Search Criteria: Research Area is "Research Tools: Cre-lox System (Cre-Recombinase Expression: Inducible)"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 005623 | B6.129S-Shhtm2(cre/ESR1)Cjt/J | Repository- Live |
| This strain expresses a fusion product involving Cre recombinase and a mutant form of the human estrogen receptor ligand binding domain from the endogenous Shh locus. The mutant human estrogen receptor does not bind natural ligand at physiological concentrations but will bind the synthetic ligand, 4-hydroxytamoxifen. Restricted to the cytoplasm, the Cre/ESR1 protein can only gain access to the nuclear compartment after exposure to tamoxifen. Tamoxifen administration induces Cre recombinase expression in all cells that express the endogenous gene resulting in the deletion of the first 35 base pairs following the ATG. Homozygous mice are not viable or fertile. Heterozygous mutant mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain may be useful in studies of limb patterning and development. | ||
| 006230 | B6.Cg-Cebpatm1Dgt Tg(Mx1-cre)1Cgn/J | Repository- Live |
| Mice homozygous for this C/EBPalpha "floxed" allele (C/EBPalphaF) and hemizygous for the Mx1-cre transgene are viable and fertile, and exhibit no abnormalities in the hematopoietic system. In the absence of cre expression, the C/EBPalphaF allele functions similarly to the wildtype allele. Mx1-Cre transgene expression can be induced by administration of either interferon (alpha or beta) or synthetic double-stranded RNA (such as poly I:C), leading to deletion of the "floxed" gene. Following 3-4.5 weeks of poly I:C treatment, deletion efficiency is greater than 95% in hematopoietic tissues, and C/EBPalpha protein is undetectable in bone marrow. These poly I:C-treated, mice have defective myeloid cell development, increased hematopoietic stem cell repopulating activity, and a significantly increased myeloblast population in the bone marrow compartment. These mutant mice may be useful in studies of hematopoietic cell (e.g. myeloid and basophil progenitor cell) d
..... For more information please see the full descriiption on the strain data sheet | ||
| 004682 | B6.Cg-Tg(CAG-cre/Esr1)5Amc/J | Repository- Live |
| These transgenic mice have a tamoxifen-inducible cre-mediated recombination system driven by the chicken beta actin promoter/enhancer coupled with the cytomegalovirus (CMV) immediate-early enhancer. The transgene insert contains a fusion product involving Cre recombinase and a mutant form of the mouse estrogen receptor ligand binding domain. The mutant mouse estrogen receptor does not bind natural ligand at physiological concentrations but will bind the synthetic ligand, 4-hydroxytamoxifen. Restricted to the cytoplasm, the cre/Esr1 protein can only gain access to the nuclear compartment after exposure to tamoxifen. When crossed with a strain containing a loxP site flanked sequence of interest, the offspring are useful for generating tamoxifen-induced, Cre-mediated targeted deletions. Tamoxifen administration will also induce Cre recombination in developing embryos of treated mothers and in cultured cells derived from transgenic mice. Homozygous mice are not viable or fertile. Heterozyg
..... For more information please see the full descriiption on the strain data sheet | ||
| 003556 | B6.Cg-Tg(Mx1-cre)1Cgn/J | Repository- Live |
| The Cre recombinase is under the control of the Mx1 promoter. This promoter is silent in healthy mice, but can be induced to high levels of transcription by administration of interferon alpha, interferon beta, or synthetic double-stranded RNA (such as poly I:C). When combined with a mutant carrying a gene that has been flanked by loxP recognition sites, the expression of Cre recombinase causes the flanked gene to be removed. This provides researchers with the capability to induce the "knockout" at any time during development. There was ~1% background recombination seen in mice not treated with interferon. The percent deletion of the targeted gene varied depending on tissue type, presumably due to the amount of interferon-responsive cells present or to the availability of interferon in each organ.
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
..... | ||
| 005657 | B6.Cg-Tg(Myh6-cre/Esr1)1Jmk/J | Repository- Live |
| Mice that are homozygous for this "MerCreMer" double fusion protein are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Cre expression in heart tissue is confirmed by western blot. Southern blot confirmed heart cell specificity compared to brain, kidney, lung, liver, and skeletal muscle. Insertion of this transgene and its protein show no changes in echocardiography, heart mass or pathology, or hypertrophy marker genes compared to nontransgenic littermates. Of note, this double fusion protein has substantially greater Cre recombinase activity with less promiscuity compared with a single CreMer fusion protein. As the cre is flanked on each end with a mutated murine estrogen receptor ligand binding domain (amino acids 281-599, G525R); Cre expression is tamoxifen inducible yet estrogen insensitive. Inducible expression of cre in cardiac cells makes this strain suitable for creating bitransgenic mice for use in studies of te
..... For more information please see the full descriiption on the strain data sheet | ||
| 005975 | B6.Cg-Tg(Plp1-cre/ESR1)3.16Pop/J | Repository- Live |
| These transgenic mice have a tamoxifen inducible Cre-mediated recombination system driven by the mouse Plp1, proteolipid protein (myelin) 1 promoter. The transgene insert contains a fusion product involving Cre recombinase and a mutant form of the mouse estrogen receptor ligand binding domain. The mutant mouse estrogen receptor does not bind natural ligand at physiological concentrations but will bind the synthetic ligand, 4-hydroxytamoxifen. Restricted to the cytoplasm, the Cre/Esr1 protein can only gain access to the nuclear compartment after exposure to tamoxifen. When crossed with a strain containing a loxP site flanked sequence of interest, the offspring are useful for generating tamoxifen-induced, Cre-mediated targeted deletions. Tamoxifen administration allows for ablation of predetermined genes in oligodendrocytes and Schwann cells, and will also induce Cre recombination in developing embryos of treated mothers and in cultured cells derived from transgenic mice. M
..... For more information please see the full descriiption on the strain data sheet | ||
| 006361 | B6.Cg-Tg(Sp7-tTA,tetO-EGFP/cre)1Amc/J | Repository- Live |
| Mice hemizygous for this Osx1-GFP::Cre transgene are viable and fertile.
The transgene carries both tTA under the regulation of the osterix (Sp7) promoter and, just downstream, a tetracycline responsive element (TRE; tetO)-controlled GFP/Cre fusion protein. In the absence of the tetracycline analog doxycycline, EGFP-Cre fusion protein expression is restricted to the osteoblast lineage throughout embryonic and early postnatal development. Fusion protein activity is largely absent from chondrocytes. When these transgenic animals are mated to transgenic strains that carry loxP-flanked (floxed) conditional alleles, Cre-mediated recombination of the floxed allele in the double mutant animals is placed under the regulation of doxycycline (dox) such that dox adminstration prevents fusion protein expression and recombination. The donating investigator suggests that the mice be maintained on dox-treated water to avoid incidental effects of tTA expression. These Osx1-GFP::Cre mut
..... For more information please see the full descriiption on the strain data sheet | ||
| 007606 | B6.Cg-Tg(Thy1-cre/ESR1,-EYFP)AGfng/J | Repository- Live |
| These transgenic mice ("SLICK" for single-neuron labeling with inducible Cre-mediated knock-out) have a tamoxifen inducible Cre-mediated recombination system and Enhanced Yellow Fluorescent Protein driven by 2 bidirectional copies of the mouse thymus cell antigen 1 promoter. Hemizygotes are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The Donating Investigator has not attempted to make the strain homozygous. When crossed with a strain containing a loxP site flanked sequence of interest, the offspring are useful for generating tamoxifen-induced, Cre-mediated targeted neuron-specific deletions only in neurons where the Thy1 promoter is active. These cells will be evident by the expression of Yellow Fluorescent Protein. Transgenic mice express YFP constitutively in neurons. The Donating Investigator reports that founder line A mice express the transgene in small subsets of motor neurons and dorsal root ganglion neurons.
..... For more information please see the full descriiption on the strain data sheet | ||
| 008085 | B6.Cg-Tg(UBC-cre/ESR1)1Ejb/J | Repository- Live |
| Mice hemizygous for this Cre-ERT2 transgene are viable and fertile. Mice from this founder line have strong tamoxifen-inducible cre activity in all reported tissue types. The Cre-ERT2 fusion protein consists of Cre recombinase fused to a triple mutant form of the human estrogen receptor; which does not bind its natural ligand (17β-estradiol) at physiological concentrations but will bind the synthetic estrogen receptor ligands 4-hydroxytamoxifen (OHT) and, with lesser sensitivity, ICI 182780. Restricted to the cytoplasm, Cre-ERT2 can only gain access to the nuclear compartment after exposure to OHT. To counteract the mixed estrogen agonist effects of tamoxifen injections, which can result in late fetal abortions in pregnant mice, progesterone may be coadministered. When these Cre-ERT2 mice are bred with mice containing a loxP-flanked sequence of interest, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the flanked sequences in widespread cel
..... For more information please see the full descriiption on the strain data sheet | ||
| 006234 | B6.Cg-Tg(tetO-cre)1Jaw/J | Repository- Live |
| Hemizygous transgenic mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express Cre recombinase under the control of a tetracycline-responsive promoter element (TRE; tetO). When hemizygotes are bred with another transgenic mouse expressing either reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA) under the control of tissue-specific promoters, Cre recombinase expression and Cre-mediated recombination in the appropriate tissues of the bitransgenic offspring can be regulated with the tetracycline analog, doxycycline. This strain represents an effective tool for generating inducible tissue specific-targeted mutants to study cell lineage during development.
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 fi
..... | ||
| 005650 | B6129-Tg(Myh6-cre/Esr1)1Jmk/J | Repository- Live |
| Mice that are homozygous for the transgene are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Cre expression in heart tissue is confirmed by western blot. Southern blot confirmed heart cell specificity compared to brain, kidney, lung, liver, and skeletal muscle. Insertion of this transgene and its protein show no changes in echocardiography, heart mass or pathology, or hypertrophy marker genes compared to nontransgenic littermates. Of note, this double fusion protein has substantially greater Cre recombinase activity with less promiscuity compared with a single CreMer fusion protein. Inducible expression of cre in cardiac cells makes this strain suitable for creating bitransgenic mice for use in studies of temporally regulated deletion of loxP-flanked targeted genes. | ||
| 004847 | B6;129-Gt(ROSA)26Sortm1(cre/Esr1)Nat/J | Repository- Live |
| These R26CreER mutant mice have a tamoxifen-inducible Cre-mediated recombination system driven by the endogenous mouse Gt(ROSA)26Sor promoter. The mutant allele consists of a fusion product involving Cre recombinase and an altered version of the mouse estrogen receptor ligand binding domain. The mutant ligand binding domain does not bind natural ligand at physiological concentrations but will bind the synthetic ligand, 4-hydroxytamoxifen. Restricted to the cytoplasm, the CRE/ESR1 protein can only gain access to the nuclear compartment to mediate recombination after exposure to tamoxifen. Tamoxifen administration will also induce Cre recombination in the developing embryos of treated mothers. When crossed with a strain containing a loxP site-flanked sequence of interest, this mutant is useful for generating tamoxifen-induced, Cre-mediated targeted deletions. Homozygous mutant mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnor
..... For more information please see the full descriiption on the strain data sheet | ||
| 007001 | B6;129S-Tg(UBC-cre/ESR1)1Ejb/J | Repository- Live |
| Mice hemizygous for this Cre-ERT2 transgene are viable and fertile. Mice from this founder line have strong tamoxifen-inducible cre activity in all reported tissue types. The Cre-ERT2 fusion protein consists of Cre recombinase fused to a triple mutant form of the human estrogen receptor; which does not bind its natural ligand (17β-estradiol) at physiological concentrations but will bind the synthetic estrogen receptor ligands 4-hydroxytamoxifen (OHT) and, with lesser sensitivity, ICI 182780. Restricted to the cytoplasm, Cre-ERT2 can only gain access to the nuclear compartment after exposure to OHT. To counteract the mixed estrogen agonist effects of tamoxifen injections, which can result in late fetal abortions in pregnant mice, progesterone may be coadministered. When these Cre-ERT2 mice are bred with mice containing a loxP-flanked sequence of interest, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the flanked sequences in widespread cel
..... For more information please see the full descriiption on the strain data sheet | ||
| 005249 | B6;SJL-Tg(Krt1-15-cre/PGR)22Cot/J | Repository- Live |
| Mice hemizygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice have a synthetic steroid RU 486 inducible Cre-mediated recombination system driven by the mouse keratin complex 1, acidic, gene 15 promoter. The transgene insert contains a fusion product involving Cre recombinase and a mutant form of the human progesterone receptor. The mutant human progesterone receptor does not bind natural ligand at physiological concentrations but will bind the synthetic ligand, RU 486. Restricted to the cytoplasm, the Cre/PGR protein can only gain access to the nuclear compartment after exposure to RU 486. When crossed with a strain containing a loxP site flanked sequence of interest, the offspring are useful for generating RU 486-induced, Cre-mediated targeted deletions. This strain represents an effective tool for generating tissue-specific targeted mutants that would be useful to study epi
..... For more information please see the full descriiption on the strain data sheet | ||
| 007610 | B6;SJL-Tg(Thy1-cre/ESR1,-EYFP)VGfng/J | Repository- Live |
| These transgenic mice ("SLICK" for single-neuron labeling with inducible Cre-mediated knock-out) have a tamoxifen inducible Cre-mediated recombination system and Enhanced Yellow Fluorescent Protein driven by 2 bidirectional copies of the mouse thymus cell antigen 1 promoter. Hemizygotes are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The Donating Investigator has not attempted to make the strain homozygous. When crossed with a strain containing a loxP site flanked sequence of interest, the offspring are useful for generating tamoxifen-induced, Cre-mediated targeted neuron-specific deletions only in neurons where the Thy1 is active. These cells will be evident by the expression of Yellow Fluorescent Protein. Transgenic mice express YFP constitutively in neurons. The Donating Investigator reports that founder line V mice express the transgene sparsely in neurons of the central nervous system.
This strain is one of
..... | ||
| 006244 | C.Cg-Tg(tetO-cre)1Jaw/J | Repository- Live |
| Hemizygous transgenic mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express Cre recombinase under the control of a tetracycline-responsive promoter element (TRE; tetO). When hemizygotes are bred with another transgenic mouse expressing either reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA) under the control of tissue-specific promoters, Cre recombinase expression and Cre-mediated recombination in the appropriate tissues of the bitransgenic offspring can be regulated with the tetracycline analog, doxycycline. This strain represents an effective tool for generating inducible tissue specific-targeted mutants to study cell lineage during development.
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 wa
..... | ||
| 006774 | FVB-Tg(Col2a1-cre/ESR1)KA3Smac/J | Repository- Live |
| Mice hemizygous or homozygous for the Col2CreERT transgene are viable and fertile. Mice from this founder line (line K from founder mouse A3) have strong tamoxifen-inducible cre expression directed to cells of the chondrogenic lineage (cartilage), with minimal (<0.1%) cre activity in the absence of tamoxifen. The CreERT protein consists of Cre recombinase fused to a mutant form of the human estrogen receptor; which does not bind its natural ligand (17β-estradiol) at physiological concentrations but will bind the synthetic estrogen receptor ligand 4-hydroxytamoxifen. Restricted to the cytoplasm, CreERT can only gain access to the nuclear compartment after exposure to tamoxifen. To counteract the mixed estrogen agonist effects of tamoxifen injections, which can result in late fetal abortions in pregnant mice, progesterone may be coadministered. When these Col2CreERT mice are bred with mice containing a loxP-flanked seq
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..... For more information please see the full descriiption on the strain data sheet | ||
| 008244 | FVB.Cg-Tg(tetO-cre)1Jaw/J | Repository- Live |
| Hemizygous transgenic mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express Cre recombinase under the control of a tetracycline-responsive promoter element (TRE; tetO). When hemizygotes are bred with another transgenic mouse expressing either reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA) under the control of tissue-specific promoters, Cre recombinase expression and Cre-mediated recombination in the appropriate tissues of the bitransgenic offspring, can be regulated with the tetracycline analog, doxycycline. This strain represents an effective tool for generating inducible, tissue-specific-targeted mutants to study cell lineage during development. Importation of this model was supported by the Boomer Esiason Foundation. | ||
| 007913 | STOCK Gli1tm3(cre/ESR1)Alj/J | Repository- Live |
| Mice homozygous for this Gli1-CreERT2 targeted allele are viable and fertile (although homozygous males are reported to have breeding problems). Under control of the endogenous upstream promoter/enhancer elements, tamoxifen-inducible cre activity is observed in cells that have received positive Hedgehog/Sonic Hedgehog signaling. The Cre-ERT2 fusion protein consists of Cre recombinase fused to a triple mutant form of the human estrogen receptor which does not bind its natural ligand (17β-estradiol) at physiological concentrations but will bind the synthetic estrogen receptor ligands 4-hydroxytamoxifen and, with lesser sensitivity, ICI 182780. Restricted to the cytoplasm, Cre-ERT2 can only gain access to the nuclear compartment after exposure to tamoxifen. To counteract the mixed estrogen agonist effects of tamoxifen injections, which can result in late fetal abortions in pregnant mice, progesterone may be coadministered. When these Gli1-CreERT2 mice are
..... For more information please see the full descriiption on the strain data sheet | ||
| 007684 | STOCK Tg(Atoh1-cre/ESR1)14Fsh/J | Repository- Live |
| Mice hemizygous for this Math1-CreERT2 transgene are viable and fertile. Under control of the Math1 (Atoh1) enhancer, tamoxifen-inducible cre activity is observed in neural progenitors of the cerebellar rhombic lip, dorsal hindbrain and spinal cord, as well as in inner-ear primordia (with a limited amount of ectopic expression in the primordium of the hippocampus but not the cortex). The Cre-ERT2 fusion protein consists of Cre recombinase fused to a triple mutant form of the human estrogen receptor; which does not bind its natural ligand (17β-estradiol) at physiological concentrations but will bind the synthetic estrogen receptor ligands 4-hydroxytamoxifen and, with lesser sensitivity, ICI 182780. Restricted to the cytoplasm, Cre-ERT2 can only gain access to the nuclear compartment after exposure to tamoxifen. To counteract the mixed estrogen agonist effects of tamoxifen injections, which can result in late fetal abortions in pregnant mice, progesterone ma
..... For more information please see the full descriiption on the strain data sheet | ||
| 008122 | STOCK Tg(Ins2-cre/Esr1)1Dam/J | Repository- Live |
| These RIP-CreER transgenic mice have a tamoxifen inducible Cre-mediated recombination system driven by the rat insulin 2, Ins2, promoter. The transgene insert contains a fusion product involving Cre recombinase and a mutant form of the mouse estrogen receptor ligand binding domain. The mutant mouse estrogen receptor does not bind natural ligand at physiological concentrations but will bind the synthetic ligand, 4-hydroxytamoxifen. Restricted to the cytoplasm, the Cre/Esr1 protein can only gain access to the nuclear compartment after exposure to tamoxifen. When crossed with a strain containing a loxP site flanked sequence of interest, the offspring are useful for generating tamoxifen-induced, Cre-mediated targeted deletions. Tamoxifen administration induces Cre recombination in islet cells of the pancreas. Hemizygous mutant mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The Donating Investigator has not attempted
..... For more information please see the full descriiption on the strain data sheet | ||
| 005107 | STOCK Tg(KRT14-cre/Esr1)20Efu/J | Repository- Live |
| These transgenic mice have a tamoxifen inducible Cre-mediated recombination system driven by the human keratin 14 (KRT14) promoter. The transgene insert contains a fusion product involving Cre recombinase and a mutant form of the mouse estrogen receptor ligand binding domain. The mutant mouse estrogen receptor does not bind natural ligand at physiological concentrations but will bind the synthetic ligand, 4-hydroxytamoxifen (tamoxifen). Restricted to the cytoplasm, the cre/Esr1 protein can only gain access to the nuclear compartment after exposure to tamoxifen. When crossed with a strain containing a loxP site flanked sequence of interest, the offspring are useful for generating tamoxifen-induced, Cre-mediated targeted keratinocyte-specific deletions. Oral tamoxifen administration induces Cre recombination in toe, back skin and tongue. Topically administered tamoxifen induces Cre-mediated recombination in a specific localized area of the skin, occuring in 50 to 60% of the
..... For more information please see the full descriiption on the strain data sheet | ||
| 008119 | STOCK Tg(Neurog3-cre/Esr1)1Dam/J | Repository- Live |
| These transgenic mice have a tamoxifen inducible Cre-mediated recombination system driven by the mouse neurogenin 3, Neurog3, promoter. The transgene insert contains a fusion product involving Cre recombinase and a mutant form of the mouse estrogen receptor ligand binding domain. The mutant mouse estrogen receptor does not bind natural ligand at physiological concentrations but will bind the synthetic ligand, 4-hydroxytamoxifen. Restricted to the cytoplasm, the Cre/Esr1 protein can only gain access to the nuclear compartment after exposure to tamoxifen. When crossed with a strain containing a loxP site flanked sequence of interest, the offspring are useful for generating tamoxifen-induced, Cre-mediated targeted deletions. Tamoxifen administration induces Cre recombination in islet cells of the pancreas, undifferentiated spermatogonia and other Neurog3 expressing cells. Transgene expression closely patterns endogenous gene expression as analyzed by in situ hybridiza
..... For more information please see the full descriiption on the strain data sheet | ||
| 006224 | STOCK Tg(tetO-cre)1Jaw/J | Repository- Live |
| Hemizygous transgenic mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express Cre recombinase under the control of a tetracycline-responsive promoter element (TRE; tetO). When hemizygotes are bred with another transgenic mouse expressing either reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA) under the control of tissue-specific promoters, Cre recombinase expression and Cre-mediated recombination in the appropriate tissues of the bitransgenic offspring, can be regulated with the tetracycline analog, doxycycline. This strain represents an effective tool for generating inducible, tissue-specific-targeted mutants to study cell lineage during development. Importation of this model was supported by the Boomer Esiason Foundation. | ||
| 005673 | C.Cg-Tg(Mx1-cre)1Cgn/J | Repository-Cryopreserved |
| The Cre recombinase is under the control of the Mx1 promoter. This promoter is silent in healthy mice, but can be induced to high levels of transcription by administration of interferon alpha, interferon beta, or synthetic double-stranded RNA (such as poly I:C). When combined with a mutant carrying a gene that has been flanked by loxP recognition sites, the expression of Cre recombinase causes the flanked gene to be removed. This provides researchers with the capability to induce the "knockout" at any time during development. There is ~1% background recombination seen in mice not treated with interferon. The percent deletion of the targeted gene varies depending on tissue type, presumably due to the amount of interferon-responsive cells present or to the availability of interferon in each organ.
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 a
..... | ||
| 003855 | NOD/ShiLt-Tg(Ins2-cre)5Lt/LtJ | Repository-Cryopreserved |
| This strain expresses Cre recombinase under the control of the rat insulin II promoter. Hemizygous mice carrying this transgene are phenotypically normal and overexpresss cre specifically in pancreatic beta cells. Homozygous transgenic mice experience delayed onset diabetes compared to wildtype controls. This transgenic strain is used in combination with mice carrying floxed targeted mutations to create various pancreatic beta cell-specific gene knockouts using the Cre/loxP system. | ||
| 004192 | STOCK Mttptm2Sgy Ldlrtm1Her Apobtm2Sgy Tg(Mx1-cre)1Cgn/J | Repository-Cryopreserved |
| These mice are homozygous for four different induced mutations. The cumulative result of these mutations is a mouse model in which hypercholesterolemia can be reversed. By themselves, the combined presence of the Ldlrtm1Sgy and Apobtm1Sgy targeted alleles results in mice with a high susceptibility to atherosclerosis and total plasma cholesterol levels of approximately 300 mg/dl. A functional microsomal triglyceride transfer protein gene (Mttp) is essential for establishing a hypercholesterolemic condition. By flanking the Mttp gene with loxP sites and including a Mx1-Cre transgene, it is possible to reduce total plasma cholesterol levels from 300 mg/dl to 30 mg/dl upon induction of the Cre recombinase by administering interferon alpha, interferon beta, or synthetic double-stranded RNA. This unique model is useful in research related to the mechanisms and events of atherosclerotic reversal. Mice homozygous for the targeted
..... For more information please see the full descriiption on the strain data sheet | ||
| 004453 | STOCK Tg(CAG-cre/Esr1)5Amc/J | Repository-Cryopreserved |
| These transgenic mice have a tamoxifen-inducible cre-mediated recombination system driven by the chicken beta actin promoter/enhancer coupled with the cytomegalovirus (CMV) immediate-early enhancer. The transgene insert contains a fusion product involving Cre recombinase and a mutant form of the mouse estrogen receptor ligand binding domain. The mutant mouse estrogen receptor does not bind natural ligand at physiological concentrations but will bind the synthetic ligand, 4-hydroxytamoxifen. Restricted to the cytoplasm, the Cre/ESR1 protein can only gain access to the nuclear compartment after exposure to tamoxifen. When crossed with a strain containing a loxP site flanked sequence of interest, the offspring are useful for generating tamoxifen-induced, Cre-mediated targeted deletions. Tamoxifen administration will also induce Cre recombination in developing embryos of treated mothers and in cultured cells derived from transgenic mice. Homozygous mice are not viable or fertile. He
..... For more information please see the full descriiption on the strain data sheet | ||
| 002527 | STOCK Tg(Mx1-cre)1Cgn/J | Repository-Cryopreserved |
| The Cre recombinase is under the control of the Mx1 promoter. This promoter is silent in healthy mice, but can be induced to high levels of transcription by administration of interferon alpha, interferon beta, or synthetic double-stranded RNA. When combined with a mutant carrying a gene that has been flanked by loxP recognition sites, the expression of Cre recombinase causes the flanked gene to be removed. This provides researchers with the capability to induce the "knockout" at any time during development. There was ~1% background recombination seen in mice not treated with interferon. The percent deletion of the targeted gene varied depending on tissue type, presumably due to the amount of interferon-responsive cells present or to the availability of interferon in each organ. | ||
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