Search Criteria: Research Area is "Developmental Biology Research: Internal/Organ Defects (heart: vasculature)"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 008444 | 129S4.129S2(B6)-Fn1tm1Hyn/J | Repository-Cryopreserved |
| Mice homozygous for the Fn1tm1Hyn targeted mutation die during early embryonic development. Blastocyst development and implantation of homozygotes is normal. Gastrulation is initiated and appears normal, including extensive mesodermal movement. From embryonic day eight onwards homozygous mutant embryos deteriorate through the 10th and 11th days of gestation. Homozygous mutant embryos have a shortened anterior-posterior axes, fail to develop a notochord, somites, or central heart (on the 129S4/SvJae genetic background). Heterozygous mice are viable for at least two years and appear healthy and approximately the same size as wild-type littermates. Plasma levels of fibronectin in heterozygotes are 50% lower than normal wild-type siblings. 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 st
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| 008445 | B6.129S-Fn1tm1Hyn/2J | Repository-Cryopreserved |
| These mice carry a targeted mutation in the fibronectin 1 gene identical to that found in Stock No. 002270.
This line, backcrossed more than 13 times to C57BL/6J in the donating investigator's colony, has been used in a search for cardiac development modifier genes demonstrating phenotypic differences on C57BL/6J and 129S4/SvJae genetic backgrounds (Astrof, 2007). In the majority of 129S4 background homozygous targeted mutant embryos, heart progenitors remain at their anterior bilateral positions and fail to fuse at the midline to form a heart tube. However, on the C57BL/6J genetic background, cardiac development progresses further and results in a centrally-positioned looped heart. Linkage analysis led to the identification of a 1-Mbp interval on mouse Chromosome 4 containing 21 genes, including five that are differentially expressed between C57BL/6J and 129S4/SvJae. This strain may be helpful in studies of
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| 002270 | B6.129S-Fn1tm1Hyn/J | Repository-Cryopreserved |
| Mice homozygous for the Fn1tm1Hyn targeted mutation die during early embryonic development. Blastocyst development and implantation of homozygotes is normal. Gastrulation is initiated and appears normal, including extensive mesodermal movement. From embryonic day 8 onwards homozygous mutant embryos deteriorate through the 10th and 11th days of gestation. Homozygous mutant embryos have a shortened anterior-posterior axes, fail to develop a notochord or somites, and have abnormal development of the heart, blood vessels, and yolk sac indicating a general deficiency in mesodermally derived tissues. Heterozygous mice are viable for at least 2 years and appear healthy and approximately the same size as wild-type littermates. Plasma levels of fibronectin in heterozygotes are 50% lower than normal wildtype siblings. | ||
| 006039 | B6.129S7-Efnb2tm1And/J | Repository-Cryopreserved |
| Mice homozygous for this targeted mutation show growth retardation and enlargement of the heart at embryonic day 10 (E10), with 100% lethality occurring around E11. Reporter protein expression patterns are consistent with arterial, but not venous, expression of the endogenous gene; prominent lacZ signal is observed in hindbrain and somites, with lower levels in aorta and heart as early as E8.25. Expression in the yolk sac was first detected at E8.5, and is also observed in nephrogenic mesoderm and branchial arches. Homozygous embryos show defective angiogenic remodeling at the capillary plexus stage in both yolk sac and head. Endothelial vessel support cell differentiation of the yolk sac is also defective. Homozygotes lack myocardial trabecular extensions, and capillary ingrowth into the neural tube does not occur. Heterozygous mice are viable, fertile, exhibit no behavioral defects, and have identical lacZ expression patterns. These mutant mice may be useful in studying
..... For more information please see the full descriiption on the strain data sheet | ||
| 006042 | B6.129S7-Efnb2tm2And/J | Repository-Cryopreserved |
| Mice that are homozygous for this floxed allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When bred to mice with a cre recombinase gene under the control of a promoter of interest, exon 1 of the targeted gene is deleted in the tissue of interest. These mutant mice may be useful in studying the cellular and molecular mechanisms underlying vasculogenesis and angiogenesis, the topography of neovascularization, and adult neovascularization, including tumor angiogenesis. To test the effectiveness of this model, these mutant mice were bred to an endothelial-specific Cre-expressing transgenic mice, Tg(Tek-cre)12Flv (Stock No. 004128) . Offspring homozygous for the Cre-mediated exon 1 deletion show angiogenic remodeling defects and embryonic death identical to homozygous Efnb2tm1And mice (see Stock No. For more information please see the full descriiption on the strain data sheet | ||
| 006044 | B6;129S7-Ephb4tm1And/J | Repository-Cryopreserved |
| Mice homozygous for this targeted mutation show growth retardation and lack of blood flow by embryonic day 9.5-10 (E9.5-10), with lethality occurring around this time. Expression of lacZ occurs exclusively in embryonic vascular endothelial cells and is preferentially expressed on veins. Homozygous embryos show defective angiogenic remodeling at the capillary plexus stage in both yolk sac and head. Arrested cardiac morphogenesis and defective myocardial trabecular extensions are also observed. Heterozygous mice are viable, fertile, exhibit no behavioral defects, and have identical lacZ expression patterns. These mutant mice may be useful in studying the cellular and molecular mechanisms underlying vasculogenesis and angiogenesis, the topography of neovascularization, and adult neovascularization, including tumor angiogenesis. The developmental abnormalities in homozygous mice closely resemble those observed for mutant mice bearing a lacZ-expressing null mutation
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| 000773 | B6;129T-Dnahc11iv/J | Repository-Cryopreserved |
| DNAHC11 is important for developmental control of organ positioning in the left-right axis such that homozygosity for the situs inversus viscerum (iv) mutant allele can result not only in inverse placement of the visceral and thoracic organs, but also in anomalous positioning and interactions of blood vessels (including the hepatic portal, inferior vena cava, and azygos vein) and modified shape of organs and blood vessels, including abnormal lobation of lungs or liver. Approximately 50% of mice homozygous for Dnahc11iv have situs inversus, and the likelihood of situs inversus is not impacted by whether the homozygous parent has situs inversus. This indicates that wild type Dnahc11 instructs left-right asymmetry, and in the absence of functional Dnahc11 the direction of this asymmetry is random. Heterotaxia is found in less than half of homozygotes and occurs equally in those that do and do not have situs inversus. W
..... For more information please see the full descriiption on the strain data sheet | ||
| 008443 | D2.129S2(Cg)-Fn1tm1Hyn/J | Repository-Cryopreserved |
| Mice homozygous for the Fn1tm1Hyn targeted mutation die during early embryonic development. Blastocyst development and implantation of homozygotes is normal. Gastrulation is initiated and appears normal, including extensive mesodermal movement. From embryonic day 8 onwards homozygous mutant embryos deteriorate through the 10th and 11th days of gestation. Homozygous mutant embryos have a shortened anterior-posterior axes, fail to develop a notochord or somites, and have abnormal development of the heart, blood vessels, and yolk sac indicating a general deficiency in mesodermally derived tissues. Heterozygous mice are viable for at least 2 years and appear healthy and approximately the same size as wild-type littermates. Plasma levels of fibronectin in heterozygotes are 50% lower than normal wild-type siblings. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from t
..... | ||
| 006768 | D2.Cg-Tg(Myh6-Zfpm2)1Sho/EiJ | Repository-Cryopreserved |
| 001045 | SI/Col Tyrp1b Dnahc11iv/J | Repository-Cryopreserved |
| DNAHC11 is important for developmental control of organ positioning in the left-right axis such that homozygosity for the situs inversus viscerum (iv) mutant allele can result not only in inverse placement of the visceral and thoracic organs, but also in anomalous positioning and interactions of blood vessels (including the hepatic portal, inferior vena cava, and azygos vein) and modified shape of organs and blood vessels, including abnormal lobation of lungs or liver. Approximately 50% of mice homozygous for Dnahc11iv have situs inversus, and the likelihood of situs inversus is not impacted by whether the homozygous parent has situs inversus. This indicates that wild type Dnahc11 instructs left-right asymmetry, and in the absence of functional Dnahc11 the direction of this asymmetry is random. Heterotaxia is found in less than half of homozygotes and occurs equally in those that do and do not have situs inversus. W
..... For more information please see the full descriiption on the strain data sheet | ||
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