JAX Mouse Strain Datasheet - 007561

B6.129-Hif1a^tm3Rsjo/J

Stock No:: 007561 |; HIF1α^flox

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Overview

Also Known As: HIF1α^flox

When these Hif1a^tm3Rsjo 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.

Donating Investigator

Randall Johnson, UC-San Diego

Genetic overview

Genetic Background	Generation
	N12+N2F7 (27-JUN-16)

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

Research Tools

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Base Price

Starting at:

$255.00 Domestic price for female

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Details

Detailed 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 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):4010-5. PubMed: 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-1alpha^+f; HIF-1alpha^F; HIF1a^f+; HIF1alpha^flox; Hif-1alpha 2-lox; Hif1a^2lox; Hif1a^fl; Hif1a^loxP; Hif^+f; Hif^f; I.1-^lox
Gene Symbol and Name	Hif1a, hypoxia inducible factor 1, alpha subunit
Gene Synonym(s)	AA959795; HIF-1-alpha; HIF-1A; HIF-1alpha; HIF1; HIF1-ALPHA; HIF1alpha; MOP1; PASD8; bHLHe78; expressed sequence AA959795
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

Research Areas By Genotype

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
involves: 129S1/Sv * 129X1/SvJ

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

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

liver/biliary system phenotype

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

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

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

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
- TPA-treated ears exhibit reduced inflammatory infiltration and edema compared with similarly treated wild-type cells
- 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

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

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

skeleton phenotype

decreased susceptibility to induced arthritis

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

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

mortality/aging

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
- 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 miceh similarly treated wild-type mice

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

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

cardiovascular system phenotype

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

Genotype: Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Vhl^tm1Jae/Vhl^tm1Jae Tg(Alb-cre)21Mgn/0
involves: 129 * BALB/c * C57BL/6 * DBA

liver/biliary system phenotype

hepatic steatosis
- severe steatosis

cardiovascular system phenotype

abnormal vasodilation
- hepatic vascular angiectasia

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

muscle phenotype

abnormal vasodilation
- hepatic vascular angiectasia

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

muscle phenotype

abnormal muscle physiology
- increase in muscle damage following exercise

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

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

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
- 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 Hif1aally 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
- 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 markerstion markers
- 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 conditionsthan cells under normoxic conditions
- stimulation by LPS does not further enhance expression of maturation markers as it does in BMDCs grown under normoxic conditions

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
- 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 Hif1aally 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

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
- 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 Hif1aally 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 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
- 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

cardiovascular system phenotype

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

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
- 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

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

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

homeostasis/metabolism phenotype

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

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
- 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

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

homeostasis/metabolism phenotype

delayed wound healing
- with reduced capillary sprouting

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

immune system phenotype

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

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):4010-5. PubMed: 10945599 MGI: J:78980

Additional - Hif1a^tm3Rsjo 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: J:177485
Albers J; Danzer C; Rechsteiner M; Lehmann H; Brandt LP; Hejhal T; Catalano A; Busenhart P; Goncalves AF; Brandt S; Bode PK; Bode-Lesniewska B; Wild PJ; Frew IJ. 2015. A versatile modular vector system for rapid combinatorial mammalian genetics. J Clin Invest 125(4):1603-19. PubMed: 25751063 MGI: J:222097
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: J:126336
Aro E; Khatri R; Gerard-O'Riley R; Mangiavini L; Myllyharju J; Schipani E. 2012. Hypoxia-inducible factor-1 (HIF-1) but not HIF-2 is essential for hypoxic induction of collagen prolyl 4-hydroxylases in primary newborn mouse epiphyseal growth plate chondrocytes. J Biol Chem 287(44):37134-44. PubMed: 22930750 MGI: J:214713
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: 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: 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: 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: 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: J:93322
Bouaziz W; Sigaux J; Modrowski D; Devignes CS; Funck-Brentano T; Richette P; Ea HK; Provot S; Cohen-Solal M; Hay E. 2016. Interaction of HIF1alpha and beta-catenin inhibits matrix metalloproteinase 13 expression and prevents cartilage damage in mice. Proc Natl Acad Sci U S A 113(19):5453-8. PubMed: 27122313 MGI: J:232188
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: J:145307
Bryant AJ; Carrick RP; McConaha ME; Jones BR; Shay SD; Moore CS; Blackwell TR; Gladson S; Penner NL; Burman A; Tanjore H; Hemnes AR; Karwandyar AK; Polosukhin VV; Talati MA; Dong HJ; Gleaves LA; Carrier EJ; Gaskill C; Scott EW; Majka SM; Fessel JP; Haase VH; West JD; Blackwell TS; Lawson WE. 2016. Endothelial HIF signaling regulates pulmonary fibrosis-associated pulmonary hypertension. Am J Physiol Lung Cell Mol Physiol 310(3):L249-62. PubMed: 26637636 MGI: J:233178
Candelario KM; Shuttleworth CW; Cunningham LA. 2013. Neural stem/progenitor cells display a low requirement for oxidative metabolism independent of hypoxia inducible factor-1alpha expression. J Neurochem 125(3):420-9. PubMed: 23410250 MGI: J:225064
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: 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: 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: 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: J:139006
Cho Y; Shin JE; Ewan EE; Oh YM; Pita-Thomas W; Cavalli V. 2015. Activating Injury-Responsive Genes with Hypoxia Enhances Axon Regeneration through Neuronal HIF-1alpha. Neuron 88(4):720-34. PubMed: 26526390 MGI: J:228750
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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: J:95245
Walter KM; Schonenberger MJ; Trotzmuller M; Horn M; Elsasser HP; Moser AB; Lucas MS; Schwarz T; Gerber PA; Faust PL; Moch H; Kofeler HC; Krek W; Kovacs WJ. 2014. Hif-2alpha promotes degradation of mammalian peroxisomes by selective autophagy. Cell Metab 20(5):882-97. PubMed: 25440060 MGI: J:218787
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: 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: 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: 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: 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: 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: 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: J:168049
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Also Known As: HIF1αflox

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Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Additional Information

Selected References

Hif1atm3Rsjo

Allele Symbol: Hif1atm3Rsjo

Disease Terms

Research Areas By Genotype

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

Mammalian Phenotype Terms by Genotype

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

homeostasis/metabolism phenotype

cellular phenotype

liver/biliary system phenotype

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

immune system phenotype

homeostasis/metabolism phenotype

skeleton phenotype

cellular phenotype

hematopoietic system phenotype

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

mortality/aging

immune system phenotype

homeostasis/metabolism phenotype

cardiovascular system phenotype

Genotype: Hif1atm3Rsjo/Hif1atm3Rsjo Vhltm1Jae/Vhltm1Jae Tg(Alb-cre)21Mgn/0involves: 129 * BALB/c * C57BL/6 * DBA

liver/biliary system phenotype

cardiovascular system phenotype

muscle phenotype

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

muscle phenotype

homeostasis/metabolism phenotype

nervous system phenotype

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

immune system phenotype

cellular phenotype

hematopoietic system phenotype

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

endocrine/exocrine gland phenotype

cardiovascular system phenotype

integument phenotype

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

mortality/aging

respiratory system phenotype

homeostasis/metabolism phenotype

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

cardiovascular system phenotype

neoplasm

homeostasis/metabolism phenotype

cellular phenotype

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

immune system phenotype

References

Additional - Hif1atm3Rsjo related

Genotyping Protocols

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Breeding Considerations

Mating System

Citation

Animal Health Reports

Live Mouse

Cryorecovery - Pricing

Progeny testing is not required

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Also Known As: HIF1α^flox

Hif1a^tm3Rsjo

Allele Symbol: Hif1a^tm3Rsjo

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

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

Genotype: Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Vhl^tm1Jae/Vhl^tm1Jae Tg(Alb-cre)21Mgn/0
involves: 129 * BALB/c * C57BL/6 * DBA

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

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

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

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

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

Additional - Hif1a^tm3Rsjo related