Strain Name:

B6.129-Hif1atm3Rsjo/J

Stock Number:

007561

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Availability:

Repository- Live

When these Hif1atm3Rsjo floxed mice are bred to mice that express Cre recombinase, resulting offspring will have exon 2 deleted in the cre-expressing tissue(s). 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.

Description

Strain Information

Type Congenic; Mutant Strain; Targeted Mutation;
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Mating SystemHomozygote x Homozygote         (Female x Male)   25-JUL-08
Specieslaboratory mouse
GenerationN12+N1F14 (11-DEC-13)
Generation Definitions
 
Donating Investigator Randall Johnson,   UC-San Diego

Description
These 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 Information

  Control
   000664 C57BL/6J
 
  Considerations for Choosing Controls

Related Strains

Strains carrying other alleles of Hif1a
024640   B6.129-Hif1atm1Kats/J
View Strains carrying other alleles of Hif1a     (1 strain)

Additional Web Information

Introduction to Cre-lox technology

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).
Von Hippel-Lindau Syndrome; VHL
- 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).
Glycogen Storage Disease V; GSD5
Glycogen Storage Disease VII; GSD7
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

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

Hif1atm3Rsjo/Hif1atm3Rsjo

        involves: 129S1/Sv * 129X1/SvJ   (conditional)
  • homeostasis/metabolism phenotype
  • abnormal gluconeogenesis
    • in mice exposed to a cre-expressing adenovirus following partial hepatectomy   (MGI Ref ID J:152724)
  • 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   (MGI Ref ID J:152724)
  • decreased glycogen level
    • in the liver of fed, but not fasted, mice exposed to a cre-expressing adenovirus 72 hours after partial hepatectomy   (MGI Ref ID J:152724)
  • 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   (MGI Ref ID J:116762)
    • decreased hepatocyte proliferation
      • in mice exposed to a cre-expressing adenovirus following partial hepatectomy   (MGI Ref ID J:152724)
  • early cellular replicative senescence
    • under normoxic conditions, adenoviral cre-treated mouse embryonic fibroblasts exhibit premature replicative senescence compared with similarly treated wild-type cells   (MGI Ref ID J:116762)
  • increased cellular sensitivity to gamma-irradiation
    • in adenoviral cre-treated mouse embryonic fibroblasts   (MGI Ref ID J:116762)
  • liver/biliary system phenotype
  • decreased hepatocyte proliferation
    • in mice exposed to a cre-expressing adenovirus following partial hepatectomy   (MGI Ref ID J:152724)
  • decreased liver regeneration
    • following exposure to a cre-expressing adenovirus, recovery from partial hepatectomy is delayed compared to in similarly treated wild-type mice   (MGI Ref ID J:152724)

The following phenotype relates to a compound genotype created using this strain.
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Hif1atm3Rsjo/Hif1atm3Rsjo Lyz2tm1(cre)Ifo/Lyz2+

        involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ   (conditional)
  • immune system phenotype
  • abnormal leukocyte physiology
    • CD44hi myeloid cells fail to promote repair of oxygen-induced retinopathy unlike wild-type cells   (MGI Ref ID J:117348)
    • abnormal macrophage physiology
      • macrophages exhibit impaired glycolysis and energy generation compared with wild-type cells   (MGI Ref ID J:107682)
      • bacteria exposed macrophages contain 7-fold more viable bacteria than similarly treated wild-type mice   (MGI Ref ID J:107682)
      • macrophages lack homotypic adhesion unlike wild-type cells   (MGI Ref ID J:107682)
      • impaired macrophage chemotaxis
        • macrophage capacity to invade matrigel is severely defective compared with wild-type mice   (MGI Ref ID J:107682)
        • macrophage migration through artificial extracellular matrix is decreased 60% compared with wild-type cells   (MGI Ref ID J:107682)
        • 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   (MGI Ref ID J:107682)
  • decreased inflammatory response
    • TPA-treated ears exhibit reduced inflammatory infiltration and edema compared with similarly treated wild-type cells   (MGI Ref ID J:107682)
    • 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   (MGI Ref ID J:107682)
  • decreased susceptibility to induced arthritis   (MGI Ref ID J:107682)
  • decreased tumor necrosis factor secretion
    • in LPS-treated macrophages   (MGI Ref ID J:107682)
  • homeostasis/metabolism phenotype
  • increased susceptibility to injury
    • following oxygen-induced retinopathy, mice exhibit decreased repair of retinal damage compared with similarly treated wild-type mice   (MGI Ref ID J:117348)
    • CD44hi myeloid cells fail to promote repair of oxygen-induced retinopathy unlike wild-type cells   (MGI Ref ID J:117348)
  • skeleton phenotype
  • decreased susceptibility to induced arthritis   (MGI Ref ID J:107682)
  • cellular phenotype
  • impaired macrophage chemotaxis
    • macrophage capacity to invade matrigel is severely defective compared with wild-type mice   (MGI Ref ID J:107682)
    • macrophage migration through artificial extracellular matrix is decreased 60% compared with wild-type cells   (MGI Ref ID J:107682)
    • 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   (MGI Ref ID J:107682)
  • hematopoietic system phenotype
  • abnormal leukocyte physiology
    • CD44hi myeloid cells fail to promote repair of oxygen-induced retinopathy unlike wild-type cells   (MGI Ref ID J:117348)
    • abnormal macrophage physiology
      • macrophages exhibit impaired glycolysis and energy generation compared with wild-type cells   (MGI Ref ID J:107682)
      • bacteria exposed macrophages contain 7-fold more viable bacteria than similarly treated wild-type mice   (MGI Ref ID J:107682)
      • macrophages lack homotypic adhesion unlike wild-type cells   (MGI Ref ID J:107682)
      • impaired macrophage chemotaxis
        • macrophage capacity to invade matrigel is severely defective compared with wild-type mice   (MGI Ref ID J:107682)
        • macrophage migration through artificial extracellular matrix is decreased 60% compared with wild-type cells   (MGI Ref ID J:107682)
        • 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   (MGI Ref ID J:107682)

Hif1atm3Rsjo/Hif1atm3Rsjo Lyz2tm1(cre)Ifo/Lyz2+

        involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6   (conditional)
  • mortality/aging
  • decreased sensitivity to xenobiotic induced morbidity/mortality
    • in LPS-treated mice compared with similarly treated wild-type mice   (MGI Ref ID J:148597)
  • immune system phenotype
  • decreased interleukin-1 alpha secretion
    • 4 hours after LPS treatment   (MGI Ref ID J:148597)
  • decreased interleukin-1 beta secretion
    • 4 hours after LPS treatment   (MGI Ref ID J:148597)
  • decreased interleukin-12 secretion
    • 4 hours after LPS treatment   (MGI Ref ID J:148597)
  • decreased interleukin-6 secretion
    • 1.5 hrs after LPS treatment   (MGI Ref ID J:148597)
  • decreased susceptibility to endotoxin shock
    • 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   (MGI Ref ID J:148597)
  • decreased tumor necrosis factor secretion
    • 1.5 and 4 hrs after LPS treatment   (MGI Ref ID J:148597)
  • homeostasis/metabolism phenotype
  • abnormal body temperature
    • LPS-treated mice develop less hypothermia compared with similarly treated wild-type mice   (MGI Ref ID J:148597)
  • decreased sensitivity to xenobiotic induced morbidity/mortality
    • in LPS-treated mice compared with similarly treated wild-type mice   (MGI Ref ID J:148597)
  • cardiovascular system phenotype
  • abnormal systemic arterial blood pressure
    • LPS-treated mice develop less hypotension compared with similarly treated wild-type mice   (MGI Ref ID J:148597)

Hif1atm3Rsjo/Hif1atm3Rsjo Vhltm1Jae/Vhltm1Jae Tg(Alb-cre)21Mgn/0

        involves: 129 * BALB/c * C57BL/6 * DBA   (conditional)
  • liver/biliary system phenotype
  • hepatic steatosis
    • severe steatosis   (MGI Ref ID J:97652)
  • cardiovascular system phenotype
  • abnormal vasodilation
    • hepatic vascular angiectasia   (MGI Ref ID J:97652)
  • increased vascular endothelial cell number
    • proliferation of endothelial cells in hepatic blood vessels   (MGI Ref ID J:97652)
  • muscle phenotype
  • abnormal vasodilation
    • hepatic vascular angiectasia   (MGI Ref ID J:97652)

Hif1atm3Rsjo/Hif1atm3Rsjo Tg(Ckmm-cre)5Khn/?

        involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * FVB   (conditional)
  • muscle phenotype
  • abnormal muscle physiology
    • increase in muscle damage following exercise   (MGI Ref ID J:97761)
  • homeostasis/metabolism phenotype
  • abnormal exercise endurance
    • increased endurance in swim tests and in the first session of running uphill (concentric exercise) but decreased endurance when running downhill (eccentric exercise)   (MGI Ref ID J:97761)
    • endurance decreased over 4 consecutive days of daily treadmill running   (MGI Ref ID J:97761)
  • abnormal glucose homeostasis
    • significant decrease in lactate accumulation after exercise   (MGI Ref ID J:97761)
  • increased circulating creatine kinase level
    • increased serum levels of the MM isoform of creatine kinase 1 day after exercise   (MGI Ref ID J:97761)
  • nervous system phenotype
  • abnormal innervation pattern to muscle
    • slight but statistically significant decrease in type IIa fibers in the soleus   (MGI Ref ID J:97761)

Hif1atm3Rsjo/Hif1atm3Rsjo Tg(Itgax-cre)1-1Reiz/0

        involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA   (conditional)
  • immune system phenotype
  • *normal* immune system phenotype
    • 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   (MGI Ref ID J:187773)
    • stimulation by LPS does not further enhance expression of maturation markers as it does in BMDCs grown under normoxic conditions   (MGI Ref ID J:187773)
    • 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   (MGI Ref ID J:187773)
    • 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   (MGI Ref ID J:187773)
    • abnormal leukocyte migration
      • 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   (MGI Ref ID J:187773)
      • 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   (MGI Ref ID J:187773)
  • 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   (MGI Ref ID J:187773)
    • abnormal leukocyte migration
      • 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   (MGI Ref ID J:187773)
      • 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   (MGI Ref ID J:187773)
  • 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   (MGI Ref ID J:187773)
  • abnormal leukocyte migration
    • 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   (MGI Ref ID J:187773)
    • 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   (MGI Ref ID J:187773)

Hif1atm3Rsjo/Hif1atm3Rsjo Tg(MMTV-cre)1Mam/0

        involves: 129S1/Sv * 129X1/SvJ * CD-1 * FVB   (conditional)
  • 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   (MGI Ref ID J:82618)
    • abnormal milk composition
      • milk water content is decreased while milk sodium and chloride ion contents are increased compared to in wild-type mice   (MGI Ref ID J:82618)
  • 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   (MGI Ref ID J:82618)
    • during lactation, mammary gland wet weight is decreased 50% compared to in wild-type mice   (MGI Ref ID J:82618)
    • abnormal mammary gland alveolus morphology
      • by day 15 of pregnancy, alveoli are smaller than normal with more prominent surrounding connective tissue than in wild-type mice   (MGI Ref ID J:82618)
      • alveolar differentiation during pregnancy is blocked   (MGI Ref ID J:82618)
      • alveolar lumens are small compared to in wild-type mice and fail to secret milk   (MGI Ref ID J:82618)
      • however, cell proliferation is normal   (MGI Ref ID J:82618)
    • abnormal mammary gland epithelium morphology
      • by day 15 of pregnancy, mammary gland epithelium lack the lacy appearance of wild-type epithelium   (MGI Ref ID J:82618)
      • during lactation, epithelial cells trap milk and fat unlike in wild-type mice   (MGI Ref ID J:82618)
      • transplanted mammary epithelium fails to grow in mice expressing the wild-type protein   (MGI Ref ID J:82618)
  • cardiovascular system phenotype
  • *normal* cardiovascular system phenotype
    • microvessel patterning and vascular density in the mammary gland are normal   (MGI Ref ID J:82618)
  • integument phenotype
  • abnormal lactation
    • female mice fail to secrete sufficient milk to support their offspring, most of whom are runted and die by P15   (MGI Ref ID J:82618)
    • abnormal milk composition
      • milk water content is decreased while milk sodium and chloride ion contents are increased compared to in wild-type mice   (MGI Ref ID J:82618)
  • 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   (MGI Ref ID J:82618)
    • during lactation, mammary gland wet weight is decreased 50% compared to in wild-type mice   (MGI Ref ID J:82618)
    • abnormal mammary gland alveolus morphology
      • by day 15 of pregnancy, alveoli are smaller than normal with more prominent surrounding connective tissue than in wild-type mice   (MGI Ref ID J:82618)
      • alveolar differentiation during pregnancy is blocked   (MGI Ref ID J:82618)
      • alveolar lumens are small compared to in wild-type mice and fail to secret milk   (MGI Ref ID J:82618)
      • however, cell proliferation is normal   (MGI Ref ID J:82618)
    • abnormal mammary gland epithelium morphology
      • by day 15 of pregnancy, mammary gland epithelium lack the lacy appearance of wild-type epithelium   (MGI Ref ID J:82618)
      • during lactation, epithelial cells trap milk and fat unlike in wild-type mice   (MGI Ref ID J:82618)
      • transplanted mammary epithelium fails to grow in mice expressing the wild-type protein   (MGI Ref ID J:82618)

Hif1atm3Rsjo/Hif1atm3Rsjo Tg(SFTPC-rtTA)5Jaw/0 Tg(tetO-cre)1Jaw/0

        involves: 129 * 129S1/Sv * 129X1/SvJ * C57BL/6   (conditional)
  • mortality/aging
  • partial neonatal lethality
    • all mice die within an hour of birth when exposed to doxycycline 8 days prior to parturition   (MGI Ref ID J:143384)
    • 85% of mice die within an hour of birth when exposed to doxycycline 4 of 6 days prior to parturition   (MGI Ref ID J:143384)
  • respiratory system phenotype
  • abnormal pulmonary alveolus morphology
    • when mice are exposed to doxycycline prior to parturition, mice exhibit reduced alveolar airspaces unlike wild-type mice   (MGI Ref ID J:143384)
    • 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   (MGI Ref ID J:143384)
      • 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   (MGI Ref ID J:143384)
  • abnormal surfactant secretion
    • when mice are exposed to doxycycline prior to parturition   (MGI Ref ID J:143384)
  • atelectasis
    • at birth when mice are exposed to doxycycline prior to parturition   (MGI Ref ID J:143384)
  • increased lung weight
    • at birth when mice are exposed to doxycycline prior to parturition   (MGI Ref ID J:143384)
  • respiratory distress
    • at birth when mice are exposed to doxycycline prior to parturition   (MGI Ref ID J:143384)
  • thick pulmonary interalveolar septum
    • at birth when mice are exposed to doxycycline prior to parturition   (MGI Ref ID J:143384)
  • homeostasis/metabolism phenotype
  • cyanosis
    • at birth when mice are exposed to doxycycline prior to parturition   (MGI Ref ID J:143384)

Hif1atm3Rsjo/Hif1atm3Rsjo Tg(Tek-cre)1Ywa/0

        involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL   (conditional)
  • cardiovascular system phenotype
  • abnormal vascular endothelial cell migration
    • endothelial cells exhibit reduced VEGF-induced migration in matrigel compared with similarly treated wild-type mice   (MGI Ref ID J:94773)
    • endothelial cells exhibit reduced VEGF-directed migration in hypoxic culture conditions compared with similarly treated wild-type cells   (MGI Ref ID J:94773)
    • however, random migration is normal   (MGI Ref ID J:94773)
  • abnormal vascular endothelial cell physiology
    • endothelial cell VEGF-induced proliferation in matrigel is reduced compared with wild-type mice   (MGI Ref ID J:94773)
  • decreased angiogenesis
    • endothelial cells exhibit reduced VEGF-induced angiogenesis compared with similarly treated wild-type mice   (MGI Ref ID J:94773)
    • transplanted tumors exhibit a 50% in tumor vessel density compared with tumors transplanted into wild-type mice   (MGI Ref ID J:94773)
    • under hypoxic culture conditions, endothelial cells exhibit reduced VEGF-induced capillary structure formation compared with similarly treated wild-type cells   (MGI Ref ID J:94773)
  • tumorigenesis
  • 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   (MGI Ref ID J:94773)
  • homeostasis/metabolism phenotype
  • delayed wound healing
    • with reduced capillary sprouting   (MGI Ref ID J:94773)
  • cellular phenotype
  • abnormal vascular endothelial cell migration
    • endothelial cells exhibit reduced VEGF-induced migration in matrigel compared with similarly treated wild-type mice   (MGI Ref ID J:94773)
    • endothelial cells exhibit reduced VEGF-directed migration in hypoxic culture conditions compared with similarly treated wild-type cells   (MGI Ref ID J:94773)
    • however, random migration is normal   (MGI Ref ID J:94773)

Hif1atm3Rsjo/Hif1atm3Rsjo Tg(UBC-cre/ERT2)1Ejb/0

        involves: 129S1/Sv * 129X1/SvJ   (conditional)
  • immune system phenotype
  • *normal* immune system phenotype
    • hematocrit levels are normal in mutants; mutants do not develop anemia   (MGI Ref ID J:119731)
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      loxP-flanked Sequences

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Hif1atm3Rsjo
Allele Name targeted mutation 3, Randall S Johnson
Allele Type Targeted (Conditional ready (e.g. floxed), No functional change)
Common Name(s) +f; HIF-1alpha+f; HIF-1alphaF; HIF1af+; HIF1alphaflox; Hif-1alpha 2-lox; Hif1a2lox; Hif1aloxP; Hif+f; Hiff; I.1-lox;
Mutation Made By Randall Johnson,   UC-San Diego
Strain of Origin(129X1/SvJ x 129S1/Sv)F1-Kitl<+>
ES Cell Line NameR1
ES Cell Line Strain(129X1/SvJ x 129S1/Sv)F1-Kitl<+>
Gene Symbol and Name Hif1a, hypoxia inducible factor 1, alpha subunit
Chromosome 12
Gene Common Name(s) AA959795; HIF-1A; HIF-1alpha; HIF1; HIF1-ALPHA; HIF1alpha; MOP1; PASD8; bHLHe78; expressed sequence AA959795;
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. [MGI Ref ID J:78980]

Genotyping

Genotyping Information

Genotyping Protocols

Hif1atm3Rsjo alternative1, Standard PCR
Hif1atm3Rsjo, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

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):4010-5. [PubMed: 10945599]  [MGI Ref ID J:78980]

Additional References

Hif1atm3Rsjo related

Adam J; Hatipoglu E; O'Flaherty L; Ternette N; Sahgal N; Lockstone H; Baban D; Nye E; Stamp GW; Wolhuter K; Stevens M; Fischer R; Carmeliet P; Maxwell PH; Pugh CW; Frizzell N; Soga T; Kessler BM; El-Bahrawy M; Ratcliffe PJ; Pollard PJ. 2011. Renal Cyst Formation in Fh1-Deficient Mice Is Independent of the Hif/Phd Pathway: Roles for Fumarate in KEAP1 Succination and Nrf2 Signaling. Cancer Cell 20(4):524-37. [PubMed: 22014577]  [MGI Ref ID J:177485]

Amarilio R; Viukov SV; Sharir A; Eshkar-Oren I; Johnson RS; Zelzer E. 2007. HIF1{alpha} regulation of Sox9 is necessary to maintain differentiation of hypoxic prechondrogenic cells during early skeletogenesis. Development 134(21):3917-28. [PubMed: 17913788]  [MGI Ref ID J:126336]

Arsenault PR; Pei F; Lee R; Kerestes H; Percy MJ; Keith B; Simon MC; Lappin TR; Khurana TS; Lee FS. 2013. A Knock-in Mouse Model of Human PHD2 Gene-associated Erythrocytosis Establishes a Haploinsufficiency Mechanism. J Biol Chem 288(47):33571-84. [PubMed: 24121508]  [MGI Ref ID J:202737]

Baranova O; Miranda LF; Pichiule P; Dragatsis I; Johnson RS; Chavez JC. 2007. Neuron-specific inactivation of the hypoxia inducible factor 1alpha increases brain injury in a mouse model of transient focal cerebral ischemia. J Neurosci 27(23):6320-32. [PubMed: 17554006]  [MGI Ref ID J:121971]

Bayele HK; Peyssonnaux C; Giatromanolaki A; Arrais-Silva WW; Mohamed HS; Collins H; Giorgio S; Koukourakis M; Johnson RS; Blackwell JM; Nizet V; Srai SK. 2007. HIF-1 regulates heritable variation and allele expression phenotypes of the macrophage immune response gene SLC11A1 from a Z-DNA forming microsatellite. Blood 110(8):3039-48. [PubMed: 17606764]  [MGI Ref ID J:148905]

Bentovim L; Amarilio R; Zelzer E. 2012. HIF1alpha is a central regulator of collagen hydroxylation and secretion under hypoxia during bone development. Development 139(23):4473-83. [PubMed: 23095889]  [MGI Ref ID J:189214]

Biju MP; Neumann AK; Bensinger SJ; Johnson RS; Turka LA; Haase VH. 2004. Vhlh gene deletion induces hif-1-mediated cell death in thymocytes. Mol Cell Biol 24(20):9038-47. [PubMed: 15456877]  [MGI Ref ID J:93322]

Boutin AT; Weidemann A; Fu Z; Mesropian L; Gradin K; Jamora C; Wiesener M; Eckardt KU; Koch CJ; Ellies LG; Haddad G; Haase VH; Simon MC; Poellinger L; Powell FL; Johnson RS. 2008. Epidermal sensing of oxygen is essential for systemic hypoxic response. Cell 133(2):223-34. [PubMed: 18423195]  [MGI Ref ID J:145307]

Cantley J; Selman C; Shukla D; Abramov AY; Forstreuter F; Esteban MA; Claret M; Lingard SJ; Clements M; Harten SK; Asare-Anane H; Batterham RL; Herrera PL; Persaud SJ; Duchen MR; Maxwell PH; Withers DJ. 2009. Deletion of the von Hippel-Lindau gene in pancreatic beta cells impairs glucose homeostasis in mice. J Clin Invest 119(1):125-35. [PubMed: 19065050]  [MGI Ref ID J:144713]

Caprara C; Thiersch M; Lange C; Joly S; Samardzija M; Grimm C. 2011. HIF1A Is Essential for the Development of the Intermediate Plexus of the Retinal Vasculature. Invest Ophthalmol Vis Sci 52(5):2109-17. [PubMed: 21212189]  [MGI Ref ID J:171540]

Chavez JC; Baranova O; Lin J; Pichiule P. 2006. The transcriptional activator hypoxia inducible factor 2 (HIF-2/EPAS-1) regulates the oxygen-dependent expression of erythropoietin in cortical astrocytes. J Neurosci 26(37):9471-81. [PubMed: 16971531]  [MGI Ref ID J:144667]

Chen Y; Doughman YQ; Gu S; Jarrell A; Aota S; Cvekl A; Watanabe M; Dunwoodie SL; Johnson RS; van Heyningen V; Kleinjan DA; Beebe DC; Yang YC. 2008. Cited2 is required for the proper formation of the hyaloid vasculature and for lens morphogenesis. Development 135(17):2939-48. [PubMed: 18653562]  [MGI Ref ID J:139006]

Ciofani M; Madar A; Galan C; Sellars M; Mace K; Pauli F; Agarwal A; Huang W; Parkurst CN; Muratet M; Newberry KM; Meadows S; Greenfield A; Yang Y; Jain P; Kirigin FK; Birchmeier C; Wagner EF; Murphy KM; Myers RM; Bonneau R; Littman DR. 2012. A validated regulatory network for th17 cell specification. Cell 151(2):289-303. [PubMed: 23021777]  [MGI Ref ID J:188993]

Clambey ET; McNamee EN; Westrich JA; Glover LE; Campbell EL; Jedlicka P; de Zoeten EF; Cambier JC; Stenmark KR; Colgan SP; Eltzschig HK. 2012. Hypoxia-inducible factor-1 alpha-dependent induction of FoxP3 drives regulatory T-cell abundance and function during inflammatory hypoxia of the mucosa. Proc Natl Acad Sci U S A 109(41):E2784-93. [PubMed: 22988108]  [MGI Ref ID J:190110]

Cowburn AS; Alexander LE; Southwood M; Nizet V; Chilvers ER; Johnson RS. 2014. Epidermal Deletion of HIF-2alpha Stimulates Wound Closure. J Invest Dermatol 134(3):801-8. [PubMed: 24037341]  [MGI Ref ID J:206050]

Cowburn AS; Takeda N; Boutin AT; Kim JW; Sterling JC; Nakasaki M; Southwood M; Goldrath AW; Jamora C; Nizet V; Chilvers ER; Johnson RS. 2013. HIF isoforms in the skin differentially regulate systemic arterial pressure. Proc Natl Acad Sci U S A 110(43):17570-5. [PubMed: 24101470]  [MGI Ref ID J:201979]

Cramer T; Yamanishi Y; Clausen BE; Forster I; Pawlinski R; Mackman N; Haase VH; Jaenisch R; Corr M; Nizet V; Firestein GS; Gerber HP; Ferrara N; Johnson RS. 2003. HIF-1alpha is essential for myeloid cell-mediated inflammation. Cell 112(5):645-57. [PubMed: 12628185]  [MGI Ref ID J:107682]

Dang EV; Barbi J; Yang HY; Jinasena D; Yu H; Zheng Y; Bordman Z; Fu J; Kim Y; Yen HR; Luo W; Zeller K; Shimoda L; Topalian SL; Semenza GL; Dang CV; Pardoll DM; Pan F. 2011. Control of T(H)17/T(reg) Balance by Hypoxia-Inducible Factor 1. Cell 146(5):772-84. [PubMed: 21871655]  [MGI Ref ID J:176230]

Diebold I; Petry A; Sabrane K; Djordjevic T; Hess J; Gorlach A. 2012. The HIF1 target gene NOX2 promotes angiogenesis through urotensin-II. J Cell Sci 125(Pt 4):956-64. [PubMed: 22399808]  [MGI Ref ID J:197690]

Doedens AL; Phan AT; Stradner MH; Fujimoto JK; Nguyen JV; Yang E; Johnson RS; Goldrath AW. 2013. Hypoxia-inducible factors enhance the effector responses of CD8(+) T cells to persistent antigen. Nat Immunol 14(11):1173-82. [PubMed: 24076634]  [MGI Ref ID J:208201]

Du J; Chen Y; Li Q; Han X; Cheng C; Wang Z; Danielpour D; Dunwoodie SL; Bunting KD; Yang YC. 2012. HIF-1alpha deletion partially rescues defects of hematopoietic stem cell quiescence caused by Cited2 deficiency. Blood 119(12):2789-98. [PubMed: 22308296]  [MGI Ref ID J:182527]

Eckle T; Brodsky K; Bonney M; Packard T; Han J; Borchers CH; Mariani TJ; Kominsky DJ; Mittelbronn M; Eltzschig HK. 2013. HIF1A reduces acute lung injury by optimizing carbohydrate metabolism in the alveolar epithelium. PLoS Biol 11(9):e1001665. [PubMed: 24086109]  [MGI Ref ID J:201805]

Eckle T; Hartmann K; Bonney S; Reithel S; Mittelbronn M; Walker LA; Lowes BD; Han J; Borchers CH; Buttrick PM; Kominsky DJ; Colgan SP; Eltzschig HK. 2012. Adora2b-elicited Per2 stabilization promotes a HIF-dependent metabolic switch crucial for myocardial adaptation to ischemia. Nat Med 18(5):774-82. [PubMed: 22504483]  [MGI Ref ID J:183926]

Eckle T; Kewley EM; Brodsky KS; Tak E; Bonney S; Gobel M; Anderson D; Glover LE; Riegel AK; Colgan SP; Eltzschig HK. 2014. Identification of hypoxia-inducible factor HIF-1A as transcriptional regulator of the A2B adenosine receptor during acute lung injury. J Immunol 192(3):1249-56. [PubMed: 24391213]  [MGI Ref ID J:207297]

Eisinger-Mathason TS; Zhang M; Qiu Q; Skuli N; Nakazawa MS; Karakasheva T; Mucaj V; Shay JE; Stangenberg L; Sadri N; Pure E; Yoon SS; Kirsch DG; Simon MC. 2013. Hypoxia-dependent modification of collagen networks promotes sarcoma metastasis. Cancer Discov 3(10):1190-205. [PubMed: 23906982]  [MGI Ref ID J:204376]

Elorza A; Soro-Arnaiz I; Melendez-Rodriguez F; Rodriguez-Vaello V; Marsboom G; de Carcer G; Acosta-Iborra B; Albacete-Albacete L; Ordonez A; Serrano-Oviedo L; Gimenez-Bachs JM; Vara-Vega A; Salinas A; Sanchez-Prieto R; Martin del Rio R; Sanchez-Madrid F;Malumbres M; Landazuri MO; Aragones J. 2012. HIF2alpha acts as an mTORC1 activator through the amino acid carrier SLC7A5. Mol Cell 48(5):681-91. [PubMed: 23103253]  [MGI Ref ID J:194004]

Fang HY; Hughes R; Murdoch C; Coffelt SB; Biswas SK; Harris AL; Johnson RS; Imityaz HZ; Simon MC; Fredlund E; Greten FR; Rius J; Lewis CE. 2009. Hypoxia-inducible factors 1 and 2 are important transcriptional effectors in primary macrophages experiencing hypoxia. Blood 114(4):844-59. [PubMed: 19454749]  [MGI Ref ID J:150747]

Franke K; Kalucka J; Mamlouk S; Singh RP; Muschter A; Weidemann A; Iyengar V; Jahn S; Wieczorek K; Geiger K; Muders M; Sykes AM; Poitz DM; Ripich T; Otto T; Bergmann S; Breier G; Baretton G; Fong GH; Greaves DR; Bornstein S; Chavakis T; Fandrey J; Gassmann M; Wielockx B. 2013. HIF-1alpha is a protective factor in conditional PHD2-deficient mice suffering from severe HIF-2alpha-induced excessive erythropoiesis. Blood 121(8):1436-45. [PubMed: 23264599]  [MGI Ref ID J:194598]

Garcia CM; Shui YB; Kamath M; DeVillar J; Johnson RS; Gerber HP; Ferrara N; Robinson ML; Beebe DC. 2009. The function of VEGF-A in lens development: formation of the hyaloid capillary network and protection against transient nuclear cataracts. Exp Eye Res 88(2):270-6. [PubMed: 18782574]  [MGI Ref ID J:146379]

Glick D; Zhang W; Beaton M; Marsboom G; Gruber M; Simon MC; Hart J; Dorn GW 2nd; Brady MJ; Macleod KF. 2012. BNip3 regulates mitochondrial function and lipid metabolism in the liver. Mol Cell Biol 32(13):2570-84. [PubMed: 22547685]  [MGI Ref ID J:186671]

Greenwood KK; Proper SP; Saini Y; Bramble LA; Jackson-Humbles DN; Wagner JG; Harkema JR; LaPres JJ. 2012. Neonatal epithelial hypoxia inducible factor-1alpha expression regulates the response of the lung to experimental asthma. Am J Physiol Lung Cell Mol Physiol 302(5):L455-62. [PubMed: 22180657]  [MGI Ref ID J:183445]

Gruber M; Hu CJ; Johnson RS; Brown EJ; Keith B; Simon MC. 2007. Acute postnatal ablation of Hif-2alpha results in anemia. Proc Natl Acad Sci U S A 104(7):2301-6. [PubMed: 17284606]  [MGI Ref ID J:119731]

Guitart AV; Subramani C; Armesilla-Diaz A; Smith G; Sepulveda C; Gezer D; Vukovic M; Dunn K; Pollard P; Holyoake TL; Enver T; Ratcliffe PJ; Kranc KR. 2013. Hif-2alpha is not essential for cell-autonomous hematopoietic stem cell maintenance. Blood 122(10):1741-5. [PubMed: 23894152]  [MGI Ref ID J:202361]

Hanna SC; Krishnan B; Bailey ST; Moschos SJ; Kuan PF; Shimamura T; Osborne LD; Siegel MB; Duncan LM; O'Brien ET 3rd; Superfine R; Miller CR; Simon MC; Wong KK; Kim WY. 2013. HIF1alpha and HIF2alpha independently activate SRC to promote melanoma metastases. J Clin Invest 123(5):2078-93. [PubMed: 23563312]  [MGI Ref ID J:201460]

Harms KM; Li L; Cunningham LA. 2010. Murine neural stem/progenitor cells protect neurons against ischemia by HIF-1alpha-regulated VEGF signaling. PLoS One 5(3):e9767. [PubMed: 20339541]  [MGI Ref ID J:158881]

Hart ML; Grenz A; Gorzolla IC; Schittenhelm J; Dalton JH; Eltzschig HK. 2011. Hypoxia-Inducible Factor-1{alpha}-Dependent Protection from Intestinal Ischemia/Reperfusion Injury Involves Ecto-5'-Nucleotidase (CD73) and the A2B Adenosine Receptor. J Immunol 186(7):4367-74. [PubMed: 21357264]  [MGI Ref ID J:170696]

Helton R; Cui J; Scheel JR; Ellison JA; Ames C; Gibson C; Blouw B; Ouyang L; Dragatsis I; Zeitlin S; Johnson RS; Lipton SA; Barlow C. 2005. Brain-specific knock-out of hypoxia-inducible factor-1alpha reduces rather than increases hypoxic-ischemic damage. J Neurosci 25(16):4099-107. [PubMed: 15843612]  [MGI Ref ID J:98637]

Herr B; Zhou J; Werno C; Menrad H; Namgaladze D; Weigert A; Dehne N; Brune B. 2009. The supernatant of apoptotic cells causes transcriptional activation of hypoxia-inducible factor-1alpha in macrophages via sphingosine-1-phosphate and transforming growth factor-beta. Blood 114(10):2140-8. [PubMed: 19549990]  [MGI Ref ID J:152258]

Higashiyama M; Hokari R; Hozumi H; Kurihara C; Ueda T; Watanabe C; Tomita K; Nakamura M; Komoto S; Okada Y; Kawaguchi A; Nagao S; Suematsu M; Goda N; Miura S. 2012. HIF-1 in T cells ameliorated dextran sodium sulfate-induced murine colitis. J Leukoc Biol 91(6):901-9. [PubMed: 22457366]  [MGI Ref ID J:184909]

Higgins DF; Biju MP; Akai Y; Wutz A; Johnson RS; Haase VH. 2004. Hypoxic induction of Ctgf is directly mediated by Hif-1. Am J Physiol Renal Physiol 287(6):F1223-32. [PubMed: 15315937]  [MGI Ref ID J:95664]

Higgins DF; Kimura K; Bernhardt WM; Shrimanker N; Akai Y; Hohenstein B; Saito Y; Johnson RS; Kretzler M; Cohen CD; Eckardt KU; Iwano M; Haase VH. 2007. Hypoxia promotes fibrogenesis in vivo via HIF-1 stimulation of epithelial-to-mesenchymal transition. J Clin Invest 117(12):3810-20. [PubMed: 18037992]  [MGI Ref ID J:130751]

Hoppe G; Lee TJ; Yoon S; Yu M; Peachey NS; Rayborn M; Zutel MJ; Trichonas G; Au J; Sears JE. 2014. Inducing a visceral organ to protect a peripheral capillary bed: stabilizing hepatic HIF-1alpha prevents oxygen-induced retinopathy. Am J Pathol 184(6):1890-9. [PubMed: 24731446]  [MGI Ref ID J:211093]

Huang TQ; Wang Y; Ebrahem Q; Chen Y; Cheng C; Doughman YQ; Watanabe M; Dunwoodie SL; Yang YC. 2012. Deletion of HIF-1alpha partially rescues the abnormal hyaloid vascular system in Cited2 conditional knockout mouse eyes. Mol Vis 18:1260-70. [PubMed: 22665973]  [MGI Ref ID J:191613]

Huang Y; Hickey RP; Yeh JL; Liu D; Dadak A; Young LH; Johnson RS; Giordano FJ. 2004. Cardiac myocyte-specific HIF-1alpha deletion alters vascularization, energy availability, calcium flux, and contractility in the normoxic heart. FASEB J 18(10):1138-40. [PubMed: 15132980]  [MGI Ref ID J:118455]

Huang Y; Lei L; Liu D; Jovin I; Russell R; Johnson RS; Di Lorenzo A; Giordano FJ. 2012. Normal glucose uptake in the brain and heart requires an endothelial cell-specific HIF-1alpha-dependent function. Proc Natl Acad Sci U S A 109(43):17478-83. [PubMed: 23047702]  [MGI Ref ID J:190364]

Ikejiri A; Nagai S; Goda N; Kurebayashi Y; Osada-Oka M; Takubo K; Suda T; Koyasu S. 2012. Dynamic regulation of Th17 differentiation by oxygen concentrations. Int Immunol 24(3):137-46. [PubMed: 22207131]  [MGI Ref ID J:182569]

Imanirad P; Solaimani Kartalaei P; Crisan M; Vink C; Yamada-Inagawa T; de Pater E; Kurek D; Kaimakis P; van der Linden R; Speck N; Dzierzak E. 2014. HIF1alpha is a regulator of hematopoietic progenitor and stem cell development in hypoxic sites of the mouse embryo. Stem Cell Res 12(1):24-35. [PubMed: 24141110]  [MGI Ref ID J:205140]

Jiang X; Khan MA; Tian W; Beilke J; Natarajan R; Kosek J; Yoder MC; Semenza GL; Nicolls MR. 2011. Adenovirus-mediated HIF-1alpha gene transfer promotes repair of mouse airway allograft microvasculature and attenuates chronic rejection. J Clin Invest 121(6):2336-49. [PubMed: 21606594]  [MGI Ref ID J:174019]

Kalucka J; Ettinger A; Franke K; Mamlouk S; Singh RP; Farhat K; Muschter A; Olbrich S; Breier G; Katschinski DM; Huttner W; Weidemann A; Wielockx B. 2013. Loss of epithelial hypoxia-inducible factor prolyl hydroxylase 2 accelerates skin wound healing in mice. Mol Cell Biol 33(17):3426-38. [PubMed: 23798557]  [MGI Ref ID J:204713]

Kapitsinou PP; Liu Q; Unger TL; Rha J; Davidoff O; Keith B; Epstein JA; Moores SL; Erickson-Miller CL; Haase VH. 2010. Hepatic HIF-2 regulates erythropoietic responses to hypoxia in renal anemia. Blood 116(16):3039-48. [PubMed: 20628150]  [MGI Ref ID J:165868]

Karhausen J; Furuta GT; Tomaszewski JE; Johnson RS; Colgan SP; Haase VH. 2004. Epithelial hypoxia-inducible factor-1 is protective in murine experimental colitis. J Clin Invest 114(8):1098-106. [PubMed: 15489957]  [MGI Ref ID J:93476]

Kim JW; Evans C; Weidemann A; Takeda N; Lee YS; Stockmann C; Branco-Price C; Brandberg F; Leone G; Ostrowski MC; Johnson RS. 2012. Loss of fibroblast HIF-1alpha accelerates tumorigenesis. Cancer Res 72(13):3187-95. [PubMed: 22556263]  [MGI Ref ID J:189318]

Kim YM; Barnes EA; Alvira CM; Ying L; Reddy S; Cornfield DN. 2013. Hypoxia-inducible factor-1alpha in pulmonary artery smooth muscle cells lowers vascular tone by decreasing myosin light chain phosphorylation. Circ Res 112(9):1230-3. [PubMed: 23513056]  [MGI Ref ID J:213312]

Kobayashi H; Gilbert V; Liu Q; Kapitsinou PP; Unger TL; Rha J; Rivella S; Schlondorff D; Haase VH. 2012. Myeloid cell-derived hypoxia-inducible factor attenuates inflammation in unilateral ureteral obstruction-induced kidney injury. J Immunol 188(10):5106-15. [PubMed: 22490864]  [MGI Ref ID J:188688]

Kocabas F; Zheng J; Thet S; Copeland NG; Jenkins NA; DeBerardinis RJ; Zhang C; Sadek HA. 2012. Meis1 regulates the metabolic phenotype and oxidant defense of hematopoietic stem cells. Blood 120(25):4963-72. [PubMed: 22995899]  [MGI Ref ID J:192126]

Kohler T; Reizis B; Johnson RS; Weighardt H; Forster I. 2012. Influence of hypoxia-inducible factor 1alpha on dendritic cell differentiation and migration. Eur J Immunol 42(5):1226-36. [PubMed: 22539295]  [MGI Ref ID J:187773]

Krishnan J; Ahuja P; Bodenmann S; Knapik D; Perriard E; Krek W; Perriard JC. 2008. Essential role of developmentally activated hypoxia-inducible factor 1alpha for cardiac morphogenesis and function. Circ Res 103(10):1139-46. [PubMed: 18849322]  [MGI Ref ID J:155281]

Krishnan J; Danzer C; Simka T; Ukropec J; Walter KM; Kumpf S; Mirtschink P; Ukropcova B; Gasperikova D; Pedrazzini T; Krek W. 2012. Dietary obesity-associated Hif1alpha activation in adipocytes restricts fatty acid oxidation and energy expenditure via suppression of the Sirt2-NAD+ system. Genes Dev 26(3):259-70. [PubMed: 22302938]  [MGI Ref ID J:181338]

Krishnan J; Suter M; Windak R; Krebs T; Felley A; Montessuit C; Tokarska-Schlattner M; Aasum E; Bogdanova A; Perriard E; Perriard JC; Larsen T; Pedrazzini T; Krek W. 2009. Activation of a HIF1alpha-PPARgamma axis underlies the integration of glycolytic and lipid anabolic pathways in pathologic cardiac hypertrophy. Cell Metab 9(6):512-24. [PubMed: 19490906]  [MGI Ref ID J:149827]

Kurihara T; Kubota Y; Ozawa Y; Takubo K; Noda K; Simon MC; Johnson RS; Suematsu M; Tsubota K; Ishida S; Goda N; Suda T; Okano H. 2010. von Hippel-Lindau protein regulates transition from the fetal to the adult circulatory system in retina. Development 137(9):1563-71. [PubMed: 20388654]  [MGI Ref ID J:160163]

Kurihara T; Westenskow PD; Bravo S; Aguilar E; Friedlander M. 2012. Targeted deletion of Vegfa in adult mice induces vision loss. J Clin Invest 122(11):4213-7. [PubMed: 23093773]  [MGI Ref ID J:194014]

Kurihara T; Westenskow PD; Krohne TU; Aguilar E; Johnson RS; Friedlander M. 2011. Astrocyte pVHL and HIF-alpha isoforms are required for embryonic-to-adult vascular transition in the eye. J Cell Biol 195(4):689-701. [PubMed: 22084310]  [MGI Ref ID J:178823]

Kusumbe AP; Ramasamy SK; Adams RH. 2014. Coupling of angiogenesis and osteogenesis by a specific vessel subtype in bone. Nature 507(7492):323-8. [PubMed: 24646994]  [MGI Ref ID J:208889]

Lange CA; Luhmann UF; Mowat FM; Georgiadis A; West EL; Abrahams S; Sayed H; Powner MB; Fruttiger M; Smith AJ; Sowden JC; Maxwell PH; Ali RR; Bainbridge JW. 2012. Von Hippel-Lindau protein in the RPE is essential for normal ocular growth and vascular development. Development 139(13):2340-50. [PubMed: 22627278]  [MGI Ref ID J:185536]

Li D; Bai T; Brorson JR. 2011. Adaptation to moderate hypoxia protects cortical neurons against ischemia-reperfusion injury and excitotoxicity independently of HIF-1alpha. Exp Neurol 230(2):302-10. [PubMed: 21619879]  [MGI Ref ID J:172731]

Li Y; Lim S; Hoffman D; Aspenstrom P; Federoff HJ; Rempe DA. 2009. HUMMR, a hypoxia- and HIF-1alpha-inducible protein, alters mitochondrial distribution and transport. J Cell Biol 185(6):1065-81. [PubMed: 19528298]  [MGI Ref ID J:150420]

Liao D; Corle C; Seagroves TN; Johnson RS. 2007. Hypoxia-inducible factor-1alpha is a key regulator of metastasis in a transgenic model of cancer initiation and progression. Cancer Res 67(2):563-72. [PubMed: 17234764]  [MGI Ref ID J:117422]

Lin M; Chen Y; Jin J; Hu Y; Zhou KK; Zhu M; Le YZ; Ge J; Johnson RS; Ma JX. 2011. Ischaemia-induced retinal neovascularisation and diabetic retinopathy in mice with conditional knockout of hypoxia-inducible factor-1 in retinal Muller cells. Diabetologia :. [PubMed: 21360191]  [MGI Ref ID J:170682]

Liu Q; Davidoff O; Niss K; Haase VH. 2012. Hypoxia-inducible factor regulates hepcidin via erythropoietin-induced erythropoiesis. J Clin Invest 122(12):4635-44. [PubMed: 23114598]  [MGI Ref ID J:193997]

Lukashev D; Klebanov B; Kojima H; Grinberg A; Ohta A; Berenfeld L; Wenger RH; Ohta A; Sitkovsky M. 2006. Cutting edge: hypoxia-inducible factor 1alpha and its activation-inducible short isoform I.1 negatively regulate functions of CD4+ and CD8+ T lymphocytes. J Immunol 177(8):4962-5. [PubMed: 17015677]  [MGI Ref ID J:117857]

Lum JJ; Bui T; Gruber M; Gordan JD; Deberardinis RJ; Covello KL; Simon MC; Thompson CB. 2007. The transcription factor HIF-1{alpha} plays a critical role in the growth factor-dependent regulation of both aerobic and anaerobic glycolysis. Genes Dev 21(9):1037-49. [PubMed: 17437992]  [MGI Ref ID J:121261]

Mason SD; Howlett RA; Kim MJ; Olfert IM; Hogan MC; McNulty W; Hickey RP; Wagner PD; Kahn CR; Giordano FJ; Johnson RS. 2004. Loss of skeletal muscle HIF-1alpha results in altered exercise endurance. PLoS Biol 2(10):e288. [PubMed: 15328538]  [MGI Ref ID J:97761]

Mason SD; Rundqvist H; Papandreou I; Duh R; McNulty WJ; Howlett RA; Olfert IM; Sundberg CJ; Denko NC; Poellinger L; Johnson RS. 2007. HIF-1alpha in endurance training: suppression of oxidative metabolism. Am J Physiol Regul Integr Comp Physiol 293(5):R2059-69. [PubMed: 17855495]  [MGI Ref ID J:145111]

Mastrogiannaki M; Matak P; Keith B; Simon MC; Vaulont S; Peyssonnaux C. 2009. HIF-2alpha, but not HIF-1alpha, promotes iron absorption in mice. J Clin Invest 119(5):1159-66. [PubMed: 19352007]  [MGI Ref ID J:149590]

Miharada K; Karlsson G; Rehn M; Rorby E; Siva K; Cammenga J; Karlsson S. 2011. Cripto regulates hematopoietic stem cells as a hypoxic-niche-related factor through cell surface receptor GRP78. Cell Stem Cell 9(4):330-44. [PubMed: 21982233]  [MGI Ref ID J:177654]

Milosevic J; Maisel M; Wegner F; Leuchtenberger J; Wenger RH; Gerlach M; Storch A; Schwarz J. 2007. Lack of hypoxia-inducible factor-1 alpha impairs midbrain neural precursor cells involving vascular endothelial growth factor signaling. J Neurosci 27(2):412-21. [PubMed: 17215402]  [MGI Ref ID J:117302]

Milovanova TN; Bhopale VM; Sorokina EM; Moore JS; Hunt TK; Hauer-Jensen M; Velazquez OC; Thom SR. 2008. Lactate stimulates vasculogenic stem cells via the thioredoxin system and engages an autocrine activation loop involving hypoxia-inducible factor 1. Mol Cell Biol 28(20):6248-61. [PubMed: 18710947]  [MGI Ref ID J:140963]

Miro-Murillo M; Elorza A; Soro-Arnaiz I; Albacete-Albacete L; Ordonez A; Balsa E; Vara-Vega A; Vazquez S; Fuertes E; Fernandez-Criado C; Landazuri MO; Aragones J. 2011. Acute Vhl Gene Inactivation Induces Cardiac HIF-Dependent Erythropoietin Gene Expression. PLoS One 6(7):e22589. [PubMed: 21811636]  [MGI Ref ID J:174924]

Miyauchi Y; Sato Y; Kobayashi T; Yoshida S; Mori T; Kanagawa H; Katsuyama E; Fujie A; Hao W; Miyamoto K; Tando T; Morioka H; Matsumoto M; Chambon P; Johnson RS; Kato S; Toyama Y; Miyamoto T. 2013. HIF1alpha is required for osteoclast activation by estrogen deficiency in postmenopausal osteoporosis. Proc Natl Acad Sci U S A 110(41):16568-73. [PubMed: 24023068]  [MGI Ref ID J:202025]

Mochizuki A; Pace A; Rockwell CE; Roth KJ; Chow A; O'Brien KM; Albee R; Kelly K; Towery K; Luyendyk JP; Copple BL. 2014. Hepatic stellate cells orchestrate clearance of necrotic cells in a hypoxia-inducible factor-1alpha-dependent manner by modulating macrophage phenotype in mice. J Immunol 192(8):3847-57. [PubMed: 24639359]  [MGI Ref ID J:209999]

Morizane Y; Thanos A; Takeuchi K; Murakami Y; Kayama M; Trichonas G; Miller J; Foretz M; Viollet B; Vavvas DG. 2011. AMP-activated Protein Kinase Suppresses Matrix Metalloproteinase-9 Expression in Mouse Embryonic Fibroblasts. J Biol Chem 286(18):16030-8. [PubMed: 21402702]  [MGI Ref ID J:172076]

Morote-Garcia JC; Rosenberger P; Kuhlicke J; Eltzschig HK. 2008. HIF-1-dependent repression of adenosine kinase attenuates hypoxia-induced vascular leak. Blood 111(12):5571-80. [PubMed: 18309031]  [MGI Ref ID J:136635]

Nakamura-Ishizu A; Kurihara T; Okuno Y; Ozawa Y; Kishi K; Goda N; Tsubota K; Okano H; Suda T; Kubota Y. 2012. The formation of an angiogenic astrocyte template is regulated by the neuroretina in a HIF-1-dependent manner. Dev Biol 363(1):106-14. [PubMed: 22226979]  [MGI Ref ID J:182708]

Neumann AK; Yang J; Biju MP; Joseph SK; Johnson RS; Haase VH; Freedman BD; Turka LA. 2005. Hypoxia inducible factor 1 alpha regulates T cell receptor signal transduction. Proc Natl Acad Sci U S A 102(47):17071-6. [PubMed: 16286658]  [MGI Ref ID J:103837]

Ochiai D; Goda N; Hishiki T; Kanai M; Senoo-Matsuda N; Soga T; Johnson RS; Yoshimura Y; Suematsu M. 2011. Disruption of HIF-1alpha in hepatocytes impairs glucose metabolism in diet-induced obesity mice. Biochem Biophys Res Commun 415(3):445-9. [PubMed: 22051049]  [MGI Ref ID J:178636]

Palazon A; Martinez-Forero I; Teijeira A; Morales-Kastresana A; Alfaro C; Sanmamed MF; Perez-Gracia JL; Penuelas I; Hervas-Stubbs S; Rouzaut A; de Landazuri MO; Jure-Kunkel M; Aragones J; Melero I. 2012. The HIF-1alpha hypoxia response in tumor-infiltrating T lymphocytes induces functional CD137 (4-1BB) for immunotherapy. Cancer Discov 2(7):608-23. [PubMed: 22719018]  [MGI Ref ID J:193060]

Pantel A; Teixeira A; Haddad E; Wood EG; Steinman RM; Longhi MP. 2014. Direct type I IFN but not MDA5/TLR3 activation of dendritic cells is required for maturation and metabolic shift to glycolysis after poly IC stimulation. PLoS Biol 12(1):e1001759. [PubMed: 24409099]  [MGI Ref ID J:207989]

Peyssonnaux C; Boutin AT; Zinkernagel AS; Datta V; Nizet V; Johnson RS. 2008. Critical role of HIF-1alpha in keratinocyte defense against bacterial infection. J Invest Dermatol 128(8):1964-8. [PubMed: 18323789]  [MGI Ref ID J:141616]

Peyssonnaux C; Cejudo-Martin P; Doedens A; Zinkernagel AS; Johnson RS; Nizet V. 2007. Cutting edge: Essential role of hypoxia inducible factor-1alpha in development of lipopolysaccharide-induced sepsis. J Immunol 178(12):7516-9. [PubMed: 17548584]  [MGI Ref ID J:148597]

Peyssonnaux C; Datta V; Cramer T; Doedens A; Theodorakis EA; Gallo RL; Hurtado-Ziola N; Nizet V; Johnson RS. 2005. HIF-1alpha expression regulates the bactericidal capacity of phagocytes. J Clin Invest 115(7):1806-15. [PubMed: 16007254]  [MGI Ref ID J:99628]

Pfander D; Kobayashi T; Knight MC; Zelzer E; Chan DA; Olsen BR; Giaccia AJ; Johnson RS; Haase VH; Schipani E. 2004. Deletion of Vhlh in chondrocytes reduces cell proliferation and increases matrix deposition during growth plate development. Development 131(10):2497-508. [PubMed: 15128677]  [MGI Ref ID J:91056]

Platero-Luengo A; Gonzalez-Granero S; Duran R; Diaz-Castro B; Piruat JI; Garcia-Verdugo JM; Pardal R; Lopez-Barneo J. 2014. An o2-sensitive glomus cell-stem cell synapse induces carotid body growth in chronic hypoxia. Cell 156(1-2):291-303. [PubMed: 24439383]  [MGI Ref ID J:205562]

Pourvali K; Matak P; Latunde-Dada GO; Solomou S; Mastrogiannaki M; Peyssonnaux C; Sharp PA. 2012. Basal expression of copper transporter 1 in intestinal epithelial cells is regulated by hypoxia-inducible factor 2alpha. FEBS Lett 586(16):2423-7. [PubMed: 22684009]  [MGI Ref ID J:186999]

Provot S; Zinyk D; Gunes Y; Kathri R; Le Q; Kronenberg HM; Johnson RS; Longaker MT; Giaccia AJ; Schipani E. 2007. Hif-1alpha regulates differentiation of limb bud mesenchyme and joint development. J Cell Biol 177(3):451-64. [PubMed: 17470636]  [MGI Ref ID J:134727]

Rankin EB; Biju MP; Liu Q; Unger TL; Rha J; Johnson RS; Simon MC; Keith B; Haase VH. 2007. Hypoxia-inducible factor-2 (HIF-2) regulates hepatic erythropoietin in vivo. J Clin Invest 117(4):1068-77. [PubMed: 17404621]  [MGI Ref ID J:121253]

Rankin EB; Higgins DF; Walisser JA; Johnson RS; Bradfield CA; Haase VH. 2005. Inactivation of the arylhydrocarbon receptor nuclear translocator (Arnt) suppresses von Hippel-Lindau disease-associated vascular tumors in mice. Mol Cell Biol 25(8):3163-72. [PubMed: 15798202]  [MGI Ref ID J:97652]

Rankin EB; Rha J; Selak MA; Unger TL; Keith B; Liu Q; Haase VH. 2009. Hypoxia-inducible factor 2 regulates hepatic lipid metabolism. Mol Cell Biol 29(16):4527-38. [PubMed: 19528226]  [MGI Ref ID J:151523]

Rankin EB; Tomaszewski JE; Haase VH. 2006. Renal cyst development in mice with conditional inactivation of the von Hippel-Lindau tumor suppressor. Cancer Res 66(5):2576-83. [PubMed: 16510575]  [MGI Ref ID J:106705]

Rankin EB; Wu C; Khatri R; Wilson TL; Andersen R; Araldi E; Rankin AL; Yuan J; Kuo CJ; Schipani E; Giaccia AJ. 2012. The HIF signaling pathway in osteoblasts directly modulates erythropoiesis through the production of EPO. Cell 149(1):63-74. [PubMed: 22464323]  [MGI Ref ID J:186085]

Regan Anderson TM; Peacock DL; Daniel AR; Hubbard GK; Lofgren KA; Girard BJ; Schorg A; Hoogewijs D; Wenger RH; Seagroves TN; Lange CA. 2013. Breast tumor kinase (Brk/PTK6) is a mediator of hypoxia-associated breast cancer progression. Cancer Res 73(18):5810-20. [PubMed: 23928995]  [MGI Ref ID J:204358]

Rempe D; Vangeison G; Hamilton J; Li Y; Jepson M; Federoff HJ. 2006. Synapsin I Cre transgene expression in male mice produces germline recombination in progeny. Genesis 44(1):44-9. [PubMed: 16419044]  [MGI Ref ID J:105271]

Riddle RC; Leslie JM; Gross TS; Clemens TL. 2011. Hypoxia-inducible Factor-1alpha Protein Negatively Regulates Load-induced Bone Formation. J Biol Chem 286(52):44449-56. [PubMed: 22081627]  [MGI Ref ID J:178824]

Ritter MR; Banin E; Moreno SK; Aguilar E; Dorrell MI; Friedlander M. 2006. Myeloid progenitors differentiate into microglia and promote vascular repair in a model of ischemic retinopathy. J Clin Invest 116(12):3266-76. [PubMed: 17111048]  [MGI Ref ID J:117348]

Rodriguez-Prados JC; Traves PG; Cuenca J; Rico D; Aragones J; Martin-Sanz P; Cascante M; Bosca L. 2010. Substrate fate in activated macrophages: a comparison between innate, classic, and alternative activation. J Immunol 185(1):605-14. [PubMed: 20498354]  [MGI Ref ID J:161403]

Saini Y; Greenwood KK; Merrill C; Kim KY; Patial S; Parameswaran N; Harkema JR; LaPres JJ. 2010. Acute cobalt-induced lung injury and the role of hypoxia-inducible factor 1alpha in modulating inflammation. Toxicol Sci 116(2):673-81. [PubMed: 20511350]  [MGI Ref ID J:162927]

Saini Y; Harkema JR; LaPres JJ. 2008. HIF1alpha is essential for normal intrauterine differentiation of alveolar epithelium and surfactant production in the newborn lung of mice. J Biol Chem 283(48):33650-7. [PubMed: 18801745]  [MGI Ref ID J:143384]

Saini Y; Kim KY; Lewandowski R; Bramble LA; Harkema JR; Lapres JJ. 2010. Role of hypoxia-inducible factor 1{alpha} in modulating cobalt-induced lung inflammation. Am J Physiol Lung Cell Mol Physiol 298(2):L139-47. [PubMed: 19915160]  [MGI Ref ID J:157680]

Sarkar K; Cai Z; Gupta R; Parajuli N; Fox-Talbot K; Darshan MS; Gonzalez FJ; Semenza GL. 2012. Hypoxia-inducible factor 1 transcriptional activity in endothelial cells is required for acute phase cardioprotection induced by ischemic preconditioning. Proc Natl Acad Sci U S A 109(26):10504-9. [PubMed: 22699503]  [MGI Ref ID J:185580]

Sarkar K; Rey S; Zhang X; Sebastian R; Marti GP; Fox-Talbot K; Cardona AV; Du J; Tan YS; Liu L; Lay F; Gonzalez FJ; Harmon JW; Semenza GL. 2012. Tie2-dependent knockout of HIF-1 impairs burn wound vascularization and homing of bone marrow-derived angiogenic cells. Cardiovasc Res 93(1):162-9. [PubMed: 22028336]  [MGI Ref ID J:194712]

Scheerer N; Dehne N; Stockmann C; Swoboda S; Baba HA; Neugebauer A; Johnson RS; Fandrey J. 2013. Myeloid hypoxia-inducible factor-1alpha is essential for skeletal muscle regeneration in mice. J Immunol 191(1):407-14. [PubMed: 23729446]  [MGI Ref ID J:205360]

Schipani E; Ryan HE; Didrickson S; Kobayashi T; Knight M; Johnson RS. 2001. Hypoxia in cartilage: HIF-1alpha is essential for chondrocyte growth arrest and survival. Genes Dev 15(21):2865-76. [PubMed: 11691837]  [MGI Ref ID J:72709]

Schmidt D; Textor B; Pein OT; Licht AH; Andrecht S; Sator-Schmitt M; Fusenig NE; Angel P; Schorpp-Kistner M. 2007. Critical role for NF-kappaB-induced JunB in VEGF regulation and tumor angiogenesis. EMBO J 26(3):710-9. [PubMed: 17255940]  [MGI Ref ID J:119917]

Scott A; Powner MB; Gandhi P; Clarkin C; Gutmann DH; Johnson RS; Ferrara N; Fruttiger M. 2010. Astrocyte-derived vascular endothelial growth factor stabilizes vessels in the developing retinal vasculature. PLoS One 5(7):e11863. [PubMed: 20686684]  [MGI Ref ID J:163069]

Seagroves TN; Hadsell D; McManaman J; Palmer C; Liao D; McNulty W; Welm B; Wagner KU; Neville M; Johnson RS. 2003. HIF1alpha is a critical regulator of secretory differentiation and activation, but not vascular expansion, in the mouse mammary gland. Development 130(8):1713-24. [PubMed: 12620994]  [MGI Ref ID J:82618]

Seagroves TN; Peacock DL; Liao D; Schwab LP; Krueger R; Handorf CR; Haase VH; Johnson RS. 2010. VHL deletion impairs mammary alveologenesis but is not sufficient for mammary tumorigenesis. Am J Pathol 176(5):2269-82. [PubMed: 20382704]  [MGI Ref ID J:160375]

Shi LZ; Wang R; Huang G; Vogel P; Neale G; Green DR; Chi H. 2011. HIF1alpha-dependent glycolytic pathway orchestrates a metabolic checkpoint for the differentiation of TH17 and Treg cells. J Exp Med 208(7):1367-76. [PubMed: 21708926]  [MGI Ref ID J:176809]

Shoham AB; Malkinson G; Krief S; Shwartz Y; Ely Y; Ferrara N; Yaniv K; Zelzer E. 2012. S1P1 inhibits sprouting angiogenesis during vascular development. Development 139(20):3859-69. [PubMed: 22951644]  [MGI Ref ID J:187683]

Shomento SH; Wan C; Cao X; Faugere MC; Bouxsein ML; Clemens TL; Riddle RC. 2010. Hypoxia-inducible factors 1alpha and 2alpha exert both distinct and overlapping functions in long bone development. J Cell Biochem 109(1):196-204. [PubMed: 19899108]  [MGI Ref ID J:161255]

Shui YB; Arbeit JM; Johnson RS; Beebe DC. 2008. HIF-1: an age-dependent regulator of lens cell proliferation. Invest Ophthalmol Vis Sci 49(11):4961-70. [PubMed: 18586877]  [MGI Ref ID J:141905]

Singh RP; Franke K; Kalucka J; Mamlouk S; Muschter A; Gembarska A; Grinenko T; Willam C; Naumann R; Anastassiadis K; Stewart AF; Bornstein S; Chavakis T; Breier G; Waskow C; Wielockx B. 2013. HIF prolyl hydroxylase 2 (PHD2) is a critical regulator of hematopoietic stem cell maintenance during steady-state and stress. Blood 121(26):5158-66. [PubMed: 23667053]  [MGI Ref ID J:200956]

Skuli N; Liu L; Runge A; Wang T; Yuan L; Patel S; Iruela-Arispe L; Simon MC; Keith B. 2009. Endothelial deletion of hypoxia-inducible factor-2alpha (HIF-2alpha) alters vascular function and tumor angiogenesis. Blood 114(2):469-77. [PubMed: 19439736]  [MGI Ref ID J:150753]

Skuli N; Majmundar AJ; Krock BL; Mesquita RC; Mathew LK; Quinn ZL; Runge A; Liu L; Kim MN; Liang J; Schenkel S; Yodh AG; Keith B; Simon MC. 2012. Endothelial HIF-2alpha regulates murine pathological angiogenesis and revascularization processes. J Clin Invest 122(4):1427-43. [PubMed: 22426208]  [MGI Ref ID J:184551]

Tajima T; Goda N; Fujiki N; Hishiki T; Nishiyama Y; Senoo-Matsuda N; Shimazu M; Soga T; Yoshimura Y; Johnson RS; Suematsu M. 2009. HIF-1alpha is necessary to support gluconeogenesis during liver regeneration. Biochem Biophys Res Commun 387(4):789-94. [PubMed: 19643083]  [MGI Ref ID J:152724]

Takubo K; Goda N; Yamada W; Iriuchishima H; Ikeda E; Kubota Y; Shima H; Johnson RS; Hirao A; Suematsu M; Suda T. 2010. Regulation of the HIF-1alpha level is essential for hematopoietic stem cells. Cell Stem Cell 7(3):391-402. [PubMed: 20804974]  [MGI Ref ID J:164436]

Takubo K; Nagamatsu G; Kobayashi CI; Nakamura-Ishizu A; Kobayashi H; Ikeda E; Goda N; Rahimi Y; Johnson RS; Soga T; Hirao A; Suematsu M; Suda T. 2013. Regulation of glycolysis by Pdk functions as a metabolic checkpoint for cell cycle quiescence in hematopoietic stem cells. Cell Stem Cell 12(1):49-61. [PubMed: 23290136]  [MGI Ref ID J:194930]

Tang N; Mack F; Haase VH; Simon MC; Johnson RS. 2006. pVHL function is essential for endothelial extracellular matrix deposition. Mol Cell Biol 26(7):2519-30. [PubMed: 16537898]  [MGI Ref ID J:106926]

Tang N; Wang L; Esko J; Giordano FJ; Huang Y; Gerber HP; Ferrara N; Johnson RS. 2004. Loss of HIF-1alpha in endothelial cells disrupts a hypoxia-driven VEGF autocrine loop necessary for tumorigenesis. Cancer Cell 6(5):485-95. [PubMed: 15542432]  [MGI Ref ID J:94773]

Thiel M; Caldwell CC; Kreth S; Kuboki S; Chen P; Smith P; Ohta A; Lentsch AB; Lukashev D; Sitkovsky MV. 2007. Targeted deletion of HIF-1alpha gene in T cells prevents their inhibition in hypoxic inflamed tissues and improves septic mice survival. PLoS ONE 2(9):e853. [PubMed: 17786224]  [MGI Ref ID J:129383]

Thiersch M; Lange C; Joly S; Heynen S; Le YZ; Samardzija M; Grimm C. 2009. Retinal neuroprotection by hypoxic preconditioning is independent of hypoxia-inducible factor-1 alpha expression in photoreceptors. Eur J Neurosci 29(12):2291-302. [PubMed: 19508692]  [MGI Ref ID J:151531]

Thom R; Rowe GC; Jang C; Safdar A; Arany Z. 2014. Hypoxic induction of vascular endothelial growth factor (VEGF) and angiogenesis in muscle by truncated peroxisome proliferator-activated receptor gamma coactivator (PGC)-1alpha. J Biol Chem 289(13):8810-7. [PubMed: 24505137]  [MGI Ref ID J:212445]

Thompson AA; Elks PM; Marriott HM; Eamsamarng S; Higgins KR; Lewis A; Williams L; Parmar S; Shaw G; McGrath EE; Formenti F; Van Eeden FJ; Kinnula VL; Pugh CW; Sabroe I; Dockrell DH; Chilvers ER; Robbins PA; Percy MJ; Simon MC; Johnson RS; Renshaw SA; Whyte MK; Walmsley SR. 2014. Hypoxia-inducible factor 2alpha regulates key neutrophil functions in humans, mice, and zebrafish. Blood 123(3):366-76. [PubMed: 24196071]  [MGI Ref ID J:207679]

Walmsley SR; Print C; Farahi N; Peyssonnaux C; Johnson RS; Cramer T; Sobolewski A; Condliffe AM; Cowburn AS; Johnson N; Chilvers ER. 2005. Hypoxia-induced neutrophil survival is mediated by HIF-1alpha-dependent NF-kappaB activity. J Exp Med 201(1):105-15. [PubMed: 15630139]  [MGI Ref ID J:95245]

Wan C; Gilbert SR; Wang Y; Cao X; Shen X; Ramaswamy G; Jacobsen KA; Alaql ZS; Eberhardt AW; Gerstenfeld LC; Einhorn TA; Deng L; Clemens TL. 2008. Activation of the hypoxia-inducible factor-1alpha pathway accelerates bone regeneration. Proc Natl Acad Sci U S A 105(2):686-91. [PubMed: 18184809]  [MGI Ref ID J:131088]

Wang H; Flach H; Onizawa M; Wei L; McManus MT; Weiss A. 2014. Negative regulation of Hif1a expression and TH17 differentiation by the hypoxia-regulated microRNA miR-210. Nat Immunol 15(4):393-401. [PubMed: 24608041]  [MGI Ref ID J:210247]

Wang R; Dillon CP; Shi LZ; Milasta S; Carter R; Finkelstein D; McCormick LL; Fitzgerald P; Chi H; Munger J; Green DR. 2011. The Transcription Factor Myc Controls Metabolic Reprogramming upon T Lymphocyte Activation. Immunity 35(6):871-82. [PubMed: 22195744]  [MGI Ref ID J:179281]

Wang Y; Wan C; Deng L; Liu X; Cao X; Gilbert SR; Bouxsein ML; Faugere MC; Guldberg RE; Gerstenfeld LC; Haase VH; Johnson RS; Schipani E; Clemens TL. 2007. The hypoxia-inducible factor alpha pathway couples angiogenesis to osteogenesis during skeletal development. J Clin Invest 117(6):1616-26. [PubMed: 17549257]  [MGI Ref ID J:122021]

Wei H; Bedja D; Koitabashi N; Xing D; Chen J; Fox-Talbot K; Rouf R; Chen S; Steenbergen C; Harmon JW; Dietz HC; Gabrielson KL; Kass DA; Semenza GL. 2012. Endothelial expression of hypoxia-inducible factor 1 protects the murine heart and aorta from pressure overload by suppression of TGF-beta signaling. Proc Natl Acad Sci U S A 109(14):E841-50. [PubMed: 22403061]  [MGI Ref ID J:182677]

Weidemann A; Kerdiles YM; Knaup KX; Rafie CA; Boutin AT; Stockmann C; Takeda N; Scadeng M; Shih AY; Haase VH; Simon MC; Kleinfeld D; Johnson RS. 2009. The glial cell response is an essential component of hypoxia-induced erythropoiesis in mice. J Clin Invest 119(11):3373-83. [PubMed: 19809162]  [MGI Ref ID J:154613]

Weidemann A; Krohne TU; Aguilar E; Kurihara T; Takeda N; Dorrell MI; Simon MC; Haase VH; Friedlander M; Johnson RS. 2010. Astrocyte hypoxic response is essential for pathological but not developmental angiogenesis of the retina. Glia 58(10):1177-85. [PubMed: 20544853]  [MGI Ref ID J:168049]

Weigert A; Weichand B; Sekar D; Sha W; Hahn C; Mora J; Ley S; Essler S; Dehne N; Brune B. 2012. HIF-1alpha is a negative regulator of plasmacytoid DC development in vitro and in vivo. Blood 120(15):3001-6. [PubMed: 22936665]  [MGI Ref ID J:192921]

Welford SM; Bedogni B; Gradin K; Poellinger L; Broome Powell M; Giaccia AJ. 2006. HIF1alpha delays premature senescence through the activation of MIF. Genes Dev 20(24):3366-71. [PubMed: 17142669]  [MGI Ref ID J:116762]

Xie L; Johnson RS; Freeman RS. 2005. Inhibition of NGF deprivation-induced death by low oxygen involves suppression of BIMEL and activation of HIF-1. J Cell Biol 168(6):911-20. [PubMed: 15767462]  [MGI Ref ID J:98249]

Zehetner J; Danzer C; Collins S; Eckhardt K; Gerber PA; Ballschmieter P; Galvanovskis J; Shimomura K; Ashcroft FM; Thorens B; Rorsman P; Krek W. 2008. pVHL is a regulator of glucose metabolism and insulin secretion in pancreatic {beta} cells. Genes Dev 22(22):3135-46. [PubMed: 19056893]  [MGI Ref ID J:142036]

Zelzer E; Mamluk R; Ferrara N; Johnson RS; Schipani E; Olsen BR. 2004. VEGFA is necessary for chondrocyte survival during bone development. Development 131(9):2161-71. [PubMed: 15073147]  [MGI Ref ID J:89363]

Zhang H; Li H; Xi HS; Li S. 2012. HIF1alpha is required for survival maintenance of chronic myeloid leukemia stem cells. Blood 119(11):2595-607. [PubMed: 22275380]  [MGI Ref ID J:182536]

Zhou J; Dehne N; Brune B. 2009. Nitric oxide causes macrophage migration via the HIF-1-stimulated small GTPases Cdc42 and Rac1. Free Radic Biol Med 47(6):741-9. [PubMed: 19523512]  [MGI Ref ID J:152571]

Zhu Y; Zhang L; Gidday JM. 2013. Role of hypoxia-inducible factor-1alpha in preconditioning-induced protection of retinal ganglion cells in glaucoma. Mol Vis 19:2360-72. [PubMed: 24319330]  [MGI Ref ID J:211869]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX10

Colony Maintenance

Breeding & HusbandryWhen maintaining a live colony, these mice are bred as homozygotes.
Mating SystemHomozygote x Homozygote         (Female x Male)   25-JUL-08
Diet Information LabDiet® 5K52/5K67

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


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

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $232.00Female or MaleHomozygous for Hif1atm3Rsjo  
Price per Pair (US dollars $)Pair Genotype
$464.00Homozygous for Hif1atm3Rsjo x Homozygous for Hif1atm3Rsjo  

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 $301.60Female or MaleHomozygous for Hif1atm3Rsjo  
Price per Pair (US dollars $)Pair Genotype
$603.20Homozygous for Hif1atm3Rsjo x Homozygous for Hif1atm3Rsjo  

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

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The Jackson Laboratory's Genotype Promise

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

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MICE, PRODUCTS AND SERVICES ARE PROVIDED “AS IS”. JACKSON EXTENDS NO WARRANTIES OF ANY KIND, EITHER EXPRESS, IMPLIED, OR STATUTORY, WITH RESPECT TO MICE, PRODUCTS OR SERVICES, INCLUDING ANY IMPLIED WARRANTY OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE, OR ANY WARRANTY OF NON-INFRINGEMENT OF ANY PATENT, TRADEMARK, OR OTHER INTELLECTUAL PROPERTY RIGHTS.

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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