JAX
Mouse Strain Datasheet - 007561
B6.129-Hif1atm3Rsjo/J
Also Known As: HIF1αflox
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.
Donating Investigator
Randall Johnson, UC-San Diego
Genetic overview
| Genetic Background | Generation |
|---|---|
|
N12+N2F7
|
Hif1atm3Rsjo
| Allele Type | Gene Symbol | Gene Name |
|---|---|---|
| Targeted (Conditional ready (e.g. floxed), No functional change) | Hif1a | hypoxia inducible factor 1, alpha subunit |
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
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.. In: . . MGI: J:78980
Hif1atm3Rsjo
Allele Symbol: Hif1atm3Rsjo
| 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-1alphaF; HIF1af+; HIF1alphaflox; Hif-1alpha 2-lox; Hif1a2lox; Hif1afl; Hif1aloxP; Hif+f; Hiff; 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 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
- Cre-lox System
Mammalian Phenotype Terms by Genotype
The following phenotype information is associated with a similar, but not exact match to this JAX® Mice strain
Genotype: Hif1atm3Rsjo/Hif1atm3Rsjo
involves: 129S1/Sv * 129X1/SvJ
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
Genotype: Hif1atm3Rsjo/Hif1atm3Rsjo Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ
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
- bacteria exposed macrophages contain 7-fold more viable bacteria than similarly treated wild-type mice (MGI Ref ID J:107682)
- macrophages exhibit impaired glycolysis and energy generation compared with wild-type cells (MGI Ref ID J:107682)
- macrophages lack homotypic adhesion unlike 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)
- impaired macrophage chemotaxis
- macrophage capacity to invade matrigel is severely defective compared with wild-type mice (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)
- macrophage migration through artificial extracellular matrix is decreased 60% compared with wild-type cells (MGI Ref ID J:107682)
homeostasis/metabolism phenotype
- increased susceptibility to injury
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 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)
- macrophage migration through artificial extracellular matrix is decreased 60% compared with 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
- bacteria exposed macrophages contain 7-fold more viable bacteria than similarly treated wild-type mice (MGI Ref ID J:107682)
- macrophages exhibit impaired glycolysis and energy generation compared with wild-type cells (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 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)
- macrophage migration through artificial extracellular matrix is decreased 60% compared with wild-type cells (MGI Ref ID J:107682)
Genotype: Hif1atm3Rsjo/Hif1atm3Rsjo Lyz2tm1(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 (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 miceh 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)
Genotype: Hif1atm3Rsjo/Hif1atm3Rsjo Vhltm1Jae/Vhltm1Jae Tg(Alb-cre)21Mgn/0
involves: 129 * BALB/c * C57BL/6 * DBA
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)
Genotype: Hif1atm3Rsjo/Hif1atm3Rsjo Tg(Ckmm-cre)5Khn/?
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * FVB/N
muscle phenotype
- abnormal muscle physiology
- increase in muscle damage following exercise (MGI Ref ID J:97761)
homeostasis/metabolism phenotype
- abnormal exercise endurance
- 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)
Genotype: Hif1atm3Rsjo/Hif1atm3Rsjo 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 (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 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 (MGI Ref ID J:187773)
- 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 (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 conditionsthan cells under normoxic conditions (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)
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 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 (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 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 (MGI Ref ID J:187773)
Genotype: Hif1atm3Rsjo/Hif1atm3Rsjo 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 (MGI Ref ID J:82618)
- abnormal mammary gland alveolus morphology
- 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)
- 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)
- 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)
- 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 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)
cardiovascular system phenotype
- 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 mammary gland alveolus morphology
- 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)
- 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)
- 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)
- 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 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)
Genotype: Hif1atm3Rsjo/Hif1atm3Rsjo Tg(SFTPC-rtTA)5Jaw/0 Tg(tetO-cre)1Jaw/0
involves: 129 * 129S1/Sv * 129X1/SvJ * C57BL/6
mortality/aging
- neonatal lethality, incomplete penetrance
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 (MGI Ref ID J:143384)
- 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 surfactant secretion
- when mice are exposed to doxycycline prior to parturition (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)
- 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)
Genotype: Hif1atm3Rsjo/Hif1atm3Rsjo 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 (MGI Ref ID J:94773)
- endothelial cells exhibit reduced VEGF-induced migration in matrigel compared with similarly treated wild-type mice (MGI Ref ID J:94773)
- however, random migration is normal (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)
- decreased vascular endothelial cell proliferation
- VEGF-induced endothelial cell proliferation in matrigel is reduced compared with wild-type mice (MGI Ref ID J:94773)
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 (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-directed migration in hypoxic culture conditions compared with similarly treated wild-type cells (MGI Ref ID J:94773)
- endothelial cells exhibit reduced VEGF-induced migration in matrigel compared with similarly treated wild-type mice (MGI Ref ID J:94773)
- however, random migration is normal (MGI Ref ID J:94773)
- decreased vascular endothelial cell proliferation
- VEGF-induced endothelial cell proliferation in matrigel is reduced compared with wild-type mice (MGI Ref ID J:94773)
Genotype: Hif1atm3Rsjo/Hif1atm3Rsjo 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 (MGI Ref ID J:119731)
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.. In: . . MGI: J:78980
Additional - 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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . MGI: J:145307
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