Overview

Also Known As:CX₃CR-1^GFP

CX₃CR-1^GFP knock-in/knock-out mice express EGFP in monocytes, dendritic cells, NK cells, and brain microglia under control of the endogenous Cx3cr1 locus. They may be useful in studies of leukocyte migration and trafficking, as well as for transplantation studies.

Donating Investigator

Dr. Dan R. Littman, New York University Medical Center

Genetic overview

Genetic Background	Generation
000664 C57BL/6J	N13F7 (2020-11-10 00:00:00)

Cx3cr1^tm1Litt

Allele Type	Gene Symbol	Gene Name
Targeted (Reporter, Null/Knockout)	Cx3cr1	chemokine (C-X3-C motif) receptor 1

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Research Applications

Research Tools
Cancer Research
Immunology, Inflammation and Autoimmunity Research
Neurobiology Research

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Base Price

Starting at:

$236.78 Domestic price for female 4-week

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Details

Detailed Description

CX₃CR-1^GFP knock-in/knock-out mice have an enhanced green fluorescent protein (EGFP) sequence replacing the first 390 bp of the coding exon (exon 2) of the chemokine (C-X3-C motif) receptor 1 (Cx3cr1) gene. RT-PCR analysis of lymphoid tissue from homozygotes detects mutant gene product (mRNA) and no wild type gene product (mRNA). Flow cytometric analysis of peripheral blood cells identified a subset of green fluorescent cells not observed in wildtype mice. EGFP, but not the endogenous gene, is expressed in monocytes, dendritic cells, NK cells, and brain microglia - mimicking endogenous gene expression. The same subset of peripheral blood cells isolated from heterozygote mice express detectable levels of EGFP. These CX₃CR-1^GFP mutant mice may be useful in studies of leukocyte migration and trafficking, as well as for transplantation studies.

Mice that are homozygous for the CX₃CR-1^GFP targeted mutation are viable and fertile.

Of note, CX₃CR-1^GFP mice are also available harboring with the CD45.1 (Ly5.1 or Ptprc^a) allele, which is atypical for the C57BL/6 congenic background (see Stock No. 008451).

When compared with GFP expression in monocytes in C57BL/6-Tg(CD68-EGFP)1Drg/J mice (Stock No. 026827) using a sterile zymosan peritonitis model, CD68-GFP monocytes retain high-level GFP expression as they differentiate to become mature macrophages, while, CX₃CR1^GFP monocytes downregulate GFP expression on differentiation into macrophages.

Development

A targeting vector containing an Enhanced Green Fluorescent Protein (EGFP, Clontech) cDNA sequence, loxP-flanked neomycin resistance gene, herpes simplex virus thymidine kinase gene, and SV40 polyadenylation site sequence was used to disrupt the first 390 bp of exon 2. The construct was electroporated into 129P2/OlaHsd derived E14.1 embryonic stem (ES) cells which were transiently transfected with a Cre recombinase vector to remove the selection cassette. ES cells that had successfully undergone Cre-mediated recombination (removing the loxP-flanked neo cassette and leaving a single loxP site downstream of EGFP) were injected into recipient blastocysts. The donating investigator reported that resulting chimeric animals were backcrossed to C57BL/6 (see SNP note below) for ten generations before being made homozygous. During the backcross, mice were likely bred to a B6.CD45.1 congenic strain (harboring the CD45.1 (Ly5.1 or Ptprc^a) allele rather than the CD45.2 (Ly5.2 or Ptprc^b) allele normally present in C57BL/6 mice). These mice, however, were bred such that they still harbor the expected CD45.2 (Ly5.2 or Ptprc^b) allele normally present in C57BL/6 mice.

In 2011, 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, 2 of 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 or a mixed C57BL/6J;C57BL/6N genetic background. In 2013, the same SNP panel analysis showed 4 of 5 markers that determine C57BL/6J from C57BL/6N were segregating. The living colony is on a mixed C57BL/6J;C57BL/6N genetic background.

Expression Data

Expressed Gene	GFP, Green Fluorescent Protein,
Site of Expression	GFP labels T and B cells in the lymphoid organs such as spleen, small intestine, and large intestine.

Control Suggestions

Approximate Controls

000664 C57BL/6J

Additional Information

Considerations for Choosing Controls

Selected References

Jung S; Aliberti J; Graemmel P; Sunshine MJ; Kreutzberg GW; Sher A; Littman DR. 2000. Analysis of fractalkine receptor CX(3)CR1 function by targeted deletion and green fluorescent protein reporter gene insertion. Mol Cell Biol 20(11):4106-14PubMed: 10805752 MGI: J:84544

View All References

Genetics

Cx3cr1^tm1Litt

Allele Symbol: Cx3cr1^tm1Litt

Allele Name	targeted mutation 1, Dan R Littman
Allele Type	Targeted (Reporter, Null/Knockout)
Allele Synonym(s)	CX3CR1^-; CX3CR1^EGFP; CX3CR1^GFP; CX3CR1-EGFP; CX3CR1-GFP; CX3CR-GFP
Gene Symbol and Name	Cx3cr1, chemokine (C-X3-C motif) receptor 1
Gene Synonym(s)
Expressed Gene	GFP, Green Fluorescent Protein,
Site of Expression	GFP labels T and B cells in the lymphoid organs such as spleen, small intestine, and large intestine.
Strain of Origin	129P2/OlaHsd
Chromosome	9
Molecular Note	The endogenous locus was disrupted by the insertion of sequence encoding green fluourescent protein (GFP), replacing the first 390 bp of the coding exon (exon 2). The deleted region encoded an amino-terminal portion of the protein that is crucial for interaction with endogenous ligand, Cx3cl1. A floxed neo gene included in the targeting vector for selection was excised prior to germline transmission, leaving a single loxP site downstream of the GFP sequence. RT-PCR and flow cytometry indicated an absence of endogenous protein and the presence GFP expression in homozygous mutant mice.
Mutations Made By	Steffen Jung, Weizmann Institute of Science

Disease/Phenotype

Disease Terms

Research Areas By Phenotype

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

Research Tools
- Immunology, Inflammation and Autoimmunity Research
  - NK Cell Deficiency
- Genetics Research
  - Tissue/Cell Markers
  - Tissue/Cell Markers: transplantation marker for embryonic and adult tissue
  - Tissue/Cell Markers: cell marker for bone marrow transplantation
  - Tissue/Cell Markers: neurons
  - Tissue/Cell Markers: glial cells
  - Tissue/Cell Markers: multiple
- Cancer Research
  - xenograft/transplant host
  - B, T, and NK cell deficiency, xenograft/transplant host
- Toxicology Research
  - xenograft/transplant host
- Developmental Biology Research
  - transplantation marker for embryonic and adult tissue
- Fluorescent Proteins
- Cell Biology Research
- Neurobiology Research
  - cell marker
Cancer Research
- Growth Factors/Receptors/Cytokines
- Toxicology
  - xenograft/transplant host
Immunology, Inflammation and Autoimmunity Research
- Growth Factors/Receptors/Cytokines
- Immunodeficiency
  - NK Cell Deficiency
Neurobiology Research
- Alzheimer's Disease

Mammalian Phenotype Terms by Genotype

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

Genotype: Cx3cr1^tm1Litt/Cx3cr1^tm1Litt
involves: 129P2/OlaHsd

digestive/alimentary phenotype

abnormal small intestinal villus morphology
- ileal villi lack intraepithelial dendritic cell extensions unlike in heterozygous mice

mortality/aging

increased susceptibility to bacterial infection induced morbidity/mortality
- S. typhimurium-infected mice exhibit a higher organ bacterial load and die within 6 days of infection unlike similarly treated heterozygous and wild-type mice

hematopoietic system phenotype

increased dendritic cell number
- antibiotic-treated mice exhibit increased numbers of all subsets of dendritic cells in the mesenteric lymph nodes as compared to untreated controls
- mice treated with antibiotic and infected with non-invasive Salmonella exhibit increased numbers of only CX3CR1 cells in the mesenteric lymph nodes and afferent lymph nodes as compared to uninfected controls

immune system phenotype

abnormal dendritic cell physiology
- Normal - however, sampling of E. coli into the Peyer Patches is normal
- laminar propria dendritic cells exhibit impaired capacity to traverse the epithelial cell monolayer unlike in heterozygous mice
- ileal villi lack intraepithelial dendritic cell extensions unlike in heterozygous mice
- laminar propria dendritic cells fail to properly sample E. coli unlike in heterozygous mice
- S. typhimurium-infected mice exhibit laminar propria dendritic cells that only form globular structures that fail to cross the epithelium unlike in similarly treated heterozygous mice
- intestinal CX3CR1+ cells show defective dendrite extension after treatment with lactic or pyruvic acid

increased susceptibility to bacterial infection induced morbidity/mortality
- S. typhimurium-infected mice exhibit a higher organ bacterial load and die within 6 days of infection unlike similarly treated heterozygous and wild-type mice

decreased inflammatory response
- intestinal CX3CR1+ cells show defective dendrite extension after treatment with lactic or pyruvic acid

increased dendritic cell number
- mice treated with antibiotic and infected with non-invasive Salmonella exhibit increased numbers of only CX3CR1 cells in the mesenteric lymph nodes and afferent lymph nodes as compared to uninfected controls
- antibiotic-treated mice exhibit increased numbers of all subsets of dendritic cells in the mesenteric lymph nodes as compared to untreated controls

Genotype: Cx3cr1^tm1Litt/Cx3cr1^tm1Litt
involves: 129P2/OlaHsd * C57BL/6

cardiovascular system phenotype

choroidal neovascularization
- following laser injury, more subretinal microglial cells accumulate adjacent to the choroid scar than in similarly treated wild-type mice and choroid neovascularization is twice as much as in similarly treated wild-type mice

mammalian phenotype

immune system phenotype
- Normal - normal Langerhans cell migration and APC function in response to contact sensitizer (oxazolone)
- Normal - normal dendritic cell migration and IL-12 production in response to a microbial antigen (STAg)

nervous system phenotype
- Normal - normal neuronal-glial cross talk indicated by microglial response to peripheral nerve injury, 129P2/OlaHsd and C57BL/6 mixed genetic background

renal/urinary system phenotype

decreased susceptibility to kidney reperfusion injury
- following kidney ischemia and reperfusion, mice exhibit decreased kidney injury, tubular cell necrosis, and macrophage recruitment compared with similarly treated heterozygous mice

vision/eye phenotype

abnormal retina morphology
- following laser injury, more subretinal microglial cells accumulate adjacent to the choroid scar than in heterozygous mice at 7 and 14 days post injury
- subretinal microglial cells accumulate with age in the retina unlike in wild-type mice

choroidal neovascularization
- following laser injury, more subretinal microglial cells accumulate adjacent to the choroid scar than in similarly treated wild-type mice and choroid neovascularization is twice as much as in similarly treated wild-type mice

cellular phenotype

impaired macrophage chemotaxis
- following kidney ischemia and reperfusion

hematopoietic system phenotype

abnormal leukocyte physiology
- following kidney ischemia and reperfusion, mice exhibit reduced monocyte egress from the blood into the inflamed kidney compared with similarly treated wild-type mice

decreased monocyte cell number
- Normal - however, expression of Tg(S100A8-BCL2)1Lgs restores monocyte numbers
- mice exhibit a reduction in the number of total monocytes compared with wild-type mice
- Gr1^low monocytes are reduced 3-fold compared to in wild-type mice

impaired macrophage chemotaxis
- following kidney ischemia and reperfusion

homeostasis/metabolism phenotype

decreased susceptibility to kidney reperfusion injury
- following kidney ischemia and reperfusion, mice exhibit decreased kidney injury, tubular cell necrosis, and macrophage recruitment compared with similarly treated heterozygous mice

immune system phenotype

abnormal leukocyte physiology
- following kidney ischemia and reperfusion, mice exhibit reduced monocyte egress from the blood into the inflamed kidney compared with similarly treated wild-type mice

impaired macrophage chemotaxis
- following kidney ischemia and reperfusion

decreased monocyte cell number
- mice exhibit a reduction in the number of total monocytes compared with wild-type mice
- Gr1^low monocytes are reduced 3-fold compared to in wild-type mice
- Normal - however, expression of Tg(S100A8-BCL2)1Lgs restores monocyte numbers

Genotype: Cx3cr1^tm1Litt/Cx3cr1^tm1Litt
C.129P2-Cx3cr1

mammalian phenotype

immune system phenotype
- Normal - normal monocyte extravasation and subsequent differentiation into macrophages in response to intraperitoneal injection of thioglycolate, a model of acute peritonitis

The following phenotype relates to a compound genotype created using this strain

Genotype: Cx3cr1^tm1Litt/Cx3cr1^tm1Litt
B6.129P2-Cx3cr1

behavior/neurological phenotype

paralysis
- following induction of experimental autoimmune encephalomyelitis, mice exhibit nonremitting spastic paralysis

hematopoietic system phenotype

abnormal microglial cell morphology
- increase in microglia numbers in the outer nuclear layer from P14 and a trend for increased microglial process number from P14 becoming significant at P90
- microglia at the level of the photoreceptor terminals exhibit normal soma size and process number with increased process length, indicating that microglia are not classically activated
- presence of microglial processes in the outer retinal is increased at P14 compared with P90, with levels further increased at P270

abnormal microglial cell physiology
- migration of microglial cells in LPS-treated mice is impaired unlike in similarly treated heterozygous mice
- Normal - however, adoptive transfer into Il1r null mice restores microglial cell migration
- microglial-cone interactions are increased in the central and peripheral retina at P21

decreased NK cell number
- in the central nervous system following induction of experimental autoimmune encephalomyelitis

abnormal leukocyte physiology
- following arterial injury, monocyte recruitment is impaired compared to in similarly treated wild-type mice

microgliosis
- intense and widespread following LPS exposure

abnormal NK cell physiology
- following induction of experimental autoimmune encephalomyelitis, recruitment of NK cells is impaired compared to in similarly treated wild-type mice

homeostasis/metabolism phenotype

increased susceptibility to dopaminergic neuron neurotoxicity
- mice treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) exhibit more severe neurotoxicity than similarly treated wild-type mice

abnormal vascular wound healing
- Normal - however, mice exhibit normal luminal and medial areas and platelet function
- following arterial injury, mice exhibit decreased intimal hyperplasia, impaired monocyte recruitment into the vascular wall, and decreased vascular smooth muscle cell proliferation compared to in similarly treated wild-type mice

immune system phenotype

abnormal leukocyte physiology
- following arterial injury, monocyte recruitment is impaired compared to in similarly treated wild-type mice

abnormal microglial cell morphology
- presence of microglial processes in the outer retinal is increased at P14 compared with P90, with levels further increased at P270
- microglia at the level of the photoreceptor terminals exhibit normal soma size and process number with increased process length, indicating that microglia are not classically activated
- increase in microglia numbers in the outer nuclear layer from P14 and a trend for increased microglial process number from P14 becoming significant at P90

abnormal microglial cell physiology
- Normal - however, adoptive transfer into Il1r null mice restores microglial cell migration
- migration of microglial cells in LPS-treated mice is impaired unlike in similarly treated heterozygous mice
- microglial-cone interactions are increased in the central and peripheral retina at P21

brain inflammation
- following induction of experimental autoimmune encephalomyelitis

increased susceptibility to experimental autoimmune encephalomyelitis
- following induction of experimental autoimmune encephalomyelitis, mice exhibit earlier onset, higher mortality, and more severe EAE symptoms (nonremitting spastic paralysis, increased hemorrhagic inflammation, and extensive demyelination) compared with similarly treated wild-type mice
- milarly treated wild-type mice
- following induction of experimental autoimmune encephalomyelitis, recruitment of NK cells is impaired compared to in similarly treated wild-type mice
- Normal - however, priming of encephalitogenic T cells and NKT cell numbers are normal

abnormal NK cell physiology
- following induction of experimental autoimmune encephalomyelitis, recruitment of NK cells is impaired compared to in similarly treated wild-type mice

decreased NK cell number
- in the central nervous system following induction of experimental autoimmune encephalomyelitis

microgliosis
- intense and widespread following LPS exposure

cardiovascular system phenotype

abnormal vascular smooth muscle physiology
- in vitro, vascular smooth muscle cells fail to proliferate in response to CXCL1 unlike similarly treated wild-type cells
- following arterial injury, vascular smooth muscle cell proliferation is decreased compared to in similarly treated wild-type mice

abnormal vascular wound healing
- Normal - however, mice exhibit normal luminal and medial areas and platelet function
- following arterial injury, mice exhibit decreased intimal hyperplasia, impaired monocyte recruitment into the vascular wall, and decreased vascular smooth muscle cell proliferation compared to in similarly treated wild-type mice

brainstem hemorrhage
- following induction of experimental autoimmune encephalomyelitis

mammalian phenotype

immune system phenotype
- Normal - mice exhibit normal response to murine cytomegalovirus infection

mortality/aging

increased sensitivity to induced morbidity/mortality
- following induction of experimental autoimmune encephalomyelitis

muscle phenotype

abnormal vascular smooth muscle physiology
- in vitro, vascular smooth muscle cells fail to proliferate in response to CXCL1 unlike similarly treated wild-type cells
- following arterial injury, vascular smooth muscle cell proliferation is decreased compared to in similarly treated wild-type mice

nervous system phenotype

abnormal photoreceptor connecting cilium morphology
- overall cilium structure is unaffected, however cilium proteins show altered distribution in the transitional zone during photoreceptor maturation

brainstem hemorrhage
- following induction of experimental autoimmune encephalomyelitis

decreased retinal cone cell number
- cone number is reduced from P30 in the periphery and in the central retina at P90
- Normal - however, outer nuclear layer thickness is not altered in either the peripheral or central retina

abnormal microglial cell physiology
- migration of microglial cells in LPS-treated mice is impaired unlike in similarly treated heterozygous mice
- Normal - however, adoptive transfer into Il1r null mice restores microglial cell migration
- microglial-cone interactions are increased in the central and peripheral retina at P21

brain inflammation
- following induction of experimental autoimmune encephalomyelitis

increased neuron apoptosis
- Normal - however, mice subjected to adoptive transfer experiments and treated with an IL1 receptor antagonist exhibit reduced neuron apoptosis
- following LPS exposure, neuron apoptosis is increased unlike in heterozygous mice
- LPS-induced neurotoxicity is cell-autonomous
- Normal - however, adoptive transfer into Il1r null mice abolishes neuron apoptosis

demyelination
- following induction of experimental autoimmune encephalomyelitis, mice exhibit more severe demyelination compared with similarly treated wild-type mice

abnormal microglial cell morphology
- presence of microglial processes in the outer retinal is increased at P14 compared with P90, with levels further increased at P270
- increase in microglia numbers in the outer nuclear layer from P14 and a trend for increased microglial process number from P14 becoming significant at P90
- microglia at the level of the photoreceptor terminals exhibit normal soma size and process number with increased process length, indicating that microglia are not classically activated

abnormal retinal photoreceptor morphology
- marker analysis indicates that photoreceptor maturation is abnormal with impaired outer segment elongation

microgliosis
- intense and widespread following LPS exposure

retinal cone cell degeneration
- from P30 on

increased susceptibility to dopaminergic neuron neurotoxicity
- mice treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) exhibit more severe neurotoxicity than similarly treated wild-type mice

short photoreceptor outer segment
- mice show shortened outer segments in P21 retina

vision/eye phenotype

abnormal retinal outer nuclear layer morphology
- microglial processes are often seen extending deep into the outer nuclear layer where photoreceptors reside

abnormal retinal photoreceptor morphology
- marker analysis indicates that photoreceptor maturation is abnormal with impaired outer segment elongation

retinal degeneration
- late-stage retinal degeneration

retinal cone cell degeneration
- from P30 on

retinal gliosis
- retina shows increased Muller cell gliosis from around eye opening at P14, becoming significant from 1 month of age, and extensive gliosis, particularly within the inner plexiform layer at 3 months of age

abnormal photoreceptor connecting cilium morphology
- overall cilium structure is unaffected, however cilium proteins show altered distribution in the transitional zone during photoreceptor maturation

decreased retinal cone cell number
- cone number is reduced from P30 in the periphery and in the central retina at P90
- Normal - however, outer nuclear layer thickness is not altered in either the peripheral or central retina

retinal outer nuclear layer degeneration
- cell loss is seen in the outer nuclear layer of 16 month old retina but not 3 month old retina

short photoreceptor outer segment
- mice show shortened outer segments in P21 retina

decreased a-wave amplitude
- 22% decrease in amplitude of the a-wave at P270 but not earlier, indicating a late onset of reduced rod-related function

decreased b-wave amplitude
- cone-related function is reduced from P17, shows no increase in response coincident with photoreceptor maturation, the functional deficit remains at P30 and P90, while no difference is seen at P270, with a decrease in b wave amplitude at P17, P30, and P90

abnormal ocular fundus morphology
- mice show numerous white/yellow fundus lesions at 16 months of age but not at 3 months

cellular phenotype

abnormal photoreceptor connecting cilium morphology
- overall cilium structure is unaffected, however cilium proteins show altered distribution in the transitional zone during photoreceptor maturation

increased neuron apoptosis
- following LPS exposure, neuron apoptosis is increased unlike in heterozygous mice
- Normal - however, adoptive transfer into Il1r null mice abolishes neuron apoptosis
- Normal - however, mice subjected to adoptive transfer experiments and treated with an IL1 receptor antagonist exhibit reduced neuron apoptosis
- LPS-induced neurotoxicity is cell-autonomous

increased susceptibility to dopaminergic neuron neurotoxicity
- mice treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) exhibit more severe neurotoxicity than similarly treated wild-type mice

Genotype: Cx3cr1^tm1Litt/Cx3cr1⁺
B6.129P2-Cx3cr1

behavior/neurological phenotype

paresis
- following induction of experimental autoimmune encephalomyelitis, mice exhibit transient flaccid paresis

hematopoietic system phenotype

microgliosis
- moderate following LPS exposure

immune system phenotype

increased susceptibility to experimental autoimmune encephalomyelitis
- following induction of experimental autoimmune encephalomyelitis (EAE), mice exhibit intermediate EAE severity (including transient flaccid paresis) compared with homozygous and wild-type mice
- mice treated with anti-NK1.1 antibodies exhibit the same severity of EAE as in homozygous mice following induction of experimental autoimmune encephalomyelitis

microgliosis
- moderate following LPS exposure

nervous system phenotype

microgliosis
- moderate following LPS exposure

Genotype: Cx3cr1^tm1Litt/Cx3cr1^tm1Litt
B6.129P2(Cg)-Cx3cr1/J

mammalian phenotype

homeostasis/metabolism phenotype
- Normal - mice exhibit normal response (dopamine nerve loss, increased body temperature, and microgliosis) to methamphetamine treatment

References

Jung S; Aliberti J; Graemmel P; Sunshine MJ; Kreutzberg GW; Sher A; Littman DR. 2000. Analysis of fractalkine receptor CX(3)CR1 function by targeted deletion and green fluorescent protein reporter gene insertion. Mol Cell Biol 20(11):4106-14PubMed: 10805752 MGI: J:84544

Additional - Cx3cr1^tm1Litt related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Standard PCR:Cx3cr1alternate1
- Probe:Cx3cr1 Probe Alternate1
- Genotyping resources and troubleshooting
Dietary Information
- LabDiet® 5K52 formulation (6% fat)
Breeding Considerations

When maintaining a live colony, these mice are bred as homozygotes.
- Additional Breeding and Husbandry Support
Mating System
- Homozygote x Homozygote
Citation
When using the CX₃CR-1^GFP mouse strain in a publication, please cite the originating article(s) and include JAX stock #005582 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

AX11 (Maximum)

Pricing & Availability

Available Now

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Live Mouse

Age

Genotype

Price

weeks

Cryorecovery - Pricing

Service/Product	Description	Price
	Heterozygous for Cx3cr1<tm1Litt>

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Frozen Mouse Embryo	B6.129P2(Cg)-Cx3cr1<tm1Litt>/J Frozen Embryos	$3373.50
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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. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.

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General Terms and Conditions

Questions about Terms of Use

Additional Use Restrictions Apply

Use of MICE by companies or for-profit entities requires a license prior to shipping.

Licensing Information

Phone: 207-288-6470

Email: TechTran@jax.org

Also Known As:CX3CR-1GFP

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Expression Data

Control Suggestions

Approximate Controls

Additional Information

Selected References

Cx3cr1tm1Litt

Allele Symbol: Cx3cr1tm1Litt

Disease Terms

Research Areas By Phenotype

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

Mammalian Phenotype Terms by Genotype

Genotype: Cx3cr1tm1Litt/Cx3cr1tm1Littinvolves: 129P2/OlaHsd

digestive/alimentary phenotype

mortality/aging

hematopoietic system phenotype

immune system phenotype

Genotype: Cx3cr1tm1Litt/Cx3cr1tm1Littinvolves: 129P2/OlaHsd * C57BL/6

cardiovascular system phenotype

mammalian phenotype

renal/urinary system phenotype

vision/eye phenotype

cellular phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

immune system phenotype

Genotype: Cx3cr1tm1Litt/Cx3cr1tm1LittC.129P2-Cx3cr1

mammalian phenotype

Genotype: Cx3cr1tm1Litt/Cx3cr1tm1LittB6.129P2-Cx3cr1

behavior/neurological phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

immune system phenotype

cardiovascular system phenotype

mammalian phenotype

mortality/aging

muscle phenotype

nervous system phenotype

vision/eye phenotype

cellular phenotype

Genotype: Cx3cr1tm1Litt/Cx3cr1+B6.129P2-Cx3cr1

behavior/neurological phenotype

hematopoietic system phenotype

immune system phenotype

nervous system phenotype

Genotype: Cx3cr1tm1Litt/Cx3cr1tm1LittB6.129P2(Cg)-Cx3cr1/J

mammalian phenotype

References

Additional - Cx3cr1tm1Litt 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

Additional Use Restrictions Apply

Licensing Information

Also Known As:CX₃CR-1^GFP

Cx3cr1^tm1Litt

Allele Symbol: Cx3cr1^tm1Litt

Genotype: Cx3cr1^tm1Litt/Cx3cr1^tm1Litt
involves: 129P2/OlaHsd

Genotype: Cx3cr1^tm1Litt/Cx3cr1^tm1Litt
involves: 129P2/OlaHsd * C57BL/6

Genotype: Cx3cr1^tm1Litt/Cx3cr1^tm1Litt
C.129P2-Cx3cr1

Genotype: Cx3cr1^tm1Litt/Cx3cr1^tm1Litt
B6.129P2-Cx3cr1

Genotype: Cx3cr1^tm1Litt/Cx3cr1⁺
B6.129P2-Cx3cr1

Genotype: Cx3cr1^tm1Litt/Cx3cr1^tm1Litt
B6.129P2(Cg)-Cx3cr1/J

Additional - Cx3cr1^tm1Litt related