Strain Name:

B6.Cg-Nfkb1tm1Bal/J

Stock Number:

006097

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Availability:

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Mice homozygous for the Nfkb1tm1Bal knock-out mutation exhibit defective B cell responses, defective responses to infection, and also defects in basal and specific antibody production. These mice may be useful in studies of inflammation and immune responses and signal transduction.

Description

Strain Information

Type Congenic; Mutant Strain; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Mating SystemHomozygote x Homozygote         (Female x Male)   14-NOV-06
Specieslaboratory mouse
GenerationN12+F18 (10-DEC-13)
Generation Definitions
 
Donating Investigator Menno de Winther,   Maastricht University

Description
Mice homozygous for the Nfkb1tm1Bal 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. These mice may be useful in studies of inflammation and immune responses and signal transduction.

In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.

Development
A targeting vector containing the PGK-neo resistance gene in opposite transcriptional orientation was designed to disrupt exon 6 of the endogenous gene. The construct was electroporated into 129P2/OlaHsd-derived E14 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6J blastocysts amd the resulting chimeric mice were crossed with C57BL/6J mice. Heterozygous mice were bred to create homozygous mice on a mixed B6;129P2 background prior to arrival at The Jackson Laboratory. Dr. Menno de Winther of Maastricht University, The Netherlands obtained JR#002849 from The Jackson Laboratory and backcrossed them to C57BL/6JIco for 12 generations.

Control Information

  Control
   000664 C57BL/6J (approximate)
 
  Considerations for Choosing Controls

Related Strains

Strains carrying   Nfkb1tm1Bal allele
002849   B6;129P-Nfkb1tm1Bal/J
024702   D2.129P2(B6)-Nfkb1tm1Bal/SjJ
View Strains carrying   Nfkb1tm1Bal     (2 strains)

Strains carrying other alleles of Nfkb1
006100   B10.Cg-H2k Tg(NFkB/Fos-luc)26Rinc/J
View Strains carrying other alleles of Nfkb1     (1 strain)

Phenotype

Phenotype Information

View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Nfkb1tm1Bal/Nfkb1tm1Bal

        B6.Cg-Nfkb1tm1Bal/J
  • 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   (MGI Ref ID J:113556)
  • 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   (MGI Ref ID J:113556)

The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.

Nfkb1tm1Bal/Nfkb1tm1Bal

        B6;129P-Nfkb1tm1Bal/J
  • hearing/vestibular/ear 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   (MGI Ref ID J:107245)
    • 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   (MGI Ref ID J:107245)
    • in contrast, no major pathological changes are seen in mutant OHCs or stria vascularis at 1 or 3 months   (MGI Ref ID J:107245)
    • all homozygotes (6 of 6) exhibit excitotoxic pathologies of afferent dendrites under the IHCs compared with 4 of 9 in wild-type mice   (MGI Ref ID J:107245)
    • 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   (MGI Ref ID J:107245)
  • decreased cochlear nerve compound action potential
    • 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   (MGI Ref ID J:107245)
    • 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   (MGI Ref ID J:107245)
    • 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   (MGI Ref ID J:107245)
    • at 3 months, no sigificant loss of distorion product otoacoustic emissions (DPOAEs) is noted when primaries are presented at 70 dB SPL   (MGI Ref ID J:107245)
    • no significant differences in mean endocochlear potential values are observed at 1, 3, and 8 months of age relative to wild-type mice   (MGI Ref ID J:107245)
  • increased susceptibility to age-related hearing loss
    • homozygotes exhibit accelerated age-related hearing loss at higher frequencies, as assessed by CAP threshold shifts at 1, 3, and 8 months of age   (MGI Ref ID J:107245)
    • 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   (MGI Ref ID J:107245)
  • 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   (MGI Ref ID J:107245)
  • 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   (MGI Ref ID J:107245)
    • 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   (MGI Ref ID J:107245)
    • in contrast, no major pathological changes are seen in mutant OHCs or stria vascularis at 1 or 3 months   (MGI Ref ID J:107245)
    • all homozygotes (6 of 6) exhibit excitotoxic pathologies of afferent dendrites under the IHCs compared with 4 of 9 in wild-type mice   (MGI Ref ID J:107245)
    • 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   (MGI Ref ID J:107245)
  • cochlear ganglion degeneration
    • at 8 months, homozygotes show a 69% loss of SGNs in the basal cochlea relative to a ~28% loss observed in wild-type mice   (MGI Ref ID J:107245)
    • at 8 months, the numbers of afferent axons per habenular opening are significantly reduced relative to those of wild-type mice   (MGI Ref ID J:107245)
    • however, no significant differences in IHC or OHC loss are noted at 8 months relative to wild-type mice   (MGI Ref ID J:107245)
  • decreased cochlear nerve compound action potential
    • 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   (MGI Ref ID J:107245)
    • 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   (MGI Ref ID J:107245)
    • 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   (MGI Ref ID J:107245)
    • at 3 months, no sigificant loss of distorion product otoacoustic emissions (DPOAEs) is noted when primaries are presented at 70 dB SPL   (MGI Ref ID J:107245)
    • no significant differences in mean endocochlear potential values are observed at 1, 3, and 8 months of age relative to wild-type mice   (MGI Ref ID J:107245)
  • homeostasis/metabolism phenotype
  • *normal* homeostasis/metabolism phenotype
    • despite altered expression of Trp53, neurons exhibit normal camptothecin-induced neuronal death   (MGI Ref ID J:91366)
    • 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   (MGI Ref ID J:107245)
  • immune system phenotype
  • *normal* immune system phenotype
    • 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   (MGI Ref ID J:118907)
    • abnormal CD4-positive 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   (MGI Ref ID J:118907)
    • abnormal cytokine secretion
      • Il-4 secretion is impaired in cultured cells upon stimulation with MOG peptide   (MGI Ref ID J:79107)
    • abnormal professional antigen presenting cell physiology   (MGI Ref ID J:118907)
      • 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   (MGI Ref ID J:118907)
      • 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   (MGI Ref ID J:118907)
    • 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   (MGI Ref ID J:118907)
  • cellular phenotype
  • increased apoptosis
    • growth factor withdrawal from cultured bone marrow dendritic cells enhances apoptosis of dendritic cells, but not granulocytes or macrophages   (MGI Ref ID J:118907)
  • muscle phenotype
  • *normal* muscle phenotype
    • myogenesis is normal   (MGI Ref ID J:135692)
  • hematopoietic system phenotype
  • abnormal CD4-positive 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   (MGI Ref ID J:118907)
  • 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   (MGI Ref ID J:118907)

Nfkb1tm1Bal/Nfkb1tm1Bal

        involves: 129P2/OlaHsd * C57BL/6
  • mortality/aging
  • 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   (MGI Ref ID J:37184)
  • 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   (MGI Ref ID J:37184)
  • premature death
    • mice die more frequently at a young age compared to wild-type mice   (MGI Ref ID J:37184)
  • immune system phenotype
  • abnormal Peyer's patch follicle morphology
    • size of interfollicluar region is reduced   (MGI Ref ID J:77049)
    • slight increase of M cells in the follicle-associated epithelium (FAE)   (MGI Ref ID J:77049)
    • 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   (MGI Ref ID J:77049)
    • abnormal Peyer's patch germinal center morphology
      • germinal centers are reduced in number and size with a low number of myeloid dentritic cells   (MGI Ref ID J:77049)
  • abnormal class switch recombination
    • B cells are defective in IgG3, IgE and IgA class switching but undergo substantial IgG1 class switching   (MGI Ref ID J:30268)
  • 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   (MGI Ref ID J:37184)
    • decreased immunoglobulin level
      • immunoglobin levels are 4-fold lower than in wild-type mice   (MGI Ref ID J:37184)
      • all isotypes except IgM are reduced   (MGI Ref ID J:37184)
      • decreased IgA level
        • IgA levels are decreased 5-fold   (MGI Ref ID J:37184)
      • decreased IgE level
        • IgE levels are decreased 50-fold   (MGI Ref ID J:37184)
      • decreased IgG1 level
        • IgG1 levels are reduced 10-fold   (MGI Ref ID J:37184)
      • decreased IgM level
        • proliferating B cells stimulated with alpha-delta-dex and IL-4 + IL-5 produce 32-fold less IgM than wild-type   (MGI Ref ID J:30268)
        • proliferating B cells stimulated wth mCD40L + IL-4 + IL-5 produce 41-fold less IgM than wild-type   (MGI Ref ID J:30268)
        • however, mlg and CD40 signaling restores B cell maturation to IgM secretion   (MGI Ref ID J:30268)
  • decreased B cell proliferation
    • B cells do not proliferate in response to LPS concentration that stimulate wild-type B cells to proliferate   (MGI Ref ID J:37184)
    • B cell proliferation following LPS and sCD40L stimulation is impaired   (MGI Ref ID J:30268)
    • however, B cells proliferate normally in response to CD40L, alpha-delta-dex and IL-4 + IL-5   (MGI Ref ID J:30268)
  • 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   (MGI Ref ID J:77049)
  • decreased interleukin-6 secretion
    • LPS-stimulated macrophages release 6-fold less IL-6   (MGI Ref ID J:37184)
  • decreased myeloid dendritic cell number
    • low number of myeloid dendritic cells in Peyer's patches   (MGI Ref ID J:77049)
  • 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   (MGI Ref ID J:37184)
  • increased susceptibility to bacterial infection
    • mice are more prone to infection than wild-type mice   (MGI Ref ID J:37184)
    • while mice efficiently clear extracellular bacteria they fail to clear intracellular bacteria   (MGI Ref ID J:37184)
    • 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   (MGI Ref ID J:37184)
    • mice die 24 hours after infection with Staphylococcus pneumoniae compared to wild-type mice that die between 36 and 72 hours after infection   (MGI Ref ID J:37184)
    • however, mice do not exhibit any abnormal response to H. influenzae and E. coli infection   (MGI Ref ID J:37184)
    • mice are more sensitive to typhlocolitis induced by H. hepaticus than wild-type mice but less sensitive than Nfkb1tm1Bal/Nfkb1tm1Bal Relatm1Bal/Rela+   (MGI Ref ID J:67107)
    • 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   (MGI Ref ID J:37184)
  • large intestinal inflammation
    • mice exhibit mild typhlocolitis   (MGI Ref ID J:67107)
    • cecum inflammation
      • mice exhibit mild typhlocolitis   (MGI Ref ID J:67107)
  • peritoneal inflammation
  • small Peyer's patches
    • Peyer's patches are smaller and contain a range of no more than 1 to 2 follicles   (MGI Ref ID J:77049)
  • digestive/alimentary phenotype
  • abnormal colon morphology
    • mice exhibit mild colonic perforations and typhlocolitis   (MGI Ref ID J:67107)
  • diarrhea
  • large intestinal inflammation
    • mice exhibit mild typhlocolitis   (MGI Ref ID J:67107)
    • cecum inflammation
      • mice exhibit mild typhlocolitis   (MGI Ref ID J:67107)
  • peritoneal inflammation
  • hematopoietic system phenotype
  • abnormal class switch recombination
    • B cells are defective in IgG3, IgE and IgA class switching but undergo substantial IgG1 class switching   (MGI Ref ID J:30268)
  • decreased B cell proliferation
    • B cells do not proliferate in response to LPS concentration that stimulate wild-type B cells to proliferate   (MGI Ref ID J:37184)
    • B cell proliferation following LPS and sCD40L stimulation is impaired   (MGI Ref ID J:30268)
    • however, B cells proliferate normally in response to CD40L, alpha-delta-dex and IL-4 + IL-5   (MGI Ref ID J:30268)
  • decreased immunoglobulin level
    • immunoglobin levels are 4-fold lower than in wild-type mice   (MGI Ref ID J:37184)
    • all isotypes except IgM are reduced   (MGI Ref ID J:37184)
    • decreased IgA level
      • IgA levels are decreased 5-fold   (MGI Ref ID J:37184)
    • decreased IgE level
      • IgE levels are decreased 50-fold   (MGI Ref ID J:37184)
    • decreased IgG1 level
      • IgG1 levels are reduced 10-fold   (MGI Ref ID J:37184)
    • decreased IgM level
      • proliferating B cells stimulated with alpha-delta-dex and IL-4 + IL-5 produce 32-fold less IgM than wild-type   (MGI Ref ID J:30268)
      • proliferating B cells stimulated wth mCD40L + IL-4 + IL-5 produce 41-fold less IgM than wild-type   (MGI Ref ID J:30268)
      • however, mlg and CD40 signaling restores B cell maturation to IgM secretion   (MGI Ref ID J:30268)
  • decreased myeloid dendritic cell number
    • low number of myeloid dendritic cells in Peyer's patches   (MGI Ref ID J:77049)

Nfkb1tm1Bal/Nfkb1tm1Bal

        involves: 129P2/OlaHsd
  • immune system phenotype
  • *normal* immune system phenotype
    • mice exhibit normal dendritic cell development and maturation   (MGI Ref ID J:113514)
    • decreased marginal zone B cell number   (MGI Ref ID J:65246)
  • hematopoietic system phenotype
  • decreased marginal zone B cell number   (MGI Ref ID J:65246)
View Research Applications

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

Cell Biology Research
Signal Transduction
Transcriptional Regulation

Immunology, Inflammation and Autoimmunity Research

Nfkb1tm1Bal related

Immunology, Inflammation and Autoimmunity Research
Immunodeficiency
      Inflammatory bowel disease

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Nfkb1tm1Bal
Allele Name targeted mutation 1, David Baltimore
Allele Type Targeted (knock-out)
Common Name(s) NF-kappaB1 KO; NF-kappaB1-; NF-kappaBtm1Bal; NFkappaB10; Nfkappab1-; Nfkb1-; p105-; p50-; p50KO;
Mutation Made ByDr. David Baltimore,   California Institute of Technology
Strain of Origin129P2/OlaHsd
ES Cell Line NameE14
ES Cell Line Strain129P2/OlaHsd
Gene Symbol and Name Nfkb1, nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105
Chromosome 3
Gene Common Name(s) EBP-1; KBF1; NF kappaB1; NF-kB; NF-kB1; NF-kappa-B; NF-kappaB; NF-kappaB p50; NFKB-p105; NFKB-p50; NFkappaB; nuclear factor kappaB p50; p105; p50; p50 subunit of NF kappaB; p50/p105;
General Note

Effect of reconstitution with Nfkb1tm1Bal 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 (Ldlrtm1Her) were lethally irradiated and transplanted with bone marrow from Nfkb1tm1Bal 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. [MGI Ref ID J:37184]

Genotyping

Genotyping Information

Genotyping Protocols

Nfkb1tm1Bal, Standard PCR
Nfkb1tm1Bal, Melt Curve Analysis


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Additional References

Nfkb1tm1Bal related

Acharyya S; Villalta SA; Bakkar N; Bupha-Intr T; Janssen PM; Carathers M; Li ZW; Beg AA; Ghosh S; Sahenk Z; Weinstein M; Gardner KL; Rafael-Fortney JA; Karin M; Tidball JG; Baldwin AS; Guttridge DC. 2007. Interplay of IKK/NF-kappaB signaling in macrophages and myofibers promotes muscle degeneration in Duchenne muscular dystrophy. J Clin Invest 117(4):889-901. [PubMed: 17380205]  [MGI Ref ID J:121279]

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):2963-73. [PubMed: 15044535]  [MGI Ref ID J:90221]

Altavilla D; Famulari C; Passaniti M; Galeano M; Macri A; Seminara P; Minutoli L; Marini H; Calo M; Venuti FS; Esposito M; Squadrito F. 2003. Attenuated cerulein-induced pancreatitis in nuclear factor-kappaB-deficient mice. Lab Invest 83(12):1723-32. [PubMed: 14691290]  [MGI Ref ID J:87079]

Artis D; Kane CM; Fiore J; Zaph C; Shapira S; Joyce K; Macdonald A; Hunter C; Scott P; Pearce EJ. 2005. Dendritic cell-intrinsic expression of NF-kappaB1 is required to promote optimal Th2 cell differentiation. J Immunol 174(11):7154-9. [PubMed: 15905559]  [MGI Ref ID J:99003]

Artis D; Shapira S; Mason N; Speirs KM; Goldschmidt M; Caamano J; Liou HC; Hunter CA; Scott P. 2002. Differential requirement for NF-kappaB family members in control of helminth infection and intestinal inflammation. J Immunol 169(8):4481-7. [PubMed: 12370384]  [MGI Ref ID J:79531]

Artis D; Speirs K; Joyce K; Goldschmidt M; Caamano J; Hunter CA; Scott P. 2003. NF-kappa B1 is required for optimal CD4+ Th1 cell development and resistance to Leishmania major. J Immunol 170(4):1995-2003. [PubMed: 12574369]  [MGI Ref ID J:106657]

Bakkar N; Wang J; Ladner KJ; Wang H; Dahlman JM; Carathers M; Acharyya S; Rudnicki MA; Hollenbach AD; Guttridge DC. 2008. IKK/NF-kappaB regulates skeletal myogenesis via a signaling switch to inhibit differentiation and promote mitochondrial biogenesis. J Cell Biol 180(4):787-802. [PubMed: 18299349]  [MGI Ref ID J:135692]

Banerjee A; Grumont R; Gugasyan R; White C; Strasser A; Gerondakis S. 2008. NF-kappaB1 and c-Rel cooperate to promote the survival of TLR4-activated B cells by neutralizing Bim via distinct mechanisms. Blood 112(13):5063-73. [PubMed: 18805964]  [MGI Ref ID J:143616]

Beg AA; Baltimore D. 1996. An essential role for NF-kappaB in preventing TNF-alpha-induced cell death [see comments] Science 274(5288):782-4. [PubMed: 8864118]  [MGI Ref ID J:36492]

Beg AA; Sha WC; Bronson RT; Baltimore D. 1995. Constitutive NF-kappa B activation, enhanced granulopoiesis, and neonatal lethality in I kappa B alpha-deficient mice. Genes Dev 9(22):2736-46. [PubMed: 7590249]  [MGI Ref ID J:30058]

Berti-Mattera LN; Kern TS; Siegel RE; Nemet I; Mitchell R. 2008. Sulfasalazine blocks the development of tactile allodynia in diabetic rats. Diabetes 57(10):2801-8. [PubMed: 18633115]  [MGI Ref ID J:142010]

Bohuslav J; Kravchenko VV; Parry GC; Erlich JH; Gerondakis S; Mackman N; Ulevitch RJ. 1998. Regulation of an essential innate immune response by the p50 subunit of NF-kappaB. J Clin Invest 102(9):1645-52. [PubMed: 9802878]  [MGI Ref ID J:115230]

Bonini SA; Ferrari-Toninelli G; Uberti D; Montinaro M; Buizza L; Lanni C; Grilli M; Memo M. 2011. Nuclear Factor {kappa}B-Dependent Neurite Remodeling Is Mediated by Notch Pathway. J Neurosci 31(32):11697-705. [PubMed: 21832199]  [MGI Ref ID J:175238]

Bosschaerts T; Morias Y; Stijlemans B; Herin M; Porta C; Sica A; Mantovani A; De Baetselier P; Beschin A. 2011. IL-10 limits production of pathogenic TNF by M1 myeloid cells through induction of nuclear NF-kappaB p50 member in Trypanosoma congolense infection-resistant C57BL/6 mice. Eur J Immunol 41(11):3270-80. [PubMed: 21805465]  [MGI Ref ID J:179528]

Bourteele S; Oesterle K; Weinzierl AO; Paxian S; Riemann M; Schmid RM; Planz O. 2007. Alteration of NF-kappaB activity leads to mitochondrial apoptosis after infection with pathological prion protein. Cell Microbiol 9(9):2202-17. [PubMed: 17573907]  [MGI Ref ID J:148571]

Burkitt MD; Williams JM; Duckworth CA; O'Hara A; Hanedi A; Varro A; Caamano JH; Pritchard DM. 2013. Signaling mediated by the NF-kappaB sub-units NF-kappaB1, NF-kappaB2 and c-Rel differentially regulate Helicobacter felis-induced gastric carcinogenesis in C57BL/6 mice. Oncogene 32(50):5563-73. [PubMed: 23975431]  [MGI Ref ID J:205159]

Campbell IK; Gerondakis S; O'Donnell K; Wicks IP. 2000. Distinct roles for the NF-kappaB1 (p50) and c-Rel transcription factors in inflammatory arthritis. J Clin Invest 105(12):1799-806. [PubMed: 10862795]  [MGI Ref ID J:120528]

Campbell IK; van Nieuwenhuijze A; Segura E; O'Donnell K; Coghill E; Hommel M; Gerondakis S; Villadangos JA; Wicks IP. 2011. Differentiation of inflammatory dendritic cells is mediated by NF-kappaB1-dependent GM-CSF production in CD4 T cells. J Immunol 186(9):5468-77. [PubMed: 21421852]  [MGI Ref ID J:172752]

Cao S; Zhang X; Edwards JP; Mosser DM. 2006. NF-kappaB1 (p50) homodimers differentially regulate pro- and anti-inflammatory cytokines in macrophages. J Biol Chem 281(36):26041-50. [PubMed: 16835236]  [MGI Ref ID J:117172]

Cariappa A; Liou HC; Horwitz BH; Pillai S. 2000. Nuclear factor kappaB is required for the development of marginal zone B lymphocytes J Exp Med 192(8):1175-82. [PubMed: 11034607]  [MGI Ref ID J:65246]

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Porta C; Rimoldi M; Raes G; Brys L; Ghezzi P; Di Liberto D; Dieli F; Ghisletti S; Natoli G; De Baetselier P; Mantovani A; Sica A. 2009. Tolerance and M2 (alternative) macrophage polarization are related processes orchestrated by p50 nuclear factor kappaB. Proc Natl Acad Sci U S A 106(35):14978-83. [PubMed: 19706447]  [MGI Ref ID J:153086]

Powolny-Budnicka I; Riemann M; Tanzer S; Schmid RM; Hehlgans T; Weih F. 2011. RelA and RelB Transcription Factors in Distinct Thymocyte Populations Control Lymphotoxin-Dependent Interleukin-17 Production in gammadelta T Cells. Immunity 34(3):364-74. [PubMed: 21419662]  [MGI Ref ID J:169863]

Raetz M; Kibardin A; Sturge CR; Pifer R; Li H; Burstein E; Ozato K; Larin S; Yarovinsky F. 2013. Cooperation of TLR12 and TLR11 in the IRF8-dependent IL-12 response to Toxoplasma gondii profilin. J Immunol 191(9):4818-27. [PubMed: 24078692]  [MGI Ref ID J:206239]

Rajendrasozhan S; Chung S; Sundar IK; Yao H; Rahman I. 2010. Targeted disruption of NF-{kappa}B1 (p50) augments cigarette smoke-induced lung inflammation and emphysema in mice: a critical role of p50 in chromatin remodeling. Am J Physiol Lung Cell Mol Physiol 298(2):L197-209. [PubMed: 19965984]  [MGI Ref ID J:157673]

Razeghi P; Wang ME; Youker KA; Golfman L; Stepkowski S; Taegtmeyer H. 2007. Lack of NF-kappaB1 (p105/p50) attenuates unloading-induced downregulation of PPARalpha and PPARalpha-regulated gene expression in rodent heart. Cardiovasc Res 74(1):133-9. [PubMed: 17276423]  [MGI Ref ID J:119766]

Robinson MJ; Beinke S; Kouroumalis A; Tsichlis PN; Ley SC. 2007. Phosphorylation of TPL-2 on serine 400 is essential for lipopolysaccharide activation of extracellular signal-regulated kinase in macrophages. Mol Cell Biol 27(21):7355-64. [PubMed: 17709378]  [MGI Ref ID J:129052]

Rodriguez-Galan MC; Bream JH; Farr A; Young HA. 2005. Synergistic effect of IL-2, IL-12, and IL-18 on thymocyte apoptosis and Th1/Th2 cytokine expression. J Immunol 174(5):2796-804. [PubMed: 15728489]  [MGI Ref ID J:97710]

Ruan Q; Kameswaran V; Tone Y; Li L; Liou HC; Greene MI; Tone M; Chen YH. 2009. Development of Foxp3(+) regulatory t cells is driven by the c-Rel enhanceosome. Immunity 31(6):932-40. [PubMed: 20064450]  [MGI Ref ID J:156177]

Rusca N; Deho L; Montagner S; Zielinski CE; Sica A; Sallusto F; Monticelli S. 2012. miR-146a and NF-kappaB1 Regulate Mast Cell Survival and T Lymphocyte Differentiation. Mol Cell Biol 32(21):4432-44. [PubMed: 22927641]  [MGI Ref ID J:189248]

Saccani A; Schioppa T; Porta C; Biswas SK; Nebuloni M; Vago L; Bottazzi B; Colombo MP; Mantovani A; Sica A. 2006. p50 nuclear factor-kappaB overexpression in tumor-associated macrophages inhibits M1 inflammatory responses and antitumor resistance. Cancer Res 66(23):11432-40. [PubMed: 17145890]  [MGI Ref ID J:116212]

Schwarz EM; Badorff C; Hiura TS; Wessely R; Badorff A; Verma IM; Knowlton KU. 1998. NF-kappaB-mediated inhibition of apoptosis is required for encephalomyocarditis virus virulence: a mechanism of resistance in p50 knockout mice. J Virol 72(7):5654-60. [PubMed: 9621024]  [MGI Ref ID J:120576]

Serre K; Mohr E; Benezech C; Bird R; Khan M; Caamano JH; Cunningham AF; Maclennan IC. 2011. Selective effects of NF-kappaB1 deficiency in CD4 T cells on Th2 and TFh induction by alum-precipitated protein vaccines. Eur J Immunol 41(6):1573-82. [PubMed: 21469117]  [MGI Ref ID J:176487]

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):321-30. [PubMed: 7834752]  [MGI Ref ID J:37184]

Shi M; Deng W; Bi E; Mao K; Ji Y; Lin G; Wu X; Tao Z; Li Z; Cai X; Sun S; Xiang C; Sun B. 2008. TRIM30 alpha negatively regulates TLR-mediated NF-kappa B activation by targeting TAB2 and TAB3 for degradation. Nat Immunol 9(4):369-77. [PubMed: 18345001]  [MGI Ref ID J:133259]

Sivakumar V; Hammond KJ; Howells N; Pfeffer K; Weih F. 2003. Differential requirement for Rel/nuclear factor kappa B family members in natural killer T cell development. J Exp Med 197(12):1613-21. [PubMed: 12810684]  [MGI Ref ID J:120660]

Snapper CM; Zelazowski P; Rosas FR; Kehry MR; Tian M; Baltimore D; Sha WC. 1996. B cells from p50/NF-kappa B knockout mice have selective defects in proliferation, differentiation, germ-line CH transcription, and Ig class switching. J Immunol 156(1):183-91. [PubMed: 8598461]  [MGI Ref ID J:30268]

Song D; Fang G; Mao SZ; Ye X; Liu G; Gong Y; Liu SF. 2012. Chronic intermittent hypoxia induces atherosclerosis by NF-kappaB-dependent mechanisms. Biochim Biophys Acta 1822(11):1650-9. [PubMed: 22846605]  [MGI Ref ID J:188032]

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):2265-73. [PubMed: 14764695]  [MGI Ref ID J:88049]

Stanic AK; Bezbradica JS; Park JJ; Van Kaer L; Boothby MR; Joyce S. 2004. Cutting edge: the ontogeny and function of Va14Ja18 natural T lymphocytes require signal processing by protein kinase C theta and NF-kappa B. J Immunol 172(8):4667-71. [PubMed: 15067039]  [MGI Ref ID J:89129]

Sweeney TE; Suliman HB; Hollingsworth JW; Welty-Wolf KE; Piantadosi CA. 2011. A toll-like receptor 2 pathway regulates the Ppargc1a/b metabolic co-activators in mice with Staphylococcal aureus sepsis. PLoS One 6(9):e25249. [PubMed: 21966468]  [MGI Ref ID J:177656]

Takahashi Y; Katai N; Murata T; Taniguchi SI; Hayashi T. 2007. Development of spontaneous optic neuropathy in NF-kappaBetap50-deficient mice: requirement for NF-kappaBetap50 in ganglion cell survival. Neuropathol Appl Neurobiol 33(6):692-705. [PubMed: 17931357]  [MGI Ref ID J:150242]

Tang T; Zhang J; Yin J; Staszkiewicz J; Gawronska-Kozak B; Jung DY; Ko HJ; Ong H; Kim JK; Mynatt R; Martin RJ; Keenan M; Gao Z; Ye J. 2010. Uncoupling of inflammation and insulin resistance by NF-kappaB in transgenic mice through elevated energy expenditure. J Biol Chem 285(7):4637-44. [PubMed: 20018865]  [MGI Ref ID J:159756]

Tato CM; Mason N; Artis D; Shapira S; Caamano JC; Bream JH; Liou HC; Hunter CA. 2006. Opposing roles of NF-{kappa}B family members in the regulation of NK cell proliferation and production of IFN-{gamma}. Int Immunol 18(4):505-13. [PubMed: 16481345]  [MGI Ref ID J:107069]

TeKippe M; Harrison DE; Chen J. 2003. Expansion of hematopoietic stem cell phenotype and activity in Trp53-null mice. Exp Hematol 31(6):521-7. [PubMed: 12829028]  [MGI Ref ID J:115677]

Tharappel JC; Nalca A; Owens AB; Ghabrial L; Konz EC; Glauert HP; Spear BT. 2003. Cell proliferation and apoptosis are altered in mice deficient in the NF-kappaB p50 subunit after treatment with the peroxisome proliferator ciprofibrate. Toxicol Sci 75(2):300-8. [PubMed: 12883078]  [MGI Ref ID J:126216]

Tharappel JC; Spear BT; Glauert HP. 2008. Effect of phenobarbital on hepatic cell proliferation and apoptosis in mice deficient in the p50 subunit of NF-kappaB. Toxicol Appl Pharmacol 226(3):338-44. [PubMed: 17963809]  [MGI Ref ID J:132189]

Thomas HE; Angstetra E; Fernandes RV; Mariana L; Irawaty W; Jamieson EL; Dudek NL; Kay TW. 2006. Perturbations in nuclear factor-kappaB or c-Jun N-terminal kinase pathways in pancreatic beta cells confer susceptibility to cytokine-induced cell death. Immunol Cell Biol 84(1):20-7. [PubMed: 16277639]  [MGI Ref ID J:105855]

Thomas PG; Carter MR; Da'dara AA; DeSimone TM; Harn DA. 2005. A helminth glycan induces APC maturation via alternative NF-kappa B activation independent of I kappa B alpha degradation. J Immunol 175(4):2082-90. [PubMed: 16081774]  [MGI Ref ID J:107518]

Tomczak MF; Erdman SE; Davidson A; Wang YY; Nambiar PR; Rogers AB; Rickman B; Luchetti D; Fox JG; Horwitz BH. 2006. Inhibition of Helicobacter hepaticus-induced colitis by IL-10 requires the p50/p105 subunit of NF-kappa B. J Immunol 177(10):7332-9. [PubMed: 17082652]  [MGI Ref ID J:140612]

Tomczak MF; Gadjeva M; Wang YY; Brown K; Maroulakou I; Tsichlis PN; Erdman SE; Fox JG; Horwitz BH. 2006. Defective activation of ERK in macrophages lacking the p50/p105 subunit of NF-kappaB is responsible for elevated expression of IL-12 p40 observed after challenge with Helicobacter hepaticus. J Immunol 176(2):1244-51. [PubMed: 16394015]  [MGI Ref ID J:126439]

Tsutsuki H; Yahiro K; Suzuki K; Suto A; Ogura K; Nagasawa S; Ihara H; Shimizu T; Nakajima H; Moss J; Noda M. 2012. Subtilase Cytotoxin Enhances Escherichia coli Survival in Macrophages by Suppression of Nitric Oxide Production through the Inhibition of NF-kappaB Activation. Infect Immun 80(11):3939-51. [PubMed: 22949549]  [MGI Ref ID J:187974]

Valenzuela JO; Iclozan C; Hossain MS; Prlic M; Hopewell E; Bronk CC; Wang J; Celis E; Engelman RW; Blazar BR; Bevan MJ; Waller EK; Yu XZ; Beg AA. 2009. PKCtheta is required for alloreactivity and GVHD but not for immune responses toward leukemia and infection in mice. J Clin Invest 119(12):3774-86. [PubMed: 19907075]  [MGI Ref ID J:155103]

Vang KB; Yang J; Pagan AJ; Li LX; Wang J; Green JM; Beg AA; Farrar MA. 2010. Cutting edge: CD28 and c-Rel-dependent pathways initiate regulatory T cell development. J Immunol 184(8):4074-7. [PubMed: 20228198]  [MGI Ref ID J:159880]

Wang Y; Meng A; Lang H; Brown SA; Konopa JL; Kindy MS; Schmiedt RA; Thompson JS; Zhou D. 2004. Activation of nuclear factor kappaB In vivo selectively protects the murine small intestine against ionizing radiation-induced damage. Cancer Res 64(17):6240-6. [PubMed: 15342410]  [MGI Ref ID J:92410]

Wang YJ; Wang JT; Fan QX; Geng JG. 2007. Andrographolide inhibits NF-kappaBeta activation and attenuates neointimal hyperplasia in arterial restenosis. Cell Res 17(11):933-41. [PubMed: 17943075]  [MGI Ref ID J:133635]

Weih F; Durham SK; Barton DS; Sha WC; Baltimore D; Bravo R. 1996. Both multiorgan inflammation and myeloid hyperplasia in RelB-deficient mice are T cell dependent. J Immunol 157(9):3974-9. [PubMed: 8892630]  [MGI Ref ID J:110829]

Weih F; Durham SK; Barton DS; Sha WC; Baltimore D; Bravo R. 1997. p50-NF-kappaB complexes partially compensate for the absence of RelB: severely increased pathology in p50(-/-)relB(-/-) double-knockout mice. J Exp Med 185(7):1359-70. [PubMed: 9104822]  [MGI Ref ID J:39508]

Williams JM; Duckworth CA; Watson AJ; Frey MR; Miguel JC; Burkitt MD; Sutton R; Hughes KR; Hall LJ; Caamano JH; Campbell BJ; Pritchard DM. 2013. A mouse model of pathological small intestinal epithelial cell apoptosis and shedding induced by systemic administration of lipopolysaccharide. Dis Model Mech 6(6):1388-99. [PubMed: 24046352]  [MGI Ref ID J:205156]

Wu CL; Kandarian SC; Jackman RW. 2011. Identification of genes that elicit disuse muscle atrophy via the transcription factors p50 and Bcl-3. PLoS One 6(1):e16171. [PubMed: 21249144]  [MGI Ref ID J:180832]

Wuerffel RA; Ma L; Kenter AL. 2001. NF-kappa B p50-dependent in vivo footprints at Ig S gamma 3 DNA are correlated with mu-->gamma 3 switch recombination. J Immunol 166(7):4552-9. [PubMed: 11254712]  [MGI Ref ID J:123765]

Xing L; Carlson L; Story B; Tai Z; Keng P; Siebenlist U; Boyce BF. 2003. Expression of either NF-kappaB p50 or p52 in osteoclast precursors is required for IL-1-induced bone resorption. J Bone Miner Res 18(2):260-9. [PubMed: 12568403]  [MGI Ref ID J:111245]

Yamamoto M; Yamazaki S; Uematsu S; Sato S; Hemmi H; Hoshino K; Kaisho T; Kuwata H; Takeuchi O; Takeshige K; Saitoh T; Yamaoka S; Yamamoto N; Yamamoto S; Muta T; Takeda K; Akira S. 2004. Regulation of Toll/IL-1-receptor-mediated gene expression by the inducible nuclear protein IkappaBzeta. Nature 430(6996):218-22. [PubMed: 15241416]  [MGI Ref ID J:91297]

Yamashita T; Yao Z; Li F; Zhang Q; Badell IR; Schwarz EM; Takeshita S; Wagner EF; Noda M; Matsuo K; Xing L; Boyce BF. 2007. NF-kappaB p50 and p52 regulate receptor activator of NF-kappaB ligand (RANKL) and tumor necrosis factor-induced osteoclast precursor differentiation by activating c-Fos and NFATc1. J Biol Chem 282(25):18245-53. [PubMed: 17485464]  [MGI Ref ID J:123379]

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):669-78. [PubMed: 15343385]  [MGI Ref ID J:92596]

Yang HT; Papoutsopoulou S; Belich M; Brender C; Janzen J; Gantke T; Handley M; Ley SC. 2012. Coordinate regulation of TPL-2 and NF-kappaB signaling in macrophages by NF-kappaB1 p105. Mol Cell Biol 32(17):3438-51. [PubMed: 22733995]  [MGI Ref ID J:196528]

Yang HT; Wang Y; Zhao X; Demissie E; Papoutsopoulou S; Mambole A; O'Garra A; Tomczak MF; Erdman SE; Fox JG; Ley SC; Horwitz BH. 2011. NF-(kappa)B1 inhibits TLR-induced IFN-(beta) production in macrophages through TPL-2-dependent ERK activation. J Immunol 186(4):1989-96. [PubMed: 21217011]  [MGI Ref ID J:169175]

Yang L; Boldin MP; Yu Y; Liu CS; Ea CK; Ramakrishnan P; Taganov KD; Zhao JL; Baltimore D. 2012. miR-146a controls the resolution of T cell responses in mice. J Exp Med 209(9):1655-70. [PubMed: 22891274]  [MGI Ref ID J:191831]

Yang L; Cohn L; Zhang DH; Homer R; Ray A; Ray P. 1998. Essential role of nuclear factor kappaB in the induction of eosinophilia in allergic airway inflammation. J Exp Med 188(9):1739-50. [PubMed: 9802985]  [MGI Ref ID J:50763]

Yao Z; Xing L; Qin C; Schwarz EM; Boyce BF. 2008. Osteoclast precursor interaction with bone matrix induces osteoclast formation directly by an interleukin-1-mediated autocrine mechanism. J Biol Chem 283(15):9917-24. [PubMed: 18250170]  [MGI Ref ID J:135323]

Ye B; Zhou PY; Jia M; Cheng XS; Jia YT; Xu SG. 2013. Absence of NF-kappaB subunit p50 ameliorates cold immobilization stress-induced gastric ulcers. Biochem Biophys Res Commun 434(3):547-51. [PubMed: 23583384]  [MGI Ref ID J:201859]

Yilmaz ZB; Weih DS; Sivakumar V; Weih F. 2003. RelB is required for Peyer's patch development: differential regulation of p52-RelB by lymphotoxin and TNF. EMBO J 22(1):121-30. [PubMed: 12505990]  [MGI Ref ID J:81255]

Yu Z; Zhou D; Bruce-Keller AJ; Kindy MS; Mattson MP. 1999. Lack of the p50 subunit of nuclear factor-kappaB increases the vulnerability of hippocampal neurons to excitotoxic injury. J Neurosci 19(20):8856-65. [PubMed: 10516305]  [MGI Ref ID J:119905]

Yu Z; Zhou D; Cheng G; Mattson MP. 2000. Neuroprotective role for the p50 subunit of NF-kappaB in an experimental model of Huntington's disease. J Mol Neurosci 15(1):31-44. [PubMed: 11211235]  [MGI Ref ID J:117914]

Zarnegar B; He JQ; Oganesyan G; Hoffmann A; Baltimore D; Cheng G. 2004. Unique CD40-mediated biological program in B cell activation requires both type 1 and type 2 NF-kappaB activation pathways. Proc Natl Acad Sci U S A 101(21):8108-13. [PubMed: 15148378]  [MGI Ref ID J:90663]

Zarnegar BJ; Wang Y; Mahoney DJ; Dempsey PW; Cheung HH; He J; Shiba T; Yang X; Yeh WC; Mak TW; Korneluk RG; Cheng G. 2008. Noncanonical NF-kappaB activation requires coordinated assembly of a regulatory complex of the adaptors cIAP1, cIAP2, TRAF2 and TRAF3 and the kinase NIK. Nat Immunol 9(12):1371-8. [PubMed: 18997794]  [MGI Ref ID J:143167]

Zelazowski P; Shen Y; Snapper CM. 2000. NF-kappaB/p50 and NF-kappaB/c-Rel differentially regulate the activity of the 3'alphaE-hsl,2 enhancer in normal murine B cells in an activation-dependent manner. Int Immunol 12(8):1167-72. [PubMed: 10917891]  [MGI Ref ID J:110506]

Zhan Y; Gerondakis S; Coghill E; Bourges D; Xu Y; Brady JL; Lew AM. 2008. Glucocorticoid-induced TNF receptor expression by T cells is reciprocally regulated by NF-kappaB and NFAT. J Immunol 181(8):5405-13. [PubMed: 18832697]  [MGI Ref ID J:140766]

Zhang J; Gao Z; Ye J. 2013. Phosphorylation and degradation of S6K1 (p70S6K1) in response to persistent JNK1 Activation. Biochim Biophys Acta 1832(12):1980-8. [PubMed: 23816567]  [MGI Ref ID J:204115]

Zhang J; Warren MA; Shoemaker SF; Ip MM. 2007. NFkappaB1/p50 is not required for tumor necrosis factor-stimulated growth of primary mammary epithelial cells: implications for NFkappaB2/p52 and RelB. Endocrinology 148(1):268-78. [PubMed: 17008396]  [MGI Ref ID J:129561]

Zhang LX; Zhao Y; Cheng G; Guo TL; Chin YE; Liu PY; Zhao TC. 2010. Targeted deletion of NF-kappaB p50 diminishes the cardioprotection of histone deacetylase inhibition. Am J Physiol Heart Circ Physiol 298(6):H2154-63. [PubMed: 20382965]  [MGI Ref ID J:160338]

Zhang Q; Guo R; Lu Y; Zhao L; Zhou Q; Schwarz EM; Huang J; Chen D; Jin ZG; Boyce BF; Xing L. 2008. VEGF-C, a lymphatic growth factor, is a RANKL target gene in osteoclasts that enhances osteoclastic bone resorption through an autocrine mechanism. J Biol Chem 283(19):13491-9. [PubMed: 18359770]  [MGI Ref ID J:137099]

Zhao JL; Rao DS; Boldin MP; Taganov KD; O'Connell RM; Baltimore D. 2011. NF-{kappa}B dysregulation in microRNA-146a-deficient mice drives the development of myeloid malignancies. Proc Natl Acad Sci U S A 108(22):9184-9. [PubMed: 21576471]  [MGI Ref ID J:173230]

Zheng S; Abraham C. 2013. NF-kappaB1 inhibits NOD2-induced cytokine secretion through ATF3-dependent mechanisms. Mol Cell Biol 33(24):4857-71. [PubMed: 24100018]  [MGI Ref ID J:206079]

Zhu M; Chin RK; Christiansen PA; Lo JC; Liu X; Ware C; Siebenlist U; Fu YX. 2006. NF-kappaB2 is required for the establishment of central tolerance through an Aire-dependent pathway. J Clin Invest 116(11):2964-71. [PubMed: 17039258]  [MGI Ref ID J:115011]

de Groot D; Haverslag RT; Pasterkamp G; de Kleijn DP; Hoefer IE. 2010. Targeted deletion of the inhibitory NF-kappaB p50 subunit in bone marrow-derived cells improves collateral growth after arterial occlusion. Cardiovasc Res 88(1):179-85. [PubMed: 20495189]  [MGI Ref ID J:183211]

dos Santos NR; Williame M; Gachet S; Cormier F; Janin A; Weih D; Weih F; Ghysdael J. 2008. RelB-dependent stromal cells promote T-cell leukemogenesis. PLoS ONE 3(7):e2555. [PubMed: 18596915]  [MGI Ref ID J:137965]

von Vietinghoff S; Asagiri M; Azar D; Hoffmann A; Ley K. 2010. Defective regulation of CXCR2 facilitates neutrophil release from bone marrow causing spontaneous inflammation in severely NF-kappaB-deficient mice. J Immunol 185(1):670-8. [PubMed: 20519647]  [MGI Ref ID J:161430]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX10

Colony Maintenance

Breeding & HusbandryWhen maintaining a live colony, these mice are bred as homozygotes.
Mating SystemHomozygote x Homozygote         (Female x Male)   14-NOV-06
Diet Information LabDiet® 5K52/5K67

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


Pricing for USA, Canada and Mexico shipping destinations View International Pricing

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $195.00Female or MaleHomozygous for Nfkb1tm1Bal  
Price per Pair (US dollars $)Pair Genotype
$390.00Homozygous for Nfkb1tm1Bal x Homozygous for Nfkb1tm1Bal  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1500 unique mouse models across a vast array of research areas. Breeding colonies provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. If a Repository strain is not immediately available, then within 2 to 3 business days, you will receive an estimated availability timeframe for your inquiry or order along with various delivery options. Repository strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping. We will note and try to accommodate requests for specific ages of Repository strains but cannot guarantee provision of these strains at specific ages. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, please let us know.

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $253.50Female or MaleHomozygous for Nfkb1tm1Bal  
Price per Pair (US dollars $)Pair Genotype
$507.00Homozygous for Nfkb1tm1Bal x Homozygous for Nfkb1tm1Bal  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1500 unique mouse models across a vast array of research areas. Breeding colonies provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. If a Repository strain is not immediately available, then within 2 to 3 business days, you will receive an estimated availability timeframe for your inquiry or order along with various delivery options. Repository strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping. We will note and try to accommodate requests for specific ages of Repository strains but cannot guarantee provision of these strains at specific ages. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, please let us know.

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1500 unique mouse models across a vast array of research areas. Breeding colonies provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. If a Repository strain is not immediately available, then within 2 to 3 business days, you will receive an estimated availability timeframe for your inquiry or order along with various delivery options. Repository strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping. We will note and try to accommodate requests for specific ages of Repository strains but cannot guarantee provision of these strains at specific ages. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, please let us know.

Control Information

  Control
   000664 C57BL/6J (approximate)
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

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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.
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"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "RECIPIENT" means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.

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In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.

No Liability

In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. Unless prohibited by law, in purchasing or receiving MICE, PRODUCTS or services from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.

MICE and PRODUCTS are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.

The foregoing represents the General Terms and Conditions applicable to JACKSON’s MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and services by JACKSON, and by its licensees and distributors.

Acceptance of delivery of MICE, PRODUCTS or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or services by JACKSON.


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