Overview

Also Known As:IR^Lox

These IR^lox mutant mice have loxP sites flanking exon 4 of the targeted gene. When bred to Cre-recombinase expressing mice, offspring will have a deletion of exon 4 in the cre expressing tissue(s). These floxed mice may be useful in studying insulin receptor function in several different tissues (including pancreas, liver, and skeletal muscle), as well as diabetes and glucose regulation.

Donating Investigator

C. Ronald Kahn, Joslin Diabetes Center

Genetic overview

Genetic Background	Generation
	N11+N1F7 (2020-03-19 00:00:00)

Insr^tm1Khn

Allele Type	Gene Symbol	Gene Name
Targeted (Conditional ready (e.g. floxed), No functional change)	Insr	insulin receptor

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Research Applications

Research Tools
Diabetes and Obesity Research

View All Research Applications

Base Price

Starting at:

$255.00 Domestic price for female 4-week

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Details

Detailed Description

Mice homozygous for this IR^lox allele are viable and fertile. These mutant mice have loxP sites flanking exon 4 of the targeted gene. When bred to Cre-recombinase expressing mice, offspring will have a deletion of exon 4 in the cre expressing tissue(s). These "floxed" mice may be useful in studying insulin receptor function in several different tissues (including pancreas, liver, and skeletal muscle), as well as diabetes and glucose regulation.

For example, when crossed to a strain expressing Cre recombinase in the central and peripheral nervous system (see Stock No. 003771), this mutant mouse strain may be useful in studies of glucose homeostasis.

When crossed to a strain expressing Cre recombinase in skeletal and cardiac muscle (see Stock No. 006475), this mutant mouse strain may be useful in studies of diabetes.

When crossed to a strain expressing Cre recombinase in the liver (see Stock No. 003574), this mutant mouse strain may be useful in studies of insulin resistance.

When crossed to a strain expressing Cre recombinase in pancreatic beta cells (see Stock No. 003573), this mutant mouse strain may be useful in studies of diabetes.

Development

A targeting vector was designed to insert a loxP-flanked neomycin cassette downstream of exon 4, as well as a single loxP site 80 bp downstream of exon 4 of the targeted gene. The construct was electroporated into the 129S4/SvJae-derived J1 embryonic stem (ES) cells. ES cell were transiently transfected with a Cre-recombinase plasmid to delete the selection cassette, leaving single loxP sites upstream and downstream of exon 4. Correctly targeted ES cells were injected into C57BL/6J blastocysts, which were injected into pseudopregnant CD-1 foster females. The resulting mutant mice (IR^lox) were backcrossed to C57BL/6J inbred mice. At some point, mice were bred to Mck-Cre transgenic mice (FVB genetic background, see Stock No. 006405). The double mutants were backcrossed for 10 generations to C57BL/6 mice and then selected for the IR^lox (and against the transgene) prior to arrival at The Jackson Laboratory.

A 32 SNP (single nucleotide polymorphism) panel analysis, with 27 markers covering all 19 chromosomes and the X chromosome, as well as 5 markers that distinguish between the C57BL/6J and C57BL/6N substrains, was performed on the rederived living colony at The Jackson Laboratory Repository. While the 27 markers throughout the genome suggested a C57BL/6 genetic background, all 5 markers that determine C57BL/6J from C57BL/6N were found to be segregating. These data suggest the mice sent to The Jackson Laboratory Repository were on a C57BL/6N genetic background.

Control Suggestions

Approximate Controls

Additional Information

Considerations for Choosing Controls

Selected References

Bruning JC; Michael MD; Winnay JN; Hayashi T; Horsch D; Accili D; Goodyear LJ; Kahn CR. 1998. A muscle-specific insulin receptor knockout exhibits features of the metabolic syndrome of NIDDM without altering glucose tolerance. Mol Cell 2(5):559-69PubMed: 9844629 MGI: J:51266

View All References

Genetics

Insr^tm1Khn

Allele Symbol: Insr^tm1Khn

Allele Name	targeted mutation 1, Ronald Kahn
Allele Type	Targeted (Conditional ready (e.g. floxed), No functional change)
Allele Synonym(s)	targeted mutation 1, Ronald Kahn; Insr^tm1Khn
Gene Symbol and Name	Insr, insulin receptor
Gene Synonym(s)	RIKEN cDNA 4932439J01 gene; D630014A15Rik; D630014A15Rik; HHF5; RIKEN cDNA D630014A15 gene; IR-A; CD220; 4932439J01Rik; IR; IR-B; 4932439J01Rik
Strain of Origin	129S4/SvJae
Chromosome	8
General Note	In conjunction with Tg(Mycha-cre)1Abel, this allele is knocked out specifically in cardiac muscle. The resulting mice are referred to as "Cardiac-specific insulin receptor knockout mice" or CIRKO. In conjunction with Tg(Ckmm-cre)5Khn, this allele is disrupted specifically in skeletal muscle. The resulting mice are referred to as "Muscle-specific insulin receptor knockout mice" or MIRKO.
Molecular Note	Exon 4 was left flanked by single loxP sites after a downstream floxed neo cassette was removed via in vitro cre mediated recombination. Deletion of the resultant floxed fragment will result in a frameshift mutation that introduces a stop codon. Translation, if it were to occur, would putatively produce a truncated peptide consisting of 308 amino terminal residues and lacking the high affinity binding site, transmembrane domain, and kinase domain.
Mutations Made By	C. Ronald Kahn, Joslin Diabetes Center

Disease/Phenotype

Disease Terms

Research Areas By Phenotype

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

Research Tools
- Diabetes and Obesity Research
  - loxP
- Cre-lox System
  - loxP-flanked Sequences
Diabetes and Obesity Research
- Insulin Receptors and Growth Factors

Mammalian Phenotype Terms by Genotype

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

Genotype: Insr^tm1Khn/Insr^tm1Khn Tg(Ckmm-cre)5Khn/0
involves: 129S4/SvJae * C57BL/6J * FVB

adipose tissue phenotype

abnormal fat pad morphology
- larger than normal fat depots in fat pads, including the perianal, subcutaneous and perigonadal fat pads

homeostasis/metabolism phenotype

increased fatty acid level
- 20% elevation in serum free fatty acids (FFAs)

increased triglyceride level
- greater than70% elevated, observed from ages 4 to 11 months

mammalian phenotype

homeostasis/metabolism phenotype
- Normal - normal concentrations of serum insulin
- Normal - normal glucose tolerance
- Normal - normal serum cholesterol levels
- Normal - normoglycemia, up to 11 months of age

Genotype: Insr^tm1Khn/Insr^tm1Dac Tg(Ckmm-cre)5Khn/0
involves: 129S4/SvJae * C57BL/6J * FVB

homeostasis/metabolism phenotype

hyperglycemia
- in the fed state, incomplete penetrance

increased circulating insulin level

Genotype: Insr^tm1Khn/Insr^tm1Khn Speer6-ps1^{Tg(Alb-cre)21Mgn}/Speer6-ps1⁺
involves: 129S4/SvJae * C57BL/6J * DBA/2 * FVB

cellular phenotype

increased mitochondria size
- at 6 months, mutant hepatocytes exhibit giant mitochondria

endocrine/exocrine gland phenotype

enlarged gallbladder
- at 6- to 12-months of age, mutant gall bladders appear enlarged

increased insulin secretion
- at 6 months, female mutants show a have 5- to 6-fold increase in pancreatic insulin content measured in acid-ethanol extracts

increased pancreatic beta cell mass
- at 6 months, increased pancreatic insulin content is associated with a 6-fold increase in pancreatic beta cell mass
- at 6 months, mutant mice show a ~4-fold increase in pancreatic beta cell mass, as a compensatory response to insulin resistance

pancreatic islet hyperplasia
- at 6 months, mutant mice show an adaptive islet hyperplastic response to insulin resistance

liver/biliary system phenotype

abnormal hepatocyte morphology
- at 6 months, mutant hepatocytes exhibit a moderate increase in lipid accumulation; only a few electron-dense glycogen granules are observed

abnormal liver morphology
- at 2 months, mutant livers appear a little darker in color, with areas of focal dysplasia and reduced glycogen storage in the parenchyma; no steatosis is observed
- at 6- to 12-months of age, mutant livers display multiple hyperplastic pale nodules scattered throughout all lobes
- by 12 months, the normal lobular structure is disrupted; hyperplastic nodules consist of highly vacuolated cells that compress the adjacent normal tissue, in the absence of fibrosis

abnormal liver physiology
- insulin resistance in liver results in elevated expression of PEPCK, the rate-limiting enzyme for gluconeogenesis, and reduced expression of glucokinase and liver pyruvate kinase, two enzymes critical for glucose utilization
- the mutant liver appears to be chronically geared toward glucose production; early insulin signaling events, such as IRS-1 and IRS-2 phosphorylation, are lost

enlarged gallbladder
- at 6- to 12-months of age, mutant gall bladders appear enlarged

small liver
- at 2 months, mutant livers are 40% smaller than those of age- and gender-matched controls; liver size decreases significantly with increasing age

growth/size/body region phenotype

postnatal growth retardation
- newborn mutant mice appear normal, nurse successfully, and survive well upon weaning but display a mild growth deficit postweaning
- this moderate growth deficit appears to result from defects in the growth hormone-IGF axis (unpublished data)

homeostasis/metabolism phenotype

abnormal circulating serum albumin level
- at 6 months, mutant mice display a 50% reduction in serum albumin levels

abnormal glucose homeostasis
- at 2 months, male mutants fail to suppress hepatic glucose output in response to insulin administration, despite intact insulin signaling in adipose tissue and nearly normal insulin signaling in muscle

abnormal insulin clearance
- in addition to increased insulin secretion, 11-week-old male mutants show a 75% reduction in the C-peptide:insulin ratio, indicating decreased insulin clearance

abnormal lipid homeostasis

decreased circulating free fatty acid level
- at 2 months, male mutants show a 40-50% reduction in the levels of serum free fatty acids

decreased circulating triglyceride level
- at 2 months, male mutants show a 40-50% reduction in the levels of serum triglycerides

hyperglycemia
- at 2 months, male mutants also display a mild hyperglycemia in the fasted state, despite a 7-fold increase in serum insulin levels
- at 2 months, male mutants exhibit significantly elevated blood glucose in the fed state, despite a 20-fold increase in insulin levels relative to control mice; in contrast, glucagon levels remain unaffected
- unexpectedly, as mutant mice age, the elevated fasting blood glucose levels progressively decline; by 6 months of age, mutants exhibit fasting hypoglycemia rather than hyperglycemia

impaired glucose tolerance
- at 2 months, fasted male mutants display pronounced glucose intolerance
- surprisingly, glucose intolerance is no longer apparent at 6 months

increased bile salt level
- mutant gallbladders show a notable increase in bile volume

increased circulating alkaline phosphatase level
- at 6 months, mutant mice show a 50% increase in alkaline phosphatase levels, suggesting biliary tract dysfunction

increased circulating aspartate transaminase level
- at 6 months, mutant mice show a 2.6-fold increase in aspartate aminotransferase levels, suggesting hepatocellular damage
- in contrast, no significant changes in levels of lactate dehydrogenase or alanine aminotransferase are observed

increased circulating insulin level
- at 2 months, male mutants exhibit an extreme increase in serum insulin levels (20-fold in fed state; 7-fold in fasted state)

increased insulin secretion
- at 6 months, female mutants show a have 5- to 6-fold increase in pancreatic insulin content measured in acid-ethanol extracts

insulin resistance
- at 2 months, random-fed male mutants are severely resistant to the blood glucose-lowering effects of exogenously administered insulin

Genotype: Insr^tm1Khn/Insr^tm1Khn Tg(Nes-cre)1Kln/0
involves: 129S4/SvJae * C57BL/6J * SJL

adipose tissue phenotype

increased white adipose tissue amount
- in females, a two-fold increase in perigonadal adipose tissue is seen
- in males, a 1.5-fold increase in adipose tissue is seen

growth/size/body region phenotype

increased body weight
- males do not exhibit weight differences on a standard chow diet, but females exhibit a 10-15% increase over controls
- on a high-fat diet, male mice exhibit a 10% weight increase at 14 weeks of age and females exhibit a 20% increase over controls

homeostasis/metabolism phenotype

decreased circulating luteinizing hormone level
- 20% of seminiferous tubules lacked a lumen and had few maturing spermatogonia
- normal pituitary morphology and LH content; treatment with lupron indicated that LH is expressed, but not secreted from the pituitary in mutant mice

increased circulating insulin level
- at 4-6 months of age, mice exhibit a 1.5 fold increase in circulating insulin levels and females exhibit a 2 fold increase
- normal glucose tolerance

increased circulating leptin level
- 1.5 fold increased in males
- 2.5 fold increased in females
- normal cholesterol concentrations

increased circulating triglyceride level
- both males and females exhibit a 30% increase in circulating triglycerides

insulin resistance
- females exhibit blunted response when injected with insulin and males performed similarly to controls

mammalian phenotype

nervous system phenotype
- Normal - brain weights and general brain histology appeared similar to controls

reproductive system phenotype

abnormal seminiferous tubule morphology
- 20% of seminiferous tubules lacked a lumen and had few maturing spermatogonia
- normal seminal vesicles, prostate, and epididymis

abnormal spermatogenesis
- impaired

decreased corpora lutea number

impaired ovarian folliculogenesis
- reduced number of antral follicles

Leydig cell hypoplasia

oligozoospermia
- 30% reduced in epididymal sperm content

reduced male fertility

behavior/neurological phenotype

polyphagia
- females exhibit a 20% increase in food intake per gram of body weight
- males did not exhibit any differences in food intake when compared to controls

cellular phenotype

oligozoospermia
- 30% reduced in epididymal sperm content

endocrine/exocrine gland phenotype

abnormal seminiferous tubule morphology
- 20% of seminiferous tubules lacked a lumen and had few maturing spermatogonia
- normal seminal vesicles, prostate, and epididymis

decreased corpora lutea number

impaired ovarian folliculogenesis
- reduced number of antral follicles

Leydig cell hypoplasia

Genotype: Insr^tm1Khn/Insr^tm1Khn Tg(Nes-cre)1Kln/0
involves: 129S4/SvJae * C57BL/6 * SJL

homeostasis/metabolism phenotype

abnormal glucose homeostasis
- insulin-induced suppression of hepatic glucose productionas assessed with a euglycemic hyperinsulinemic clamp is attenuated

Genotype: Insr^tm1Khn/Insr^tm1Khn Tg(Ckmm-cre)5Khn/0
involves: 129S4/SvJae * C57BL/6 * FVB

mammalian phenotype

cardiovascular system phenotype
- Normal - heart function and morphology is normal

growth/size/body region phenotype
- Normal - mice exhibit normal growth rates

homeostasis/metabolism phenotype
- Normal - mice exhibit normal glucose homeostasis

Genotype: Insr^tm1Khn/Insr^tm1Khn Speer6-ps1^{Tg(Alb-cre)21Mgn}/Speer6-ps1⁺ Tg(Ins2-cre)25Mgn/0
involves: 129S4/SvJae * C57BL/6 * DBA/2

behavior/neurological phenotype

polydipsia
- during terminal stages

mammalian phenotype

digestive/alimentary phenotype
- Normal - unlike mice null for Insr in beta cells mice, islet cell mass is not increased despite similar levels of elevated insulin levels

mortality/aging

premature death
- 82% of mice die by 6 weeks of age with some mice surviving a few weeks longer

renal/urinary system phenotype

polyuria
- during terminal stages

endocrine/exocrine gland phenotype

decreased insulin secretion

growth/size/body region phenotype

decreased body weight
- mice develop severe diabetes and loss 30% of their body weight in terminal stages

homeostasis/metabolism phenotype

decreased insulin secretion

hyperglycemia
- mice develop hypoglycemia at 2 weeks of age that rapidly worsens by 6 weeks of age
- mice exhibit high fasting glucose serum levels

impaired glucose tolerance

increased circulating insulin level

insulin resistance

Genotype: Insr^tm1Khn/Insr^tm1Khn Tg(Ins2-cre)25Mgn/0
involves: 129S4/SvJae * C57BL/6 * DBA/2

endocrine/exocrine gland phenotype

decreased insulin secretion

decreased pancreatic beta cell mass
- mice exhibit decreased beta cell mass when fed a normal or high fat diet

homeostasis/metabolism phenotype

decreased insulin secretion

hyperglycemia
- mice exhibit an increase in serum glucose level on a regular diet and a severe increase when fed a high fat diet

impaired glucose tolerance
- Normal - however, mice are not insulin resistant
- mice exhibit impaired glucose tolerance on a normal diet and severe intolerance when fed a high fat diet

mortality/aging

increased sensitivity to induced morbidity/mortality
- when fed a high fat diet, 30% of mice die by 16 weeks

premature death
- some mice die due to severe hyperglycemia

Genotype: Insr^tm1Khn/Insr^tm1Khn Speer6-ps1^{Tg(Alb-cre)21Mgn}/Speer6-ps1⁺
involves: 129S4/SvJae * C57BL/6 * DBA/2

endocrine/exocrine gland phenotype

increased pancreatic beta cell mass
- at 10 to 12 months of age, mice exhibit a 27-fold increase in beta cell mass due to an 8-fold increase in proliferating beta cells with a slight increase in apoptosis
- at 2 weeks beta cell mass is increased 2-fold and at 6 weeks 4-fold compared to in wild-type mice due to increased mitosis of beta cells

homeostasis/metabolism phenotype

decreased circulating glucose level
- at 10 to 12 months of age

hyperglycemia
- while mice display normoglycemia during the first 3 weeks of life, at 4 weeks mice develop hypoglycemia that lasts until week 6

impaired glucose tolerance

increased circulating insulin level

insulin resistance

References

Bruning JC; Michael MD; Winnay JN; Hayashi T; Horsch D; Accili D; Goodyear LJ; Kahn CR. 1998. A muscle-specific insulin receptor knockout exhibits features of the metabolic syndrome of NIDDM without altering glucose tolerance. Mol Cell 2(5):559-69PubMed: 9844629 MGI: J:51266

Additional References

Mezza T; Shirakawa J; Martinez R; Hu J; Giaccari A; Kulkarni RN. 2016. Nuclear Export of FoxO1 Is Associated with ERK Signaling in beta-Cells Lacking Insulin Receptors. J Biol Chem 291(41):21485-21495PubMed: 27535223 MGI: J:237303
Tarchick MJ; Cutler AH; Trobenter TD; Kozlowski MR; Makowski ER; Holoman N; Shao J; Shen B; Anand-Apte B; Samuels IS. 2019. Endogenous insulin signaling in the RPE contributes to the maintenance of rod photoreceptor function in diabetes. Exp Eye Res 180:63-74PubMed: 30543793 MGI: J:281341

Additional - Insr^tm1Khn related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Standard PCR:Insr Alternate1
- Standard PCR:Generic Neo
- Probe:Generic Neo
- Genotyping resources and troubleshooting
Dietary Information
- LabDiet® 5K52 formulation (6% fat)
Breeding Considerations

When maintaining a live colony, homozygous mice are bred.
- Additional Breeding and Husbandry Support
Mating System
- Homozygote x Homozygote
Citation
When using the IR^Lox mouse strain in a publication, please cite the originating article(s) and include JAX stock #006955 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

AX10 (Standard)

Pricing & Availability

Available

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International

Live Mouse

Age

Genotype

Price

weeks

Cryorecovery - Pricing

Service/Product	Description	Price
	Heterozygous for Insr<tm1Khn>

Related Products and Services

Frozen Mouse Embryo	B6.129S4(FVB)-Insr<tm1Khn>/J	$2595.00
Frozen Mouse Embryo	B6.129S4(FVB)-Insr<tm1Khn>/J	$2595.00
Frozen Mouse Embryo	B6.129S4(FVB)-Insr<tm1Khn>/J	$3373.50
Frozen Mouse Embryo	B6.129S4(FVB)-Insr<tm1Khn>/J	$3373.50

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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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Also Known As:IRLox

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Approximate Controls

Additional Information

Selected References

Insrtm1Khn

Allele Symbol: Insrtm1Khn

Disease Terms

Research Areas By Phenotype

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

Mammalian Phenotype Terms by Genotype

Genotype: Insrtm1Khn/Insrtm1Khn Tg(Ckmm-cre)5Khn/0involves: 129S4/SvJae * C57BL/6J * FVB

adipose tissue phenotype

homeostasis/metabolism phenotype

mammalian phenotype

Genotype: Insrtm1Khn/Insrtm1Dac Tg(Ckmm-cre)5Khn/0involves: 129S4/SvJae * C57BL/6J * FVB

homeostasis/metabolism phenotype

Genotype: Insrtm1Khn/Insrtm1Khn Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+involves: 129S4/SvJae * C57BL/6J * DBA/2 * FVB

cellular phenotype

endocrine/exocrine gland phenotype

liver/biliary system phenotype

growth/size/body region phenotype

homeostasis/metabolism phenotype

Genotype: Insrtm1Khn/Insrtm1Khn Tg(Nes-cre)1Kln/0involves: 129S4/SvJae * C57BL/6J * SJL

adipose tissue phenotype

growth/size/body region phenotype

homeostasis/metabolism phenotype

mammalian phenotype

reproductive system phenotype

behavior/neurological phenotype

cellular phenotype

endocrine/exocrine gland phenotype

Genotype: Insrtm1Khn/Insrtm1Khn Tg(Nes-cre)1Kln/0involves: 129S4/SvJae * C57BL/6 * SJL

homeostasis/metabolism phenotype

Genotype: Insrtm1Khn/Insrtm1Khn Tg(Ckmm-cre)5Khn/0involves: 129S4/SvJae * C57BL/6 * FVB

mammalian phenotype

Genotype: Insrtm1Khn/Insrtm1Khn Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+ Tg(Ins2-cre)25Mgn/0involves: 129S4/SvJae * C57BL/6 * DBA/2

behavior/neurological phenotype

mammalian phenotype

mortality/aging

renal/urinary system phenotype

endocrine/exocrine gland phenotype

growth/size/body region phenotype

homeostasis/metabolism phenotype

Genotype: Insrtm1Khn/Insrtm1Khn Tg(Ins2-cre)25Mgn/0involves: 129S4/SvJae * C57BL/6 * DBA/2

endocrine/exocrine gland phenotype

homeostasis/metabolism phenotype

mortality/aging

Genotype: Insrtm1Khn/Insrtm1Khn Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+involves: 129S4/SvJae * C57BL/6 * DBA/2

endocrine/exocrine gland phenotype

homeostasis/metabolism phenotype

References

Additional References

Additional - Insrtm1Khn related

Genotyping Protocols

Dietary Information

Breeding Considerations

Mating System

Citation

Animal Health Reports

Live Mouse

Cryorecovery - Pricing

Related Products and Services

Payment Terms and Conditions

The Jackson Laboratory's Genotype Promise

Terms Of Use

Licensing Information

JAX® Mice, Products & Services Conditions of Use

No Warranty

Credit for PRODUCTS or SERVICES

Animal Care and Use for SERVICES

No Liability

Also Known As:IR^Lox

Insr^tm1Khn

Allele Symbol: Insr^tm1Khn

Genotype: Insr^tm1Khn/Insr^tm1Khn Tg(Ckmm-cre)5Khn/0
involves: 129S4/SvJae * C57BL/6J * FVB

Genotype: Insr^tm1Khn/Insr^tm1Dac Tg(Ckmm-cre)5Khn/0
involves: 129S4/SvJae * C57BL/6J * FVB

Genotype: Insr^tm1Khn/Insr^tm1Khn Speer6-ps1^{Tg(Alb-cre)21Mgn}/Speer6-ps1⁺
involves: 129S4/SvJae * C57BL/6J * DBA/2 * FVB

Genotype: Insr^tm1Khn/Insr^tm1Khn Tg(Nes-cre)1Kln/0
involves: 129S4/SvJae * C57BL/6J * SJL

Genotype: Insr^tm1Khn/Insr^tm1Khn Tg(Nes-cre)1Kln/0
involves: 129S4/SvJae * C57BL/6 * SJL

Genotype: Insr^tm1Khn/Insr^tm1Khn Tg(Ckmm-cre)5Khn/0
involves: 129S4/SvJae * C57BL/6 * FVB

Genotype: Insr^tm1Khn/Insr^tm1Khn Speer6-ps1^{Tg(Alb-cre)21Mgn}/Speer6-ps1⁺ Tg(Ins2-cre)25Mgn/0
involves: 129S4/SvJae * C57BL/6 * DBA/2

Genotype: Insr^tm1Khn/Insr^tm1Khn Tg(Ins2-cre)25Mgn/0
involves: 129S4/SvJae * C57BL/6 * DBA/2

Genotype: Insr^tm1Khn/Insr^tm1Khn Speer6-ps1^{Tg(Alb-cre)21Mgn}/Speer6-ps1⁺
involves: 129S4/SvJae * C57BL/6 * DBA/2

Additional - Insr^tm1Khn related