Overview

Also Known As: CX3CR1-GFP

CX3CR1-GFP 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
	N13F5 (2019-06-13 00:00:00)

Cx3cr1^tm1Litt

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

View Genetics

Research Applications

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

View All Research Applications

Base Price

Starting at:

$0.00 Domestic price for male 4-week

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Details

Detailed Description

Mice that are homozygous for the CX3CR1-GFP targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. 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. Enhanced Green Fluorescent Protein (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 CX3CR1-GFP mutant mice may be useful in studies of leukocyte migration and trafficking, as well as for transplantation studies.

Of note, CX3CR1-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)	targeted mutation 1, Dan R Littman; Cx3cr1^tm1Litt
Gene Symbol and Name	Cx3cr1, chemokine (C-X3-C motif) receptor 1
Gene Synonym(s)	CMKDR1; GPR13; GPRV28; V28; CMKBRL1; CCRL1; Rbs11
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 Genotype

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

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
- Gr1^low monocytes are reduced 3-fold compared to in wild-type mice
- 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

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

decreased monocyte cell number
- Gr1^low monocytes are reduced 3-fold compared to in wild-type mice
- 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

impaired macrophage chemotaxis
- following kidney ischemia and reperfusion

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

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
- ileal villi lack intraepithelial dendritic cell extensions unlike in heterozygous mice
- laminar propria dendritic cells exhibit impaired capacity to traverse the epithelial cell monolayer 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

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

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

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

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

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

homeostasis/metabolism phenotype

abnormal vascular wound healing
- 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
- Normal - however, mice exhibit normal luminal and medial areas and platelet function

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

cardiovascular system phenotype

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

abnormal vascular wound healing
- 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
- Normal - however, mice exhibit normal luminal and medial areas and platelet function

brainstem hemorrhage
- following induction of experimental autoimmune encephalomyelitis

immune system phenotype

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

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

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

brain inflammation
- following induction of experimental autoimmune encephalomyelitis

decreased NK cell number
- in the central nervous system 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
- 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
- milarly treated wild-type mice

microgliosis
- intense and widespread following LPS exposure

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

nervous system phenotype

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

brain inflammation
- following induction of experimental autoimmune encephalomyelitis

brainstem hemorrhage
- following induction of experimental autoimmune encephalomyelitis

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

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

microgliosis
- intense and widespread following LPS exposure

cellular phenotype

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 References

Cope EC; LaMarca EA; Monari PK; Olson LB; Martinez S; Zych AD; Katchur NJ; Gould E. 2018. Microglia Play an Active Role in Obesity-Associated Cognitive Decline. J Neurosci 38(41):8889-8904PubMed: 30201764 MGI: J:266379
Rahmani W; Liu Y; Rosin NL; Kline A; Raharjo E; Yoon J; Stratton JA; Sinha S; Biernaskie J. 2018. Macrophages Promote Wound-Induced Hair Follicle Regeneration in a CX3CR1- and TGF-beta1-Dependent Manner. J Invest Dermatol 138(10):2111-2122PubMed: 29705291 MGI: J:266395
Kreisel T; Wolf B; Keshet E; Licht T. 2019. Unique role for dentate gyrus microglia in neuroblast survival and in VEGF-induced activation. Glia 67(4):594-618PubMed: 30453385 MGI: J:271655
Rotterman TM; Akhter ET; Lane AR; MacPherson KP; Garcia VV; Tansey MG; Alvarez FJ. 2019. Spinal Motor Circuit Synaptic Plasticity after Peripheral Nerve Injury Depends on Microglia Activation and a CCR2 Mechanism. J Neurosci 39(18):3412-3433PubMed: 30833511 MGI: J:274670

Additional - Cx3cr1^tm1Litt related

Technical Support

Contact Technical Support

Genotyping Protocols
- High Resolution Melting: Cx3cr1^tm1Littalternate1
- 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 CX3CR1-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

Domestic
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Live Mouse

Age

Genotype

Price

weeks

Cryorecovery - Pricing

Service	Genotype	Price
	Heterozygous for Cx3cr1<tm1Litt>

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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Also Known As: CX3CR1-GFP

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 Genotype

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

Mammalian Phenotype Terms by Genotype

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/Cx3cr1tm1Littinvolves: 129P2/OlaHsd

digestive/alimentary phenotype

mortality/aging

hematopoietic system phenotype

immune system phenotype

Genotype: Cx3cr1tm1Litt/Cx3cr1tm1LittB6.129P2-Cx3cr1

behavior/neurological phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

cardiovascular system phenotype

immune system phenotype

mammalian phenotype

mortality/aging

muscle phenotype

nervous system 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 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

JAX® Mice, Products & Services Conditions of Use

No Warranty

Credit for PRODUCTS or SERVICES

Animal Care and Use for SERVICES

No Liability

Cx3cr1^tm1Litt

Allele Symbol: Cx3cr1^tm1Litt

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

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

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

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