NSG CSF1 mice express human CSF1 [colony stimulating factor 1 (macrophage)] on the immunodeficient NSG background. In humanized NSG CSF1 mice, the human CSF1 protein improves the function of human macrophages and monocytes.
Dr. Leonard D. Shultz, The Jackson Laboratory
Genetic Background | Generation |
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?+pN1F6
|
Allele Type | Gene Symbol | Gene Name |
---|---|---|
Spontaneous | Prkdc | protein kinase, DNA activated, catalytic polypeptide |
Allele Type | Gene Symbol | Gene Name |
---|---|---|
Targeted (Null/Knockout) | Il2rg | interleukin 2 receptor, gamma chain |
Allele Type |
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Transgenic (Inserted expressed sequence, Humanized sequence) |
Starting at:
$275.89 Domestic price for male 4-week |
287.24 Domestic price for breeder pair |
NSG CSF1 mice express human CSF1 [colony stimulating factor 1 (macrophage)] on the immunodeficient NSG (Stock No. 05557) background. NSG mice carry the Prkdcscid and Il2rgtm1Wjl alleles on the NOD/LtShiJ background; they should have no mature T cells or B cells, lack functional natural killer (NK) cells, have reduced numbers of lymphocytes and myeloid dendritic cells, and be deficient in cytokine signaling. CSF1 encodes a cytokine involved in the regulation of macrophages. The NSG CSF1 strain is used to make "humanized mice", which are created by injecting human immune cells. The CSF1 protein improves the function of human macrophages and monocytes that develop in the humanized mouse. In turn, the macrophages and monocytes assist other immune cells such as Natural Killer cells.
View our Resources for the NSG mouse model, including discussion forum, immunodeficient model comparison, and categorized, up-to-date references.
A transgenic construct containing the human colony stimulating factor 1 (macrophage), CSF1, gene from the 157 Kb BAC clone RP11-19F3 was microinjected into the pronuclei of fertilized NOD.CB17-Prkdcscid/J eggs. Founder line 3 was established and mated to NOD.Cg-Prkdcscid Il2rgtm1Wjl/J (Stock No. 005557) mice. Progeny were interbred until all offspring were homozygous for scid, hemizygous/homozygous for the Il2rg targeted mutation and hemizygous for the transgene.
Expressed Gene | CSF1, colony stimulating factor 1, human |
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Site of Expression | CSF1 encodes a cytokine involved in the regulation of macrophages. |
Allele Name | severe combined immunodeficiency |
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Allele Type | Spontaneous |
Allele Synonym(s) | SCID |
Gene Symbol and Name | Prkdc, protein kinase, DNA activated, catalytic polypeptide |
Gene Synonym(s) | |
Site of Expression | T and B lymphocytes. |
Strain of Origin | C.BKa-Ighb/Icr |
Chromosome | 16 |
Molecular Note | A T-to-A transversion point mutation at a position corresponding to codon 4046 (codon 4095 in transcript ENSMUST00000023352.8) created a premature stop codon (p.Y4046*). |
Allele Name | targeted mutation 1, Warren J Leonard |
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Allele Type | Targeted (Null/Knockout) |
Allele Synonym(s) | [KO]gammac; CD132-; gammac-; gc-; Il2rgtm1Wjll; IL2Rgammanull |
Gene Symbol and Name | Il2rg, interleukin 2 receptor, gamma chain |
Gene Synonym(s) | |
Site of Expression | Primarily lymphoid cells. |
Strain of Origin | 129S4/SvJae |
Chromosome | X |
Molecular Note | A neomycin resistance cassette replaced part of exon 3 and all of exons 4 - 8 of the gene, resulting in the loss of most of the extracellular domain and all of the transmembrane and cytoplasmic domains of the protein. |
Mutations Made By | Dr. Warren Leonard, NHLBI, NIH |
Allele Name | transgene insertion 3, Leonard Shultz |
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Allele Type | Transgenic (Inserted expressed sequence, Humanized sequence) |
Allele Synonym(s) | |
Gene Symbol and Name | Tg(CSF1)3Sz, transgene insertion 3, Leonard Shultz |
Gene Synonym(s) | |
Promoter | CSF1, colony stimulating factor 1, human |
Expressed Gene | CSF1, colony stimulating factor 1, human |
Site of Expression | CSF1 encodes a cytokine involved in the regulation of macrophages. |
Strain of Origin | NOD.Cg-Prkdcscid |
Chromosome | UN |
Molecular Note | This transgene consists of a 157 kb human BAC clone, RP11-19F3, containing the entire genomic sequence of the human CSF1 gene including the endogenous promoter. CSF1 is the only gene in the plasmid. |
When maintaining a live colony, these mice are bred as Hom (scid) Hom (Il2rg) Noncarrier (no CSF1 transgene) x Hom (scid) Hemi (Il2rg) Hemi (CSF1 transgene) or reciprocal. Il2rg is located on the X chromosome. Males homozygous for the transgene do not produce viable sperm.
This strain should be housed under pathogen free conditions similar to the Prkdcscid/Prkdcscid mouse or any other immunodeficient strain.
When using the NSG CSF1 mouse strain in a publication, please cite the originating article(s) and include JAX stock #028654 in your Materials and Methods section.
Service/Product | Description | Price |
---|---|---|
Homozygous for Prkdc<scid>, homozygous females and hemizygous males for Il2rg<tm1Wjl>, hemizigous or non-carrier for Tg(CSF1)3Sz |
Frozen Mouse Embryo | NOD.Cg-Prkdc<scid> Il2rg<tm1Wjl> Tg(CSF1)3Sz/SzJ | $2595.00 |
Frozen Mouse Embryo | NOD.Cg-Prkdc<scid> Il2rg<tm1Wjl> Tg(CSF1)3Sz/SzJ | $2595.00 |
Frozen Mouse Embryo | NOD.Cg-Prkdc<scid> Il2rg<tm1Wjl> Tg(CSF1)3Sz/SzJ | $3373.50 |
Frozen Mouse Embryo | NOD.Cg-Prkdc<scid> Il2rg<tm1Wjl> Tg(CSF1)3Sz/SzJ | $3373.50 |
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The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project. 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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