JAX Mouse Strain Datasheet - 005582

B6.129P-Cx3cr1^tm1Litt/J

Stock No:: 005582 |; CX3CR1-GFP

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Overview

Also Known As: CX3CR1-GFP

These 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
	N12F10 (16-MAY-16)

Cx3cr1^tm1Litt

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

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Research Applications

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

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Base Price

Starting at:

$224.00 Domestic price for female 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 wild type 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

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):4106-14. PubMed: 10805752 MGI: J:84544

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Genetics

Cx3cr1^tm1Litt

Allele Symbol: Cx3cr1^tm1Litt

Allele Name	targeted mutation 1, Dan R Littman
Allele Type	Targeted (Null/Knockout, Reporter)
Allele Synonym(s)	CX3CR-GFP; CX3CR1-EGFP; CX3CR1-GFP; CX3CR1^-; CX3CR1^EGFP; CX3CR1^GFP; Cx3cr1^gfp
Gene Symbol and Name	Cx3cr1, chemokine (C-X3-C motif) receptor 1
Gene Synonym(s)	CCRL1; CMKBRL1; CMKDR1; GPR13; GPRV28; Rbs11; V28
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:

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
Research Tools
- Cancer Research
  - B, T, and NK cell deficiency, xenograft/transplant host
  - xenograft/transplant host
- Cell Biology Research
- Developmental Biology Research
  - transplantation marker for embryonic and adult tissue
- Fluorescent Proteins
- Genetics Research
  - Tissue/Cell Markers
  - Tissue/Cell Markers: cell marker for bone marrow transplantation
  - Tissue/Cell Markers: glial cells
  - Tissue/Cell Markers: multiple
  - Tissue/Cell Markers: neurons
  - Tissue/Cell Markers: transplantation marker for embryonic and adult tissue
- Immunology, Inflammation and Autoimmunity Research
  - NK Cell Deficiency
- Neurobiology Research
  - cell marker
- Toxicology Research
  - xenograft/transplant host

Genotype: GFP related

Research Tools
- Fluorescent Proteins

Mammalian Phenotype Terms by Genotype

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

nervous 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

behavior/neurological phenotype

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

hematopoietic system phenotype

microgliosis
- moderate following LPS exposure

Genotype: Cx3cr1^tm1Litt/Cx3cr1^tm1Litt
B6.129P-Cx3cr1^tm1Litt/J

homeostasis/metabolism phenotype

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

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

mortality/aging

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

nervous system phenotype

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

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

immune system phenotype

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

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

abnormal microglial cell physiology
- 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

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

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

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 micemilarly treated wild-type mice
- following induction of experimental autoimmune encephalomyelitis, recruitment of NK cells is impaired compared to in similarly treated wild-type mice
- however, priming of encephalitogenic T cells and NKT cell numbers are normal

microgliosis
- intense and widespread following LPS exposure

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
- however, mice exhibit normal luminal and medial areas and platelet function

brainstem hemorrhage
- following induction of experimental autoimmune encephalomyelitis

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
- 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

behavior/neurological phenotype

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

hematopoietic system phenotype

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

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

abnormal microglial cell physiology
- 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

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

microgliosis
- intense and widespread following LPS exposure

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

cellular phenotype

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

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

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

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
- 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

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

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

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

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

nervous system phenotype

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

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

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
- 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

cellular phenotype

impaired macrophage chemotaxis
- following kidney ischemia and reperfusion

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

immune system phenotype

immune system phenotype
- 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

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

immune system phenotype

abnormal dendritic cell physiology
- 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
- 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

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

digestive/alimentary phenotype

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

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):4106-14. PubMed: 10805752 MGI: J:84544

Additional - Cx3cr1^tm1Litt related

A-Gonzalez N; Guillen JA; Gallardo G; Diaz M; de la Rosa JV; Hernandez IH; Casanova-Acebes M; Lopez F; Tabraue C; Beceiro S; Hong C; Lara PC; Andujar M; Arai S; Miyazaki T; Li S; Corbi AL; Tontonoz P; Hidalgo A; Castrillo A. 2013. The nuclear receptor LXRalpha controls the functional specialization of splenic macrophages. Nat Immunol 14(8):831-9. PubMed: 23770640 MGI: J:204819
Abiega O; Beccari S; Diaz-Aparicio I; Nadjar A; Laye S; Leyrolle Q; Gomez-Nicola D; Domercq M; Perez-Samartin A; Sanchez-Zafra V; Paris I; Valero J; Savage JC; Hui CW; Tremblay ME; Deudero JJ; Brewster AL; Anderson AE; Zaldumbide L; Galbarriatu L; Marinas A; Vivanco Md; Matute C; Maletic-Savatic M; Encinas JM; Sierra A. 2016. Neuronal Hyperactivity Disturbs ATP Microgradients, Impairs Microglial Motility, and Reduces Phagocytic Receptor Expression Triggering Apoptosis/Microglial Phagocytosis Uncoupling. PLoS Biol 14(5):e1002466. PubMed: 27228556 MGI: J:236323
Acharya N; Penukonda S; Shcheglova T; Hagymasi AT; Basu S; Srivastava PK. 2017. Endocannabinoid system acts as a regulator of immune homeostasis in the gut. Proc Natl Acad Sci U S A 114(19):5005-5010. PubMed: 28439004 MGI: J:242225
Afik R; Zigmond E; Vugman M; Klepfish M; Shimshoni E; Pasmanik-Chor M; Shenoy A; Bassat E; Halpern Z; Geiger T; Sagi I; Varol C. 2016. Tumor macrophages are pivotal constructors of tumor collagenous matrix. J Exp Med 213(11):2315-2331. PubMed: 27697834 MGI: J:237417
Alt C; Runnels JM; Mortensen LJ; Zaher W; Lin CP. 2014. In vivo imaging of microglia turnover in the mouse retina after ionizing radiation and dexamethasone treatment. Invest Ophthalmol Vis Sci 55(8):5314-9. PubMed: 25082884 MGI: J:230246
An G; Wang H; Tang R; Yago T; McDaniel JM; McGee S; Huo Y; Xia L. 2008. P-selectin glycoprotein ligand-1 is highly expressed on Ly-6Chi monocytes and a major determinant for Ly-6Chi monocyte recruitment to sites of atherosclerosis in mice. Circulation 117(25):3227-37. PubMed: 18519846 MGI: J:155081
Arno B; Grassivaro F; Rossi C; Bergamaschi A; Castiglioni V; Furlan R; Greter M; Favaro R; Comi G; Becher B; Martino G; Muzio L. 2014. Neural progenitor cells orchestrate microglia migration and positioning into the developing cortex. Nat Commun 5:5611. PubMed: 25425146 MGI: J:225279
Arnold L; Henry A; Poron F; Baba-Amer Y; van Rooijen N; Plonquet A; Gherardi RK; Chazaud B. 2007. Inflammatory monocytes recruited after skeletal muscle injury switch into antiinflammatory macrophages to support myogenesis. J Exp Med 204(5):1057-69. PubMed: 17485518 MGI: J:125715
Arnold L; Perrin H; de Chanville CB; Saclier M; Hermand P; Poupel L; Guyon E; Licata F; Carpentier W; Vilar J; Mounier R; Chazaud B; Benhabiles N; Boissonnas A; Combadiere B; Combadiere C. 2015. CX3CR1 deficiency promotes muscle repair and regeneration by enhancing macrophage ApoE production. Nat Commun 6:8972. PubMed: 26632270 MGI: J:228319
Asano K; Takahashi N; Ushiki M; Monya M; Aihara F; Kuboki E; Moriyama S; Iida M; Kitamura H; Qiu CH; Watanabe T; Tanaka M. 2015. Intestinal CD169(+) macrophages initiate mucosal inflammation by secreting CCL8 that recruits inflammatory monocytes. Nat Commun 6:7802. PubMed: 26193821 MGI: J:224450
Auffray C; Fogg DK; Narni-Mancinelli E; Senechal B; Trouillet C; Saederup N; Leemput J; Bigot K; Campisi L; Abitbol M; Molina T; Charo I; Hume DA; Cumano A; Lauvau G; Geissmann F. 2009. CX3CR1+ CD115+ CD135+ common macrophage/DC precursors and the role of CX3CR1 in their response to inflammation. J Exp Med 206(3):595-606. PubMed: 19273628 MGI: J:146747
Avraham-Davidi I; Yona S; Grunewald M; Landsman L; Cochain C; Silvestre JS; Mizrahi H; Faroja M; Strauss-Ayali D; Mack M; Jung S; Keshet E. 2013. On-site education of VEGF-recruited monocytes improves their performance as angiogenic and arteriogenic accessory cells. J Exp Med 210(12):2611-25. PubMed: 24166715 MGI: J:207718
Baalman K; Marin MA; Ho TS; Godoy M; Cherian L; Robertson C; Rasband MN. 2015. Axon initial segment-associated microglia. J Neurosci 35(5):2283-92. PubMed: 25653382 MGI: J:219895
Baik SH; Kang S; Son SM; Mook-Jung I. 2016. Microglia contributes to plaque growth by cell death due to uptake of amyloid beta in the brain of Alzheimer's disease mouse model. Glia 64(12):2274-2290. PubMed: 27658617 MGI: J:236228
Baldwin KT; Carbajal KS; Segal BM; Giger RJ. 2015. Neuroinflammation triggered by beta-glucan/dectin-1 signaling enables CNS axon regeneration. Proc Natl Acad Sci U S A 112(8):2581-6. PubMed: 25675510 MGI: J:220172
Bar-On L; Birnberg T; Lewis KL; Edelson BT; Bruder D; Hildner K; Buer J; Murphy KM; Reizis B; Jung S. 2010. CX3CR1+ CD8alpha+ dendritic cells are a steady-state population related to plasmacytoid dendritic cells. Proc Natl Acad Sci U S A 107(33):14745-50. PubMed: 20679228 MGI: J:163703
Baron R; Babcock AA; Nemirovsky A; Finsen B; Monsonego A. 2014. Accelerated microglial pathology is associated with Abeta plaques in mouse models of Alzheimer's disease. Aging Cell 13(4):584-95. PubMed: 24641683 MGI: J:215081
Batti L; Sundukova M; Murana E; Pimpinella S; De Castro Reis F; Pagani F; Wang H; Pellegrino E; Perlas E; Di Angelantonio S; Ragozzino D; Heppenstall PA. 2016. TMEM16F Regulates Spinal Microglial Function in Neuropathic Pain States. Cell Rep 15(12):2608-15. PubMed: 27332874 MGI: J:238366
Bergsbaken T; Bevan MJ. 2015. Proinflammatory microenvironments within the intestine regulate the differentiation of tissue-resident CD8(+) T cells responding to infection. Nat Immunol 16(4):406-14. PubMed: 25706747 MGI: J:231497
Berta T; Park CK; Xu ZZ; Xie RG; Liu T; Lu N; Liu YC; Ji RR. 2014. Extracellular caspase-6 drives murine inflammatory pain via microglial TNF-alpha secretion. J Clin Invest 124(3):1173-86. PubMed: 24531553 MGI: J:209726
Bertrand JY; Jalil A; Klaine M; Jung S; Cumano A; Godin I. 2005. Three pathways to mature macrophages in the early mouse yolk sac. Blood 106(9):3004-11. PubMed: 16020514 MGI: J:123941
Bhaskar K; Konerth M; Kokiko-Cochran ON; Cardona A; Ransohoff RM; Lamb BT. 2010. Regulation of tau pathology by the microglial fractalkine receptor. Neuron 68(1):19-31. PubMed: 20920788 MGI: J:167757
Blomster LV; Vukovic J; Hendrickx DA; Jung S; Harvey AR; Filgueira L; Ruitenberg MJ. 2011. CX(3)CR1 deficiency exacerbates neuronal loss and impairs early regenerative responses in the target-ablated olfactory epithelium. Mol Cell Neurosci 48(3):236-45. PubMed: 21871566 MGI: J:189381
Bogunovic M; Ginhoux F; Helft J; Shang L; Hashimoto D; Greter M; Liu K; Jakubzick C; Ingersoll MA; Leboeuf M; Stanley ER; Nussenzweig M; Lira SA; Randolph GJ; Merad M. 2009. Origin of the lamina propria dendritic cell network. Immunity 31(3):513-25. PubMed: 19733489 MGI: J:152688
Bonnardel J; Da Silva C; Henri S; Tamoutounour S; Chasson L; Montanana-Sanchis F; Gorvel JP; Lelouard H. 2015. Innate and adaptive immune functions of peyer's patch monocyte-derived cells. Cell Rep 11(5):770-84. PubMed: 25921539 MGI: J:228363
Bosco A; Crish SD; Steele MR; Romero CO; Inman DM; Horner PJ; Calkins DJ; Vetter ML. 2012. Early reduction of microglia activation by irradiation in a model of chronic glaucoma. PLoS One 7(8):e43602. PubMed: 22952717 MGI: J:191663
Bosco A; Romero CO; Breen KT; Chagovetz AA; Steele MR; Ambati BK; Vetter ML. 2015. Neurodegeneration severity can be predicted from early microglia alterations monitored in vivo in a mouse model of chronic glaucoma. Dis Model Mech 8(5):443-55. PubMed: 25755083 MGI: J:221352
Bottcher JP; Beyer M; Meissner F; Abdullah Z; Sander J; Hochst B; Eickhoff S; Rieckmann JC; Russo C; Bauer T; Flecken T; Giesen D; Engel D; Jung S; Busch DH; Protzer U; Thimme R; Mann M; Kurts C; Schultze JL; Kastenmuller W; Knolle PA. 2015. Functional classification of memory CD8(+) T cells by CX3CR1 expression. Nat Commun 6:8306. PubMed: 26404698 MGI: J:227216
Bradfield PF; Scheiermann C; Nourshargh S; Ody C; Luscinskas FW; Rainger GE; Nash GB; Miljkovic-Licina M; Aurrand-Lions M; Imhof BA. 2007. JAM-C regulates unidirectional monocyte transendothelial migration in inflammation. Blood 110(7):2545-55. PubMed: 17625065 MGI: J:147010
Broz ML; Binnewies M; Boldajipour B; Nelson AE; Pollack JL; Erle DJ; Barczak A; Rosenblum MD; Daud A; Barber DL; Amigorena S; Van't Veer LJ; Sperling AI; Wolf DM; Krummel MF. 2014. Dissecting the tumor myeloid compartment reveals rare activating antigen-presenting cells critical for T cell immunity. Cancer Cell 26(5):638-52. PubMed: 25446897 MGI: J:217466
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Seyed-Razavi Y; Chinnery HR; McMenamin PG. 2014. A novel association between resident tissue macrophages and nerves in the peripheral stroma of the murine cornea. Invest Ophthalmol Vis Sci 55(3):1313-20. PubMed: 24458151 MGI: J:229287
Shechter R; London A; Kuperman Y; Ronen A; Rolls A; Chen A; Schwartz M. 2013. Hypothalamic neuronal toll-like receptor 2 protects against age-induced obesity. Sci Rep 3:1254. PubMed: 23409245 MGI: J:207263
Shechter R; Miller O; Yovel G; Rosenzweig N; London A; Ruckh J; Kim KW; Klein E; Kalchenko V; Bendel P; Lira SA; Jung S; Schwartz M. 2013. Recruitment of beneficial m2 macrophages to injured spinal cord is orchestrated by remote brain choroid plexus. Immunity 38(3):555-69. PubMed: 23477737 MGI: J:194904
Shibuya Y; Chang CC; Huang LH; Bryleva EY; Chang TY. 2014. Inhibiting ACAT1/SOAT1 in microglia stimulates autophagy-mediated lysosomal proteolysis and increases Abeta1-42 clearance. J Neurosci 34(43):14484-501. PubMed: 25339759 MGI: J:217151
Shum WW; Smith TB; Cortez-Retamozo V; Grigoryeva LS; Roy JW; Hill E; Pittet MJ; Breton S; Da Silva N. 2014. Epithelial basal cells are distinct from dendritic cells and macrophages in the mouse epididymis. Biol Reprod 90(5):90. PubMed: 24648397 MGI: J:210305
Soehnlein O; Zernecke A; Eriksson EE; Rothfuchs AG; Pham CT; Herwald H; Bidzhekov K; Rottenberg ME; Weber C; Lindbom L. 2008. Neutrophil secretion products pave the way for inflammatory monocytes. Blood 112(4):1461-71. PubMed: 18490516 MGI: J:138439
Song JW; Misgeld T; Kang H; Knecht S; Lu J; Cao Y; Cotman SL; Bishop DL; Lichtman JW. 2008. Lysosomal activity associated with developmental axon pruning. J Neurosci 28(36):8993-9001. PubMed: 18768693 MGI: J:141170
Song KH; Park J; Park JH; Natarajan R; Ha H. 2013. Fractalkine and its receptor mediate extracellular matrix accumulation in diabetic nephropathy in mice. Diabetologia 56(7):1661-9. PubMed: 23604552 MGI: J:198960
Stark K; Philippi V; Stockhausen S; Busse J; Antonelli A; Miller M; Schubert I; Hoseinpour P; Chandraratne S; von Bruhl ML; Gaertner F; Lorenz M; Agresti A; Coletti R; Antoine DJ; Heermann R; Jung K; Reese S; Laitinen I; Schwaiger M; Walch A; Sperandio M; Nawroth PP; Reinhardt C; Jackel S; Bianchi ME; Massberg S. 2016. Disulfide HMGB1 derived from platelets coordinates venous thrombosis in mice. Blood 128(20):2435-2449. PubMed: 27574188 MGI: J:237387
Staumont-Salle D; Fleury S; Lazzari A; Molendi-Coste O; Hornez N; Lavogiez C; Kanda A; Wartelle J; Fries A; Pennino D; Mionnet C; Prawitt J; Bouchaert E; Delaporte E; Glaichenhaus N; Staels B; Julia V; Dombrowicz D. 2014. CX(3)CL1 (fractalkine) and its receptor CX(3)CR1 regulate atopic dermatitis by controlling effector T cell retention in inflamed skin. J Exp Med 211(6):1185-96. PubMed: 24821910 MGI: J:213740
Stein K; Stoffels M; Lysson M; Schneiker B; Dewald O; Kronke G; Kalff JC; Wehner S. 2016. A role for 12/15-lipoxygenase-derived proresolving mediators in postoperative ileus: protectin DX-regulated neutrophil extravasation. J Leukoc Biol 99(2):231-9. PubMed: 26292977 MGI: J:242874
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Sun K; Yajjala VK; Bauer C; Talmon GA; Fischer KJ; Kielian T; Metzger DW. 2016. Nox2-derived oxidative stress results in inefficacy of antibiotics against post-influenza S. aureus pneumonia. J Exp Med 213(9):1851-64. PubMed: 27526712 MGI: J:236726
Sundberg TB; Choi HG; Song JH; Russell CN; Hussain MM; Graham DB; Khor B; Gagnon J; O'Connell DJ; Narayan K; Dancik V; Perez JR; Reinecker HC; Gray NS; Schreiber SL; Xavier RJ; Shamji AF. 2014. Small-molecule screening identifies inhibition of salt-inducible kinases as a therapeutic strategy to enhance immunoregulatory functions of dendritic cells. Proc Natl Acad Sci U S A 111(34):12468-73. PubMed: 25114223 MGI: J:213913
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Synowitz M; Glass R; Farber K; Markovic D; Kronenberg G; Herrmann K; Schnermann J; Nolte C; van Rooijen N; Kiwit J; Kettenmann H. 2006. A1 adenosine receptors in microglia control glioblastoma-host interaction. Cancer Res 66(17):8550-7. PubMed: 16951167 MGI: J:112410
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Taylor RA; Chang CF; Goods BA; Hammond MD; Mac Grory B; Ai Y; Steinschneider AF; Renfroe SC; Askenase MH; McCullough LD; Kasner SE; Mullen MT; Hafler DA; Love JC; Sansing LH. 2017. TGF-beta1 modulates microglial phenotype and promotes recovery after intracerebral hemorrhage. J Clin Invest 127(1):280-292. PubMed: 27893460 MGI: J:239742
Taylor RA; Hammond MD; Ai Y; Sansing LH. 2014. CX3CR1 signaling on monocytes is dispensable after intracerebral hemorrhage. PLoS One 9(12):e114472. PubMed: 25469644 MGI: J:225693
Thomas DM; Francescutti-Verbeem DM; Kuhn DM. 2008. Methamphetamine-induced neurotoxicity and microglial activation are not mediated by fractalkine receptor signaling. J Neurochem 106(2):696-705. PubMed: 18410508 MGI: J:139390
Tighe RM; Li Z; Potts EN; Frush S; Liu N; Gunn MD; Foster WM; Noble PW; Hollingsworth JW. 2011. Ozone inhalation promotes CX3CR1-dependent maturation of resident lung macrophages that limit oxidative stress and inflammation. J Immunol 187(9):4800-8. PubMed: 21930959 MGI: J:179462
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Vallon-Eberhard A; Landsman L; Yogev N; Verrier B; Jung S. 2006. Transepithelial pathogen uptake into the small intestinal lamina propria. J Immunol 176(4):2465-9. PubMed: 16456006 MGI: J:106225
Van Overmeire E; Stijlemans B; Heymann F; Keirsse J; Morias Y; Elkrim Y; Brys L; Abels C; Lahmar Q; Ergen C; Vereecke L; Tacke F; De Baetselier P; Van Ginderachter JA; Laoui D. 2016. M-CSF and GM-CSF Receptor Signaling Differentially Regulate Monocyte Maturation and Macrophage Polarization in the Tumor Microenvironment. Cancer Res 76(1):35-42. PubMed: 26573801 MGI: J:230585
Varol C; Landsman L; Fogg DK; Greenshtein L; Gildor B; Margalit R; Kalchenko V; Geissmann F; Jung S. 2007. Monocytes give rise to mucosal, but not splenic, conventional dendritic cells. J Exp Med 204(1):171-80. PubMed: 17190836 MGI: J:125312
Varol C; Vallon-Eberhard A; Elinav E; Aychek T; Shapira Y; Luche H; Fehling HJ; Hardt WD; Shakhar G; Jung S. 2009. Intestinal lamina propria dendritic cell subsets have different origin and functions. Immunity 31(3):502-12. PubMed: 19733097 MGI: J:152689
Varvel NH; Bhaskar K; Kounnas MZ; Wagner SL; Yang Y; Lamb BT; Herrup K. 2009. NSAIDs prevent, but do not reverse, neuronal cell cycle reentry in a mouse model of Alzheimer disease. J Clin Invest 119(12):3692-702. PubMed: 19907078 MGI: J:155100
Vessey KA; Greferath U; Jobling AI; Phipps JA; Ho T; Waugh M; Fletcher EL. 2012. Ccl2/Cx3cr1 knockout mice have inner retinal dysfunction but are not an accelerated model of AMD. Invest Ophthalmol Vis Sci 53(12):7833-46. PubMed: 23074204 MGI: J:214216
Vukovic J; Blomster LV; Chinnery HR; Weninger W; Jung S; McMenamin PG; Ruitenberg MJ. 2010. Bone marrow chimeric mice reveal a role for CXCR1 in maintenance of the monocyte-derived cell population in the olfactory neuroepithelium. J Leukoc Biol 88(4):645-54. PubMed: 20610801 MGI: J:165615
Vukovic J; Colditz MJ; Blackmore DG; Ruitenberg MJ; Bartlett PF. 2012. Microglia modulate hippocampal neural precursor activity in response to exercise and aging. J Neurosci 32(19):6435-43. PubMed: 22573666 MGI: J:184859
Waddell A; Ahrens R; Steinbrecher K; Donovan B; Rothenberg ME; Munitz A; Hogan SP. 2011. Colonic eosinophilic inflammation in experimental colitis is mediated by Ly6C(high) CCR2(+) inflammatory monocyte/macrophage-derived CCL11. J Immunol 186(10):5993-6003. PubMed: 21498668 MGI: J:173219
Wang J; Gusti V; Saraswati A; Lo DD. 2011. Convergent and divergent development among M cell lineages in mouse mucosal epithelium. J Immunol 187(10):5277-85. PubMed: 21984701 MGI: J:179643
Wang J; Kubes P. 2016. A Reservoir of Mature Cavity Macrophages that Can Rapidly Invade Visceral Organs to Affect Tissue Repair. Cell 165(3):668-78. PubMed: 27062926 MGI: J:234500
Wang K; Peng B; Lin B. 2014. Fractalkine receptor regulates microglial neurotoxicity in an experimental mouse glaucoma model. Glia 62(12):1943-54. PubMed: 24989686 MGI: J:214962
Wang Y; Cella M; Mallinson K; Ulrich JD; Young KL; Robinette ML; Gilfillan S; Krishnan GM; Sudhakar S; Zinselmeyer BH; Holtzman DM; Cirrito JR; Colonna M. 2015. TREM2 lipid sensing sustains the microglial response in an Alzheimer's disease model. Cell 160(6):1061-71. PubMed: 25728668 MGI: J:222876
Wantha S; Alard JE; Megens RT; van der Does AM; Doring Y; Drechsler M; Pham CT; Wang MW; Wang JM; Gallo RL; von Hundelshausen P; Lindbom L; Hackeng T; Weber C; Soehnlein O. 2013. Neutrophil-derived cathelicidin promotes adhesion of classical monocytes. Circ Res 112(5):792-801. PubMed: 23283724 MGI: J:212860
Weber B; Saurer L; Schenk M; Dickgreber N; Mueller C. 2011. CX3CR1 defines functionally distinct intestinal mononuclear phagocyte subsets which maintain their respective functions during homeostatic and inflammatory conditions. Eur J Immunol 41(3):773-9. PubMed: 21341263 MGI: J:175420
Willart MA; Jan de Heer H; Hammad H; Soullie T; Deswarte K; Clausen BE; Boon L; Hoogsteden HC; Lambrecht BN. 2009. The lung vascular filter as a site of immune induction for T cell responses to large embolic antigen. J Exp Med 206(12):2823-35. PubMed: 19858325 MGI: J:154860
Wojcik AJ; Skaflen MD; Srinivasan S; Hedrick CC. 2008. A Critical Role for ABCG1 in Macrophage Inflammation and Lung Homeostasis. J Immunol 180(6):4273-82. PubMed: 18322240 MGI: J:132952
Wolf Y; Shemer A; Polonsky M; Gross M; Mildner A; Yona S; David E; Kim KW; Goldmann T; Amit I; Heikenwalder M; Nedospasov S; Prinz M; Friedman N; Jung S. 2017. Autonomous TNF is critical for in vivo monocyte survival in steady state and inflammation. J Exp Med 214(4):905-917. PubMed: 28330904 MGI: J:241862
Wong HS; Jaumouille V; Freeman SA; Doodnauth SA; Schlam D; Canton J; Mukovozov IM; Saric A; Grinstein S; Robinson LA. 2016. Chemokine Signaling Enhances CD36 Responsiveness toward Oxidized Low-Density Lipoproteins and Accelerates Foam Cell Formation. Cell Rep 14(12):2859-71. PubMed: 26997267 MGI: J:234880
Woodfin A; Voisin MB; Beyrau M; Colom B; Caille D; Diapouli FM; Nash GB; Chavakis T; Albelda SM; Rainger GE; Meda P; Imhof BA; Nourshargh S. 2011. The junctional adhesion molecule JAM-C regulates polarized transendothelial migration of neutrophils in vivo. Nat Immunol 12(8):761-9. PubMed: 21706006 MGI: J:174437
Wu LJ; Vadakkan KI; Zhuo M. 2007. ATP-induced chemotaxis of microglial processes requires P2Y receptor-activated initiation of outward potassium currents. Glia 55(8):810-21. PubMed: 17357150 MGI: J:156095
Wu LJ; Wu G; Akhavan Sharif MR; Baker A; Jia Y; Fahey FH; Luo HR; Feener EP; Clapham DE. 2012. The voltage-gated proton channel Hv1 enhances brain damage from ischemic stroke. Nat Neurosci 15(4):565-73. PubMed: 22388960 MGI: J:191259
Xi H; Katschke KJ Jr; Helmy KY; Wark PA; Kljavin N; Clark H; Eastham-Anderson J; Shek T; Roose-Girma M; Ghilardi N; van Lookeren Campagne M. 2010. Negative regulation of autoimmune demyelination by the inhibitory receptor CLM-1. J Exp Med 207(1):7-16, S1-5. PubMed: 20038601 MGI: J:156819
Xiong Z; Leme AS; Ray P; Shapiro SD; Lee JS. 2011. CX3CR1+ Lung Mononuclear Phagocytes Spatially Confined to the Interstitium Produce TNF-{alpha} and IL-6 and Promote Cigarette Smoke-Induced Emphysema. J Immunol 186(5):3206-14. PubMed: 21278339 MGI: J:169385
Yamasaki R; Fujii T; Wang B; Masaki K; Kido MA; Yoshida M; Matsushita T; Kira JI. 2016. Allergic Inflammation Leads to Neuropathic Pain via Glial Cell Activation. J Neurosci 36(47):11929-11945. PubMed: 27881779 MGI: J:237192
Yamasaki R; Lu H; Butovsky O; Ohno N; Rietsch AM; Cialic R; Wu PM; Doykan CE; Lin J; Cotleur AC; Kidd G; Zorlu MM; Sun N; Hu W; Liu L; Lee JC; Taylor SE; Uehlein L; Dixon D; Gu J; Floruta CM; Zhu M; Charo IF; Weiner HL; Ransohoff RM. 2014. Differential roles of microglia and monocytes in the inflamed central nervous system. J Exp Med 211(8):1533-49. PubMed: 25002752 MGI: J:214724
Yang J; Yang H; Liu Y; Li X; Qin L; Lou H; Duan S; Wang H. 2016. Astrocytes contribute to synapse elimination via type 2 inositol 1,4,5-trisphosphate receptor-dependent release of ATP. Elife 5:. PubMed: 27067238 MGI: J:232107
Yin N; Xu J; Ginhoux F; Randolph GJ; Merad M; Ding Y; Bromberg JS. 2012. Functional specialization of islet dendritic cell subsets. J Immunol 188(10):4921-30. PubMed: 22508930 MGI: J:188667
Yona S; Kim KW; Wolf Y; Mildner A; Varol D; Breker M; Strauss-Ayali D; Viukov S; Guilliams M; Misharin A; Hume DA; Perlman H; Malissen B; Zelzer E; Jung S. 2013. Fate Mapping Reveals Origins and Dynamics of Monocytes and Tissue Macrophages under Homeostasis. Immunity 38(1):79-91. PubMed: 23273845 MGI: J:193038
Yun TJ; Lee JS; Machmach K; Shim D; Choi J; Wi YJ; Jang HS; Jung IH; Kim K; Yoon WK; Miah MA; Li B; Chang J; Bego MG; Pham TN; Loschko J; Fritz JH; Krug AB; Lee SP; Keler T; Guimond JV; Haddad E; Cohen EA; Sirois MG; El-Hamamsy I; Colonna M; Oh GT; Choi JH; Cheong C. 2016. Indoleamine 2,3-Dioxygenase-Expressing Aortic Plasmacytoid Dendritic Cells Protect against Atherosclerosis by Induction of Regulatory T Cells. Cell Metab 23(5):852-66. PubMed: 27166946 MGI: J:235369
Zabel MK; Zhao L; Zhang Y; Gonzalez SR; Ma W; Wang X; Fariss RN; Wong WT. 2016. Microglial phagocytosis and activation underlying photoreceptor degeneration is regulated by CX3CL1-CX3CR1 signaling in a mouse model of retinitis pigmentosa. Glia 64(9):1479-91. PubMed: 27314452 MGI: J:234182
Zawislak CL; Beaulieu AM; Loeb GB; Karo J; Canner D; Bezman NA; Lanier LL; Rudensky AY; Sun JC. 2013. Stage-specific regulation of natural killer cell homeostasis and response against viral infection by microRNA-155. Proc Natl Acad Sci U S A 110(17):6967-72. PubMed: 23572582 MGI: J:196148
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Also Known As: CX3CR1-GFP

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Cx3cr1tm1Litt

Allele Symbol: Cx3cr1tm1Litt

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

Genotype: GFP related

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

nervous system phenotype

immune system phenotype

behavior/neurological phenotype

hematopoietic system phenotype

Genotype: Cx3cr1tm1Litt/Cx3cr1tm1LittB6.129P-Cx3cr1tm1Litt/J

homeostasis/metabolism phenotype

Genotype: Cx3cr1tm1Litt/Cx3cr1tm1LittB6.129P2-Cx3cr1tm1Litt

mortality/aging

nervous system phenotype

immune system phenotype

cardiovascular system phenotype

homeostasis/metabolism phenotype

behavior/neurological phenotype

hematopoietic system phenotype

muscle phenotype

cellular phenotype

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

immune system phenotype

homeostasis/metabolism phenotype

vision/eye phenotype

renal/urinary system phenotype

nervous system phenotype

cardiovascular system phenotype

hematopoietic system phenotype

cellular phenotype

Genotype: Cx3cr1tm1Litt/Cx3cr1tm1LittC.129P2-Cx3cr1tm1Litt

immune system phenotype

Genotype: Cx3cr1tm1Litt/Cx3cr1tm1Littinvolves: 129P2/OlaHsd

mortality/aging

immune system phenotype

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hematopoietic system phenotype

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Cx3cr1^tm1Litt

Allele Symbol: Cx3cr1^tm1Litt

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

Genotype: Cx3cr1^tm1Litt/Cx3cr1^tm1Litt
B6.129P-Cx3cr1^tm1Litt/J

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

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

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

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

Additional - Cx3cr1^tm1Litt related