Strain Name:

STOCK Fgf2tm1Doe/J

Stock Number:

003256

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Availability:

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Description

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Strain Information

Type Mutant Stock; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Specieslaboratory mouse
 
Donating Investigator Thomas Doetschman,   University of Arizona

Description
Mice homozygous for the Fgf2tm1Doe targeted-mutant allele have low blood pressure, presumably resulting from low vascular tone, increased megakaryocyte colony stimulation activity-induced megakaryocyte colony formation; increased platelet counts, and decreased IL3-induced colony formation. Vessel layer hypertrophy following vessel injury is not altered in the absence of FGF2. Cardiac hypertrophic response to induced high blood pressure is severely blunted in the absence of FGF2. Both sexes of the mutant exhibit no discernible morphologic or behavioral defects and have a normal life span. Both sexes are fertile and fecundity is normal.

Development
In the mutant allele, an Hprt minigene replaces 0.5kb of sequence containing 121bp of the proximal promoter region and exon 1. The targeting construct was electroporated into 129P2/OlaHsd-derived E14TG2a embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6-derived blastocysts, and the resulting chimeric mice were bred to outbred Black Swiss mice.

Control Information

  Control
   Wild-type from the colony
 
  Considerations for Choosing Controls

Related Strains

Strains carrying other alleles of Fgf2
010698   STOCK Fgf2tm2Doe/J
010720   STOCK Fgf2tm3Doe/J
View Strains carrying other alleles of Fgf2     (2 strains)

Phenotype

Phenotype Information

View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Fgf2tm1Doe/Fgf2tm1Doe

        involves: 129P2/OlaHsd * Black Swiss
  • cardiovascular system phenotype
  • abnormal cardiac muscle relaxation
    • -dP/dt (derivative of change in relaxation pressure over time) is increased as compared to wild type following ischemic-reperfusion injury in DMSO treated hearts   (MGI Ref ID J:119652)
  • decreased cardiac muscle contractility
    • recovery of contractile function in DMSO-treated heart following ischemia-reperfusion injury is decreased as compared to wild type (39 +/-4% vs 60 +/-7%)   (MGI Ref ID J:119652)
    • +dP/dt (derivative of change in contractile pressure over time) is decreased following ischemic-reperfusion injury in DMSO treated hearts   (MGI Ref ID J:119652)
  • decreased left ventricle developed pressure
    • 98.3+/-5.6 mmHg compared to 123.2+/-7.8 mmHg in wild-type mice   (MGI Ref ID J:45775)
    • maximal rate of ventricular contraction is decreased 7011.6+/-567 mmHg/s compared to 8631.6+/-746.6 mmHg/s in wild-type mice while maximum rate of ventricular relaxation is increased -7616.5+/-499.3 mmHg/s compared to -10716+/-713.8 mmHg/s in wild-type mice   (MGI Ref ID J:45775)
  • decreased left ventricle systolic pressure
    • LVSP is decreased as compared to wild type following ischemic-reperfusion injury in DMSO treated hearts   (MGI Ref ID J:119652)
  • decreased mean systemic arterial blood pressure
    • 78.0+/-5.9 mmHg compared to 98.9+/-5.6 mmHg in wild-type mice   (MGI Ref ID J:45775)
  • decreased vasoconstriction
    • in the portal vein spontaneous contractile activity and force generated are decreased   (MGI Ref ID J:45775)
    • however, sensitivity to phenylephrine and injury-induced vascular hyperplasia are normal   (MGI Ref ID J:45775)
  • increased cardiomyocyte apoptosis
    • mice exhibit an increase TUNEL-positive cells (indicator of late stage apoptosis) in non-ischemic hearts as compared to wild-type   (MGI Ref ID J:119652)
    • following ischemia-reperfusion injury mice exhibit an increase TUNEL-positive cells (indicator of late stage apoptosis) in DMSO- treated hearts as compared to wild-type   (MGI Ref ID J:119652)
  • hematopoietic system phenotype
  • abnormal common myeloid progenitor cell morphology
    • when cultured on methylcellulose bone marrow cells generate fewer IL-3-producing colonies and increased megakaryocyte colony-stimulating activity-induced megakaryocyte colonies compared to wild-type cells   (MGI Ref ID J:45775)
    • however, bone marrow cell culture response to granulocyte monocyte colony stimulating factor (GM-CSF) and erythropoietin, mitogen promoting granulocyte/macrophage and erythroid lineages, respectively, is normal   (MGI Ref ID J:45775)
  • increased platelet cell number
    • 669+/-87x103/mm3 compared to 472+/-68x103/mm3 in wild-type mice   (MGI Ref ID J:45775)
    • however, platelet aggregation is normal   (MGI Ref ID J:45775)
  • muscle phenotype
  • abnormal cardiac muscle relaxation
    • -dP/dt (derivative of change in relaxation pressure over time) is increased as compared to wild type following ischemic-reperfusion injury in DMSO treated hearts   (MGI Ref ID J:119652)
  • decreased cardiac muscle contractility
    • recovery of contractile function in DMSO-treated heart following ischemia-reperfusion injury is decreased as compared to wild type (39 +/-4% vs 60 +/-7%)   (MGI Ref ID J:119652)
    • +dP/dt (derivative of change in contractile pressure over time) is decreased following ischemic-reperfusion injury in DMSO treated hearts   (MGI Ref ID J:119652)
  • decreased vasoconstriction
    • in the portal vein spontaneous contractile activity and force generated are decreased   (MGI Ref ID J:45775)
    • however, sensitivity to phenylephrine and injury-induced vascular hyperplasia are normal   (MGI Ref ID J:45775)
  • increased cardiomyocyte apoptosis
    • mice exhibit an increase TUNEL-positive cells (indicator of late stage apoptosis) in non-ischemic hearts as compared to wild-type   (MGI Ref ID J:119652)
    • following ischemia-reperfusion injury mice exhibit an increase TUNEL-positive cells (indicator of late stage apoptosis) in DMSO- treated hearts as compared to wild-type   (MGI Ref ID J:119652)
  • nervous system phenotype
  • abnormal neuron morphology
    • neuron density in the surpragranular layer is decreased by 60% compared to in wild-type mice   (MGI Ref ID J:126973)
    • mice exhibit a 45% decrease in SMI-32+ cell density in the infragranular layer with a decrease in neurophil staining of the frontal and parietal cortices   (MGI Ref ID J:126973)
    • abnormal cerebral cortex pyramidal cell morphology
      • pyramidal cell somata in the frontal and parietal cortices are smaller than in wild-type mice   (MGI Ref ID J:126973)
      • pyramidal cell dendritic staining is decreased compared to in wild-type mice   (MGI Ref ID J:126973)
      • decreased cerebral cortex pyramidal cell number
        • the number of pyramidal neurons in the cortex is decreased in all cortical layers   (MGI Ref ID J:126973)
        • however, the number of interneurons is unchanged   (MGI Ref ID J:126973)
        • no change in pyramidal or granule cell number is detected in the hippocampus   (MGI Ref ID J:126973)
    • abnormal neuron differentiation
      • neurogenesis following treatment with kainic acid or middle cerebral artery occlusion (MCAO) is less than in wild-type mice at days 9 and 16 post-treatment   (MGI Ref ID J:126024)
      • the number of proliferating cells following treatment with kainic acid is increased 2.4-fold compared to 6.8-fold in wild-type mice   (MGI Ref ID J:126024)
      • the number of proliferating cells following MCAO is increased 1.6-fold compared to 4.2-fold in wild-type mice   (MGI Ref ID J:126024)
      • the proportion of differentiating cells induced by kainic acid and MCAO reduced compared to in wild-type mice   (MGI Ref ID J:126024)
      • however, mice do not display an increase seizure following kainic acid treatment or difference in blood flow, mean arterial blood pressure or infarct size following MCAO   (MGI Ref ID J:126024)
    • loss of glutamate neurons
      • glutamate-immunoreactive cells in the dorsolateral prefrontal and parietal cortices are reduced in number   (MGI Ref ID J:126973)
      • however, glutamate cell density in the occipital cortex is normal   (MGI Ref ID J:126973)
      • the number of excitatory neurons (glutamate+) is decreased by 38% compared to in wild-type mice   (MGI Ref ID J:126973)
      • fewer glutamate staining cells are found in the entire cerebral cortex compared to in wild-type mice with anterior cortical region exhibiting a more pronounced lack than the posterior region   (MGI Ref ID J:126973)
  • behavior/neurological phenotype
  • abnormal sleep pattern
    • in 3 to 4 month old male mice treated with PTB (a GABA receptor agonist), sleep time is increased (218+/-7 minutes compared to 159+/-904 minutes for wild-type mice)   (MGI Ref ID J:126973)
    • in 4 to 5 month old female mice treated with PTB (a GABA receptor agonist), sleep time is increased (118+/-19 minutes compared to 88+/-15 for wild-type mice)   (MGI Ref ID J:126973)
  • cellular phenotype
  • abnormal neuron differentiation
    • neurogenesis following treatment with kainic acid or middle cerebral artery occlusion (MCAO) is less than in wild-type mice at days 9 and 16 post-treatment   (MGI Ref ID J:126024)
    • the number of proliferating cells following treatment with kainic acid is increased 2.4-fold compared to 6.8-fold in wild-type mice   (MGI Ref ID J:126024)
    • the number of proliferating cells following MCAO is increased 1.6-fold compared to 4.2-fold in wild-type mice   (MGI Ref ID J:126024)
    • the proportion of differentiating cells induced by kainic acid and MCAO reduced compared to in wild-type mice   (MGI Ref ID J:126024)
    • however, mice do not display an increase seizure following kainic acid treatment or difference in blood flow, mean arterial blood pressure or infarct size following MCAO   (MGI Ref ID J:126024)
  • increased cardiomyocyte apoptosis
    • mice exhibit an increase TUNEL-positive cells (indicator of late stage apoptosis) in non-ischemic hearts as compared to wild-type   (MGI Ref ID J:119652)
    • following ischemia-reperfusion injury mice exhibit an increase TUNEL-positive cells (indicator of late stage apoptosis) in DMSO- treated hearts as compared to wild-type   (MGI Ref ID J:119652)

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

Fgf2tm1Doe/Fgf2tm1Doe

        B6.129P2-Fgf2tm1Doe
  • cardiovascular system phenotype
  • abnormal vascular endothelial cell migration
    • following de-endothelialization and treatment with 17beta-Estradiol (E2), mice fail to re-endothelialize the site of injury unlike wild-type mice   (MGI Ref ID J:114567)
    • endothelial precursor cell migration in response to E2 is disrupted   (MGI Ref ID J:114567)
  • cellular phenotype
  • abnormal vascular endothelial cell migration
    • following de-endothelialization and treatment with 17beta-Estradiol (E2), mice fail to re-endothelialize the site of injury unlike wild-type mice   (MGI Ref ID J:114567)
    • endothelial precursor cell migration in response to E2 is disrupted   (MGI Ref ID J:114567)

Fgf2tm1Doe/Fgf2tm1Doe

        involves: 129P2/OlaHsd * C57BL/6
  • cardiovascular system phenotype
  • altered response to myocardial infarction
    • left ventricle chamber is increased 10-fold 4 weeks after infarct induction compared to wild-type mice in which dilation is 6-fold   (MGI Ref ID J:126804)
    • expansion index at 4 weeks post-infarct induction is twice as much as in wild-type mice   (MGI Ref ID J:126804)
    • following infarct induction mice exhibit less cardiomyocyte hypertrophy (4% increase in cross-section area compared to 19% increase in cross-section area in wild-type mice)   (MGI Ref ID J:126804)
    • fibroblast proliferation at 4 days and 1 week post-infarct induction is decreased 33% and 59%, respectively, compared to in wild-type mice   (MGI Ref ID J:126804)
    • interstitial fibrosis fails to increase as in wild-type mice after infarct induction   (MGI Ref ID J:126804)
    • the decline in vascular density declines more dramatically following myocardial infarct induction compared to in wild-type mice (74% versus 25% at week 1 week, 91% versus 75% at 4 weeks)   (MGI Ref ID J:126804)
    • following myocardial infarct induction, the average area per vessel is increased 10-fold compared to in wild-type mice (122.9+/-23.4 um2 compared to 38.7+/-7.9 um2 in wild-type mice and these large sinusoidal vessels often lack smooth muscle/pericyte investment   (MGI Ref ID J:126804)
    • however, vessel area is unchanged even after myocardial infarct induction   (MGI Ref ID J:126804)
    • following infarct induction, left ventricular function is decreased 20% compared to 11% in wild-type mice   (MGI Ref ID J:126804)
    • increased myocardial infarction size
      • cardiac infarcts fail to undergo scar contraction after 4 weeks as in wild-type mice   (MGI Ref ID J:126804)
      • however, there is no difference in infarct composition or initial size   (MGI Ref ID J:126804)
  • homeostasis/metabolism phenotype
  • altered response to myocardial infarction
    • left ventricle chamber is increased 10-fold 4 weeks after infarct induction compared to wild-type mice in which dilation is 6-fold   (MGI Ref ID J:126804)
    • expansion index at 4 weeks post-infarct induction is twice as much as in wild-type mice   (MGI Ref ID J:126804)
    • following infarct induction mice exhibit less cardiomyocyte hypertrophy (4% increase in cross-section area compared to 19% increase in cross-section area in wild-type mice)   (MGI Ref ID J:126804)
    • fibroblast proliferation at 4 days and 1 week post-infarct induction is decreased 33% and 59%, respectively, compared to in wild-type mice   (MGI Ref ID J:126804)
    • interstitial fibrosis fails to increase as in wild-type mice after infarct induction   (MGI Ref ID J:126804)
    • the decline in vascular density declines more dramatically following myocardial infarct induction compared to in wild-type mice (74% versus 25% at week 1 week, 91% versus 75% at 4 weeks)   (MGI Ref ID J:126804)
    • following myocardial infarct induction, the average area per vessel is increased 10-fold compared to in wild-type mice (122.9+/-23.4 um2 compared to 38.7+/-7.9 um2 in wild-type mice and these large sinusoidal vessels often lack smooth muscle/pericyte investment   (MGI Ref ID J:126804)
    • however, vessel area is unchanged even after myocardial infarct induction   (MGI Ref ID J:126804)
    • following infarct induction, left ventricular function is decreased 20% compared to 11% in wild-type mice   (MGI Ref ID J:126804)
    • increased myocardial infarction size
      • cardiac infarcts fail to undergo scar contraction after 4 weeks as in wild-type mice   (MGI Ref ID J:126804)
      • however, there is no difference in infarct composition or initial size   (MGI Ref ID J:126804)
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Research Applications
This mouse can be used to support research in many areas including:

Fgf2tm1Doe related

Cancer Research
Genes Regulating Growth and Proliferation

Cardiovascular Research
Hypotension
Vascular Defects

Cell Biology Research
Genes Regulating Growth and Proliferation

Hematological Research
Hematopoietic Defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Fgf2tm1Doe
Allele Name targeted mutation 1, Thomas Doetschman
Allele Type Targeted (Null/Knockout)
Common Name(s) FGF-2-; Fgf2-;
Mutation Made By Thomas Doetschman,   University of Arizona
Strain of Origin129P2/OlaHsd
ES Cell Line NameE14TG2a
ES Cell Line Strain129P2/OlaHsd
Gene Symbol and Name Fgf2, fibroblast growth factor 2
Chromosome 3
Gene Common Name(s) BFGF; FGF-2; FGFB; Fgf-2; Fgfb; HBGF-2; fibroblast growth factor, basic;
Molecular Note An Hprt minigene replaced 0.5kb of sequence containing 121bp of the proximal promoter region and exon 1. Northern blot analysis of E13.5 embryos demonstrated that no mRNA containing exon 2 and 3 sequences is detectable in homozygous mutant mice. Western blot analysis on brain tissue from homozygous mutant mice showed that the protein is absent. [MGI Ref ID J:45775]

Genotyping

Genotyping Information

Genotyping Protocols

Fgf2tm1Doe, Separated PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Zhou M; Sutliff RL; Paul RJ; Lorenz JN; Hoying JB; Haudenschild CC ; Yin M ; Coffin JD ; Kong L ; Kranias EG ; Luo W ; Boivin GP ; Duffy JJ ; Pawlowski SA ; Doetschman T. 1998. Fibroblast growth factor 2 control of vascular tone. Nat Med 4(2):201-7. [PubMed: 9461194]  [MGI Ref ID J:45775]

Additional References

Jungnickel J; Claus P; Gransalke K; Timmer M; Grothe C. 2004. Targeted disruption of the FGF-2 gene affects the response to peripheral nerve injury. Mol Cell Neurosci 25(3):444-52. [PubMed: 15033172]  [MGI Ref ID J:89373]

Montero A; Okada Y; Tomita M; Ito M; Tsurukami H; Nakamura T; Doetschman T; Coffin JD; Hurley MM. 2000. Disruption of the fibroblast growth factor-2 gene results in decreased bone mass and bone formation. J Clin Invest 105(8):1085-93. [PubMed: 10772653]  [MGI Ref ID J:78866]

Fgf2tm1Doe related

Armstrong RC; Le TQ; Frost EE; Borke RC; Vana AC. 2002. Absence of fibroblast growth factor 2 promotes oligodendroglial repopulation of demyelinated white matter. J Neurosci 22(19):8574-85. [PubMed: 12351731]  [MGI Ref ID J:79214]

Billon-Gales A; Krust A; Fontaine C; Abot A; Flouriot G; Toutain C; Berges H; Gadeau AP; Lenfant F; Gourdy P; Chambon P; Arnal JF. 2011. Activation function 2 (AF2) of estrogen receptor-alpha is required for the atheroprotective action of estradiol but not to accelerate endothelial healing. Proc Natl Acad Sci U S A 108(32):13311-6. [PubMed: 21788522]  [MGI Ref ID J:175619]

Cheng Y; Black IB; DiCicco-Bloom E. 2002. Hippocampal granule neuron production and population size are regulated by levels of bFGF. Eur J Neurosci 15(1):3-12. [PubMed: 11860501]  [MGI Ref ID J:107796]

Fadda P; Bedogni F; Fresu A; Collu M; Racagni G; Riva MA. 2007. Reduction of corticostriatal glutamatergic fibers in basic fibroblast growth factor deficient mice is associated with hyperactivity and enhanced dopaminergic transmission. Biol Psychiatry 62(3):235-42. [PubMed: 17161387]  [MGI Ref ID J:129589]

Fei Y; Xiao L; Doetschman T; Coffin DJ; Hurley MM. 2011. Fibroblast growth factor 2 stimulation of osteoblast differentiation and bone formation is mediated by modulation of the wnt signaling pathway. J Biol Chem 286(47):40575-83. [PubMed: 21987573]  [MGI Ref ID J:178146]

Fei Y; Xiao L; Hurley MM. 2011. The impaired bone anabolic effect of PTH in the absence of endogenous FGF2 is partially due to reduced ATF4 expression. Biochem Biophys Res Commun 412(1):160-4. [PubMed: 21806973]  [MGI Ref ID J:175755]

Fontaine V; Filipe C; Werner N; Gourdy P; Billon A; Garmy-Susini B; Brouchet L; Bayard F; Prats H; Doetschman T; Nickenig G; Arnal JF. 2006. Essential role of bone marrow fibroblast growth factor-2 in the effect of estradiol on reendothelialization and endothelial progenitor cell mobilization. Am J Pathol 169(5):1855-62. [PubMed: 17071606]  [MGI Ref ID J:114567]

Garmy-Susini B; Delmas E; Gourdy P; Zhou M; Bossard C; Bugler B; Bayard F; Krust A; Prats AC; Doetschman T; Prats H; Arnal JF. 2004. Role of fibroblast growth factor-2 isoforms in the effect of estradiol on endothelial cell migration and proliferation. Circ Res 94(10):1301-9. [PubMed: 15073041]  [MGI Ref ID J:94550]

Haul S; Godecke A; Schrader J; Haas HL; Luhmann HJ. 1999. Impairment of neocortical long-term potentiation in mice deficient of endothelial nitric oxide synthase. J Neurophysiol 81(2):494-7. [PubMed: 10036253]  [MGI Ref ID J:103986]

House SL; Bolte C; Zhou M; Doetschman T; Klevitsky R; Newman G; Schultz Jel J. 2003. Cardiac-specific overexpression of fibroblast growth factor-2 protects against myocardial dysfunction and infarction in a murine model of low-flow ischemia. Circulation 108(25):3140-8. [PubMed: 14656920]  [MGI Ref ID J:102944]

Hurley MM; Okada Y; Xiao L; Tanaka Y; Ito M; Okimoto N; Nakamura T; Rosen CJ; Doetschman T; Coffin JD. 2006. Impaired bone anabolic response to parathyroid hormone in Fgf2-/- and Fgf2+/- mice. Biochem Biophys Res Commun 341(4):989-94. [PubMed: 16455048]  [MGI Ref ID J:105866]

Itkin T; Ludin A; Gradus B; Gur-Cohen S; Kalinkovich A; Schajnovitz A; Ovadya Y; Kollet O; Canaani J; Shezen E; Coffin DJ; Enikolopov GN; Berg T; Piacibello W; Hornstein E; Lapidot T. 2012. FGF-2 expands murine hematopoietic stem and progenitor cells via proliferation of stromal cells, c-Kit activation, and CXCL12 down-regulation. Blood 120(9):1843-55. [PubMed: 22645180]  [MGI Ref ID J:189114]

Jungnickel J; Claus P; Gransalke K; Timmer M; Grothe C. 2004. Targeted disruption of the FGF-2 gene affects the response to peripheral nerve injury. Mol Cell Neurosci 25(3):444-52. [PubMed: 15033172]  [MGI Ref ID J:89373]

Jungnickel J; Haastert K; Grzybek M; Thau N; Lipokatic-Takacs E; Ratzka A; Nolle A; Claus P; Grothe C. 2010. Mice lacking basic fibroblast growth factor showed faster sensory recovery. Exp Neurol 223(1):166-72. [PubMed: 19520074]  [MGI Ref ID J:162374]

Jungnickel J; Klutzny A; Guhr S; Meyer K; Grothe C. 2005. Regulation of neuronal death and calcitonin gene-related peptide by fibroblast growth factor-2 and FGFR3 after peripheral nerve injury: evidence from mouse mutants. Neuroscience 134(4):1343-50. [PubMed: 16009496]  [MGI Ref ID J:104421]

Korada S; Zheng W; Basilico C; Schwartz ML; Vaccarino FM. 2002. Fibroblast growth factor 2 is necessary for the growth of glutamate projection neurons in the anterior neocortex. J Neurosci 22(3):863-75. [PubMed: 11826116]  [MGI Ref ID J:126973]

Lavine KJ; Yu K; White AC; Zhang X; Smith C; Partanen J; Ornitz DM. 2005. Endocardial and epicardial derived FGF signals regulate myocardial proliferation and differentiation in vivo. Dev Cell 8(1):85-95. [PubMed: 15621532]  [MGI Ref ID J:95803]

Li CF; Hughes-Fulford M. 2006. Fibroblast growth factor-2 is an immediate-early gene induced by mechanical stress in osteogenic cells. J Bone Miner Res 21(6):946-55. [PubMed: 16753025]  [MGI Ref ID J:128095]

Liao S; Porter D; Scott A; Newman G; Doetschman T; Schultz Jel J. 2007. The cardioprotective effect of the low molecular weight isoform of fibroblast growth factor-2: the role of JNK signaling. J Mol Cell Cardiol 42(1):106-20. [PubMed: 17150229]  [MGI Ref ID J:119652]

Montero A; Okada Y; Tomita M; Ito M; Tsurukami H; Nakamura T; Doetschman T; Coffin JD; Hurley MM. 2000. Disruption of the fibroblast growth factor-2 gene results in decreased bone mass and bone formation. J Clin Invest 105(8):1085-93. [PubMed: 10772653]  [MGI Ref ID J:78866]

Murtie JC; Zhou YX; Le TQ; Armstrong RC. 2005. In vivo analysis of oligodendrocyte lineage development in postnatal FGF2 null mice. Glia 49(4):542-54. [PubMed: 15578654]  [MGI Ref ID J:104940]

Murtie JC; Zhou YX; Le TQ; Vana AC; Armstrong RC. 2005. PDGF and FGF2 pathways regulate distinct oligodendrocyte lineage responses in experimental demyelination with spontaneous remyelination. Neurobiol Dis 19(1-2):171-82. [PubMed: 15837572]  [MGI Ref ID J:105115]

Naganawa T; Xiao L; Abogunde E; Sobue T; Kalajzic I; Sabbieti M; Agas D; Hurley MM. 2006. In vivo and in vitro comparison of the effects of FGF-2 null and haplo-insufficiency on bone formation in mice. Biochem Biophys Res Commun 339(2):490-8. [PubMed: 16298332]  [MGI Ref ID J:103985]

Okada Y; Montero A; Zhang X; Sobue T; Lorenzo J; Doetschman T; Coffin JD; Hurley MM. 2003. Impaired osteoclast formation in bone marrow cultures of Fgf2 null mice in response to parathyroid hormone. J Biol Chem 278(23):21258-66. [PubMed: 12665515]  [MGI Ref ID J:133244]

Raballo R; Rhee J; Lyn-Cook R; Leckman JF; Schwartz ML; Vaccarino FM. 2000. Basic fibroblast growth factor (Fgf2) is necessary for cell proliferation and neurogenesis in the developing cerebral cortex. J Neurosci 20(13):5012-23. [PubMed: 10864959]  [MGI Ref ID J:63176]

Reuss B; Dono R; Unsicker K. 2003. Functions of fibroblast growth factor (FGF)-2 and FGF-5 in astroglial differentiation and blood-brain barrier permeability: evidence from mouse mutants. J Neurosci 23(16):6404-12. [PubMed: 12878680]  [MGI Ref ID J:84705]

Rottlaender A; Villwock H; Addicks K; Kuerten S. 2011. Neuroprotective role of fibroblast growth factor-2 in experimental autoimmune encephalomyelitis. Immunology 133(3):370-8. [PubMed: 21564095]  [MGI Ref ID J:176190]

Schultz JE; Witt SA; Nieman ML; Reiser PJ; Engle SJ; Zhou M; Pawlowski SA; Lorenz JN; Kimball TR; Doetschman T. 1999. Fibroblast growth factor-2 mediates pressure-induced hypertrophic response. J Clin Invest 104(6):709-19. [PubMed: 10491406]  [MGI Ref ID J:57630]

Seitz M; Grosheva M; Skouras E; Angelova SK; Ankerne J; Jungnickel J; Grothe C; Klimaschewski L; Hubbers CU; Dunlop SA; Angelov DN. 2011. Poor functional recovery and muscle polyinnervation after facial nerve injury in fibroblast growth factor-2-/- mice can be improved by manual stimulation of denervated vibrissal muscles. Neuroscience 182:241-7. [PubMed: 21440044]  [MGI Ref ID J:173958]

Sullivan CJ; Doetschman T; Hoying JB. 2002. Targeted disruption of the Fgf2 gene does not affect vascular growth in the mouse ischemic hindlimb. J Appl Physiol 93(6):2009-17. [PubMed: 12391121]  [MGI Ref ID J:103383]

Sullivan CJ; Hoying JB. 2002. Flow-dependent remodeling in the carotid artery of fibroblast growth factor-2 knockout mice. Arterioscler Thromb Vasc Biol 22(7):1100-5. [PubMed: 12117723]  [MGI Ref ID J:103193]

Tanaka T; Saika S; Ohnishi Y; Ooshima A; McAvoy JW; Liu CY; Azhar M; Doetschman T; Kao WW. 2004. Fibroblast growth factor 2: roles of regulation of lens cell proliferation and epithelial-mesenchymal transition in response to injury. Mol Vis 10:462-7. [PubMed: 15273655]  [MGI Ref ID J:91701]

Timmer M; Cesnulevicius K; Winkler C; Kolb J; Lipokatic-Takacs E; Jungnickel J; Grothe C. 2007. Fibroblast growth factor (FGF)-2 and FGF receptor 3 are required for the development of the substantia nigra, and FGF-2 plays a crucial role for the rescue of dopaminergic neurons after 6-hydroxydopamine lesion. J Neurosci 27(3):459-71. [PubMed: 17234579]  [MGI Ref ID J:117417]

Virag JA; Rolle ML; Reece J; Hardouin S; Feigl EO; Murry CE. 2007. Fibroblast growth factor-2 regulates myocardial infarct repair: effects on cell proliferation, scar contraction, and ventricular function. Am J Pathol 171(5):1431-40. [PubMed: 17872976]  [MGI Ref ID J:126804]

Xiao L; Sobue T; Esliger A; Kronenberg MS; Coffin JD; Doetschman T; Hurley MM. 2010. Disruption of the Fgf2 gene activates the adipogenic and suppresses the osteogenic program in mesenchymal marrow stromal stem cells. Bone 47(2):360-70. [PubMed: 20510392]  [MGI Ref ID J:162103]

Yoshimura S; Takagi Y; Harada J; Teramoto T; Thomas SS; Waeber C; Bakowska JC; Breakefield XO; Moskowitz MA. 2001. FGF-2 regulation of neurogenesis in adult hippocampus after brain injury. Proc Natl Acad Sci U S A 98(10):5874-9. [PubMed: 11320217]  [MGI Ref ID J:126024]

Zhao M; Ross JT; Itkin T; Perry JM; Venkatraman A; Haug JS; Hembree MJ; Deng CX; Lapidot T; He XC; Li L. 2012. FGF signaling facilitates postinjury recovery of mouse hematopoietic system. Blood 120(9):1831-42. [PubMed: 22802336]  [MGI Ref ID J:189159]

Zheng W; Nowakowski RS; Vaccarino FM. 2004. Fibroblast growth factor 2 is required for maintaining the neural stem cell pool in the mouse brain subventricular zone. Dev Neurosci 26(2-4):181-96. [PubMed: 15711059]  [MGI Ref ID J:104899]

Health & husbandry

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Health & Colony Maintenance Information

Animal Health Reports

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

Colony Maintenance

Breeding & HusbandryHomozygotes are viable and fertile. Prior to its arrival at The Jackson Laboratory, the donating investigator maintained the strain as an advanced intercross line by breeding non-sibling heterozygotes to avoid inbreeding. At The Jackson Laboratory, the strain was maintained similarly by intercrossing non-sibling heterozygotes. The donating investigator indicated that mice that carry this mutation may manifest developmental defects on a C57BL/6 background. Expected coat color from breeding: agouti and chinchilla.

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


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

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $2525.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Frozen Products

Price (US dollars $)
Frozen Embryo $1650.00

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryopreserved Embryos
    Available to most shipping destinations1
    This strain is also available as cryopreserved embryos2. Orders for cryopreserved embryos may be placed with our Customer Service Department. Experienced technicians at The Jackson Laboratory have recovered frozen embryos of this strain successfully. We will provide you enough embryos to perform two embryo transfers. The Jackson Laboratory does not guarantee successful recovery at your facility. For complete information on purchasing embryos, please visit our Cryopreserved Embryos web page.

    1 Shipments cannot be made to Australia due to Australian government import restrictions.
    2 Embryos for most strains are cryopreserved at the two cell stage while some strains are cryopreserved at the eight cell stage. If this information is important to you, please contact Customer Service.
  • Cryorecovery - Standard.
    Progeny testing is not required.

    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $3283.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Frozen Products

Price (US dollars $)
Frozen Embryo $2145.00

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryopreserved Embryos
    Available to most shipping destinations1
    This strain is also available as cryopreserved embryos2. Orders for cryopreserved embryos may be placed with our Customer Service Department. Experienced technicians at The Jackson Laboratory have recovered frozen embryos of this strain successfully. We will provide you enough embryos to perform two embryo transfers. The Jackson Laboratory does not guarantee successful recovery at your facility. For complete information on purchasing embryos, please visit our Cryopreserved Embryos web page.

    1 Shipments cannot be made to Australia due to Australian government import restrictions.
    2 Embryos for most strains are cryopreserved at the two cell stage while some strains are cryopreserved at the eight cell stage. If this information is important to you, please contact Customer Service.
  • Cryorecovery - Standard.
    Progeny testing is not required.

    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Control Information

  Control
   Wild-type from the colony
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

Payment Terms and Conditions

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


See Terms of Use tab for General Terms and Conditions


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.
Ordering Information
JAX® Mice
Surgical and Preconditioning Services
JAX® Services
Customer Services and Support
Tel: 1-800-422-6423 or 1-207-288-5845
Fax: 1-207-288-6150
Technical Support Email Form

Terms of Use

Terms of Use


General Terms and Conditions


Contact information

General inquiries regarding Terms of Use

Contracts Administration

phone:207-288-6470

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.

No Warranty

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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