B6.Cg-Hprt1tm1(Cd68-BCL2)Ple/Orl
Status | Available to order |
EMMA ID | EM:04748 |
Citation information | RRID:IMSR_EM:04748 Research Resource Identifiers (RRID) are persistent unique ID numbers assigned to help researchers cite key resources (e.g. antibodies, model organisms and software projects) in the biomedical literature to improve transparency and reproducibility in research. See https://www.rrids.org/ for more information. |
International strain name | B6.Cg-Hprt1tm1(Cd68-BCL2)Ple/Orl |
Alternative name | Tg CD68 hBcl2 |
Strain type | Targeted Mutant Strains : Knock-in |
Allele/Transgene symbol | Hprt1tm1(Cd68-BCL2)Ple |
Gene/Transgene symbol | Hprt1 |
Information from provider
Provider | philippe Lesnik |
Provider affiliation | INSERM Unit 939, Hôpital de la Pitié-Salpêtrière |
Genetic information | Using homologous recombination in embryonic stem (ES) cells, a transgene made of the anti-apoptotic protein hBcl2 under the macrophage-specific promoter Cd68 was inserted at a defined site in the mouse genome as described previously (Farhadi et al.). Site-specific and single-copy integration of the transgene was achieved at the hypoxanthine phosphoribosyl transferase (Hprt1) locus on the X chromosome. |
Phenotypic information | Macrophages with enhanced longevity and resistance to apoptosis. Immune system is functional. |
Breeding history | The transgene was introduced by electroporation into BPES ES cells (hybrid C57BL/6 x 129). Targeted ES cells were injected into blastocysts, implanted into pseudopregnant females and chimeric mice generated. These chimeras transmitted the transgene through their germ line, and a number of mice bearing the transgene were obtained. Then, the transgenic mice were backcrossed 6 times to C57BL/6 genetic background. Currently continuing the backcross to C57BL/6. |
References |
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Homozygous fertile | not known |
Homozygous viable | not known |
Homozygous matings required | no |
Immunocompromised | no |
Information from EMMA
Archiving centre | Institut de Transgenose, INTRAGENE, Orléans, France |
Animals used for archiving | heterozygous C57BL/6J males |
Disease and phenotype information
IMPC phenotypes (gene matching)
MGI phenotypes (gene matching)
- decreased hematocrit / MGI
- increased leukocyte cell number / MGI
- increased neutrophil cell number / MGI
- abnormal small intestine morphology / MGI
- abnormal liver morphology / MGI
- abnormal branching of the mammary ductal tree / MGI
- enlarged spleen / MGI
- spleen hyperplasia / MGI
- enlarged lymph nodes / MGI
- tremors / MGI
- convulsive seizures / MGI
- abnormal lung morphology / MGI
- decreased body weight / MGI
- decreased anxiety-related response / MGI
- ataxia / MGI
- hypoactivity / MGI
- impaired coordination / MGI
- abnormal gait / MGI
- short stride length / MGI
- decreased exploration in new environment / MGI
- limb grasping / MGI
- abnormal motor coordination/balance / MGI
- abnormal hematopoietic system physiology / MGI
- hyperglycemia / MGI
- anemia / MGI
- cardiac hypertrophy / MGI
- increased mammary adenocarcinoma incidence / MGI
- abnormal reflex / MGI
- seizures / MGI
- abnormal motor capabilities/coordination/movement / MGI
- premature death / MGI
- abnormal definitive hematopoiesis / MGI
- abnormal brain morphology / MGI
- no abnormal phenotype detected / MGI
- neurodegeneration / MGI
- abnormal spleen white pulp morphology / MGI
- abnormal hematopoietic system morphology/development / MGI
- abnormal megakaryocyte progenitor cell morphology / MGI
- hepatic steatosis / MGI
- decreased vertical activity / MGI
- increased heart weight / MGI
- increased systemic arterial blood pressure / MGI
- albuminuria / MGI
- decreased erythrocyte cell number / MGI
- increased urine protein level / MGI
- impaired social transmission of food preference / MGI
- no phenotypic analysis / MGI
- phenotypic reversion / MGI
- abnormal dopaminergic neuron morphology / MGI
- astrocytosis / MGI
- abnormal depression-related behavior / MGI
- decreased tumor growth/size / MGI
- abnormal nervous system morphology / MGI
- abnormal cardiac muscle relaxation / MGI
- neuronal intranuclear inclusions / MGI
- abnormal myocardial fiber physiology / MGI
- abnormal Paneth cell morphology / MGI
- decreased B cell number / MGI
- decreased cardiac muscle contractility / MGI
- glomerulosclerosis / MGI
- abnormal podocyte morphology / MGI
- muscle phenotype / MGI
- homeostasis/metabolism phenotype / MGI
- endocrine/exocrine gland phenotype / MGI
- behavior/neurological phenotype / MGI
- immune system phenotype / MGI
- taste/olfaction phenotype / MGI
- hematopoietic system phenotype / MGI
- jerky movement / MGI
- thrombocytosis / MGI
- decreased ventricle muscle contractility / MGI
- decreased mean corpuscular hemoglobin concentration / MGI
- decreased dopamine level / MGI
- abnormal podocyte slit diaphragm morphology / MGI
- absent podocyte slit diaphragm / MGI
- podocyte foot process effacement / MGI
- increased megakaryocyte cell number / MGI
- abnormal spatial reference memory / MGI
- abnormal spatial working memory / MGI
- abnormal splenic cell ratio / MGI
- abnormal physiological response to xenobiotic / MGI
- abnormal enterocyte proliferation / MGI
- abnormal enterocyte apoptosis / MGI
- abnormal neuron differentiation / MGI
- increased mammary gland tumor incidence / MGI
- myeloid hyperplasia / MGI
- expanded mesangial matrix / MGI
- mesangial cell hyperplasia / MGI
- abnormal habituation to a new environment / MGI
- abnormal ceramide level / MGI
- decreased brain choline acetyltransferase activity / MGI
- decreased brain tyrosine 3-monooxygenase activity / MGI
- decreased vascular endothelial cell proliferation / MGI
Literature references
- Macrophage apoptosis exerts divergent effects on atherogenesis as a function of lesion stage.;Gautier Emmanuel L, Huby Thierry, Witztum Joseph L, Ouzilleau Betty, Miller Elizabeth R, Saint-Charles Flora, Aucouturier Pierre, Chapman M John, Lesnik Philippe, ;2009;Circulation;119;1795-804; 19307478
- A combinatorial network of evolutionarily conserved myelin basic protein regulatory sequences confers distinct glial-specific phenotypes.;Farhadi Hooman F, Lepage Pierre, Forghani Reza, Friedman Hana C H, Orfali Wayel, Jasmin Luc, Miller Webb, Hudson Thomas J, Peterson Alan C, ;2003;The Journal of neuroscience : the official journal of the Society for Neuroscience;23;10214-23; 14614079
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