces tumor burden, with a reduction in both number of hyperplastic areas and adenomas and size of the tumors
- presence of atypical adenomatous hyperplasia after Cre-adenovirus treatment

increased lung tumor incidence
- 20% and 100% of mice develop lung lesions at 6 weeks and 20 weeks, respectively, post intranasal adenoviral cre administration
- treatment with adenoviral Cre to induce oncogenic Kras expression results in lung tumor development, but causes a lower tumor burden and decreased overall tumor area compared to induced mutants on a Spry2-null background
- cre adenovirus-treated mice develop fewer tumors than in Kras^tm4Tyj/Kras⁺ Rb1^tm3Tyj/Rb1^tm3Tyj mice
- cre adenovirus-treated mice develop lung adenocarcinomas, papillary adenomas and bronchiolar hyperplasia and dysplasia
- large tumors easily visible on the surface of the lungs at eight weeks after Cre-adenovirus treatment
- mice treated with adenovirus cre develop lung lesions in 4 to 6 months

abnormal bronchiole morphology
- cre adenovirus-treated mice develop bronchiolar hyperplasia and dysplasia unlike wild-type mice

bronchiolar epithelial hyperplasia
- in cre adenovirus-treated mice

increased lung carcinoma incidence
- the most common lesion is adenocarcinoma after Cre-adenovirus treatment

lung epithelium hyperplasia
- presence of epithelial hyperplasia after Cre-adenovirus treatment

thick pulmonary interalveolar septum
- in cre adenovirus-treated mice

Genotype: Kras^tm4Tyj/Kras⁺ Lyz2^tm1(cre)Ifo/Lyz2⁺
involves: 129P2/OlaHsd * 129S4/SvJae

mortality/aging

postnatal lethality, complete penetrance
- the maximum survival is 24 days

neoplasm

increased lung tumor incidence

respiratory system phenotype

increased lung tumor incidence

increased lung weight
- lung weight is 10-fold higher than that in control mice at 3 weeks old

Genotype: Kras^tm4Tyj/Kras⁺ Tg(Tyr-cre/ERT2)13Bos/0
involves: 129S4/SvJae * FVB

neoplasm

increased melanoma incidence
- 1 in 14 tamoxifen treated mice develops melanoma with a median tumor latency greater than 52 weeks

pigmentation phenotype

abnormal melanocyte morphology
- tamoxifen-treated mice exhibit melanocytic proliferation unlike wild-type mice

hyperpigmentation
- tamoxifen-treated mice develop pigmented macules in the paws and tail unlike wild-type mice

Genotype: Kras^tm4Tyj/Kras⁺
either: (involves: 129S4/SvJae) or (involves: 129S4/SvJae * C3H/HeJ)

endocrine/exocrine gland phenotype

abnormal ovary morphology
- after ovarian intrabursal injection of an adenovirus expressing Cre, mutants develop benign ovarian endometriosis-like lesions, however no invasive ovarian tumors are seen up to 10 months following adenoviral injection

growth/size/body region phenotype

abnormal peritoneum morphology
- 47% of mutants develop peritoneal endometriosis following ovarian intrabursal injection of an adenovirus expressing Cre
- Normal - however, mice injected with adenovirus expressing Cre directly into the peritoneum do not develop peritoneal endometriosis

reproductive system phenotype

abnormal ovary morphology
- after ovarian intrabursal injection of an adenovirus expressing Cre, mutants develop benign ovarian endometriosis-like lesions, however no invasive ovarian tumors are seen up to 10 months following adenoviral injection

Genotype: Kras^tm4Tyj/Kras⁺ Tg(Gfap-cre)77.6Mvs/0
involves: 129 * BALB/c * C57BL/6NHsd

mammalian phenotype

neoplasm
- Normal - mutants do not develop tumors

Genotype: Kras^tm4Tyj/Kras⁺ Tg(Krt1-15-cre/PGR)22Cot/0
involves: 129S4/SvJae * C57BL/6J * SJL/J

craniofacial phenotype

increased facial tumor incidence
- 2-4 months following RU486 treatment, tumors develop in the face in 35% of treated mutants

increased lip tumor incidence
- 2-4 months following RU486 treatment, lip tumors develop in 57% of treated mice

growth/size/body region phenotype

increased facial tumor incidence
- 2-4 months following RU486 treatment, tumors develop in the face in 35% of treated mutants

increased lip tumor incidence
- 2-4 months following RU486 treatment, lip tumors develop in 57% of treated mice

integument phenotype

increased skin papilloma incidence
- double mutants not treated with tamoxifen develop some papillomas but with increased latency (>6 months)
- skin tumors are benign papillomas with no sign of malignant transformtion seen up to 4 months after treatment with RU486

increased skin tumor incidence
- 2-4 months following RU486 treatment, tumors develop in the back skin in 14% of treated mice

neoplasm

increased facial tumor incidence
- 2-4 months following RU486 treatment, tumors develop in the face in 35% of treated mutants

increased lip tumor incidence
- 2-4 months following RU486 treatment, lip tumors develop in 57% of treated mice

increased skin papilloma incidence
- double mutants not treated with tamoxifen develop some papillomas but with increased latency (>6 months)
- skin tumors are benign papillomas with no sign of malignant transformtion seen up to 4 months after treatment with RU486

increased skin tumor incidence
- 2-4 months following RU486 treatment, tumors develop in the back skin in 14% of treated mice

Genotype: Kras^tm4Tyj/Kras⁺ Shh^{tm2(cre/ERT2)Cjt}/Shh⁺
involves: 129S4/SvJae * 129S6/SvEvTac

mammalian phenotype

integument phenotype
- Normal - no epidermal defects or tumor formation are observed with tamoxifen treatment at day 28 (during period of up to 4 months after cre induction) when hair follicles are in full anlagen

Genotype: Kras^tm4Tyj/Kras⁺
B6.129S4-Kras

mortality/aging

premature death
- mutants with an intranasal instillation of an adenovirus expressing Cre recombinase have a median survival of 79 days

neoplasm

increased lung adenocarcinoma incidence
- ction
- mutants with an intranasal instillation of an adenovirus expressing Cre recombinase develop noninvasive adenoma and adenocarcinoma over a 6-10 week period, characterized by epithelial cell proliferation without destruction of alveolar walls or stromal reaction

increased lung adenoma incidence
- ction
- mutants with an intranasal instillation of an adenovirus expressing Cre recombinase develop noninvasive adenoma and adenocarcinoma over a 6-10 week period, characterized by epithelial cell proliferation without destruction of alveolar walls or stromal reaction

respiratory system phenotype

increased lung adenocarcinoma incidence
- ction
- mutants with an intranasal instillation of an adenovirus expressing Cre recombinase develop noninvasive adenoma and adenocarcinoma over a 6-10 week period, characterized by epithelial cell proliferation without destruction of alveolar walls or stromal reaction

increased lung adenoma incidence
- ction
- mutants with an intranasal instillation of an adenovirus expressing Cre recombinase develop noninvasive adenoma and adenocarcinoma over a 6-10 week period, characterized by epithelial cell proliferation without destruction of alveolar walls or stromal reaction

Genotype: Kras^tm4Tyj/Kras⁺ Speer6-ps1^{Tg(Alb-cre)21Mgn}/Speer6-ps1⁺
involves: 129S4/SvJae * C57BL/6 * DBA

liver/biliary system phenotype

increased cholangiocarcinoma incidence
- mutants develop invasive intrahepatic cholangiocarcinoma with low penetrance (1 of 8 mutants) and long latency (at 36 weeks of age)

increased liver tumor incidence
- mice develop liver tumors at 12 months of age and do not show obvious symptoms up to 18 months of age
- tumors resemble hepatocellular dysplasia

neoplasm

increased cholangiocarcinoma incidence
- mutants develop invasive intrahepatic cholangiocarcinoma with low penetrance (1 of 8 mutants) and long latency (at 36 weeks of age)

increased liver tumor incidence
- mice develop liver tumors at 12 months of age and do not show obvious symptoms up to 18 months of age
- tumors resemble hepatocellular dysplasia

Genotype: Kras^tm4Tyj/Kras^tm4Tyj
B6.129S4-Kras

cellular phenotype

increased cell proliferation
- primary mouse embryonic fibroblast treated with adenoviral-cre exhibit enhanced growth rate compared with wild-type cells

Genotype: Kras^tm4Tyj/Kras⁺
involves: 129S4/SvJae * C57BL/6

neoplasm

increased lung adenoma incidence
- lung adenocarcinomas cover 11% of lung area 9 weeks after administration of a Cre-recombinase expressing adenovirus

respiratory system phenotype

increased lung adenoma incidence
- lung adenocarcinomas cover 11% of lung area 9 weeks after administration of a Cre-recombinase expressing adenovirus

Genotype: Kras^tm4Tyj/Kras⁺ Tg(Krt1-15-cre/PGR)22Cot/0
involves: 129S4/SvJae * C57BL/6 * C57BL/6J * SJL/J

neoplasm

increased papilloma incidence
- mice develop benign papillomas without progressing to malignancy following topical application of RU486 to the back of skin at 3 weeks of age for 5 days

Genotype: Kras^tm4Tyj/Kras⁺ Tg(Mx1-cre)1Cgn/0
involves: 129S4/SvJae * C57BL/6 * CBA

cellular phenotype

increased splenocyte proliferation
- increase in the number of proliferating splenocytes in pIpC treated mice; most of these proliferating cells are Mac1+/Gr1 lo or Ter119+

hematopoietic system phenotype

abnormal erythropoiesis
- bone marrow from pIpC treated mice forms abnormally large BFU-E colonies characterized by both erythropoietin-independent growth and hypersensitivity to erythropoietin
- mice treated with pIpC show large numbers of proliferating splenic Ter199+ cells, indicating that erythropoiesis is ineffective
- pIpC treated mice show normal numbers of early erythroid cells in the bone marrow but a paucity of all the more mature TER119 hi populations, indicating an inefficient transition from TER119- to TER119 hi stages of erythropoiesis
- spleen of pIpC treated mice contains increase of immature CD71 hi TER119-/lo cells and large numbers of TER119 hi erythroblasts
- the erythroid progenitor compartment is massively expanded in the spleen of pIpC treated mice

abnormal myelopoiesis
- bone marrow mononuclear cells from pIpC treated mice form significant numbers of colony-forming unit granulocyte-macrophage (CFU-GM) colonies in the absence of exogenous cytokines while wild-type cells do not
- CFU-GM shows an increased proliferative response without added cytokines (9-fold) or to GM-CSF (19-fold increase) or IL-3 (37-fold increase)
- pIpC injected mice develop a myeloproliferative disease with excess monocytes

anemia
- Normal - however, normal platelet counts are seen in pIpC injected mice
- pups injected with pIpC develop anemia

anisopoikilocytosis
- in pIpC treated mice

decreased mean corpuscular hemoglobin
- in pIpC treated mice

enlarged spleen
- in pIpC treated mice
- spleens of pIpC-treated moribund mice are massively enlarged

increased leukocyte cell number
- pups injected with pIpC at 21 days of age develop progressive leukocytosis that is evident 3 weeks after pIpC injection

increased monocyte cell number
- mice show an expanded population of Mac-1+, Gr-1 lo cells, indicating an expansion of immature monocytic cells

increased splenocyte proliferation
- increase in the number of proliferating splenocytes in pIpC treated mice; most of these proliferating cells are Mac1+/Gr1 lo or Ter119+

myeloid hyperplasia
- mice show abundant myeloid cells at various stages of differentiation after pIpC injection

polychromatophilia
- in pIpC treated mice

reticulocytosis
- in pIpC treated mice

homeostasis/metabolism phenotype

increased circulating erythropoietin level
- serum erythropoietin levels are increased in proportion to anemia in pIpC treated mice

immune system phenotype

abnormal myelopoiesis
- bone marrow mononuclear cells from pIpC treated mice form significant numbers of colony-forming unit granulocyte-macrophage (CFU-GM) colonies in the absence of exogenous cytokines while wild-type cells do not
- CFU-GM shows an increased proliferative response without added cytokines (9-fold) or to GM-CSF (19-fold increase) or IL-3 (37-fold increase)
- pIpC injected mice develop a myeloproliferative disease with excess monocytes

enlarged spleen
- in pIpC treated mice
- spleens of pIpC-treated moribund mice are massively enlarged

increased leukocyte cell number
- pups injected with pIpC at 21 days of age develop progressive leukocytosis that is evident 3 weeks after pIpC injection

increased monocyte cell number
- mice show an expanded population of Mac-1+, Gr-1 lo cells, indicating an expansion of immature monocytic cells

increased splenocyte proliferation
- increase in the number of proliferating splenocytes in pIpC treated mice; most of these proliferating cells are Mac1+/Gr1 lo or Ter119+

myeloid hyperplasia
- mice show abundant myeloid cells at various stages of differentiation after pIpC injection

liver/biliary system phenotype

enlarged liver
- pIpC injected mice show moderate hepatomegaly with myeloid infiltration, particularly in periportal areas

mortality/aging

premature death
- mice survive for a median of 84 days after pIpC injection

Genotype: Kras^tm4Tyj/Kras⁺ Tg(CAG-Bgeo,-tsA58T)T26Ichi/0 Tg(Pdx1-cre)6Tuv/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB/N

endocrine/exocrine gland phenotype

increased pancreatic ductal adenocarcinoma incidence
- at P16, pancreatic ductal adenocarcinoma progresses to occupy the whole pancreas and to invade the muscular wall of the duodenum
- mice develop highly aggressive adenocarcinoma with a ductal cell phenotype and inflammation resembling human pancreatic ductal adenocarcinoma within a short period (5 and 10 days after birth) and die within 3 weeks

increased pancreatic intraepithelial neoplasia incidence
- PanIN-3 are detected in the pancreas with inflammation at P3 and P4

pancreatic acinar-to-ductal metaplasia
- invasive features of pancreatic ductal adenocarcinoma are seen containing acinoductal metaplasia at P5-P10

homeostasis/metabolism phenotype

hemorrhagic ascites
- hemorrhagic ascites are seen by P16

mortality/aging

postnatal lethality, complete penetrance
- mice do not survive beyond P21

neoplasm

increased pancreatic ductal adenocarcinoma incidence
- at P16, pancreatic ductal adenocarcinoma progresses to occupy the whole pancreas and to invade the muscular wall of the duodenum
- mice develop highly aggressive adenocarcinoma with a ductal cell phenotype and inflammation resembling human pancreatic ductal adenocarcinoma within a short period (5 and 10 days after birth) and die within 3 weeks

increased pancreatic intraepithelial neoplasia incidence
- PanIN-3 are detected in the pancreas with inflammation at P3 and P4

Genotype: Kras^tm4Tyj/Kras⁺
involves: 129S4/SvJae * C57BL/6 * FVB/N

mortality/aging

premature death
- mice inoculated with an adenovirus expressing cre recombinase (ad-cre) by inhalation have a median survival of 24 weeks after ad-cre inoculation

neoplasm

increased lung adenocarcinoma incidence
- all tumors of ad-cre inoculated mice are adenocarincomas
- metastasis or local invasion is not seen in ad-cre inoculated mice
- mice inoculated with ad-cre by inhalation develop lung tumors with high multiplicity, long latency, and low aggressiveness

respiratory system phenotype

increased lung adenocarcinoma incidence
- all tumors of ad-cre inoculated mice are adenocarincomas
- metastasis or local invasion is not seen in ad-cre inoculated mice
- mice inoculated with ad-cre by inhalation develop lung tumors with high multiplicity, long latency, and low aggressiveness

Genotype: Kras^tm4Tyj/Kras⁺ Tg(KRT14-cre/ERT)20Efu/0
involves: 129S4/SvJae * C57BL/6 * CD-1 * FVB/N

digestive/alimentary phenotype

increased mouth tumor incidence
- tamoxifen treated mice develop oral tumors

neoplasm

increased mouth tumor incidence
- tamoxifen treated mice develop oral tumors

References

Jackson EL; Willis N; Mercer K; Bronson RT; Crowley D; Montoya R; Jacks T; Tuveson DA. 2001. Analysis of lung tumor initiation and progression using conditional expression of oncogenic K-ras. Genes Dev 15(24):3243-8PubMed: 11751630 MGI: J:73445

Additional - Kras^tm4Tyj related

Technical Support

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Genotyping Protocols
- MELT: Kras^tm4Tyj Alt1
- Genotyping resources and troubleshooting
Breeding Considerations

When maintained as a live colony, heterozygotes may be bred. Homozygotes are embryonic lethal.
- Additional Breeding and Husbandry Support
Mating System
- Heterozygote x Wild-type
- Wild-type x Heterozygote
Citation
When using the B6N.Cg-Kras^tm4Tyj/CjDswJ mouse strain in a publication, please cite the originating article(s) and include JAX stock #019104 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

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

Pricing & Availability

Cryo Recovery

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Genotype

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weeks

Cryorecovery - Pricing

Service	Genotype	Price
	Heterozygous or wild type for Kras<tm4Tyj>

We will fulfill your order by providing at least two carriers for each strain ordered. The total number, sex, and genotypes provided will vary, although typically 8 or more animals are provided. Please check genotypes which will be recovered. While the genotypes of all animals produced will be communicated to you prior to scheduling shipment, the genotypes of animals provided may not reflect the mating scheme and genotypes described in the strain description. Animals are typically ready to ship in 11-14 weeks. If a second recovery is required to produce the minimum number of animals, then delivery time would increase to approximately 25 weeks. If we fail to produce animals of the correct genotype, you will not be charged. We cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation.

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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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Donating Investigator

Genetic overview

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Detailed Description

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Additional Information

Selected References

Krastm4Tyj

Allele Symbol: Krastm4Tyj

Disease Terms

Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).

Model with phenotypic similarity to human disease where etiologies are distinct. Human genes are associated with this disease. Orthologs of these genes do not appear in the mouse genotype(s).

Characteristics of this human disease are associated with transgenes and other mutation types in the mouse.

Models with phenotypic similarity to human diseases where etiology is unknown or involving genes where ortholog is unknown.

No similarity to the expected human disease phenotype was found. One or more human genes are associated with this human disease. The mouse genotype may involve mutations to orthologs of one or more of these genes, but the phenotype did not resemble the disease.

Research Areas By Genotype

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

Mammalian Phenotype Terms by Genotype

Genotype: Krastm4Tyj/Kras+ Tg(Mx1-cre)1Cgn/0involves: 129S4/SvJae * BALB/c * C57BL/6 * CBA

digestive/alimentary phenotype

immune system phenotype

integument phenotype

liver/biliary system phenotype

mortality/aging

endocrine/exocrine gland phenotype

neoplasm

respiratory system phenotype

growth/size/body region phenotype

hematopoietic system phenotype

Genotype: Krastm4Tyj/Kras+ Tg(MMTV-cre)4Mam/0involves: 129S4/SvJae * FVB

digestive/alimentary phenotype

endocrine/exocrine gland phenotype

Genotype: Krastm4Tyj/Kras+ Tg(Prm-cre)58Og/0involves: 129S4/SvJae

cardiovascular system phenotype

mortality/aging

cellular phenotype

embryo phenotype

Genotype: Krastm4Tyj/Kras+ Tg(Tek-cre)12Flv/0involves: 129S4/SvJae * C3H * C57BL/6

mammalian phenotype

Genotype: Krastm4Tyj/Kras+ Tg(SFTPC-rtTA)5Jaw/0 Tg(tetO-cre)1Jaw/0involves: 129/Sv * C57BL/6

mortality/aging

respiratory system phenotype

Genotype: Krastm4Tyj/Kras+ Meox2tm1(cre)Sor/Meox2+involves: 129S4/SvJae * 129S4/SvJaeSor

cardiovascular system phenotype

homeostasis/metabolism phenotype

integument phenotype

liver/biliary system phenotype

mammalian phenotype

mortality/aging

respiratory system phenotype

cellular phenotype

embryo phenotype

hematopoietic system phenotype

Genotype: Krastm4Tyj/Kras+involves: 129S4/SvJae

neoplasm

hematopoietic system phenotype

reproductive system phenotype

immune system phenotype

mortality/aging

respiratory system phenotype

Genotype: Krastm4Tyj/Kras+ Lyz2tm1(cre)Ifo/Lyz2+involves: 129P2/OlaHsd * 129S4/SvJae

mortality/aging

neoplasm

respiratory system phenotype

Genotype: Krastm4Tyj/Kras+ Tg(Tyr-cre/ERT2)13Bos/0involves: 129S4/SvJae * FVB

neoplasm

pigmentation phenotype

Genotype: Krastm4Tyj/Kras+either: (involves: 129S4/SvJae) or (involves: 129S4/SvJae * C3H/HeJ)

endocrine/exocrine gland phenotype

growth/size/body region phenotype

reproductive system phenotype

Genotype: Krastm4Tyj/Kras+ Tg(Gfap-cre)77.6Mvs/0involves: 129 * BALB/c * C57BL/6NHsd

mammalian phenotype

Genotype: Krastm4Tyj/Kras+ Tg(Krt1-15-cre/PGR)22Cot/0involves: 129S4/SvJae * C57BL/6J * SJL/J

craniofacial phenotype

growth/size/body region phenotype

integument phenotype

neoplasm

Kras^tm4Tyj

Allele Symbol: Kras^tm4Tyj

Genotype: Kras^tm4Tyj/Kras⁺ Tg(Mx1-cre)1Cgn/0
involves: 129S4/SvJae * BALB/c * C57BL/6 * CBA

Genotype: Kras^tm4Tyj/Kras⁺ Tg(MMTV-cre)4Mam/0
involves: 129S4/SvJae * FVB

Genotype: Kras^tm4Tyj/Kras⁺ Tg(Prm-cre)58Og/0
involves: 129S4/SvJae

Genotype: Kras^tm4Tyj/Kras⁺ Tg(Tek-cre)12Flv/0
involves: 129S4/SvJae * C3H * C57BL/6

Genotype: Kras^tm4Tyj/Kras⁺ Tg(SFTPC-rtTA)5Jaw/0 Tg(tetO-cre)1Jaw/0
involves: 129/Sv * C57BL/6

Genotype: Kras^tm4Tyj/Kras⁺ Meox2^tm1(cre)Sor/Meox2⁺
involves: 129S4/SvJae * 129S4/SvJaeSor

Genotype: Kras^tm4Tyj/Kras⁺
involves: 129S4/SvJae

Genotype: Kras^tm4Tyj/Kras⁺ Lyz2^tm1(cre)Ifo/Lyz2⁺
involves: 129P2/OlaHsd * 129S4/SvJae

Genotype: Kras^tm4Tyj/Kras⁺ Tg(Tyr-cre/ERT2)13Bos/0
involves: 129S4/SvJae * FVB

Genotype: Kras^tm4Tyj/Kras⁺
either: (involves: 129S4/SvJae) or (involves: 129S4/SvJae * C3H/HeJ)

Genotype: Kras^tm4Tyj/Kras⁺ Tg(Gfap-cre)77.6Mvs/0
involves: 129 * BALB/c * C57BL/6NHsd

Genotype: Kras^tm4Tyj/Kras⁺ Tg(Krt1-15-cre/PGR)22Cot/0
involves: 129S4/SvJae * C57BL/6J * SJL/J

Genotype: Kras^tm4Tyj/Kras⁺ Shh^{tm2(cre/ERT2)Cjt}/Shh⁺
involves: 129S4/SvJae * 129S6/SvEvTac

Genotype: Kras^tm4Tyj/Kras⁺
B6.129S4-Kras

Genotype: Kras^tm4Tyj/Kras⁺ Speer6-ps1^{Tg(Alb-cre)21Mgn}/Speer6-ps1⁺
involves: 129S4/SvJae * C57BL/6 * DBA

Genotype: Kras^tm4Tyj/Kras^tm4Tyj
B6.129S4-Kras

Genotype: Kras^tm4Tyj/Kras⁺
involves: 129S4/SvJae * C57BL/6

Genotype: Kras^tm4Tyj/Kras⁺ Tg(Krt1-15-cre/PGR)22Cot/0
involves: 129S4/SvJae * C57BL/6 * C57BL/6J * SJL/J

Genotype: Kras^tm4Tyj/Kras⁺ Tg(Mx1-cre)1Cgn/0
involves: 129S4/SvJae * C57BL/6 * CBA

Genotype: Kras^tm4Tyj/Kras⁺ Tg(CAG-Bgeo,-tsA58T)T26Ichi/0 Tg(Pdx1-cre)6Tuv/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB/N

Genotype: Kras^tm4Tyj/Kras⁺
involves: 129S4/SvJae * C57BL/6 * FVB/N

Genotype: Kras^tm4Tyj/Kras⁺ Tg(KRT14-cre/ERT)20Efu/0
involves: 129S4/SvJae * C57BL/6 * CD-1 * FVB/N

Additional - Kras^tm4Tyj related