Overview

In addition to the Tlr4^Lps-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 Lps^d on BALB/c, a strain susceptible to infection, neoplastic disease including the induction of plasmacytomas and other tumors.

Genetic overview

Genetic Background	Generation

Tlr4^Lps-d

Allele Type	Gene Symbol	Gene Name
Spontaneous	Tlr4	toll-like receptor 4

View Genetics

Research Applications

Immunology, Inflammation and Autoimmunity Research

View All Research Applications

Base Price

Starting at:

$2,854.50 Domestic price Cryo Recovery

View Price List

Details

Detailed Description

In addition to the Tlr4^Lps-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 Lps^d 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 Tlr4^Lps-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 Tyr^c allele, were selected at each generation to continue the backcross. At N6 intercrossing made the strain homozygous for Tlr4^Lps-d and Tyrp1^B. Backcrossing to BALB/cAnPt was resumed from N6F22. When backcrossing reached N20, the strain was intercrossed to generate this strain homozygous for Tlr4^Lps-d and Tyrp1^B but not Tyr^c. The congenic interval encompassing Tyrp1^B and Tlr4^Lps-d includes at least from D4Mit151 through D4Mit26. This strain was imported into The Jackson Laboratory from Dr.Stefanie Vogel at Uniformed Services University of the Health Sciences in 1997.

Control Suggestions

Approximate Controls

001026 BALB/cByJ

Additional Information

Considerations for Choosing Controls

Genetics

Tlr4^Lps-d

Allele Symbol: Tlr4^Lps-d

Allele Name	defective lipopolysaccharide response
Allele Type	Spontaneous
Allele Synonym(s)	lps^d; mutant TLR4; Tlr^Lps-d; Tlr4^-; Tlr4^d; TLR4^lps-def; TLR4d; TLR4-M; TLR4-Mu
Gene Symbol and Name	Tlr4, toll-like receptor 4
Gene Synonym(s)
Strain of Origin	C3H/HeJ
Chromosome	4
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 Tlr4^lps-n allele; others, including Tlr4^Lps-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 coding tide position 2135 (c.2135C>A) results in an amino acid substitution that replaces proline with histidine at position 712 (p.P712H).

Disease/Phenotype

Disease Terms

Research Areas By Phenotype

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

Genotype: Tlr4^Lps-d related

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

Mammalian Phenotype Terms by Genotype

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

Genotype: Tlr4^Lps-d/Tlr4^Lps-d
involves: C3H/HeJ

homeostasis/metabolism phenotype

abnormal circulating enzyme level
- myeloperoxidase levels are reduced after 90 minutes of liver ischemia followed by 6 hours of reperfusion
- increased HO-1 expression

decreased circulating alanine transaminase level
- serum levels decreased after 90 minutes of liver ischemia followed by 6 hours of reperfusion

abnormal tumor necrosis factor level
- macrophage primary but not secondary necrotic cells with residual stimulatory affect on TNF alpha production by macrophage
- diminished TNF alpha expression after 90 minutes of liver ischemia followed by 6 hours of reperfusion

immune system phenotype

abnormal osteoclast differentiation
- lipopolysaccharide fails to inhibit RANKL induced osteoclast formation as it does in controls
- antibody to IFN-beta or to IFNAR1 reverses inhibition of osteoclast formation induced by RANKL

abnormal tumor necrosis factor level
- diminished TNF alpha expression after 90 minutes of liver ischemia followed by 6 hours of reperfusion
- macrophage primary but not secondary necrotic cells with residual stimulatory affect on TNF alpha production by macrophage

increased susceptibility to bacterial infection
- increased K. pneumoniae levels in the lung
- increased sensitivity to gram (-) infection
- significantly shortened survival after infection with Klebsiella pneumoniae
- low responsiveness of spleen cells to lipopolysaccharides

increased susceptibility to induced arthritis
- reduced susceptibility to arthritis induced by type II collagen

abnormal T-helper 2 physiology
- Th2 responses elevated after induction of autoimmune arthritis

behavior/neurological phenotype

increased thermal nociceptive threshold
- attenuated response to heat

hyporesponsive to tactile stimuli
- reduced mechanical allodynia after nerve injury

mammalian phenotype

muscle phenotype
- Normal - MCP-1 (monocyte chemoattractant protein-1) release from isolated mouse aorta smooth muscle cells (MAoSMC) by stimulation with dsRNA is normal relative to controls

hearing/vestibular/ear phenotype
- Normal - cisplatin and lipopolysaccharide treatment does not lead to significant increases in auditory brainstem response as is observed in controls

nervous system phenotype

abnormal glial cell apoptosis
- isolated microglia exposed to LPS are resistant to apoptosis

skeleton phenotype

abnormal osteoclast differentiation
- lipopolysaccharide fails to inhibit RANKL induced osteoclast formation as it does in controls
- antibody to IFN-beta or to IFNAR1 reverses inhibition of osteoclast formation induced by RANKL

increased susceptibility to induced arthritis
- reduced susceptibility to arthritis induced by type II collagen

cellular phenotype

abnormal osteoclast differentiation
- antibody to IFN-beta or to IFNAR1 reverses inhibition of osteoclast formation induced by RANKL
- lipopolysaccharide fails to inhibit RANKL induced osteoclast formation as it does in controls

abnormal glial cell apoptosis
- isolated microglia exposed to LPS are resistant to apoptosis

hematopoietic system phenotype

abnormal osteoclast differentiation
- lipopolysaccharide fails to inhibit RANKL induced osteoclast formation as it does in controls
- antibody to IFN-beta or to IFNAR1 reverses inhibition of osteoclast formation induced by RANKL

abnormal T-helper 2 physiology
- Th2 responses elevated after induction of autoimmune arthritis

Genotype: Tlr4^Lps-d/Tlr4^Lps-d
C3H/HeJ-Tlr4

cellular phenotype

abnormal macrophage chemotaxis
- robust macrophage response at the site of spinal injury

abnormal muscle cell glucose uptake
- insulin stimulated glucose uptake by soleus muscle is not affected by palmitate treatment or by other fatty acids

focal hepatic necrosis

decreased neuron apoptosis
- neurons are resistant to apoptosis caused by glucose deficiency

decreased hepatocyte apoptosis
- hepatocyte cell death is reduced compared to controls after BDL

respiratory system phenotype

lung inflammation
- no increase in white blood cells or neutrophiles in bronchoalveolar fluid
- white blood cells and neutrophiles are not detected by myeloperoxidase assay

abnormal pulmonary alveolus morphology
- destruction of normal alveolar structures

abnormal respiratory system morphology

dilated pulmonary alveolar ducts
- enlarged air spaces distal to the terminal bronchioles

pulmonary edema
- less protein leakage into bronchoalveolar lavage fluid after lipopolysaccharide inhalation
- resistant to lipopolysaccharide induced lung interstitial edema

abnormal respiratory system physiology

enlarged lung
- significantly increased lung volume at 3 months of age in contrast to normal body weights through 12 months

skeleton phenotype

decreased susceptibility to bone fracture
- bones resistant to fracture

increased bone mass
- increased bone area of the tibia

increased bone mineral density
- density continues to increase over time
- significantly increased bone mineral density at 20 weeks

increased bone mineral content
- greater mineral content

digestive/alimentary phenotype

rectal hemorrhage
- recover from bleeding after 10 days of treatment when 50% of controls are dead
- rectal bleeding after 7 days of dextrose sodium sulfate treatment is reduced relative to controls

growth/size/body region phenotype

decreased body weight
- lower body weight than controls after 8 weeks on a high fat diet
- food intake comparable to controls
- weights are 15% lower than controls after 8 months on a high fat diet

decreased body size
- always smaller than controls

enlarged lung
- significantly increased lung volume at 3 months of age in contrast to normal body weights through 12 months

decreased susceptibility to weight loss
- reduced weight loss following infection with Vac-GFL

hematopoietic system phenotype

abnormal phagocyte morphology
- Normal - however, response to stimulation with TLR9 or TLR7 and TLR8 with their ligands (CpG and R848, respectively) is similar to in wild-type cells
- phagocytes fail to respond to LPS stimulation

abnormal microglial cell physiology
- resistant to lipopolysaccharide induced apoptosis

abnormal macrophage chemotaxis
- robust macrophage response at the site of spinal injury

abnormal spleen weight
- spleen weight fails to increase with dextran sodium sulfate treatment as it does in controls

adipose tissue phenotype

decreased fat cell size
- adipocyte size reduced 30% relative to controls on a high fat diet
- reduced aggregation of macrophage around dying adipocytes than in controls

decreased epididymal fat pad weight
- weight similar to controls on a normal diet
- reduced 40% compared to controls when on a high fat diet

decreased percent body fat/body weight
- 70% less body fat

homeostasis/metabolism phenotype

abnormal cytokine level
- macrophage inflammatory protein-2 levels in lungs are unaffected by lipopolysaccharide
- keratinocyte derived cytokine levels in lungs are unaffected by lipopolysaccharide

abnormal gas homeostasis

abnormal tumor necrosis factor level
- less increase in TNF alpha on a high fat diet than in controls
- TNF alpha levels in lungs are unaffected by lipopolysaccharide

decreased liver triglyceride level
- less increase in hepatic triglycerides on a high fat diet than in controls

abnormal circulating glucose level
- faster disappearance of glucose in response to insulin when on a high fat diet

decreased circulating insulin level
- lower blood insulin levels when on a high fat diet

decreased respiratory quotient
- lower respiratory exchange ratio

increased circulating interleukin-6 level
- increased levels after 7 days of dextran sodium sulfate treatment

abnormal interleukin level
- Il-6 levels in lungs are unaffected by lipopolysaccharide
- il6 levels increase less on a high fat diet than in controls

abnormal lipid level

abnormal fatty acids level
- less elevated than for controls on a high fat diet

decreased body temperature
- more severe reduction in body temperature following infection with Vac-GFL

improved glucose tolerance
- lower blood glucose in a glucose tolerance test when on a high fat diet

abnormal glucose homeostasis

decreased susceptibility to ischemic brain injury
- reduced neurological impairment after cerebral ischemia/reperfusion
- less inflammation after cerebral ischemia/reperfusion
- less nerve cell swelling after cerebral ischemia/reperfusion
- reduced brain edema after cerebral ischemia/reperfusion

increased oxygen consumption
- oxygen consumption is higher after 8 weeks on a high fat diet than controls

pulmonary edema
- less protein leakage into bronchoalveolar lavage fluid after lipopolysaccharide inhalation
- resistant to lipopolysaccharide induced lung interstitial edema

abnormal circulating leptin level
- increase in blood leptin on a high fat diet is 36% less than in controls

increased adiponectin level
- levels remain elevated on a high fat diet

decreased cerebral infarct size
- damage due to middle cerebral artery occlusion is considerably reduced
- infarctions due to cerebral ischemia/reperfusion are smaller in size

behavior/neurological phenotype

abnormal locomotor behavior
- locomotor recovery impaired as measured 4-6 weeks after spinal cord injury

abnormal motor coordination/balance
- impaired recovery of fore-limb-hindlimb coordination as measured 4-6 weeks after spinal cord injury

immune system phenotype

abnormal microglial cell physiology
- resistant to lipopolysaccharide induced apoptosis

abnormal susceptibility to infection
- days afteinfection and viral replication is increased
- 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

liver inflammation
- after BDL, necroinflammatory foci and lymphocytic infiltration are obviously less than in controls

abnormal cytokine level
- keratinocyte derived cytokine levels in lungs are unaffected by lipopolysaccharide
- macrophage inflammatory protein-2 levels in lungs are unaffected by lipopolysaccharide

increased susceptibility to Poxviridae 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

abnormal phagocyte morphology
- Normal - however, response to stimulation with TLR9 or TLR7 and TLR8 with their ligands (CpG and R848, respectively) is similar to in wild-type cells
- phagocytes fail to respond to LPS stimulation

abnormal tumor necrosis factor level
- TNF alpha levels in lungs are unaffected by lipopolysaccharide
- less increase in TNF alpha on a high fat diet than in controls

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

abnormal interleukin level
- Il-6 levels in lungs are unaffected by lipopolysaccharide
- il6 levels increase less on a high fat diet than in controls

abnormal macrophage chemotaxis
- robust macrophage response at the site of spinal injury

abnormal spleen weight
- spleen weight fails to increase with dextran sodium sulfate treatment as it does in controls

lung inflammation
- no increase in white blood cells or neutrophiles in bronchoalveolar fluid
- white blood cells and neutrophiles are not detected by myeloperoxidase assay

increased circulating interleukin-6 level
- increased levels after 7 days of dextran sodium sulfate treatment

liver/biliary system phenotype

liver inflammation
- after BDL, necroinflammatory foci and lymphocytic infiltration are obviously less than in controls

decreased hepatocyte apoptosis
- hepatocyte cell death is reduced compared to controls after BDL

decreased liver triglyceride level
- less increase in hepatic triglycerides on a high fat diet than in controls

abnormal hepatocyte morphology
- confluent foci of feathery hepatocyte degeneration due to bile acid cytotoxicity are significantly reduced compared to controls 24 hours after BDL

abnormal liver physiology
- liver protected from ischemia/reperfusion injury

focal hepatic necrosis

mammalian phenotype

hematopoietic system phenotype
- Normal - B cell apoptosis in Peyer's patch is not observed after bile duct ligation (BDL)

immune system phenotype
- Normal - mice inoculated with Candida albicans show vaginal fungal burden and polymorphonuclear neutrophil migration to the vagina that are similar to that seen in wild-type mice

homeostasis/metabolism phenotype
- Normal - after BDL, serum alanine transaminase levels are not different from controls

mortality/aging

decreased sensitivity to induced morbidity/mortality
- heat-inactivated E. coli exposure results in fatal toxemia as in wild type mice
- systemic challenge with Myr₃-CSK₄ (a synthetic lipopeptide) after D-galactosamine induces lethal shock in wild-type mice, but mutants are protected
- Normal - heat-inactivated E. coli exposure results in fatal toxemia as in wild-type mice
- Normal - 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

increased susceptibility to Poxviridae 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

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

cardiovascular system phenotype

rectal hemorrhage
- rectal bleeding after 7 days of dextrose sodium sulfate treatment is reduced relative to controls
- recover from bleeding after 10 days of treatment when 50% of controls are dead

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

nervous system phenotype

abnormal microglial cell physiology
- resistant to lipopolysaccharide induced apoptosis

decreased susceptibility to ischemic brain injury
- reduced brain edema after cerebral ischemia/reperfusion
- reduced neurological impairment after cerebral ischemia/reperfusion
- less nerve cell swelling after cerebral ischemia/reperfusion
- less inflammation after cerebral ischemia/reperfusion

abnormal nervous system morphology

abnormal myelin sheath morphology
- no clear delineation between injured and spared tissues
- increased myelin destruction at site of spinal cord injury

decreased cerebral infarct size
- infarctions due to cerebral ischemia/reperfusion are smaller in size
- damage due to middle cerebral artery occlusion is considerably reduced

decreased neuron apoptosis
- neurons are resistant to apoptosis caused by glucose deficiency

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

Genotype: Tlr4^Lps-d/Tlr4^Lps-d
C.C3-Tlr4/J

cardiovascular system phenotype

decreased angiogenesis
- perfusion restoration is significantly reduced 7 days after femoral artery ligation

decreased response of heart to induced stress
- exhibit reduced cardiac hypertrophy following pressure overload compared to controls
- exhibit no significant myocardial interstitial fibrosis or cardiac myocyte death following pressure overload unlike wild-type

skeleton phenotype

increased bone mineral density
- significantly increased bone mineral density at 20 weeks
- density continues to increase over time

increased bone mass
- increased bone area of the tibia

increased bone mineral content
- greater mineral content but not yet significant at 6 weeks

abnormal bone structure

homeostasis/metabolism phenotype

decreased response of heart to induced stress
- exhibit reduced cardiac hypertrophy following pressure overload compared to controls
- exhibit no significant myocardial interstitial fibrosis or cardiac myocyte death following pressure overload unlike wild-type

References

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):4527-34PubMed: 15034070 MGI: 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):2061-6PubMed: 792337 MGI: 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):3392-7PubMed: 15322203 MGI: J:92712
Moeller GR; Terry L; Snyderman R. 1978. The inflammatory response and resistance to endotoxin in mice. J Immunol 120(1):116-23PubMed: 627714 MGI: 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):2085-8PubMed: 9851930 MGI: 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):4454-9PubMed: 7927709 MGI: J:20449

Additional - Tlr4^Lps-d related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Pyrosequencing:Tyr c
- End Point Analysis:Tyr c-EP
- End Point Analysis:Tlr4 Alternate 4
- Sanger sequencing:Tlr4 SEQ
- Genotyping resources and troubleshooting
The Tlr4^Lps-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)
Breeding Considerations

This strain is a good breeder.
- Additional Breeding and Husbandry Support
Appearance
- agouti
  Related Genotype: A/A Tyrp1⁺/Tyrp1⁺
Citation
When using the C.C3-Tlr4^Lps-d/J mouse strain in a publication, please cite the originating article(s) and include JAX stock #002930 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

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

Pricing & Availability

Cryo Recovery

Domestic
International

Live Mouse

Age

Genotype

Price

weeks

Cryorecovery - Pricing

Service/Product	Description	Price
> >	Homozygous for Tlr4<Lps-d>, 1 pair minimum

Payment Terms and Conditions

Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.

The Jackson Laboratory's Genotype Promise

The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.

Terms Of Use

General Terms and Conditions

Questions about Terms of Use

Licensing Information

Phone: 207-288-6470

Email: TechTran@jax.org

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Approximate Controls

Additional Information

Tlr4Lps-d

Allele Symbol: Tlr4Lps-d

Disease Terms

Research Areas By Phenotype

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

Genotype: Tlr4Lps-d related

Mammalian Phenotype Terms by Genotype

Genotype: Tlr4Lps-d/Tlr4Lps-dinvolves: C3H/HeJ

homeostasis/metabolism phenotype

immune system phenotype

behavior/neurological phenotype

mammalian phenotype

nervous system phenotype

skeleton phenotype

cellular phenotype

hematopoietic system phenotype

Genotype: Tlr4Lps-d/Tlr4Lps-dC3H/HeJ-Tlr4

cellular phenotype

respiratory system phenotype

skeleton phenotype

digestive/alimentary phenotype

growth/size/body region phenotype

hematopoietic system phenotype

adipose tissue phenotype

homeostasis/metabolism phenotype

behavior/neurological phenotype

immune system phenotype

liver/biliary system phenotype

mammalian phenotype

mortality/aging

cardiovascular system phenotype

muscle phenotype

nervous system phenotype

Genotype: Tlr4Lps-d/Tlr4Lps-dC.C3-Tlr4/J

cardiovascular system phenotype

skeleton phenotype

homeostasis/metabolism phenotype

References

Additional References

Additional - Tlr4Lps-d related

Genotyping Protocols

Breeding Considerations

Appearance

Citation

Animal Health Reports

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

Live Mouse

Cryorecovery - Pricing

Payment Terms and Conditions

The Jackson Laboratory's Genotype Promise

Terms Of Use

Licensing Information

Tlr4^Lps-d

Allele Symbol: Tlr4^Lps-d

Genotype: Tlr4^Lps-d related

Genotype: Tlr4^Lps-d/Tlr4^Lps-d
involves: C3H/HeJ

Genotype: Tlr4^Lps-d/Tlr4^Lps-d
C3H/HeJ-Tlr4

Genotype: Tlr4^Lps-d/Tlr4^Lps-d
C.C3-Tlr4/J

Additional - Tlr4^Lps-d related