Overview

These integrin beta 3 targeted mutant mice exhibit significant embryonic lethality attributed to fetal hemorrhaging and placental defects. This mutant mouse strain represents a model that may be useful in studies related to Glanzmann thrombasthenia.

Donating Investigator

Dr. Richard Hynes, Massachusetts Institute of Technology

Genetic overview

Genetic Background	Generation

Itgb3^tm1Hyn

Allele Type	Gene Symbol	Gene Name
Targeted (Null/Knockout)	Itgb3	integrin beta 3

View Genetics

Research Applications

Cardiovascular Research
Hematological Research
Developmental Biology Research
Internal/Organ Research

View All Research Applications

Base Price

Starting at:

$2,854.50 Domestic price Cryo Recovery

View Price List

Details

Detailed Description

Mice that are homozygous for this targeted allele are viable and fertile. No gene product (protein) is detected on the surface of platelets. Significant (50%) embryonic lethality attributed to fetal hemorrhaging and placental defects is observed. Until three weeks of age, additional pup loss may occur due to hemorrhaging in the skin and gastrointestinal tract. Gastrointestinal tract bleeding is commonly observed in adults and is frequently associated with an enlarged spleen. Erythrocyte number, hemoglobin, hematocrits and thrombus formation are all reduced while bleeding time is prolonged. Varying degrees of liver and kidney necrosis are also observed. Although increased numbers of osteoclasts are observed (3.5 fold over that seen in heterozygotes) they appear to be dysfunctional, having a reduced ability to resorb whale dentin in vitro. Mice are osteosclerotic and hypocalcemic. Enhanced tumor angiogenesis and vascular endothelial growth factor-induced blood vessel growth are observed. This mutant mouse strain represents a model that may be useful in studies related to Glanzmann thrombasthenia.

In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.

Development

A targeting vector containing a neomycin resistance gene driven by the mouse phosphoglycerate kinase promoter was used to disrupt exons 1 and 2 of the targeted gene. The construct was transfected into 129S2/SvPas-derived D3 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6J blastocysts. The resulting chimeric animals were backcrossed to 129S4/AvJae for more than 7 generations by the donating laboratory.

Selected References

Hodivala-Dilke KM; McHugh KP; Tsakiris DA; Rayburn H; Crowley D; Ullman-Cullere M; Ross FP; Coller BS; Teitelbaum S; Hynes RO. 1999. Beta3-integrin-deficient mice are a model for Glanzmann thrombasthenia showing placental defects and reduced survival. J Clin Invest 103(2):229-38PubMed: 9916135 MGI: J:52262

View All References

Genetics

Itgb3^tm1Hyn

Allele Symbol: Itgb3^tm1Hyn

Allele Name	targeted mutation 1, Richard Hynes
Allele Type	Targeted (Null/Knockout)
Allele Synonym(s)	Itgb3^tm1Hyn; targeted mutation 1, Richard Hynes
Gene Symbol and Name	Itgb3, integrin beta 3
Gene Synonym(s)	BDPLT16; CD61; GT; platelet glycoprotein IIIa (GP3A); GPIIIa; GP3A; BDPLT2
Strain of Origin	129S2/SvPas
Chromosome	11
Molecular Note	A PGK-neomycin resistance cassette replaced 1.4 kb of sequence including exons I and II. FACS, immunoprecipitation, and immunofluorescence analyses did not detect protein expression in platelets and MEFs from homozygous mutant animals.
Mutations Made By	Dr. Richard Hynes, Massachusetts Institute of Technology

Disease/Phenotype

Disease Terms

Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).

platelet-type bleeding disorder 16

Research Areas By Genotype

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

Genotype: Itgb3^tm1Hyn related

Cardiovascular Research
- Vascular Defects
Hematological Research
- Clotting Defects
- Platelet Defects

Developmental Biology Research
- Embryonic Lethality (Homozygous)
  - incomplete
Internal/Organ Research
- Skeleton
  - Bone

Mammalian Phenotype Terms by Genotype

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

Genotype: Itgb3^tm1Hyn/Itgb3^tm1Hyn
involves: 129S2/SvPas * C57BL/6

cardiovascular system phenotype

abnormal cardiac muscle relaxation
- diastolic relaxation is impaired (dP/dt min and tau (Glantz) are significantly increased)

abnormal induced retinal neovascularization
- hypoxia-induced retinal neovascularization is significantly elevated as measure by numbers of vascular glomeruli at P17

abnormal tumor vascularization
- significantly elevated numbers of vessels per square millimeter of tumors, from injected cells, when compared with wild-type controls

cardiac hypertrophy
- in 12-week-old spontaneous cardiac hypertrophy occurs in the absence of provocative stimulation

decreased cardiac muscle contractility
- a significantly impaired contractile response to infusion of the inotropic agent Dobutamine

decreased heart rate
- heart rate is significantly decreased 7 days after pressure overload by transverse aortic constriction surgery (TAC) compared to wild-type

decreased left ventricle systolic pressure
- 12-week-old mice have reduced systolic function compared to wild-type littermates
- left ventricular peak systolic pressure is decreased in 12-week-old mice
- left ventricular peak systolic pressure is significantly decreased 7 days after pressure overload by transverse aortic constriction surgery (TAC) compared to wild-type

gastrointestinal hemorrhage
- in some homozygous newborn pups which die before weaning and in many of the surviving homozygous adult mice

heart left ventricle hypertrophy

hemorrhage
- some homozygous embryos and newborn pups displayed hemorrhage in the skin, in petechiae and in purpura, and appeared anemic

increased angiogenesis
- blood-vessel infiltration of matrigel implants impregnated with VEGF is significantly elevated
- however, no increase in vessel density is seen on scruff skin
- in the presence of VEGF, the total number of vessel sprouts in aortic rings embedded in Matrigel is significantly higher compared to wild-type

increased heart weight
- heart weight to body weight ratio is increased

increased left ventricle diastolic pressure
- left ventricular end-diastolic pressure is significantly increased 7 days after pressure overload by transverse aortic constriction surgery (TAC) compared to wild-type
- minimal change in pressure per unit time is significantly increased 7 days after pressure overload by TAC surgery compared to wild-type
- the maximal change in pressure per unit time is significantly decreased 7 days after pressure overload by TAC surgery compared to wild-type

increased left ventricle weight
- left ventricle weight to body weight ratio is increased by 4 weeks of age

increased response of heart to induced stress
- cardiac tissue exhibits marked round cell infiltration 7 days after transverse aortic constriction surgery
- impairment of systolic and diastolic function after transverse aortic constriction is more severe than in wild-type controls

petechiae
- petechiae are observed around the mouth, indicating bleeding under the epidermis

purpura
- purpura are observed on the forelimb, indicating bleeding within the dermis

uterine hemorrhage

cellular phenotype

abnormal cell adhesion
- endothelial cells showed background levels of adhesion and no migration on vitronectin

abnormal cell migration
- endothelial cells showed background levels of adhesion and no migration on vitronectin

hepatic necrosis
- centrilobular necrosis of the liver are found secondary to the excessive bleeding

impaired macrophage chemotaxis
- peritoneal macrophages migrate less efficiently

renal necrosis
- enlarged glomeruli and dilated and necrotic proximal tubules containing proteinaceous deposits are found secondary to the excessive bleeding

digestive/alimentary phenotype

gastrointestinal hemorrhage
- in some homozygous newborn pups which die before weaning and in many of the surviving homozygous adult mice

embryo phenotype

abnormal placenta labyrinth morphology
- thickened cell layers in the labyrinth layer in approximately 25% of placentae of homozygous pregnant females which were associated with dead embryos
- within affected placentae, the space between endothelial layers was reduced with evidence of increased necrosis

abnormal trophoblast giant cell morphology
- within affected placentae of homozygous pregnant females, trophoblastic cells sometimes invaded the labyrinthine part of the placenta

pale placenta

hematopoietic system phenotype

abnormal macrophage physiology
- peritoneal macrophages express significantly more Tnf and Il1b

abnormal platelet activation
- platelet isolated from homozygous mice did not aggregate after ADP-induced activation in vitro
- platelet isolated from homozygous mice shows reduced clot retraction and greatly reduced fibrinogen uptake in vitro
- reduced formation of thrombi in Shwartzman-like reaction, an experimental model of hemorrhagic vasculitis induced by subcutaneous injection of LPS followed 24 h later by an injection of TNF-alpha in the same place

anemia
- secondary to the excessive bleeding

decreased erythrocyte cell number
- in 8-12-week-old mice

decreased hematocrit
- in 8-12-week-old mice

decreased hemoglobin content
- in 8-12-week-old mice

enlarged spleen
- commonly associated with gastrointestinal bleeding

extramedullary hematopoiesis
- found in animals with splenomegaly

impaired macrophage chemotaxis
- peritoneal macrophages migrate less efficiently

increased monocyte cell number
- the monocyte count is dramatically increased in peripheral blood

reticulocytosis
- in 8-12-week-old mice

homeostasis/metabolism phenotype

abnormal platelet activation
- platelet isolated from homozygous mice did not aggregate after ADP-induced activation in vitro
- platelet isolated from homozygous mice shows reduced clot retraction and greatly reduced fibrinogen uptake in vitro
- reduced formation of thrombi in Shwartzman-like reaction, an experimental model of hemorrhagic vasculitis induced by subcutaneous injection of LPS followed 24 h later by an injection of TNF-alpha in the same place

increased bleeding time
- impaired hemostasis as evidenced by failure to arrest bleeding within 10 minutes following tail resection

increased response of heart to induced stress
- cardiac tissue exhibits marked round cell infiltration 7 days after transverse aortic constriction surgery
- impairment of systolic and diastolic function after transverse aortic constriction is more severe than in wild-type controls

immune system phenotype

abnormal macrophage physiology
- peritoneal macrophages express significantly more Tnf and Il1b

dermatitis
- ulcerative dermatitis in some homozygous animals undergoing crisis

enlarged spleen
- commonly associated with gastrointestinal bleeding

impaired macrophage chemotaxis
- peritoneal macrophages migrate less efficiently

increased monocyte cell number
- the monocyte count is dramatically increased in peripheral blood

myositis
- cardiac tissue exhibits marked round cell infiltration 7 days after transverse aortic constriction surgery

integument phenotype

dermatitis
- ulcerative dermatitis in some homozygous animals undergoing crisis

petechiae
- petechiae are observed around the mouth, indicating bleeding under the epidermis

purpura
- purpura are observed on the forelimb, indicating bleeding within the dermis

liver/biliary system phenotype

hepatic necrosis
- centrilobular necrosis of the liver are found secondary to the excessive bleeding

mammalian phenotype

vision/eye phenotype
- Normal - the patterns of neovascularization in P7 retinas isolated from wild-type or homozygous mutant mice showed no obvious differences

mortality/aging

postnatal lethality, incomplete penetrance
- significant loss of homozygous pups up to three weeks of age due to hemorrhage

premature death
- some homozygous animals suffered acute blood loss and crisis which lead to premature death

muscle phenotype

abnormal cardiac muscle relaxation
- diastolic relaxation is impaired (dP/dt min and tau (Glantz) are significantly increased)

decreased cardiac muscle contractility
- a significantly impaired contractile response to infusion of the inotropic agent Dobutamine

heart left ventricle hypertrophy

myositis
- cardiac tissue exhibits marked round cell infiltration 7 days after transverse aortic constriction surgery

neoplasm

abnormal tumor vascularization
- significantly elevated numbers of vessels per square millimeter of tumors, from injected cells, when compared with wild-type controls

increased tumor growth/size
- tumor size is enhanced significantly when injected with murine melanoma (B16F0) or lung carcinoma (CMT19T) cells

renal/urinary system phenotype

renal necrosis
- enlarged glomeruli and dilated and necrotic proximal tubules containing proteinaceous deposits are found secondary to the excessive bleeding

reproductive system phenotype

abnormal miscarriage rate
- 9.5% of the embryos carried by homozygous mothers were found dead in utero at E14 and E17

abnormal uterine environment
- compromised survival of embryos in homozygous mother as a result of placental defects and intrauterine hemorrhage

reduced female fertility
- litter sizes of homozygous female were reduced significantly compared to wild-type

uterine hemorrhage

vision/eye phenotype

abnormal induced retinal neovascularization
- hypoxia-induced retinal neovascularization is significantly elevated as measure by numbers of vascular glomeruli at P17

Genotype: Itgb3^tm1Hyn/Itgb3⁺
involves: 129S2/SvPas * C57BL/6

cardiovascular system phenotype

cardiac hypertrophy
- the hypertrophy phenotype is intermediate between homozygous null and wild-type mice

decreased heart rate
- heart rate is significantly decreased 7 days after pressure overload by transverse aortic constriction surgery (TAC) compared to wild-type

heart left ventricle hypertrophy
- spontaneous

increased heart weight
- heart weight to body weight ratio is increased

increased left ventricle weight
- left ventricle weight to body weight ratio is increased

increased response of heart to induced stress
- heart rate is significantly decreased 7 days after pressure overload by transverse aortic constriction surgery (TAC) compared to wild-type
- impairment of systolic and diastolic function after transverse aortic constriction is more severe than in wild-type controls

muscle phenotype

heart left ventricle hypertrophy
- spontaneous

homeostasis/metabolism phenotype

increased response of heart to induced stress
- heart rate is significantly decreased 7 days after pressure overload by transverse aortic constriction surgery (TAC) compared to wild-type
- impairment of systolic and diastolic function after transverse aortic constriction is more severe than in wild-type controls

Genotype: Itgb3^tm1Hyn/Itgb3^tm1Hyn
involves: 129S2/SvPas * BALB/c

cellular phenotype

maternal effect
- gotes
- heterozygous pups from non-immunized females mated with wild-type males exhibit normal platelets counts, indicating that maternal antibodies of the pregnant females and not pup genotype is responsible for the reduced platelets and hemorrhaging in heterozygotes
- loimmune thrombocytopenia
- pups and fetuses from homozygous females immunized two or four times with wild-type platelets, respectively, and mated with wild-type males exhibit hemorrhaging, reduced platelets and increased mortality, a phenotype similar to human fetal and neonatal alloimmune thrombocytopenia

mortality/aging

pregnancy-related premature death
- one of three homozygous females immunized four times with wild-type platelets and mated with a wild-type male, died during delivery after a 3-week pregnancy

reproductive system phenotype

abnormal miscarriage rate
- homozygous females immunized with wild-type platelets and mated with wild-type males, exhibit miscarriages due to internal organ bleeding of fetuses; females immunized 4 times show more miscarriages than females immunized 2 times with wild-type platelets

hematopoietic system phenotype

increased IgG level
- however, homozygous preimmunized females do not show any detectable anti-Itgb3 IgG after the first and second deliveries after mating with wild-type males; low levels of anti-Itgb3 antibodies are seen in the third and subsequent deliveries
- titer of maternal IgG against Itgb3 in homozygous females increases with the number of times females are immunized with wild-type platelets

immune system phenotype

increased IgG level
- however, homozygous preimmunized females do not show any detectable anti-Itgb3 IgG after the first and second deliveries after mating with wild-type males; low levels of anti-Itgb3 antibodies are seen in the third and subsequent deliveries
- titer of maternal IgG against Itgb3 in homozygous females increases with the number of times females are immunized with wild-type platelets

mammalian phenotype

immune system phenotype
- Normal - both T-helper 1 and T-helper 2 immune responses to platelet Itgb3 antigen exist in mutants

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

Genotype: Itgb3^tm1Hyn/Itgb3^tm1Hyn
involves: 129S2/SvPas

cardiovascular system phenotype

abnormal physiological neovascularization
- increase in vascularization in wounds after 7 days of healing

immune system phenotype

abnormal osteoclast morphology
- actin rings fail to form and actin is diffusely distributed, in a punctate pattern
- the ruffled membrane is thick with blunted projections

abnormal osteoclast physiology
- bone marrow macrophages differentiate into osteoclasts that fail to spread

decreased macrophage cell number
- number of macrophage in wounds is significantly lower than in wild-type wounds

increased osteoclast cell number
- about a 3 fold increase per mm trabecular bone surface

integument phenotype

decreased keratinocyte proliferation
- in the hyperproliferative epidermal region 3 days after wounding

cellular phenotype

decreased keratinocyte proliferation
- in the hyperproliferative epidermal region 3 days after wounding

skeleton phenotype

abnormal osteoclast morphology
- actin rings fail to form and actin is diffusely distributed, in a punctate pattern
- the ruffled membrane is thick with blunted projections

abnormal osteoclast physiology
- bone marrow macrophages differentiate into osteoclasts that fail to spread

increased compact bone thickness
- increased bone mass

increased osteoclast cell number
- about a 3 fold increase per mm trabecular bone surface

increased trabecular bone thickness
- decreased ability of bone marrow macrophage derived osteoclasts to excavate whale dentin and produce well defined resorption lacunae

osteosclerosis
- increased bone mass

hematopoietic system phenotype

abnormal osteoclast morphology
- actin rings fail to form and actin is diffusely distributed, in a punctate pattern
- the ruffled membrane is thick with blunted projections

abnormal osteoclast physiology
- bone marrow macrophages differentiate into osteoclasts that fail to spread

abnormal platelet physiology
- platelets release twofold more TGF

decreased macrophage cell number
- number of macrophage in wounds is significantly lower than in wild-type wounds

increased osteoclast cell number
- about a 3 fold increase per mm trabecular bone surface

homeostasis/metabolism phenotype

abnormal platelet physiology
- platelets release twofold more TGF

decreased circulating calcium level

enhanced wound healing
- dermal fibroblast recruitment in wounded tissue is significantly elevated with enhanced fibronectin and vitronectin deposition in granulation tissue
- re-epithelialization is accelerated significantly

increased transforming growth factor level
- platelets release twofold more TGF

References

Hodivala-Dilke KM; McHugh KP; Tsakiris DA; Rayburn H; Crowley D; Ullman-Cullere M; Ross FP; Coller BS; Teitelbaum S; Hynes RO. 1999. Beta3-integrin-deficient mice are a model for Glanzmann thrombasthenia showing placental defects and reduced survival. J Clin Invest 103(2):229-38PubMed: 9916135 MGI: J:52262

Additional - Itgb3^tm1Hyn related

Technical Support

Contact Technical Support

Genotyping Protocols
- Genotyping resources and troubleshooting
Breeding Considerations

When maintained as a live colony, homozygotes or heterozygotes may be bred.
- Additional Breeding and Husbandry Support
Citation
When using the 129S-Itgb3^tm1Hyn/J mouse strain in a publication, please cite the originating article(s) and include JAX stock #008700 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

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

Pricing & Availability

Cryo Recovery

Domestic
International

Live Mouse

Age

Genotype

Price

weeks

Cryorecovery - Pricing

Service	Genotype	Price
	Heterozygous for Itgb3<tm1Hyn>

We will fulfill your order by providing at least two carriers for each strain ordered. The total number, sex, and genotypes provided will vary, although typically 8 or more animals are provided. Please check genotypes which will be recovered. While the genotypes of all animals produced will be communicated to you prior to scheduling shipment, the genotypes of animals provided may not reflect the mating scheme and genotypes described in the strain description. Animals are typically ready to ship in 11-14 weeks. If a second recovery is required to produce the minimum number of animals, then delivery time would increase to approximately 25 weeks. If we fail to produce animals of the correct genotype, you will not be charged. We 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.

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.

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.

Terms Of Use

Terms of Use

General Terms and Conditions

Questions about Terms of Use

Additional Use Restrictions Apply

Use of MICE by companies or for-profit entities requires a license prior to shipping.

Licensing Information

Phone: 207-288-6470

Email: TechTran@jax.org

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"). "PRODUCT(S)" means biological materials supplied by JACKSON, and their derivatives. "SERVICES" means projects conducted by JACKSON for other parties that may include but are not limited to the use of MICE or PRODUCTS. "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 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, PRODUCTS or SERVICES 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.

Credit for PRODUCTS or SERVICES

In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of, PRODUCTS or SERVICES, JACKSON will, at its option, provide credit or replacement for the PRODUCT received or the SERVICES provided; JACKSON makes no other representations and this shall be the exclusive remedy of the purchaser. Please note specific policy for live mice.

Animal Care and Use for SERVICES

Consistent with the requirement for a written understanding regarding animal care and use, the JACKSON Animal Care and Use Committee will review the animal care and use protocol(s) associated with any SERVICES to be performed at JACKSON, and JACKSON shall have ultimate responsibility and authority for the care of animals while on site or in JACKSON custody.

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, PRODUCTS or SERVICES 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.

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Selected References

Itgb3tm1Hyn

Allele Symbol: Itgb3tm1Hyn

Disease Terms

Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).

Research Areas By Genotype

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

Genotype: Itgb3tm1Hyn related

Mammalian Phenotype Terms by Genotype

Genotype: Itgb3tm1Hyn/Itgb3tm1Hyninvolves: 129S2/SvPas * C57BL/6

cardiovascular system phenotype

cellular phenotype

digestive/alimentary phenotype

embryo phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

immune system phenotype

integument phenotype

liver/biliary system phenotype

mammalian phenotype

mortality/aging

muscle phenotype

neoplasm

renal/urinary system phenotype

reproductive system phenotype

vision/eye phenotype

Genotype: Itgb3tm1Hyn/Itgb3+involves: 129S2/SvPas * C57BL/6

cardiovascular system phenotype

muscle phenotype

homeostasis/metabolism phenotype

Genotype: Itgb3tm1Hyn/Itgb3tm1Hyninvolves: 129S2/SvPas * BALB/c

cellular phenotype

mortality/aging

reproductive system phenotype

hematopoietic system phenotype

immune system phenotype

mammalian phenotype

Genotype: Itgb3tm1Hyn/Itgb3tm1Hyninvolves: 129S2/SvPas

cardiovascular system phenotype

immune system phenotype

integument phenotype

cellular phenotype

skeleton phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

References

Additional - Itgb3tm1Hyn related

Genotyping Protocols

Breeding Considerations

Citation

Animal Health Reports

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

Live Mouse

Cryorecovery - Pricing

Payment Terms and Conditions

The Jackson Laboratory's Genotype Promise

Terms of Use

Additional Use Restrictions Apply

Licensing Information

JAX® Mice, Products & Services Conditions of Use

No Warranty

Credit for PRODUCTS or SERVICES

Animal Care and Use for SERVICES

No Liability

Itgb3^tm1Hyn

Allele Symbol: Itgb3^tm1Hyn

Genotype: Itgb3^tm1Hyn related

Genotype: Itgb3^tm1Hyn/Itgb3^tm1Hyn
involves: 129S2/SvPas * C57BL/6

Genotype: Itgb3^tm1Hyn/Itgb3⁺
involves: 129S2/SvPas * C57BL/6

Genotype: Itgb3^tm1Hyn/Itgb3^tm1Hyn
involves: 129S2/SvPas * BALB/c

Genotype: Itgb3^tm1Hyn/Itgb3^tm1Hyn
involves: 129S2/SvPas

Additional - Itgb3^tm1Hyn related