Strain Name:

C.C3-Tlr4Lps-d/J

Stock Number:

002930

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Availability:

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In addition to the Tlr4Lps-d congenic interval from C3H/HeJ, this strain is also congenic for the wild type tyrosinase allele from C3H/HeJ on chromosome 7. This strain provides a tool for analysis of markers in the region and for examining functional effects of Lpsd on BALB/c, a strain susceptible to infection, neoplastic disease including the induction of plasmacytomas and other tumors.

Description

Strain Information

Type Congenic; Mutant Strain;
Additional information on Genetically Engineered and Mutant Mice.
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Additional information on Congenic nomenclature.
Mating SystemHomozygote x Homozygote         (Female x Male)   01-MAR-06
Breeding Considerations This strain is a good breeder.
Specieslaboratory mouse
Background Strain BALB/cAnPt
Donor Strain C3H/HeJ

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Appearance
agouti
Related Genotype: A/A Tyrp1+/Tyrp1+

Description
In addition to the Tlr4Lps-d congenic interval from C3H/HeJ, this strain is also congenic for the wild type tyrosinase allele from C3H/HeJ on chromosome 7. This strain provides a tool for analysis of markers in the region and for examining functional effects of Lpsd on BALB/c, a strain susceptible to infection, neoplastic disease including the induction of plasmacytomas and other tumors.

Development
The Lps-d mutation arose in C3H/HeJ sometime between 1960 and 1968. In 1977 a C3H/HeJ female, derived from the colony of David Sachs at NIH, was crossed with a BALB/cAnPt male and the Tlr4Lps-d allele was transferred onto the BALB/cAnPt background by continued backcrossing. At that time it was thought that Tlr4 and Tyrp1 were tightly linked so the agouti mice, those that would be carrying the C3H/HeJ-derived dominant B (wild-type) allele of Typr1 rather than being homozygous for the BALB/cAnPt-derived recessive b allele and Tyrc allele, were selected at each generation to continue the backcross. At N6 intercrossing made the strain homozygous for Tlr4Lps-d and Tyrp1B. Backcrossing to BALB/cAnPt was resumed from N6F22. When backcrossing reached N20, the strain was intercrossed to generate this strain homozygous for Tlr4Lps-d and Tyrp1B but not Tyrc. The congenic interval encompassing Tyrp1B and Tlr4Lps-d includes at least from D4Mit151 through D4Mit26. In March 1977, this strain was imported into The Jackson Laboratory from Dr. Stephanie Vogel at Uniformed Services University of the Health Sciences.

Control Information

  Control
   001026 BALB/cByJ (approximate)
 
  Considerations for Choosing Controls

Related Strains

Strains carrying   Tlr4Lps-d allele
005973   C3Bir.129P2(B6)-Il10C3Bir/LtJ
004326   C3Bir.129P2(B6)-Il10tm1Cgn/Lt
003968   C3Bir.129P2(B6)-Il10tm1Cgn/LtJ
000659   C3H/HeJ
005972   C3H/HeJBirLtJ
View Strains carrying   Tlr4Lps-d     (5 strains)

Strains carrying other alleles of Tlr4
024872   B6(Cg)-Tlr4tm1.1Karp/J
007227   B6.B10ScN-Tlr4lps-del/JthJ
000029   BXD29-Tlr4lps-2J/J
003752   C57BL/10ScNJ
View Strains carrying other alleles of Tlr4     (4 strains)

Additional Web Information

JAX® NOTES, Summer 2005; 498. Toll-like Receptor JAX® Mice for Immunological Research.

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).
Toll-Like Receptor 4; TLR4
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Macular Degeneration, Age-Related, 10; ARMD10   (TLR4)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Tlr4Lps-d/Tlr4Lps-d

        C.C3-Tlr4Lps-d/J
  • cardiovascular system phenotype
  • decreased angiogenesis
    • perfusion restoration is significantly reduced 7 days after femoral artery ligation   (MGI Ref ID J:171028)
  • decreased response of heart to induced stress
    • exhibit reduced cardiac hypertrophy following pressure overload compared to controls   (MGI Ref ID J:106358)
    • exhibit no significant myocardial interstitial fibrosis or cardiac myocyte death following pressure overload unlike wild-type   (MGI Ref ID J:106358)
  • homeostasis/metabolism phenotype
  • decreased response of heart to induced stress
    • exhibit reduced cardiac hypertrophy following pressure overload compared to controls   (MGI Ref ID J:106358)
    • exhibit no significant myocardial interstitial fibrosis or cardiac myocyte death following pressure overload unlike wild-type   (MGI Ref ID J:106358)
  • skeleton phenotype
  • abnormal bone structure   (MGI Ref ID J:118467)
    • increased bone mass
      • increased bone area of the tibia   (MGI Ref ID J:118467)
    • increased bone mineral content
      • greater mineral content but not yet significant at 6 weeks   (MGI Ref ID J:118467)
    • increased bone mineral density
      • significantly increased bone mineral density at 20 weeks   (MGI Ref ID J:118467)
      • density continues to increase over time   (MGI Ref ID J:118467)

The following phenotype information is associated with a similar, but not exact match to this JAX® Mice strain.

Tlr4Lps-d/Tlr4Lps-d

        involves: C3H/HeJ
  • immune system phenotype
  • abnormal T-helper 2 physiology
    • Th2 responses elevated after induction of autoimmune arthritis   (MGI Ref ID J:96356)
  • abnormal osteoclast differentiation
    • lipopolysaccharide fails to inhibit RANKL induced osteoclast formation as it does in controls   (MGI Ref ID J:131353)
    • antibody to IFN-beta or to IFNAR1 reverses inhibition of osteoclast formation induced by RANKL   (MGI Ref ID J:131353)
  • abnormal tumor necrosis factor level
    • diminished TNF alpha expression after 90 minutes of liver ischemia followed by 6 hours of reperfusion   (MGI Ref ID J:114368)
    • macrophage primary but not secondary necrotic cells with residual stimulatory affect on TNF alpha production by macrophage   (MGI Ref ID J:124334)
  • increased susceptibility to bacterial infection
    • low responsiveness of spleen cells to lipopolysaccharides   (MGI Ref ID J:5721)
    • increased sensitivity to gram (-) infection   (MGI Ref ID J:51522)
    • significantly shortened survival after infection with Klebsiella pneumoniae   (MGI Ref ID J:87807)
    • increased K. pneumoniae levels in the lung   (MGI Ref ID J:87807)
  • increased susceptibility to induced arthritis
    • reduced susceptibility to arthritis induced by type II collagen   (MGI Ref ID J:96356)
  • behavior/neurological phenotype
  • hyporesponsive to tactile stimuli
    • reduced mechanical allodynia after nerve injury   (MGI Ref ID J:97819)
  • increased thermal nociceptive threshold
    • attenuated response to heat   (MGI Ref ID J:97819)
  • skeleton phenotype
  • abnormal osteoclast differentiation
    • lipopolysaccharide fails to inhibit RANKL induced osteoclast formation as it does in controls   (MGI Ref ID J:131353)
    • antibody to IFN-beta or to IFNAR1 reverses inhibition of osteoclast formation induced by RANKL   (MGI Ref ID J:131353)
  • increased susceptibility to induced arthritis
    • reduced susceptibility to arthritis induced by type II collagen   (MGI Ref ID J:96356)
  • muscle phenotype
  • *normal* muscle phenotype
    • MCP-1 (monocyte chemoattractant protein-1) release from isolated mouse aorta smooth muscle cells (MAoSMC) by stimulation with dsRNA is normal relative to controls   (MGI Ref ID J:116310)
  • integument phenotype
  • hyporesponsive to tactile stimuli
    • reduced mechanical allodynia after nerve injury   (MGI Ref ID J:97819)
  • increased thermal nociceptive threshold
    • attenuated response to heat   (MGI Ref ID J:97819)
  • nervous system phenotype
  • abnormal glial cell apoptosis
    • isolated microglia exposed to LPS are resistant to apoptosis   (MGI Ref ID J:99051)
  • homeostasis/metabolism phenotype
  • abnormal circulating enzyme level
    • myeloperoxidase levels are reduced after 90 minutes of liver ischemia followed by 6 hours of reperfusion   (MGI Ref ID J:114368)
    • increased HO-1 expression   (MGI Ref ID J:114368)
    • decreased circulating alanine transaminase level
      • serum levels decreased after 90 minutes of liver ischemia followed by 6 hours of reperfusion   (MGI Ref ID J:114368)
  • abnormal tumor necrosis factor level
    • diminished TNF alpha expression after 90 minutes of liver ischemia followed by 6 hours of reperfusion   (MGI Ref ID J:114368)
    • macrophage primary but not secondary necrotic cells with residual stimulatory affect on TNF alpha production by macrophage   (MGI Ref ID J:124334)
  • hematopoietic system phenotype
  • abnormal T-helper 2 physiology
    • Th2 responses elevated after induction of autoimmune arthritis   (MGI Ref ID J:96356)
  • abnormal osteoclast differentiation
    • lipopolysaccharide fails to inhibit RANKL induced osteoclast formation as it does in controls   (MGI Ref ID J:131353)
    • antibody to IFN-beta or to IFNAR1 reverses inhibition of osteoclast formation induced by RANKL   (MGI Ref ID J:131353)
  • cellular phenotype
  • abnormal glial cell apoptosis
    • isolated microglia exposed to LPS are resistant to apoptosis   (MGI Ref ID J:99051)
  • abnormal osteoclast differentiation
    • lipopolysaccharide fails to inhibit RANKL induced osteoclast formation as it does in controls   (MGI Ref ID J:131353)
    • antibody to IFN-beta or to IFNAR1 reverses inhibition of osteoclast formation induced by RANKL   (MGI Ref ID J:131353)
  • hearing/vestibular/ear phenotype
  • *normal* hearing/vestibular/ear phenotype
    • cisplatin and lipopolysaccharide treatment does not lead to significant increases in auditory brainstem response as is observed in controls   (MGI Ref ID J:168789)

Tlr4Lps-d/Tlr4Lps-d

        C3H/HeJ-Tlr4Lps-d
  • mortality/aging
  • decreased sensitivity to induced morbidity/mortality
    • bacterial lipoteichoic acid exposure after priming by IFNgamma and sensitization with D-galactosamine induces lethal shock in Tlr4-deficient mutants, while Tlr2- and Tlr2/4-doubly deficient mice are protected   (MGI Ref ID J:121930)
    • systemic challenge with Myr3-CSK4 (a synthetic lipopeptide) after D-galactosamine induces lethal shock in wild-type mice, but mutants are protected   (MGI Ref ID J:121930)
    • heat-inactivated E. coli exposure results in fatal toxemia as in wild type mice heat-inactivated E. coli exposure results in fatal toxemia as in wild-type mice   (MGI Ref ID J:121930)
  • increased susceptibility to viral infection induced morbidity/mortality
    • 10 days after intranasal infection with 5 x 105 pfu Vac-GFL 70% of mice succumb unlike wild-type controls that all survive   (MGI Ref ID J:162716)
  • growth/size/body phenotype
  • decreased body size
    • always smaller than controls   (MGI Ref ID J:118467)
    • decreased body weight
      • lower body weight than controls after 8 weeks on a high fat diet   (MGI Ref ID J:126488)
      • weights are 15% lower than controls after 8 months on a high fat diet   (MGI Ref ID J:126488)
      • food intake comparable to controls   (MGI Ref ID J:126488)
  • decreased percent body fat
    • 70% less body fat   (MGI Ref ID J:118467)
  • decreased susceptibility to weight loss
    • reduced weight loss following infection with Vac-GFL   (MGI Ref ID J:162716)
  • immune system phenotype
  • abnormal cytokine level
    • keratinocyte derived cytokine levels in lungs are unaffected by lipopolysaccharide   (MGI Ref ID J:96680)
    • macrophage inflammatory protein-2 levels in lungs are unaffected by lipopolysaccharide   (MGI Ref ID J:96680)
    • abnormal interleukin level
      • Il-6 levels in lungs are unaffected by lipopolysaccharide   (MGI Ref ID J:96680)
      • il6 levels increase less on a high fat diet than in controls   (MGI Ref ID J:96680)
      • increased circulating interleukin-6 level
        • increased levels after 7 days of dextran sodium sulfate treatment   (MGI Ref ID J:37271)
    • abnormal tumor necrosis factor level
      • TNF alpha levels in lungs are unaffected by lipopolysaccharide   (MGI Ref ID J:96680)
      • less increase in TNF alpha on a high fat diet than in controls   (MGI Ref ID J:96680)
  • abnormal macrophage chemotaxis
    • robust macrophage response at the site of spinal injury   (MGI Ref ID J:122597)
  • abnormal microglial cell physiology
    • resistant to lipopolysaccharide induced apoptosis   (MGI Ref ID J:99051)
  • abnormal phagocyte morphology
    • phagocytes fail to respond to LPS stimulation   (MGI Ref ID J:125179)
    • however, response to stimulation with TLR9 or TLR7 and TLR8 with their ligands (CpG and R848, respectively) is similar to in wild-type cells   (MGI Ref ID J:125179)
  • abnormal spleen weight
    • spleen weight fails to increase with dextran sodium sulfate treatment as it does in controls   (MGI Ref ID J:37271)
  • altered susceptibility to infection
    • following intranasal infection with 1x104 pfu Vac-GFL (a recombinant vaccinia virus that expresses a reporter protein) weight loss is reduced at 1 - 3 and 7 - 8 days after infection but the decrease in body temperature is more severe at 4 - 7 days afteinfection and viral replication is increased   (MGI Ref ID J:162716)
    • increased susceptibility to viral infection induced morbidity/mortality
      • 10 days after intranasal infection with 5 x 105 pfu Vac-GFL 70% of mice succumb unlike wild-type controls that all survive   (MGI Ref ID J:162716)
  • liver inflammation
    • after BDL, necroinflammatory foci and lymphocytic infiltration are obviously less than in controls   (MGI Ref ID J:135830)
  • lung inflammation
    • no increase in white blood cells or neutrophiles in bronchoalveolar fluid   (MGI Ref ID J:96680)
    • white blood cells and neutrophiles are not detected by myeloperoxidase assay   (MGI Ref ID J:96680)
  • hematopoietic system phenotype
  • *normal* hematopoietic system phenotype
    • B cell apoptosis in Peyer's patch is not observed after bile duct ligation (BDL)   (MGI Ref ID J:135830)
    • abnormal macrophage chemotaxis
      • robust macrophage response at the site of spinal injury   (MGI Ref ID J:122597)
    • abnormal microglial cell physiology
      • resistant to lipopolysaccharide induced apoptosis   (MGI Ref ID J:99051)
    • abnormal phagocyte morphology
      • phagocytes fail to respond to LPS stimulation   (MGI Ref ID J:125179)
      • however, response to stimulation with TLR9 or TLR7 and TLR8 with their ligands (CpG and R848, respectively) is similar to in wild-type cells   (MGI Ref ID J:125179)
    • abnormal spleen weight
      • spleen weight fails to increase with dextran sodium sulfate treatment as it does in controls   (MGI Ref ID J:37271)
  • homeostasis/metabolism phenotype
  • *normal* homeostasis/metabolism phenotype
    • after BDL, serum alanine transaminase levels are not different from controls   (MGI Ref ID J:135830)
    • abnormal circulating leptin level
      • increase in blood leptin on a high fat diet is 36% less than in controls   (MGI Ref ID J:126488)
    • abnormal cytokine level
      • keratinocyte derived cytokine levels in lungs are unaffected by lipopolysaccharide   (MGI Ref ID J:96680)
      • macrophage inflammatory protein-2 levels in lungs are unaffected by lipopolysaccharide   (MGI Ref ID J:96680)
      • abnormal interleukin level
        • Il-6 levels in lungs are unaffected by lipopolysaccharide   (MGI Ref ID J:96680)
        • il6 levels increase less on a high fat diet than in controls   (MGI Ref ID J:96680)
        • increased circulating interleukin-6 level
          • increased levels after 7 days of dextran sodium sulfate treatment   (MGI Ref ID J:37271)
      • abnormal tumor necrosis factor level
        • TNF alpha levels in lungs are unaffected by lipopolysaccharide   (MGI Ref ID J:96680)
        • less increase in TNF alpha on a high fat diet than in controls   (MGI Ref ID J:96680)
    • abnormal gas homeostasis   (MGI Ref ID J:126488)
      • decreased respiratory quotient
        • lower respiratory exchange ratio   (MGI Ref ID J:126488)
      • increased oxygen consumption
        • oxygen consumption is higher after 8 weeks on a high fat diet than controls   (MGI Ref ID J:126488)
    • abnormal glucose homeostasis   (MGI Ref ID J:126488)
      • abnormal circulating glucose level
        • faster disappearance of glucose in response to insulin when on a high fat diet   (MGI Ref ID J:126488)
      • decreased circulating insulin level
        • lower blood insulin levels when on a high fat diet   (MGI Ref ID J:126488)
      • improved glucose tolerance
        • lower blood glucose in a glucose tolerance test when on a high fat diet   (MGI Ref ID J:126488)
    • abnormal lipid level   (MGI Ref ID J:126488)
      • abnormal fatty acid level
        • less elevated than for controls on a high fat diet   (MGI Ref ID J:126488)
      • decreased liver triglyceride level
        • less increase in hepatic triglycerides on a high fat diet than in controls   (MGI Ref ID J:126488)
    • decreased body temperature
      • more severe reduction in body temperature following infection with Vac-GFL   (MGI Ref ID J:162716)
    • decreased susceptibility to ischemic brain injury
      • reduced brain edema after cerebral ischemia/reperfusion   (MGI Ref ID J:117223)
      • less inflammation after cerebral ischemia/reperfusion   (MGI Ref ID J:117223)
      • less nerve cell swelling after cerebral ischemia/reperfusion   (MGI Ref ID J:117223)
      • reduced neurological impairment after cerebral ischemia/reperfusion   (MGI Ref ID J:117223)
      • decreased cerebral infarction size
        • infarctions due to cerebral ischemia/reperfusion are smaller in size   (MGI Ref ID J:117223)
        • damage due to middle cerebral artery occlusion is considerably reduced   (MGI Ref ID J:124100)
    • increased adiponectin level
      • levels remain elevated on a high fat diet   (MGI Ref ID J:126488)
    • pulmonary edema
      • resistant to lipopolysaccharide induced lung interstitial edema   (MGI Ref ID J:96680)
      • less protein leakage into bronchoalveolar lavage fluid after lipopolysaccharide inhalation   (MGI Ref ID J:96680)
  • liver/biliary system phenotype
  • abnormal hepatocyte morphology
    • confluent foci of feathery hepatocyte degeneration due to bile acid cytotoxicity are significantly reduced compared to controls 24 hours after BDL   (MGI Ref ID J:135830)
  • abnormal liver physiology
    • liver protected from ischemia/reperfusion injury   (MGI Ref ID J:98036)
    • decreased hepatocyte apoptosis
      • hepatocyte cell death is reduced compared to controls after BDL   (MGI Ref ID J:135830)
    • liver inflammation
      • after BDL, necroinflammatory foci and lymphocytic infiltration are obviously less than in controls   (MGI Ref ID J:135830)
  • decreased liver triglyceride level
    • less increase in hepatic triglycerides on a high fat diet than in controls   (MGI Ref ID J:126488)
  • focal hepatic necrosis   (MGI Ref ID J:135830)
  • adipose tissue phenotype
  • decreased epididymal fat pad weight
    • reduced 40% compared to controls when on a high fat diet   (MGI Ref ID J:126488)
    • weight similar to controls on a normal diet   (MGI Ref ID J:126488)
  • decreased fat cell size
    • adipocyte size reduced 30% relative to controls on a high fat diet   (MGI Ref ID J:126488)
    • reduced aggregation of macrophage around dying adipocytes than in controls   (MGI Ref ID J:126488)
  • decreased percent body fat
    • 70% less body fat   (MGI Ref ID J:118467)
  • cardiovascular system phenotype
  • rectal hemorrhage
    • rectal bleeding after 7 days of dextrose sodium sulfate treatment is reduced relative to controls   (MGI Ref ID J:37271)
    • recover from bleeding after 10 days of treatment when 50% of controls are dead   (MGI Ref ID J:37271)
  • digestive/alimentary phenotype
  • rectal hemorrhage
    • rectal bleeding after 7 days of dextrose sodium sulfate treatment is reduced relative to controls   (MGI Ref ID J:37271)
    • recover from bleeding after 10 days of treatment when 50% of controls are dead   (MGI Ref ID J:37271)
  • respiratory system phenotype
  • abnormal respiratory system morphology   (MGI Ref ID J:114985)
    • abnormal pulmonary alveolus morphology
      • destruction of normal alveolar structures   (MGI Ref ID J:114985)
    • dilated pulmonary alveolar ducts
      • enlarged air spaces distal to the terminal bronchioles   (MGI Ref ID J:114985)
    • enlarged lung
      • significantly increased lung volume at 3 months of age in contrast to normal body weights through 12 months   (MGI Ref ID J:114985)
  • abnormal respiratory system physiology   (MGI Ref ID J:96680)
    • lung inflammation
      • no increase in white blood cells or neutrophiles in bronchoalveolar fluid   (MGI Ref ID J:96680)
      • white blood cells and neutrophiles are not detected by myeloperoxidase assay   (MGI Ref ID J:96680)
    • pulmonary edema
      • resistant to lipopolysaccharide induced lung interstitial edema   (MGI Ref ID J:96680)
      • less protein leakage into bronchoalveolar lavage fluid after lipopolysaccharide inhalation   (MGI Ref ID J:96680)
  • nervous system phenotype
  • abnormal microglial cell physiology
    • resistant to lipopolysaccharide induced apoptosis   (MGI Ref ID J:99051)
  • abnormal nervous system morphology   (MGI Ref ID J:124100)
    • abnormal myelin sheath morphology
      • increased myelin destruction at site of spinal cord injury   (MGI Ref ID J:122597)
      • no clear delineation between injured and spared tissues   (MGI Ref ID J:122597)
  • decreased neuron apoptosis
    • neurons are resistant to apoptosis caused by glucose deficiency   (MGI Ref ID J:124100)
  • decreased susceptibility to ischemic brain injury
    • reduced brain edema after cerebral ischemia/reperfusion   (MGI Ref ID J:117223)
    • less inflammation after cerebral ischemia/reperfusion   (MGI Ref ID J:117223)
    • less nerve cell swelling after cerebral ischemia/reperfusion   (MGI Ref ID J:117223)
    • reduced neurological impairment after cerebral ischemia/reperfusion   (MGI Ref ID J:117223)
    • decreased cerebral infarction size
      • infarctions due to cerebral ischemia/reperfusion are smaller in size   (MGI Ref ID J:117223)
      • damage due to middle cerebral artery occlusion is considerably reduced   (MGI Ref ID J:124100)
  • behavior/neurological phenotype
  • abnormal locomotor behavior
    • locomotor recovery impaired as measured 4-6 weeks after spinal cord injury   (MGI Ref ID J:122597)
  • abnormal motor coordination/ balance
    • impaired recovery of fore-limb-hindlimb coordination as measured 4-6 weeks after spinal cord injury   (MGI Ref ID J:122597)
  • skeleton phenotype
  • decreased susceptibility to bone fracture
    • bones resistant to fracture   (MGI Ref ID J:118467)
  • increased bone mass
    • increased bone area of the tibia   (MGI Ref ID J:118467)
  • increased bone mineral content
    • greater mineral content   (MGI Ref ID J:118467)
  • increased bone mineral density
    • significantly increased bone mineral density at 20 weeks   (MGI Ref ID J:118467)
    • density continues to increase over time   (MGI Ref ID J:118467)
  • muscle phenotype
  • abnormal muscle cell glucose uptake
    • insulin stimulated glucose uptake by soleus muscle is not affected by palmitate treatment or by other fatty acids   (MGI Ref ID J:126488)
  • cellular phenotype
  • abnormal macrophage chemotaxis
    • robust macrophage response at the site of spinal injury   (MGI Ref ID J:122597)
  • abnormal muscle cell glucose uptake
    • insulin stimulated glucose uptake by soleus muscle is not affected by palmitate treatment or by other fatty acids   (MGI Ref ID J:126488)
  • decreased hepatocyte apoptosis
    • hepatocyte cell death is reduced compared to controls after BDL   (MGI Ref ID J:135830)
  • decreased neuron apoptosis
    • neurons are resistant to apoptosis caused by glucose deficiency   (MGI Ref ID J:124100)
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Research Applications
This mouse can be used to support research in many areas including:

Tlr4Lps-d related

Immunology, Inflammation and Autoimmunity Research
CD Antigens, Antigen Receptors, and Histocompatibility Markers
      Tlr deficiency
Immunodeficiency
      Tlr deficiency
Inflammation
      Tlr deficiency

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Tlr4Lps-d
Allele Name defective lipopolysaccharide response
Allele Type Spontaneous
Common Name(s) TLR4-M; TLR4-Mu; TLR4lps-def; TLR4d; Tlr4-; Tlr4d; TlrLps-d; lpsd; mutant TLR4;
Strain of OriginC3H/HeJ
Gene Symbol and Name Tlr4, toll-like receptor 4
Chromosome 4
Gene Common Name(s) ARMD10; CD284; Lps; RAS-like, family 2, locus 8; Rasl2-8; TLR-4; TOLL; lipopolysaccharide response;
General Note C3H/HeJ mice carry this allele. Various combinations of Lps-associated traits have been followed in crosses between C3H/HeJ and other C3H substrains, and the traits have in all cases segregated together (J:30692, J:5557, J:5593, J:5938). Some of the traits show dominance of the Tlr4lps-n allele; others, including Tlr4Lps-d, show codominance.

Genbank ID for this allele: AF095353

Molecular Note This allele corresponds to a mutation in the third exon of the gene. A C to A substitution at nucleotide position 2342 results in an amino acid substitution that replaces proline with histidine at position 712. [MGI Ref ID J:51522] [MGI Ref ID J:53519] [MGI Ref ID J:57938]

Genotyping

Genotyping Information

Genotyping Protocols

Tlr4Lps-d-Alternate 2, End Point Analysis
Tyr c, Pyrosequencing
Tyr c-EP, End Point Analysis

The Tlr4Lps-d mutation arises from an A to C at substitution (Poltorak A et al. 1998. Science 282(5396):2085-8.[PMID: 9851930]) A single-strand conformation polymorphism (SSCP)-based assay for the Tlr mutation has been described in the following reference: Vogel SN et al. 1999. J Immunol 162:5666-5670. (PMID: 10229796)

Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Additional References

Eisenbarth SC; Zhadkevich A; Ranney P; Herrick CA; Bottomly K. 2004. IL-4-dependent Th2 collateral priming to inhaled antigens independent of Toll-like receptor 4 and myeloid differentiation factor 88. J Immunol 172(7):4527-34. [PubMed: 15034070]  [MGI Ref ID J:88724]

Glode LM; Rosenstreich DL. 1976. Genetic control of B cell activation by bacterial lipopolysaccharide is mediated by multiple distinct genes or alleles. J Immunol 117(6):2061-6. [PubMed: 792337]  [MGI Ref ID J:5724]

Jang S; Uematsu S; Akira S; Salgame P. 2004. IL-6 and IL-10 induction from dendritic cells in response to Mycobacterium tuberculosis is predominantly dependent on TLR2-mediated recognition. J Immunol 173(5):3392-7. [PubMed: 15322203]  [MGI Ref ID J:92712]

Moeller GR; Terry L; Snyderman R. 1978. The inflammatory response and resistance to endotoxin in mice. J Immunol 120(1):116-23. [PubMed: 627714]  [MGI Ref ID J:5936]

Poltorak A; He X; Smirnova I; Liu MY; Huffel CV; Du X; Birdwell D; Alejos E; Silva M; Galanos C; Freudenberg M; Ricciardi-Castagnoli P; Layton B; Beutler B. 1998. Defective LPS signaling in C3H/HeJ and C57BL/10ScCr mice: mutations in Tlr4 gene. Science 282(5396):2085-8. [PubMed: 9851930]  [MGI Ref ID J:51522]

Vogel SN; Wax JS; Perera PY; Padlan C; Potter M; Mock BA. 1994. Construction of a BALB/c congenic mouse, C.C3H-Lpsd, that expresses the Lpsd allele: analysis of chromosome 4 markers surrounding the Lps gene. Infect Immun 62(10):4454-9. [PubMed: 7927709]  [MGI Ref ID J:20449]

Tlr4Lps-d related

Abel B; Thieblemont N; Quesniaux VJ; Brown N; Mpagi J; Miyake K; Bihl F; Ryffel B. 2002. Toll-like receptor 4 expression is required to control chronic Mycobacterium tuberculosis infection in mice. J Immunol 169(6):3155-62. [PubMed: 12218133]  [MGI Ref ID J:78959]

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Timmers L; Sluijter JP; van Keulen JK; Hoefer IE; Nederhoff MG; Goumans MJ; Doevendans PA; van Echteld CJ; Joles JA; Quax PH; Piek JJ; Pasterkamp G; de Kleijn DP. 2008. Toll-like receptor 4 mediates maladaptive left ventricular remodeling and impairs cardiac function after myocardial infarction. Circ Res 102(2):257-64. [PubMed: 18007026]  [MGI Ref ID J:145592]

Tjota MY; Williams JW; Lu T; Clay BS; Byrd T; Hrusch CL; Decker DC; de Araujo CA; Bryce PJ; Sperling AI. 2013. IL-33-dependent induction of allergic lung inflammation by FcgammaRIII signaling. J Clin Invest 123(5):2287-97. [PubMed: 23585480]  [MGI Ref ID J:201453]

Treml LS; Carlesso G; Hoek KL; Stadanlick JE; Kambayashi T; Bram RJ; Cancro MP; Khan WN. 2007. TLR stimulation modifies BLyS receptor expression in follicular and marginal zone B cells. J Immunol 178(12):7531-9. [PubMed: 17548587]  [MGI Ref ID J:148596]

Tsukumo DM; Carvalho-Filho MA; Carvalheira JB; Prada PO; Hirabara SM; Schenka AA; Araujo EP; Vassallo J; Curi R; Velloso LA; Saad MJ. 2007. Loss-of-function mutation in Toll-like receptor 4 prevents diet-induced obesity and insulin resistance. Diabetes 56(8):1986-98. [PubMed: 17519423]  [MGI Ref ID J:126488]

Tsung A; Hoffman RA; Izuishi K; Critchlow ND; Nakao A; Chan MH; Lotze MT; Geller DA; Billiar TR. 2005. Hepatic ischemia/reperfusion injury involves functional TLR4 signaling in nonparenchymal cells. J Immunol 175(11):7661-8. [PubMed: 16301676]  [MGI Ref ID J:122164]

Tsung A; Klune JR; Zhang X; Jeyabalan G; Cao Z; Peng X; Stolz DB; Geller DA; Rosengart MR; Billiar TR. 2007. HMGB1 release induced by liver ischemia involves Toll-like receptor 4 dependent reactive oxygen species production and calcium-mediated signaling. J Exp Med 204(12):2913-23. [PubMed: 17984303]  [MGI Ref ID J:128522]

Tsung A; Sahai R; Tanaka H; Nakao A; Fink MP; Lotze MT; Yang H; Li J; Tracey KJ; Geller DA; Billiar TR. 2005. The nuclear factor HMGB1 mediates hepatic injury after murine liver ischemia-reperfusion. J Exp Med 201(7):1135-43. [PubMed: 15795240]  [MGI Ref ID J:98036]

Tsung A; Zheng N; Jeyabalan G; Izuishi K; Klune JR; Geller DA; Lotze MT; Lu L; Billiar TR. 2007. Increasing numbers of hepatic dendritic cells promote HMGB1-mediated ischemia-reperfusion injury. J Leukoc Biol 81(1):119-28. [PubMed: 17062605]  [MGI Ref ID J:117230]

Vazquez-Torres A; Vallance BA; Bergman MA; Finlay BB; Cookson BT; Jones-Carson J; Fang FC. 2004. Toll-like receptor 4 dependence of innate and adaptive immunity to Salmonella: importance of the Kupffer cell network. J Immunol 172(10):6202-8. [PubMed: 15128808]  [MGI Ref ID J:89854]

Velazquez P; Wei B; McPherson M; Mendoza LM; Nguyen SL; Turovskaya O; Kronenberg M; Huang TT; Schrage M; Lobato LN; Fujiwara D; Brewer S; Arditi M; Cheng G; Sartor RB; Newberry RD; Braun J. 2008. Villous B cells of the small intestine are specialized for invariant NK T cell dependence. J Immunol 180(7):4629-38. [PubMed: 18354186]  [MGI Ref ID J:133099]

Vogel SN; Johnson D; Perera PY; Medvedev A; Lariviere L; Qureshi ST ; Malo D. 1999. Cutting edge: functional characterization of the effect of the C3H/HeJ defect in mice that lack an Lpsn gene: in vivo evidence for a dominant negative mutation. J Immunol 162(10):5666-70. [PubMed: 10229796]  [MGI Ref ID J:54987]

Vogl T; Tenbrock K; Ludwig S; Leukert N; Ehrhardt C; van Zoelen MA; Nacken W; Foell D; van der Poll T; Sorg C; Roth J. 2007. Mrp8 and Mrp14 are endogenous activators of Toll-like receptor 4, promoting lethal, endotoxin-induced shock. Nat Med 13(9):1042-9. [PubMed: 17767165]  [MGI Ref ID J:125179]

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Wang S; Schmaderer C; Kiss E; Schmidt C; Bonrouhi M; Porubsky S; Gretz N; Schaefer L; Kirschning CJ; Popovic ZV; Grone HJ. 2010. Recipient Toll-like receptors contribute to chronic graft dysfunction by both MyD88- and TRIF-dependent signaling. Dis Model Mech 3(1-2):92-103. [PubMed: 20038715]  [MGI Ref ID J:157656]

Wang X; Moser C; Louboutin JP; Lysenko ES; Weiner DJ; Weiser JN; Wilson JM. 2002. Toll-like receptor 4 mediates innate immune responses to Haemophilus influenzae infection in mouse lung. J Immunol 168(2):810-5. [PubMed: 11777976]  [MGI Ref ID J:73739]

Wang XM; Kim HP; Nakahira K; Ryter SW; Choi AM. 2009. The heme oxygenase-1/carbon monoxide pathway suppresses TLR4 signaling by regulating the interaction of TLR4 with caveolin-1. J Immunol 182(6):3809-18. [PubMed: 19265160]  [MGI Ref ID J:145914]

Wang Y; Han G; Wang K; Liu G; Wang R; Xiao H; Li X; Hou C; Shen B; Guo R; Li Y; Chen G. 2014. Tumor-derived GM-CSF promotes inflammatory colon carcinogenesis via stimulating epithelial release of VEGF. Cancer Res 74(3):716-26. [PubMed: 24366884]  [MGI Ref ID J:208169]

Wang ZY; Yang D; Chen Q; Leifer CA; Segal DM; Su SB; Caspi RR; Howard ZO; Oppenheim JJ. 2006. Induction of dendritic cell maturation by pertussis toxin and its B subunit differentially initiate Toll-like receptor 4-dependent signal transduction pathways. Exp Hematol 34(8):1115-24. [PubMed: 16863919]  [MGI Ref ID J:111901]

Wantia N; Rodriguez N; Cirl C; Ertl T; Durr S; Layland LE; Wagner H; Miethke T. 2011. Toll-like receptors 2 and 4 regulate the frequency of IFNgamma-producing CD4+ T-cells during pulmonary infection with Chlamydia pneumoniae. PLoS One 6(11):e26101. [PubMed: 22096480]  [MGI Ref ID J:180980]

Warger T; Hilf N; Rechtsteiner G; Haselmayer P; Carrick DM; Jonuleit H; von Landenberg P; Rammensee HG; Nicchitta CV; Radsak MP; Schild H. 2006. Interaction of TLR2 and TLR4 ligands with the N-terminal domain of Gp96 amplifies innate and adaptive immune responses. J Biol Chem 281(32):22545-53. [PubMed: 16754684]  [MGI Ref ID J:116459]

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Weighardt H; Kaiser-Moore S; Vabulas RM; Kirschning CJ; Wagner H; Holzmann B. 2002. Cutting edge: myeloid differentiation factor 88 deficiency improves resistance against sepsis caused by polymicrobial infection. J Immunol 169(6):2823-7. [PubMed: 12218091]  [MGI Ref ID J:120435]

Whitaker SM; Colmenares M; Pestana KG; McMahon-Pratt D. 2008. Leishmania pifanoi proteoglycolipid complex P8 induces macrophage cytokine production through Toll-like receptor 4. Infect Immun 76(5):2149-56. [PubMed: 18299340]  [MGI Ref ID J:134478]

Wong PM; Kang A; Chen H; Yuan Q; Fan P; Sultzer BM; Kan YW; Chung SW. 1999. Lps(d)/Ran of endotoxin-resistant C3H/HeJ mice is defective in mediating lipopolysaccharide endotoxin responses. Proc Natl Acad Sci U S A 96(20):11543-8. [PubMed: 10500213]  [MGI Ref ID J:57938]

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Wu SC; Yang JC; Rau CS; Chen YC; Lu TH; Lin MW; Tzeng SL; Wu YC; Wu CJ; Hsieh CH. 2013. Profiling circulating microRNA expression in experimental sepsis using cecal ligation and puncture. PLoS One 8(10):e77936. [PubMed: 24205035]  [MGI Ref ID J:209241]

Xiang M; Yin L; Li Y; Xiao G; Vodovotz Y; Billiar TR; Wilson MA; Fan J. 2011. Hemorrhagic shock activates lung endothelial reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase via neutrophil NADPH oxidase. Am J Respir Cell Mol Biol 44(3):333-40. [PubMed: 20418360]  [MGI Ref ID J:183358]

Yang HZ; Wang JP; Mi S; Liu HZ; Cui B; Yan HM; Yan J; Li Z; Liu H; Hua F; Lu W; Hu ZW. 2012. TLR4 activity is required in the resolution of pulmonary inflammation and fibrosis after acute and chronic lung injury. Am J Pathol 180(1):275-92. [PubMed: 22062220]  [MGI Ref ID J:180182]

Yang R; Murillo FM; Delannoy MJ; Blosser RL; Yutzy WH 4th; Uematsu S; Takeda K; Akira S; Viscidi RP; Roden RB. 2005. B lymphocyte activation by human papillomavirus-like particles directly induces Ig class switch recombination via TLR4-MyD88. J Immunol 174(12):7912-9. [PubMed: 15944297]  [MGI Ref ID J:100870]

Yang X; Murthy V; Schultz K; Tatro JB; Fitzgerald KA; Beasley D. 2006. Toll-like receptor 3 signaling evokes a proinflammatory and proliferative phenotype in human vascular smooth muscle cells. Am J Physiol Heart Circ Physiol 291(5):H2334-43. [PubMed: 16782847]  [MGI Ref ID J:116310]

Yano J; Palmer GE; Eberle KE; Peters BM; Vogl T; McKenzie AN; Fidel PL Jr. 2014. Vaginal epithelial cell-derived S100 alarmins induced by Candida albicans via pattern recognition receptor interactions are sufficient but not necessary for the acute neutrophil response during experimental vaginal candidiasis. Infect Immun 82(2):783-92. [PubMed: 24478092]  [MGI Ref ID J:209808]

Yao C; Purwanti N; Karabasil MR; Azlina A; Javkhlan P; Hasegawa T; Akamatsu T; Hosoi T; Ozawa K; Hosoi K. 2010. Potential down-regulation of salivary gland AQP5 by LPS via cross-coupling of NF-kappaB and p-c-Jun/c-Fos. Am J Pathol 177(2):724-34. [PubMed: 20522648]  [MGI Ref ID J:163414]

Yohe HC; O'Hara KA; Hunt JA; Kitzmiller TJ; Wood SG; Bement JL; Bement WJ; Szakacs JG; Wrighton SA; Jacobs JM; Kostrubsky V; Sinclair PR; Sinclair JF. 2006. Involvement of Toll-like receptor 4 in acetaminophen hepatotoxicity. Am J Physiol Gastrointest Liver Physiol 290(6):G1269-79. [PubMed: 16439473]  [MGI Ref ID J:111091]

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Yu H; Ha T; Liu L; Wang X; Gao M; Kelley J; Kao R; Williams D; Li C. 2012. Scavenger receptor A (SR-A) is required for LPS-induced TLR4 mediated NF-kappaB activation in macrophages. Biochim Biophys Acta 1823(7):1192-8. [PubMed: 22627090]  [MGI Ref ID J:185204]

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Yvan-Charvet L; Welch C; Pagler TA; Ranalletta M; Lamkanfi M; Han S; Ishibashi M; Li R; Wang N; Tall AR. 2008. Increased inflammatory gene expression in ABC transporter-deficient macrophages: free cholesterol accumulation, increased signaling via toll-like receptors, and neutrophil infiltration of atherosclerotic lesions. Circulation 118(18):1837-47. [PubMed: 18852364]  [MGI Ref ID J:165622]

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Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX11

Colony Maintenance

Mating SystemHomozygote x Homozygote         (Female x Male)   01-MAR-06
Breeding Considerations This strain is a good breeder.

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 $135.00Female or MaleHomozygous for Tlr4Lps-d  
Price per Pair (US dollars $)Pair Genotype
$270.00Homozygous for Tlr4Lps-d x Homozygous for Tlr4Lps-d  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $175.50Female or MaleHomozygous for Tlr4Lps-d  
Price per Pair (US dollars $)Pair Genotype
$351.00Homozygous for Tlr4Lps-d x Homozygous for Tlr4Lps-d  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

Control Information

  Control
   001026 BALB/cByJ (approximate)
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

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See Terms of Use tab for General Terms and Conditions


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.
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Terms of Use


General Terms and Conditions


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JAX® Mice, Products & Services Conditions of Use

"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.

No Warranty

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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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