Overview

Also Known As:p50^-

Mice homozygous for Nfkb1^tm1Bal exhibit defective B cell responses, defective responses to infection, and also defects in basal and specific antibody production.

Donating Investigator

Dr. David Baltimore, California Institute of Technology

Genetic overview

Genetic Background	Generation

Nfkb1^tm1Bal

Allele Type	Gene Symbol	Gene Name
Targeted (Null/Knockout)	Nfkb1	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105

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Research Applications

Immunology, Inflammation and Autoimmunity Research

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Base Price

Starting at:

$2,854.50 Domestic price Cryo Recovery

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Details

Detailed Description

Mice homozygous for the Nfkb1^tm1Bal targeted mutation are viable and fertile. Homozygous mutant mice exhibit defective B cell responses, defective responses to infection, and also defects in basal and specific antibody production.

Development

Exon 6 of the Nfkb1 gene was disrupted by insertion of a vector containing the neo resistance gene. The construct was electroporated into 129P2/OlaHsd-derived E14 embryonic stem (ES) cells. Correctly targeted ES cells were injected into blastocysts. The resulting chimeric animals were bred to crossed to C57BL/6J.

Control Suggestions

Approximate Controls

100903 B6129PF2/J

Additional Information

Considerations for Choosing Controls

Selected References

Sha WC; Liou HC; Tuomanen EI; Baltimore D. 1995. Targeted disruption of the p50 subunit of NF-kappa B leads to multifocal defects in immune responses. Cell 80(2):321-30PubMed: 7834752 MGI: J:37184

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Genetics

Nfkb1^tm1Bal

Allele Symbol: Nfkb1^tm1Bal

Allele Name	targeted mutation 1, David Baltimore
Allele Type	Targeted (Null/Knockout)
Allele Synonym(s)	NF-kappaB^tm1Bal; Nfkappab1-; NF-kappaB1 KO; NF-kappaB1^-; NFkappaB1⁰; Nfkb1-; p105^-; p50^-; p50^KO
Gene Symbol and Name	Nfkb1, nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105
Gene Synonym(s)
Strain of Origin	129P2/OlaHsd
Chromosome	3
General Note	Effect of reconstitution with Nfkb1^tm1Bal homozygous hematopoietic cells on atherogenesis in atherosclerosis prone mice To assess the role of NFKB1 in atherogenesis, mice homozygous for a mutation of the low density lipoprotein receptor (Ldlr^tm1Her) were lethally irradiated and transplanted with bone marrow from Nfkb1^tm1Bal homozygous mice and 4 weeks later placed on a high-fat diet for 10 weeks. Aortic root lesion area of mice with NFKB1-deficient hematopoietic cells was 41% smaller than in control mice. Whereas control lesions contained primarily large foam cells, lesions of mice reconstituted with NFKB1-deficient bone marrow contained large numbers of small, inflammatory cells and very few foam cells. 3-fold as many cells attached to the lesion cap in transplanted mice. Most cells in control lesions were macrophages, while in transplanted mice there was a preponderance of T and B lymphocytes. Macrophages induced to differentiate in culture from NFKB1-deficient bone marrow exhibited differences compared to control macrophages in the secretion patterns of several cytokines following lipopolysaccharide (LPS) stimulation. Whereas control macrophages expressed high levels of scavenger receptor class A (SR-A) in response to LPS, this response was greatly attenuated in mice with NFKB1-deficient hematopoietic systems; uptake of oxidized low density lipoprotein (oxLDL) was similarly diminished, although neither parameter differed between transplant and control macrophages in the absence of stimulation. J:87639
Molecular Note	Insertion of a PGK-neomycin resistance cassette into exon 6 disrupted the gene. Exon 6 encodes the p105 precursor of the p50 subunit of the encoded transcription factor. The authors predict that this allele produces a truncated polypeptide that cannot bind with DNA, or dimerize with itself or other kappaB binding motifs.
Mutations Made By	Dr. David Baltimore, California Institute of Technology

Disease/Phenotype

Disease Terms

Research Areas By Phenotype

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

Genotype: Nfkb1^tm1Bal related

Immunology, Inflammation and Autoimmunity Research
- Immunodeficiency
  - Inflammatory bowel 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: Nfkb1^tm1Bal/Nfkb1^tm1Bal
B6.Cg-Nfkb1/J

hematopoietic system phenotype

abnormal B cell physiology
- addition of Tnfsf13b (BAFF) to the in vitro B cell cultures does not elevate survival of B cells for the first 12 hours but provides benefits when present for 24 hours or longer

immune system phenotype

abnormal B cell physiology
- addition of Tnfsf13b (BAFF) to the in vitro B cell cultures does not elevate survival of B cells for the first 12 hours but provides benefits when present for 24 hours or longer

Genotype: Nfkb1^tm1Bal/Nfkb1^tm1Bal
involves: 129P2/OlaHsd

hematopoietic system phenotype

decreased marginal zone B cell number

immune system phenotype

decreased marginal zone B cell number

mammalian phenotype

immune system phenotype
- Normal - mice exhibit normal dendritic cell development and maturation

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

Genotype: Nfkb1^tm1Bal/Nfkb1^tm1Bal
involves: 129P2/OlaHsd * C57BL/6

hematopoietic system phenotype

abnormal class switch recombination
- B cells are defective in IgG3, IgE and IgA class switching but undergo substantial IgG1 class switching

decreased B cell proliferation
- B cell proliferation following LPS and sCD40L stimulation is impaired
- Normal - however, B cells proliferate normally in response to CD40L, alpha-delta-dex and IL-4 + IL-5
- B cells do not proliferate in response to LPS concentration that stimulate wild-type B cells to proliferate

decreased myeloid dendritic cell number
- low number of myeloid dendritic cells in Peyer's patches

decreased IgM level
- proliferating B cells stimulated with alpha-delta-dex and IL-4 + IL-5 produce 32-fold less IgM than wild-type
- proliferating B cells stimulated wth mCD40L + IL-4 + IL-5 produce 41-fold less IgM than wild-type
- Normal - however, mlg and CD40 signaling restores B cell maturation to IgM secretion

decreased IgA level
- IgA levels are decreased 5-fold

decreased immunoglobulin level
- immunoglobin levels are 4-fold lower than in wild-type mice
- all isotypes except IgM are reduced

decreased IgE level
- IgE levels are decreased 50-fold

decreased IgG1 level
- IgG1 levels are reduced 10-fold

immune system phenotype

abnormal Peyer's patch T cell area morphology
- CD3+ T cell numbers are reduced and T-cell areas of Peyer's patches are underrepresented and small in size

cecum inflammation
- mice exhibit mild typhlocolitis

abnormal humoral immune response
- total NP-binding following exposure to NP15-CG is lower than in wild-type mice and NP-specific antibodies of all isotypes are decreased compared to in wild-type mice

abnormal class switch recombination
- B cells are defective in IgG3, IgE and IgA class switching but undergo substantial IgG1 class switching

abnormal Peyer's patch follicle morphology
- size of interfollicluar region is reduced
- slight increase of M cells in the follicle-associated epithelium (FAE)

decreased IgA level
- IgA levels are decreased 5-fold

increased susceptibility to bacterial infection
- mice are more prone to infection than wild-type mice
- mice die 24 hours after infection with Staphylococcus pneumoniae compared to wild-type mice that die between 36 and 72 hours after infection
- mice are more sensitive to typhlocolitis induced by H. hepaticus than wild-type mice but less sensitive than Nfkb1^tm1Bal/Nfkb1^tm1Bal Rela^tm1Bal/Rela⁺
- 6 days after infection with Listeria monocytogenes, mice exhibit no peritoneal bacterial but several thousand splenic bacteria compared to wild-type mice that exhibit neither
- while mice efficiently clear extracellular bacteria they fail to clear intracellular bacteria
- Normal - however, mice do not exhibit any abnormal response to H. influenzae and E. coli infection

peritoneal inflammation
- mild

decreased susceptibility to Picornaviridae infection induced morbidity/mortality
- mice are more resistant to EMC virus infection than wild-type mice and exhibit mortality at a 10-fold higher titer with a slower progression towards fatal encephalopathy

decreased IgM level
- proliferating B cells stimulated with alpha-delta-dex and IL-4 + IL-5 produce 32-fold less IgM than wild-type
- Normal - however, mlg and CD40 signaling restores B cell maturation to IgM secretion
- proliferating B cells stimulated wth mCD40L + IL-4 + IL-5 produce 41-fold less IgM than wild-type

decreased immunoglobulin level
- all isotypes except IgM are reduced
- immunoglobin levels are 4-fold lower than in wild-type mice

large intestinal inflammation
- mice exhibit mild typhlocolitis

decreased B cell proliferation
- B cell proliferation following LPS and sCD40L stimulation is impaired
- B cells do not proliferate in response to LPS concentration that stimulate wild-type B cells to proliferate
- Normal - however, B cells proliferate normally in response to CD40L, alpha-delta-dex and IL-4 + IL-5

decreased IgG1 level
- IgG1 levels are reduced 10-fold

decreased interleukin-6 secretion
- LPS-stimulated macrophages release 6-fold less IL-6

decreased susceptibility to viral infection induced morbidity/mortality
- mice are more resistant to EMC virus infection than wild-type mice and exhibit mortality at a 10-fold higher titer with a slower progression towards fatal encephalopathy

small Peyer's patches
- Peyer's patches are smaller and contain a range of no more than 1 to 2 follicles

decreased myeloid dendritic cell number
- low number of myeloid dendritic cells in Peyer's patches

increased susceptibility to bacterial infection induced morbidity/mortality
- mice die 24 hours after infection with Staphylococcus pneumoniae compared to wild-type mice that die between 36 and 72 hours after infection

abnormal Peyer's patch germinal center morphology
- germinal centers are reduced in number and size with a low number of myeloid dentritic cells

decreased IgE level
- IgE levels are decreased 50-fold

decreased Peyer's patch number
- average of 2 to 4 Peyer's patches per mouse compared to an observed average of 7 to 10 per control mouse

cellular phenotype

decreased B cell proliferation
- Normal - however, B cells proliferate normally in response to CD40L, alpha-delta-dex and IL-4 + IL-5
- B cell proliferation following LPS and sCD40L stimulation is impaired
- B cells do not proliferate in response to LPS concentration that stimulate wild-type B cells to proliferate

digestive/alimentary phenotype

abnormal colon morphology
- mice exhibit mild colonic perforations and typhlocolitis

large intestinal inflammation
- mice exhibit mild typhlocolitis

diarrhea
- mild

peritoneal inflammation
- mild

cecum inflammation
- mice exhibit mild typhlocolitis

mortality/aging

decreased susceptibility to Picornaviridae infection induced morbidity/mortality
- mice are more resistant to EMC virus infection than wild-type mice and exhibit mortality at a 10-fold higher titer with a slower progression towards fatal encephalopathy

premature death
- mice die more frequently at a young age compared to wild-type mice

decreased susceptibility to viral infection induced morbidity/mortality
- mice are more resistant to EMC virus infection than wild-type mice and exhibit mortality at a 10-fold higher titer with a slower progression towards fatal encephalopathy

increased susceptibility to bacterial infection induced morbidity/mortality
- mice die 24 hours after infection with Staphylococcus pneumoniae compared to wild-type mice that die between 36 and 72 hours after infection

Genotype: Nfkb1^tm1Bal/Nfkb1^tm1Bal
B6;129P-Nfkb1/J

cellular phenotype

increased apoptosis
- growth factor withdrawal from cultured bone marrow dendritic cells enhances apoptosis of dendritic cells, but not granulocytes or macrophages

hematopoietic system phenotype

abnormal CD4-positive, alpha-beta T cell physiology
- splenocytes treated with anti-CD3 with or without anti-CD28 antibodies produce reduced levels of interferon gamma and Il-2 (Th1 cytokines) but increased levels of Il-4 and Il-10 (Th2 cytokines) while wild-type splenocytes produce both Th1 and Th2 cytokines
- s

abnormal macrophage physiology
- peritoneal macrophages produce less Il-6, Il-12p40, TNF alpha, and nitric oxide compared to wild-type cells upon stimulation with interferon gamma and/or LPS

homeostasis/metabolism phenotype

abnormal calcium ion homeostasis
- at 8 months, the immunoreactivity for a set of calcium-buffering proteins is significantly increased in mutant spiral ganglion neurons, suggesting impaired calcium ion homeostasis

immune system phenotype

abnormal professional antigen presenting cell physiology

abnormal CD4-positive, alpha-beta T cell physiology
- splenocytes treated with anti-CD3 with or without anti-CD28 antibodies produce reduced levels of interferon gamma and Il-2 (Th1 cytokines) but increased levels of Il-4 and Il-10 (Th2 cytokines) while wild-type splenocytes produce both Th1 and Th2 cytokines
- s

abnormal cytokine secretion
- Il-4 secretion is impaired in cultured cells upon stimulation with MOG peptide

abnormal dendritic cell physiology
- bone marrow-derived dendritic cells stimulated with LPS produce significantly less Il-12p40 and TNF alpha than stimulated wild-type dendritic cells

abnormal macrophage physiology
- peritoneal macrophages produce less Il-6, Il-12p40, TNF alpha, and nitric oxide compared to wild-type cells upon stimulation with interferon gamma and/or LPS

decreased susceptibility to autoimmune diabetes
- >70% of control mice treated with low dose streptozotocin for 5 days develop diabetes starting ~8 and 12 days after the first injection, but only 23% of mutants develop diabetes

mammalian phenotype

immune system phenotype
- Normal - most pancreatic islet cells appear normal in mutants not developing diabetes after streptozotocin treatment, while control pancreatic islets display insulitis; mutants developing diabetes after treatment display insulis in many islets

homeostasis/metabolism phenotype
- Normal - despite altered expression of Trp53, neurons exhibit normal camptothecin-induced neuronal death

muscle phenotype
- Normal - myogenesis is normal

nervous system phenotype

abnormal cochlear inner hair cell morphology
- at 1 and 3 months, vacuole-like spaces replace the afferent terminals of the inner radial nerves while efferent inner spiral fibers appear intact
- in contrast, no major pathological changes are seen in mutant OHCs or stria vascularis at 1 or 3 months
- at 1 and 3 months, edematous-appearing extracellular spaces are noted between the IHC and supporting cells; the cytoplasm in the base of IHCs consists of numerous small vesicles infiltrated with mitochondria and short profiles of cisternae
- homozygotes show a significantly higher number of swollen dendritic terminals per IHC region relative to wild-type mice; only type I ganglion neurons are involved
- all homozygotes (6 of 6) exhibit excitotoxic pathologies of afferent dendrites under the IHCs compared with 4 of 9 in wild-type mice

cochlear ganglion degeneration
- however, no significant differences in IHC or OHC loss are noted at 8 months relative to wild-type mice
- at 8 months, the numbers of afferent axons per habenular opening are significantly reduced relative to those of wild-type mice
- at 8 months, homozygotes show a 69% loss of SGNs in the basal cochlea relative to a ~28% loss observed in wild-type mice

decreased cochlear nerve compound action potential
- by 8 months of age, most homozygotes no longer respond to auditory stimuli at high frequencies (90 dB SPL), whereas wild-type mice retain CAP responses at most test frequencies
- at 1 month of age, CAP thresholds in homozygotes are elevated by 6-20 dB SPL relative to wild-type mice at almost all frequencies
- at 3 months, no sigificant loss of distorion product otoacoustic emissions (DPOAEs) is noted when primaries are presented at 70 dB SPL
- no significant differences in mean endocochlear potential values are observed at 1, 3, and 8 months of age relative to wild-type mice
- at 3 months of age, mutant CAP thresholds are increased by ~20 dB SPL at low frequencies and by ~30 dB at high frequencies relative to wild-type

hearing/vestibular/ear phenotype

decreased cochlear nerve compound action potential
- at 3 months, no sigificant loss of distorion product otoacoustic emissions (DPOAEs) is noted when primaries are presented at 70 dB SPL
- at 3 months of age, mutant CAP thresholds are increased by ~20 dB SPL at low frequencies and by ~30 dB at high frequencies relative to wild-type
- no significant differences in mean endocochlear potential values are observed at 1, 3, and 8 months of age relative to wild-type mice
- at 1 month of age, CAP thresholds in homozygotes are elevated by 6-20 dB SPL relative to wild-type mice at almost all frequencies
- by 8 months of age, most homozygotes no longer respond to auditory stimuli at high frequencies (90 dB SPL), whereas wild-type mice retain CAP responses at most test frequencies

increased susceptibility to age-related hearing loss
- accelerated hearing loss is highly associated with an exacerbated excitotoxic-like damage in afferent dendrites under IHCs and an accelerated loss of spiral ganglion neurons
- homozygotes exhibit accelerated age-related hearing loss at higher frequencies, as assessed by CAP threshold shifts at 1, 3, and 8 months of age

abnormal cochlear inner hair cell morphology
- at 1 and 3 months, vacuole-like spaces replace the afferent terminals of the inner radial nerves while efferent inner spiral fibers appear intact
- homozygotes show a significantly higher number of swollen dendritic terminals per IHC region relative to wild-type mice; only type I ganglion neurons are involved
- all homozygotes (6 of 6) exhibit excitotoxic pathologies of afferent dendrites under the IHCs compared with 4 of 9 in wild-type mice
- in contrast, no major pathological changes are seen in mutant OHCs or stria vascularis at 1 or 3 months
- at 1 and 3 months, edematous-appearing extracellular spaces are noted between the IHC and supporting cells; the cytoplasm in the base of IHCs consists of numerous small vesicles infiltrated with mitochondria and short profiles of cisternae

increased susceptibility to noise-induced hearing loss
- at 2 hrs after exposure to a wideband, low-level noise at 70 dB SPL, 1-month-old homozygotes display 7-15 dB SPL threshold shifts across most test frequencies whereas wild-type mice show no significant CAP threshold shifts

References

Sha WC; Liou HC; Tuomanen EI; Baltimore D. 1995. Targeted disruption of the p50 subunit of NF-kappa B leads to multifocal defects in immune responses. Cell 80(2):321-30PubMed: 7834752 MGI: J:37184

Additional References

Aleyasin H; Cregan SP; Iyirhiaro G; O'Hare MJ; Callaghan SM; Slack RS; Park DS. 2004. Nuclear factor-(kappa)B modulates the p53 response in neurons exposed to DNA damage. J Neurosci 24(12):2963-73PubMed: 15044535 MGI: J:90221
Das G; Augustine MM; Das J; Bottomly K; Ray P; Ray A. 2003. An important regulatory role for CD4+CD8 alpha alpha T cells in the intestinal epithelial layer in the prevention of inflammatory bowel disease. Proc Natl Acad Sci U S A 100(9):5324-9PubMed: 12695566 MGI: J:83283
Hilliard BA; Mason N; Xu L; Sun J; Lamhamedi-Cherradi SE; Liou HC; Hunter C; Chen YH. 2002. Critical roles of c-Rel in autoimmune inflammation and helper T cell differentiation. J Clin Invest 110(6):843-50PubMed: 12235116 MGI: J:79107
Hunot S; Vila M; Teismann P; Davis RJ; Hirsch EC; Przedborski S; Rakic P; Flavell RA. 2004. JNK-mediated induction of cyclooxygenase 2 is required for neurodegeneration in a mouse model of Parkinson's disease. Proc Natl Acad Sci U S A 101(2):665-70PubMed: 14704277 MGI: J:87428
Kassed CA; Willing AE; Garbuzova-Davis S; Sanberg PR; Pennypacker KR. 2002. Lack of NF-kappaB p50 exacerbates degeneration of hippocampal neurons after chemical exposure and impairs learning. Exp Neurol 176(2):277-88PubMed: 12359170 MGI: J:78419
Kenter AL; Wuerffel R; Dominguez C; Shanmugam A; Zhang H. 2004. Mapping of a functional recombination motif that defines isotype specificity for mu-->gamma3 switch recombination implicates NF-kappaB p50 as the isotype-specific switching factor. J Exp Med 199(5):617-27PubMed: 14993249 MGI: J:90466
Paxian S; Merkle H; Riemann M; Wilda M; Adler G; Hameister H; Liptay S; Pfeffer K; Schmid RM. 2002. Abnormal organogenesis of Peyer's patches in mice deficient for NF-kappaB1, NF-kappaB2, and Bcl-3. Gastroenterology 122(7):1853-68PubMed: 12055593 MGI: J:77049
Stanic AK; Bezbradica JS; Park JJ; Matsuki N; Mora AL; Van Kaer L; Boothby MR; Joyce S. 2004. NF-kappa B controls cell fate specification, survival, and molecular differentiation of immunoregulatory natural T lymphocytes. J Immunol 172(4):2265-73PubMed: 14764695 MGI: J:88049
Waterfield M; Jin W; Reiley W; Zhang M; Sun SC. 2004. IkappaB kinase is an essential component of the Tpl2 signaling pathway. Mol Cell Biol 24(13):6040-8PubMed: 15199157 MGI: J:91588
Waterfield MR; Zhang M; Norman LP; Sun SC. 2003. NF-kappaB1/p105 regulates lipopolysaccharide-stimulated MAP kinase signaling by governing the stability and function of the Tpl2 kinase. Mol Cell 11(3):685-94PubMed: 12667451 MGI: J:82762
Yang G; Abate A; George AG; Weng YH; Dennery PA. 2004. Maturational differences in lung NF-kappaB activation and their role in tolerance to hyperoxia. J Clin Invest 114(5):669-78PubMed: 15343385 MGI: J:92596

Additional - Nfkb1^tm1Bal related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Standard PCR:Nfkb1
- Standard PCR:Nfkb1
- Genotyping resources and troubleshooting
Breeding Considerations

While maintaining a live colony, these mice are maintained by mating homozygote siblings.
- Additional Breeding and Husbandry Support
Appearance
- pink-eyed light-bellied agouti, yellow coat
  Related Genotype: A^w/A^w Oca2^p/Oca2^p
Citation
When using the p50^- mouse strain in a publication, please cite the originating article(s) and include JAX stock #002849 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200

Pricing & Availability

Cryo Recovery

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Live Mouse

Age

Genotype

Price

weeks

Cryorecovery - Pricing

Service/Product	Description	Price
> >	Heterozygous or wildtype for Nfkb1<tm1Bal>

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Frozen Mouse Embryo	B6;129P-Nfkb1<tm1Bal>/J	$2595.00
Frozen Mouse Embryo	B6;129P-Nfkb1<tm1Bal>/J	$2595.00
Frozen Mouse Embryo	B6;129P-Nfkb1<tm1Bal>/J	$3373.50
Frozen Mouse Embryo	B6;129P-Nfkb1<tm1Bal>/J	$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

Licensing Information

Phone: 207-288-6470

Email: TechTran@jax.org

Also Known As:p50-

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Approximate Controls

Additional Information

Selected References

Nfkb1tm1Bal

Allele Symbol: Nfkb1tm1Bal

Effect of reconstitution with Nfkb1tm1Bal homozygous hematopoietic cells on atherogenesis in atherosclerosis prone mice

Disease Terms

Research Areas By Phenotype

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

Genotype: Nfkb1tm1Bal related

Mammalian Phenotype Terms by Genotype

Genotype: Nfkb1tm1Bal/Nfkb1tm1BalB6.Cg-Nfkb1/J

hematopoietic system phenotype

immune system phenotype

Genotype: Nfkb1tm1Bal/Nfkb1tm1Balinvolves: 129P2/OlaHsd

hematopoietic system phenotype

immune system phenotype

mammalian phenotype

Genotype: Nfkb1tm1Bal/Nfkb1tm1Balinvolves: 129P2/OlaHsd * C57BL/6

hematopoietic system phenotype

immune system phenotype

cellular phenotype

digestive/alimentary phenotype

mortality/aging

Genotype: Nfkb1tm1Bal/Nfkb1tm1BalB6;129P-Nfkb1/J

cellular phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

immune system phenotype

mammalian phenotype

nervous system phenotype

hearing/vestibular/ear phenotype

References

Additional References

Additional - Nfkb1tm1Bal related

Genotyping Protocols

Breeding Considerations

Appearance

Citation

Animal Health Reports

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200

Live Mouse

Cryorecovery - Pricing

Related Products and Services

Payment Terms and Conditions

The Jackson Laboratory's Genotype Promise

Terms Of Use

Licensing Information

Also Known As:p50^-

Nfkb1^tm1Bal

Allele Symbol: Nfkb1^tm1Bal

Effect of reconstitution with Nfkb1^tm1Bal homozygous hematopoietic cells on atherogenesis in atherosclerosis prone mice

Genotype: Nfkb1^tm1Bal related

Genotype: Nfkb1^tm1Bal/Nfkb1^tm1Bal
B6.Cg-Nfkb1/J

Genotype: Nfkb1^tm1Bal/Nfkb1^tm1Bal
involves: 129P2/OlaHsd

Genotype: Nfkb1^tm1Bal/Nfkb1^tm1Bal
involves: 129P2/OlaHsd * C57BL/6

Genotype: Nfkb1^tm1Bal/Nfkb1^tm1Bal
B6;129P-Nfkb1/J

Additional - Nfkb1^tm1Bal related