Overview

Also Known As:HIF1α^flox

HIF1α^flox mice have loxP sites flanking exon 2 of the hypoxia inducible factor 1, alpha subunit gene (Hif1a). Exposure to Cre recombinase removes the floxed sequence - creating a null allele. Mice from this strain can be crossed to strains expressing Cre recombinase in various tissues and may be useful for studies of the role of HIF transcription factors in von Hippel-Landau syndrome, adult erythropoiesis, inflammation, mammary epithelium, tumor angiogenesis, and lung development as examples.

Donating Investigator

Randall Johnson, UC-San Diego

Genetic overview

Genetic Background	Generation
	N12+N2F13 (2019-12-31 00:00:00)

Hif1a^tm3Rsjo

Allele Type	Gene Symbol	Gene Name
Targeted (Conditional ready (e.g. floxed), No functional change)	Hif1a	hypoxia inducible factor 1, alpha subunit

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Research Applications

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Base Price

Starting at:

$255.00 Domestic price for female 4-week

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Details

Detailed Description

These HIF1α^flox mice possess loxP sites on either side of exon 2 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 2 deleted in the cre-expressing tissue(s).

For example, when crossed to a strain expressing Cre recombinase in skeletal and cardiac muscle (see Stock No. 006475), this mutant mouse strain may be useful in studies of the metabolic control of muscle function.

When bred to a strain with the targeted null allele in von Hippel-Lindau syndrome homolog, Vhlh (Stock No. 004081) and a strain expressing Cre recombinase in liver (Stock No. 003574), this mutant mouse strain may be useful in the role of HIF transcription factors in von Hippel-Landau syndrome.

When crossed to a tamoxifen inducible strain with widespread Cre recombinase expression (see Stock No. 008085), this mutant mouse strain may be useful in studies of adult erythropoiesis.

When bred to a strain expressing Cre recombinase in the myeloid cell lineage (see Stock No. 004781 for example), this mutant mouse strain may be useful in studies of inflammation.

When bred to a strain expressing Cre recombinase in the mammary gland and other secretory tissues (see Stock No. 003551 for example), this mutant mouse strain may be useful in studies of mammary epithelium.

When bred to a strain expressing Cre recombinase in vascular endothelial cells (see Stock No. 008863 for example), this mutant mouse strain may be useful in studies of tumor angiogenesis.

When bred to a strain expressing Cre recombinase under the control of a tetracycline-responsive promoter element and a strain expressing a tetracycline-controlled activator protein in lung epithelial cells (see Stock No. 006234 and 006235 respectively), this mutant mouse strain may be useful in studies of lung development.

Development

Similarly oriented loxP sites were placed upstream of exon 2 and flanking the neomycin resistance cassette (located in intron 2). The construct was electroporated into (129X1/SvJ x 129S1/Sv)F1-derived R1 embryonic stem (ES) cells. Correctly targeted ES cells were transiently transfected with a cre expression plasmid for the purpose of removing the selectable marker cassette. ES cells that had successfully undergone Cre-mediated recombination and no longer retained the cassette but did retain the loxP flanked exon 2 were injected in C57BL/6 blastocysts. The donating investigator reported that the resulting chimeric male animals were backcrossed to wildtype C57BL/6J mice (see SNP note below) for 12 generations. A speed congenic protocol was used for the first 6 generations of backcrossing, after which the mice were backcrossed an additional 6 generations to C57BL/6J (see SNP note below) prior to arriving at The Jackson Laboratory. The Y chromosome may not have been fixed to the C57BL/6J genetic background.

A 32 SNP (single nucleotide polymorphism) panel analysis, with 27 markers covering all 19 chromosomes and the X chromosome, as well as 5 markers that distinguish between the C57BL/6J and C57BL/6N substrains, was performed on the rederived living colony at The Jackson Laboratory Repository. While the 27 markers throughout the genome suggested a C57BL/6 genetic background, at least 2 of 5 markers that determine C57BL/6J from C57BL/6N were found to be segregating. These data suggest the mice sent to The Jackson Laboratory Repository were on a mixed C57BL/6J ; C57BL/6N genetic background.

Control Suggestions

000664 C57BL/6J

Additional Information

Considerations for Choosing Controls

Selected References

Ryan HE; Poloni M; McNulty W; Elson D; Gassmann M; Arbeit JM; Johnson RS. 2000. Hypoxia-inducible factor-1alpha is a positive factor in solid tumor growth. Cancer Res 60(15):4010-5PubMed: 10945599 MGI: J:78980

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Genetics

Hif1a^tm3Rsjo

Allele Symbol: Hif1a^tm3Rsjo

Allele Name	targeted mutation 3, Randall S Johnson
Allele Type	Targeted (Conditional ready (e.g. floxed), No functional change)
Allele Synonym(s)	+^f; Hif^+f; Hif^f; Hif1a^2lox; HIF1a^f+; Hif1a^fl; Hif1a^loxP; Hif-1alpha 2-lox; HIF-1alpha^+f; HIF-1alpha^F; HIF1alpha^flox; I.1-^lox
Gene Symbol and Name	Hif1a, hypoxia inducible factor 1, alpha subunit
Gene Synonym(s)
Strain of Origin	(129X1/SvJ x 129S1/Sv)F1-Kitl⁺
Chromosome	12
Molecular Note	A loxP site was inserted in intron 1 and a floxed neomycin resistance cassette was placed in intron 2. Exon 2 was left flanked by loxP sites after the neo cassette was excised by in vitro expression of cre recombinase.
Mutations Made By	Randall Johnson, UC-San Diego

Disease/Phenotype

Disease Terms

Model with phenotypic similarity to human disease where etiologies are distinct. Human genes are associated with this disease. Orthologs of these genes do not appear in the mouse genotype(s).

Characteristics of this human disease are associated with transgenes and other mutation types in the mouse.

von Hippel-Lindau disease

Research Areas By Phenotype

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

Research Tools
- Cre-lox System
  - loxP-flanked Sequences

Mammalian Phenotype Terms by Genotype

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

Genotype: Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(Ckmm-cre)5Khn/?
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * FVB/N

homeostasis/metabolism phenotype

abnormal exercise endurance
- endurance decreased over 4 consecutive days of daily treadmill running
- increased endurance in swim tests and in the first session of running uphill (concentric exercise) but decreased endurance when running downhill (eccentric exercise)

abnormal glucose homeostasis
- significant decrease in lactate accumulation after exercise

increased circulating creatine kinase level
- increased serum levels of the MM isoform of creatine kinase 1 day after exercise

muscle phenotype

abnormal muscle physiology
- increase in muscle damage following exercise

nervous system phenotype

abnormal innervation pattern to muscle
- slight but statistically significant decrease in type IIa fibers in the soleus

Genotype: Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Vhl^tm1Jae/Vhl^tm1Jae Speer6-ps1^{Tg(Alb-cre)21Mgn}/Speer6-ps1⁺
involves: 129 * BALB/c * C57BL/6 * DBA

cardiovascular system phenotype

abnormal vasodilation
- hepatic vascular angiectasia

increased vascular endothelial cell number
- proliferation of endothelial cells in hepatic blood vessels

liver/biliary system phenotype

hepatic steatosis
- severe steatosis

muscle phenotype

abnormal vasodilation
- hepatic vascular angiectasia

Genotype: Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Ndor1^{Tg(UBC-cre/ERT2)1Ejb}/0
involves: 129S1/Sv * 129X1/SvJ

mammalian phenotype

immune system phenotype
- hematocrit levels are normal in mutants; mutants do not develop anemia

Genotype: Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Lyz2^tm1(cre)Ifo/Lyz2⁺
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ

cellular phenotype

impaired macrophage chemotaxis
- macrophage capacity to invade matrigel is severely defective compared with wild-type mice
- macrophage exhibit reduced directed motility in the absence of matrigel by 50% at normoxia and 75% under hypoxic conditions compared with similarly treated wild-type cells
- macrophage migration through artificial extracellular matrix is decreased 60% compared with wild-type cells

homeostasis/metabolism phenotype

increased susceptibility to injury
- CD44^hi myeloid cells fail to promote repair of oxygen-induced retinopathy unlike wild-type cells
- following oxygen-induced retinopathy, mice exhibit decreased repair of retinal damage compared with similarly treated wild-type mice

immune system phenotype

abnormal leukocyte physiology
- CD44^hi myeloid cells fail to promote repair of oxygen-induced retinopathy unlike wild-type cells

abnormal macrophage physiology
- bacteria exposed macrophages contain 7-fold more viable bacteria than similarly treated wild-type mice
- macrophages exhibit impaired glycolysis and energy generation compared with wild-type cells
- macrophages lack homotypic adhesion unlike wild-type cells

decreased inflammatory response
- following disruption of barrier function with 5% SDS (chronic cutaneous inflammation), mice fail to exhibit an inflammatory response as in similarly treated wild-type mice
- TPA-treated ears exhibit reduced inflammatory infiltration and edema compared with similarly treated wild-type cells

decreased susceptibility to induced arthritis

decreased tumor necrosis factor secretion
- in LPS-treated macrophages

impaired macrophage chemotaxis
- macrophage capacity to invade matrigel is severely defective compared with wild-type mice
- macrophage exhibit reduced directed motility in the absence of matrigel by 50% at normoxia and 75% under hypoxic conditions compared with similarly treated wild-type cells
- macrophage migration through artificial extracellular matrix is decreased 60% compared with wild-type cells

skeleton phenotype

decreased susceptibility to induced arthritis

hematopoietic system phenotype

abnormal leukocyte physiology
- CD44^hi myeloid cells fail to promote repair of oxygen-induced retinopathy unlike wild-type cells

abnormal macrophage physiology
- bacteria exposed macrophages contain 7-fold more viable bacteria than similarly treated wild-type mice
- macrophages exhibit impaired glycolysis and energy generation compared with wild-type cells
- macrophages lack homotypic adhesion unlike wild-type cells

impaired macrophage chemotaxis
- macrophage capacity to invade matrigel is severely defective compared with wild-type mice
- macrophage exhibit reduced directed motility in the absence of matrigel by 50% at normoxia and 75% under hypoxic conditions compared with similarly treated wild-type cells
- macrophage migration through artificial extracellular matrix is decreased 60% compared with wild-type cells

Genotype: Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(MMTV-cre)1Mam/0
involves: 129S1/Sv * 129X1/SvJ * CD-1 * FVB

endocrine/exocrine gland phenotype

abnormal lactation
- female mice fail to secrete sufficient milk to support their offspring, most of whom are runted and die by P15

abnormal mammary gland alveolus morphology
- alveolar differentiation during pregnancy is blocked
- alveolar lumens are small compared to in wild-type mice and fail to secret milk
- by day 15 of pregnancy, alveoli are smaller than normal with more prominent surrounding connective tissue than in wild-type mice
- Normal - however, cell proliferation is normal

abnormal mammary gland epithelium morphology
- by day 15 of pregnancy, mammary gland epithelium lack the lacy appearance of wild-type epithelium
- during lactation, epithelial cells trap milk and fat unlike in wild-type mice
- transplanted mammary epithelium fails to grow in mice expressing the wild-type protein

abnormal mammary gland morphology
- at day 1 of lactation, mammary glands have fewer alveoli, fewer milk granules, and increased trapping of lipid droplets within epithelial cells compared to in wild-type mice
- during lactation, mammary gland wet weight is decreased 50% compared to in wild-type mice

abnormal milk composition
- milk water content is decreased while milk sodium and chloride ion contents are increased compared to in wild-type mice

abnormal milk sodium level
- milk sodium ion content is significantly increased at mid-lactation

homeostasis/metabolism phenotype

abnormal milk sodium level
- milk sodium ion content is significantly increased at mid-lactation

integument phenotype

abnormal lactation
- female mice fail to secrete sufficient milk to support their offspring, most of whom are runted and die by P15

abnormal mammary gland alveolus morphology
- alveolar differentiation during pregnancy is blocked
- alveolar lumens are small compared to in wild-type mice and fail to secret milk
- by day 15 of pregnancy, alveoli are smaller than normal with more prominent surrounding connective tissue than in wild-type mice
- Normal - however, cell proliferation is normal

abnormal mammary gland epithelium morphology
- by day 15 of pregnancy, mammary gland epithelium lack the lacy appearance of wild-type epithelium
- during lactation, epithelial cells trap milk and fat unlike in wild-type mice
- transplanted mammary epithelium fails to grow in mice expressing the wild-type protein

abnormal mammary gland morphology
- at day 1 of lactation, mammary glands have fewer alveoli, fewer milk granules, and increased trapping of lipid droplets within epithelial cells compared to in wild-type mice
- during lactation, mammary gland wet weight is decreased 50% compared to in wild-type mice

abnormal milk composition
- milk water content is decreased while milk sodium and chloride ion contents are increased compared to in wild-type mice

abnormal milk sodium level
- milk sodium ion content is significantly increased at mid-lactation

mammalian phenotype

cardiovascular system phenotype
- Normal - microvessel patterning and vascular density in the mammary gland are normal

Genotype: Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(Tek-cre)1Ywa/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL

cardiovascular system phenotype

abnormal vascular endothelial cell migration
- endothelial cells exhibit reduced VEGF-directed migration in hypoxic culture conditions compared with similarly treated wild-type cells
- endothelial cells exhibit reduced VEGF-induced migration in matrigel compared with similarly treated wild-type mice
- Normal - however, random migration is normal

decreased angiogenesis
- endothelial cells exhibit reduced VEGF-induced angiogenesis compared with similarly treated wild-type mice
- transplanted tumors exhibit a 50% in tumor vessel density compared with tumors transplanted into wild-type mice
- under hypoxic culture conditions, endothelial cells exhibit reduced VEGF-induced capillary structure formation compared with similarly treated wild-type cells

decreased vascular endothelial cell proliferation
- VEGF-induced endothelial cell proliferation in matrigel is reduced compared with wild-type mice

homeostasis/metabolism phenotype

delayed wound healing
- with reduced capillary sprouting

neoplasm

decreased tumor growth/size
- transplanted tumors are 60% lighter than those transplanted into wild-type mice with severe central necrosis due to decreased tumor angiogenesis

cellular phenotype

abnormal vascular endothelial cell migration
- endothelial cells exhibit reduced VEGF-directed migration in hypoxic culture conditions compared with similarly treated wild-type cells
- endothelial cells exhibit reduced VEGF-induced migration in matrigel compared with similarly treated wild-type mice
- Normal - however, random migration is normal

decreased vascular endothelial cell proliferation
- VEGF-induced endothelial cell proliferation in matrigel is reduced compared with wild-type mice

Genotype: Hif1a^tm3Rsjo/Hif1a^tm3Rsjo
involves: 129S1/Sv * 129X1/SvJ

cellular phenotype

decreased cell proliferation
- adenoviral cre-treated mouse embryonic fibroblasts exhibit reduced proliferation under normoxic or hypoxic conditions compared with similarly treated wild-type cells

decreased hepatocyte proliferation
- in mice exposed to a cre-expressing adenovirus following partial hepatectomy

early cellular replicative senescence
- under normoxic conditions, adenoviral cre-treated mouse embryonic fibroblasts exhibit premature replicative senescence compared with similarly treated wild-type cells

increased cellular sensitivity to gamma-irradiation
- in adenoviral cre-treated mouse embryonic fibroblasts

homeostasis/metabolism phenotype

abnormal gluconeogenesis
- in mice exposed to a cre-expressing adenovirus following partial hepatectomy

decreased circulating glucose level
- following partial hepatectomy, fed or fasted mice exposed to a cre-expressing adenovirus exhibit a greater decrease in circulating glucose levels compared with similarly treated wild-type mice

decreased liver glycogen level
- decreased glycogen level in the liver of fed, but not fasted, mice exposed to a cre-expressing adenovirus 72 hours after partial hepatectomy

liver/biliary system phenotype

decreased hepatocyte proliferation
- in mice exposed to a cre-expressing adenovirus following partial hepatectomy

decreased liver glycogen level
- decreased glycogen level in the liver of fed, but not fasted, mice exposed to a cre-expressing adenovirus 72 hours after partial hepatectomy

decreased liver regeneration
- following exposure to a cre-expressing adenovirus, recovery from partial hepatectomy is delayed compared to in similarly treated wild-type mice

Genotype: Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Lyz2^tm1(cre)Ifo/Lyz2⁺
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6

cardiovascular system phenotype

abnormal systemic arterial blood pressure
- LPS-treated mice develop less hypotension compared with similarly treated wild-type mice

mortality/aging

decreased sensitivity to xenobiotic induced morbidity/mortality
- in LPS-treated mice compared with similarly treated wild-type mice

homeostasis/metabolism phenotype

abnormal body temperature
- LPS-treated mice develop less hypothermia compared with similarly treated wild-type mice

decreased sensitivity to xenobiotic induced morbidity/mortality
- in LPS-treated mice compared with similarly treated wild-type mice

immune system phenotype

decreased interleukin-1 alpha secretion
- 4 hours after LPS treatment

decreased interleukin-1 beta secretion
- 4 hours after LPS treatment

decreased interleukin-12 secretion
- 4 hours after LPS treatment

decreased interleukin-6 secretion
- 1.5 hrs after LPS treatment

decreased susceptibility to endotoxin shock
- h similarly treated wild-type mice
- LPS-treated mice exhibit less hypothermia, hypotension, and mortality; improved hemodynamic parameter, shock index, and heart rate to systolic blood pressure; and decreased macrophage cytokine production (TNF-alpha, IL6, IL12, IL1a, and IL1b) compared with similarly treated wild-type mice

decreased tumor necrosis factor secretion
- 1.5 and 4 hrs after LPS treatment

Genotype: Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(SFTPC-rtTA)5Jaw/0 Tg(tetO-cre)1Jaw/0
involves: 129 * 129S1/Sv * 129X1/SvJ * C57BL/6

growth/size/body region phenotype

increased lung weight
- at birth when mice are exposed to doxycycline prior to parturition

homeostasis/metabolism phenotype

cyanosis
- at birth when mice are exposed to doxycycline prior to parturition

mortality/aging

neonatal lethality, incomplete penetrance
- 85% of mice die within an hour of birth when exposed to doxycycline 4 of 6 days prior to parturition
- all mice die within an hour of birth when exposed to doxycycline 8 days prior to parturition

respiratory system phenotype

abnormal pulmonary alveolus epithelial cell morphology
- when mice are exposed to doxycycline prior to parturition, the alveolar surface is lined with immature pneumocytes unlike in wild-type mice

abnormal pulmonary alveolus morphology
- when mice are exposed to doxycycline prior to parturition, mice exhibit reduced alveolar airspaces unlike wild-type mice

abnormal surfactant secretion
- when mice are exposed to doxycycline prior to parturition

abnormal type II pneumocyte morphology
- when mice are exposed to doxycycline prior to parturition, the alveolar septa has only a few scattered type II cells unlike in wild-type mice

atelectasis
- at birth when mice are exposed to doxycycline prior to parturition

increased lung weight
- at birth when mice are exposed to doxycycline prior to parturition

respiratory distress
- at birth when mice are exposed to doxycycline prior to parturition

thick pulmonary interalveolar septum
- at birth when mice are exposed to doxycycline prior to parturition

Genotype: Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(Itgax-cre)1-1Reiz/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA

cellular phenotype

abnormal cell physiology
- reduced amounts of ATP are detected in lysates of mutant BMDCs cultured under hypoxic conditions compared to control cells under hypoxia suggesting an energy metabolism defect with Hif1a deletion

abnormal leukocyte migration
- ally well to draining lymph nodes while control cells generated under hypoxia display enhanced migration relative to control cells from normoxic cultures, indicating migration under under hypoxic conditons is dependent on Hif1a
- fewer mutant BMDCs generated under hypoxic conditions migrate toward CCL19 in a transwell chamber assay than control cells grown under hypoxic conditions; migration toward CXCL12 is not different from controls under hypoxic or normoxic conditions
- mutant BMDCs generated under hypoxic conditions injected into mouse footpads show reduced migration to popliteal lymph nodes compared to control BMDCs grown under hypoxic conditions; mutant and control BMDCs generated under normoxic conditions migrate equally well to draining lymph nodes while control cells generated under hypoxia display enhanced migration relative to control cells from normoxic cultures, indicating migration under under hypoxic conditons is dependent on Hif1a

mammalian phenotype

immune system phenotype
- Normal - bone marrow derived dendritic cells (BMDCs) cultured under hypoxic conditions (1% oxygen) show upregulation of maturation markers such as MHCII, CD86, with CD80 only slightly enhanced; control BMDCs grown in hypoxic conditions show similar enhanced maturation markers
- Normal - production of Il12p70, Il10, Il6, and Il23 is decreased in mutant and control BMDCs under hypoxic conditions, with Il22 upregulated compared to normoxic cells; mutant and control BMDCs generated under hypoxic conditions produce less TNFalpha and Il-1beta than cells under normoxic conditions
- Normal - stimulation by LPS does not further enhance expression of maturation markers as it does in BMDCs grown under normoxic conditions
- Normal - than cells under normoxic conditions
- Normal - tion markers

hematopoietic system phenotype

abnormal dendritic cell number
- bone marrow dendritic cells (BMDCs) differentiated under hypoxic conditions display reduced growth (proliferation) compared to control cells grown in hypoxia or mutant and control cells grown under normoxic (21% oxygen) conditions

abnormal leukocyte migration
- ally well to draining lymph nodes while control cells generated under hypoxia display enhanced migration relative to control cells from normoxic cultures, indicating migration under under hypoxic conditons is dependent on Hif1a
- fewer mutant BMDCs generated under hypoxic conditions migrate toward CCL19 in a transwell chamber assay than control cells grown under hypoxic conditions; migration toward CXCL12 is not different from controls under hypoxic or normoxic conditions
- mutant BMDCs generated under hypoxic conditions injected into mouse footpads show reduced migration to popliteal lymph nodes compared to control BMDCs grown under hypoxic conditions; mutant and control BMDCs generated under normoxic conditions migrate equally well to draining lymph nodes while control cells generated under hypoxia display enhanced migration relative to control cells from normoxic cultures, indicating migration under under hypoxic conditons is dependent on Hif1a

immune system phenotype

abnormal dendritic cell number
- bone marrow dendritic cells (BMDCs) differentiated under hypoxic conditions display reduced growth (proliferation) compared to control cells grown in hypoxia or mutant and control cells grown under normoxic (21% oxygen) conditions

abnormal leukocyte migration
- ally well to draining lymph nodes while control cells generated under hypoxia display enhanced migration relative to control cells from normoxic cultures, indicating migration under under hypoxic conditons is dependent on Hif1a
- fewer mutant BMDCs generated under hypoxic conditions migrate toward CCL19 in a transwell chamber assay than control cells grown under hypoxic conditions; migration toward CXCL12 is not different from controls under hypoxic or normoxic conditions
- mutant BMDCs generated under hypoxic conditions injected into mouse footpads show reduced migration to popliteal lymph nodes compared to control BMDCs grown under hypoxic conditions; mutant and control BMDCs generated under normoxic conditions migrate equally well to draining lymph nodes while control cells generated under hypoxia display enhanced migration relative to control cells from normoxic cultures, indicating migration under under hypoxic conditons is dependent on Hif1a

Genotype: Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Speer6-ps1^{Tg(Alb-cre)21Mgn}/Speer6-ps1^{Tg(Alb-cre)21Mgn}
B6.Cg-Hif1a Speer6-ps1

homeostasis/metabolism phenotype

decreased physiological sensitivity to xenobiotic
- mice subjected to oxygen-induced retinopathy and with treated dimethyloxaloylglycine fail to exhibit an improvement in percent avascular retina and tortuosity ratio compared with similarly treated wildtype mice

mammalian phenotype

vision/eye phenotype
- Normal - under normoxic conditions, mice exhibit normal retinal development

References

Ryan HE; Poloni M; McNulty W; Elson D; Gassmann M; Arbeit JM; Johnson RS. 2000. Hypoxia-inducible factor-1alpha is a positive factor in solid tumor growth. Cancer Res 60(15):4010-5PubMed: 10945599 MGI: J:78980

Additional References

Zhao C; Chen J; Cheng L; Xu K; Yang Y; Su X. 2020. Deficiency of HIF-1alpha enhances influenza A virus replication by promoting autophagy in alveolar type II epithelial cells. Emerg Microbes Infect 9(1):691-706PubMed: 32208814 MGI: J:290384

Additional - Hif1a^tm3Rsjo related

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Genotyping Protocols
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Dietary Information
- LabDiet® 5K52 formulation (6% fat)
Breeding Considerations

When maintaining a live colony, these mice are bred as homozygotes.
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Mating System
- Homozygote x Homozygote
Citation
When using the HIF1α^flox mouse strain in a publication, please cite the originating article(s) and include JAX stock #007561 in your Materials and Methods section.

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AX10 (Standard)

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Also Known As:HIF1αflox

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Additional Information

Selected References

Hif1atm3Rsjo

Allele Symbol: Hif1atm3Rsjo

Disease Terms

Model with phenotypic similarity to human disease where etiologies are distinct. Human genes are associated with this disease. Orthologs of these genes do not appear in the mouse genotype(s).

Characteristics of this human disease are associated with transgenes and other mutation types in the mouse.

Research Areas By Phenotype

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

Mammalian Phenotype Terms by Genotype

Genotype: Hif1atm3Rsjo/Hif1atm3Rsjo Tg(Ckmm-cre)5Khn/?involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * FVB/N

homeostasis/metabolism phenotype

muscle phenotype

nervous system phenotype

Genotype: Hif1atm3Rsjo/Hif1atm3Rsjo Vhltm1Jae/Vhltm1Jae Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+involves: 129 * BALB/c * C57BL/6 * DBA

cardiovascular system phenotype

liver/biliary system phenotype

muscle phenotype

Genotype: Hif1atm3Rsjo/Hif1atm3Rsjo Ndor1Tg(UBC-cre/ERT2)1Ejb/0involves: 129S1/Sv * 129X1/SvJ

mammalian phenotype

Genotype: Hif1atm3Rsjo/Hif1atm3Rsjo Lyz2tm1(cre)Ifo/Lyz2+involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ

cellular phenotype

homeostasis/metabolism phenotype

immune system phenotype

skeleton phenotype

hematopoietic system phenotype

Genotype: Hif1atm3Rsjo/Hif1atm3Rsjo Tg(MMTV-cre)1Mam/0involves: 129S1/Sv * 129X1/SvJ * CD-1 * FVB

endocrine/exocrine gland phenotype

homeostasis/metabolism phenotype

integument phenotype

mammalian phenotype

Genotype: Hif1atm3Rsjo/Hif1atm3Rsjo Tg(Tek-cre)1Ywa/0involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL

cardiovascular system phenotype

homeostasis/metabolism phenotype

neoplasm

cellular phenotype

Genotype: Hif1atm3Rsjo/Hif1atm3Rsjoinvolves: 129S1/Sv * 129X1/SvJ

cellular phenotype

homeostasis/metabolism phenotype

liver/biliary system phenotype

Genotype: Hif1atm3Rsjo/Hif1atm3Rsjo Lyz2tm1(cre)Ifo/Lyz2+involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6

cardiovascular system phenotype

mortality/aging

homeostasis/metabolism phenotype

immune system phenotype

Genotype: Hif1atm3Rsjo/Hif1atm3Rsjo Tg(SFTPC-rtTA)5Jaw/0 Tg(tetO-cre)1Jaw/0involves: 129 * 129S1/Sv * 129X1/SvJ * C57BL/6

growth/size/body region phenotype

homeostasis/metabolism phenotype

mortality/aging

respiratory system phenotype

Genotype: Hif1atm3Rsjo/Hif1atm3Rsjo Tg(Itgax-cre)1-1Reiz/0involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA

cellular phenotype

mammalian phenotype

hematopoietic system phenotype

immune system phenotype

Genotype: Hif1atm3Rsjo/Hif1atm3Rsjo Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1Tg(Alb-cre)21MgnB6.Cg-Hif1a Speer6-ps1

homeostasis/metabolism phenotype

mammalian phenotype

References

Additional References

Additional - Hif1atm3Rsjo related

Genotyping Protocols

Dietary Information

Breeding Considerations

Mating System

Citation

Animal Health Reports

Live Mouse

Cryorecovery - Pricing

Related Products and Services

Payment Terms and Conditions

The Jackson Laboratory's Genotype Promise

Also Known As:HIF1α^flox

Hif1a^tm3Rsjo

Allele Symbol: Hif1a^tm3Rsjo

Genotype: Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(Ckmm-cre)5Khn/?
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * FVB/N

Genotype: Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Vhl^tm1Jae/Vhl^tm1Jae Speer6-ps1^{Tg(Alb-cre)21Mgn}/Speer6-ps1⁺
involves: 129 * BALB/c * C57BL/6 * DBA

Genotype: Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Ndor1^{Tg(UBC-cre/ERT2)1Ejb}/0
involves: 129S1/Sv * 129X1/SvJ

Genotype: Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Lyz2^tm1(cre)Ifo/Lyz2⁺
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ

Genotype: Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(MMTV-cre)1Mam/0
involves: 129S1/Sv * 129X1/SvJ * CD-1 * FVB

Genotype: Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(Tek-cre)1Ywa/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL

Genotype: Hif1a^tm3Rsjo/Hif1a^tm3Rsjo
involves: 129S1/Sv * 129X1/SvJ

Genotype: Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Lyz2^tm1(cre)Ifo/Lyz2⁺
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6

Genotype: Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(SFTPC-rtTA)5Jaw/0 Tg(tetO-cre)1Jaw/0
involves: 129 * 129S1/Sv * 129X1/SvJ * C57BL/6

Genotype: Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(Itgax-cre)1-1Reiz/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA

Genotype: Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Speer6-ps1^{Tg(Alb-cre)21Mgn}/Speer6-ps1^{Tg(Alb-cre)21Mgn}
B6.Cg-Hif1a Speer6-ps1

Additional - Hif1a^tm3Rsjo related