B6 fvb tg cdh5 cre 7mlia j

Manufactured by Jackson ImmunoResearch

B6.FVB-Tg(Cdh5-cre)7Mlia/J is a transgenic mouse line that expresses Cre recombinase under the control of the Cdh5 (VE-cadherin) promoter. The Cre recombinase is specifically expressed in endothelial cells.

Automatically generated - may contain errors

Lab products found in correlation

B6 cg gt rosa 26sortm14 cag tdtomato hze j, by Jackson ImmunoResearch (1 mentions) B6.129s4 ccr2tm1ifc j, by Jackson ImmunoResearch (1 mentions) B6.129x1 gt rosa 26sortm1 eyfp cos j, by Jackson ImmunoResearch (1 mentions)

Spelling variants of this product

B6 FVB-Tg (cdh5-cre)7Mlia/J Cre mice (13 citations) Cdh5-Cre (10 citations)

7 protocols using b6 fvb tg cdh5 cre 7mlia j

Vascular Endothelial Tracing in Mice

Check if the same lab product or an alternative is used in the 5 most similar protocols

Experiments were carried out in accordance with the Israeli law and the Weizmann Institute guidelines. All experimental protocols were reviewed and approved by the Weizmann Institutional Animal Care and Use Committee.
Vecad^cre mice (B6.FVB-Tg(Cdh5-cre)7Mlia/J, Jackson) crossed with tdTomato^{flox/stop/flox} mice (B6.Cg-Gt(ROSA)26Sor^{tm14(CAG-tdTomato)Hze/J}, Jackson) were used. In the double transgenic offspring, the red fluorescent protein variant (tdTomato) is controlled by vascular endothelial cadherin (VECAD) promoter, to be expressed only by endothelial cells of both developing and mature blood vessels. Ovaries and uteri were collected from 3-weeks-old mice, 24 hours after injection of pregnant mare serum gonadotropin PMSG, (5 IU). Lungs and livers were collected from 8-weeks-old mice.

Oren R., Fellus-Alyagor L., Addadi Y., Bochner F., Gutman H., Blumenreich S., Dafni H., Dekel N., Neeman M, & Lazar S. (2018). Whole Organ Blood and Lymphatic Vessels Imaging (WOBLI). Scientific Reports, 8, 1412.

+ Open protocol

+ Expand

Endothelial-specific PHD2 Knockout Mice

Check if the same lab product or an alternative is used in the 5 most similar protocols

PHD2^flox/flox (PHD2^f/f) mice were obtained from Dr. Guo‐hua Fong at University of Connecticut. PHD2^ECKO mice were generated using the Cre‐LoxP system as we previously reported 19. In brief, exon 2 of PHD2 gene in PHD2^f/f mice was flanked with LoxP sites, for subsequent deletion by Cre recombinase. PHD2^f/f mice were crossbred with VE‐Cadherin‐Cre (Cdh5‐Cre) transgenic mice [B6.FVB‐Tg (Cdh5‐cre) 7Mlia/J] obtained from Jackson Laboratories that express Cre recombinase under the control of Cdh5 promoter in vascular ECs. The resulting Cdh5‐Cre/PHD2^flox/− heterozygous mutants were then mated with PHD2^f/f to obtain endothelial‐specific ablated PHD2 mutant mice (PHD2^ECKO) and PHD2^f/f mice. Experiments were performed on male mice at 15 months of age.

Wang S., Zeng H., Chen S.T., Zhou L., Xie X., He X., Tao Y., Tuo Q., Deng C., Liao D, & Chen J. (2017). Ablation of endothelial prolyl hydroxylase domain protein‐2 promotes renal vascular remodelling and fibrosis in mice. Journal of Cellular and Molecular Medicine, 21(9), 1967-1978.

+ Open protocol

+ Expand

Endothelial-specific Ccr2 Knockout Mice

Cited 1 time

Check if the same lab product or an alternative is used in the 5 most similar protocols

All animal experiments were performed according to the guidelines of the Swiss Animal Protection Law, and approved by the Veterinary Office of Kanton Zurich. C57BL/6J (wt) mice as well as systemic Ccr2-deficient mice, B6.129S4-Ccr2^<tm1Ifc/J>, were purchased from The Jackson Laboratory. VE-cad-Cre/Ccr2^fl/fl mouse (hereafter Ccr2^ecKO mouse) was generated by breeding the Ccr2^fl/fl mouse (25 (link)) (obtained from M. Pasparakis) with the VE-cadherin-Cre mouse, B6.FVB-Tg(Cdh5-cre)7Mlia/J, (26 (link)) (The Jackson Laboratory) in C57BL/6J background. Ccr2^fl/fl and Ccr2^ecKO littermates were used for all experiments. Mice expressing a VE-cadherin-EGFP fusion protein through a DNA construct knocked into the Cdh5 locus (27 (link)) were obtained from D. Vestweber.

Roblek M., Protsyuk D., Becker P.F., Stefanescu C., Gorzelanny C., Glaus Garzon J.F., Knopfova L., Heikenwalder M., Luckow B., Schneider S.W, & Borsig L. (2018). CCL2 is a vascular permeability factor inducing CCR2-dependent endothelial retraction during lung metastasis. Molecular cancer research : MCR, 17(3), 783-793.

+ Open protocol

+ Expand

Endothelial SIRT3 Knockout Mice Model

Cited 2 times

Check if the same lab product or an alternative is used in the 5 most similar protocols

Endothelial SIRT3 knockout (SIRT3 ECKO) mice were obtained by crossbreeding SIRT3^flox/flox mice with VE-Cadherin-Cre (Cdh5-Cre) transgenic mice [B6.FVB-Tg(Cdh5-cre)7Mlia/J from Jackson Laboratories] expressing Cre recombinase in vascular endothelial cells, as described in previous study [27 (link)]. Male SIRT3 global knockout (SIRT3 KO) or SIRT3 ECKO mice at age of 12–14 months were injected with DMOG (25 μg/g/day) intraperitoneally for 14 days as shown in Supplemental Figure S1. The number of mice used for each experiment was indicated in the figure legends. This dosage used in this study was chose based on previous studies with minor change [35 (link)–37 (link)]. Diastolic function and coronary flow reserve was monitored using echocardiography before the treatment and every 7 days. After 14 days of treatment, the mice were sacrificed, and heart tissue were harvested for Western blot and immunofluorescence staining.

He X., Zeng H., Roman R.J, & Chen J.X. (2018). Inhibition of Prolyl Hydroxylases Alters Cell Metabolism and Reverses Pre-Existing Diastolic Dysfunction in Mice. International journal of cardiology, 272, 281-287.

+ Open protocol

+ Expand

BMP7 and PLX Retinal Angiogenesis Study

Cited 1 time

Check if the same lab product or an alternative is used in the 5 most similar protocols

Experiments were carried out in 4–8 weeks old male C57BL/6J. All procedures were in accordance with the guidelines set by the Institutional Animal Care and Use Committee (IACUC) at the school of science IUPUI (protocol number SC230R). For BMP7 injection studies, n = 8 mice were used with the left eye injected with the vehicle and the right eye injected with BMP7. For the PLX studies, two groups of mice were considered, the age-matched control chow group (n = 12) and the PLX group (n = 12), kept on PLX chow diet. For the PLX BMP7 injection studies, two groups of mice were considered, the age-matched control group (n = 12) and the PLX group (n = 12), kept on the PLX diet. Both the groups were injected with the vehicle control in the left eye and BMP7 in the right eye. P30 VE-YFP mice (n = 3), which express YFP in endothelial cells, generated by crossing a line of mice containing an enhanced yellow fluorescent protein (YFP) with a floxed stop sequence upstream of the YFP (B6.129X1-Gt(ROSA)26Sor^tm1(EYFP)Cos/J; strain number 006148 Jackson laboratory) [44 (link)] with the VE-cadherin-cre line (B6.FVB-Tg(Cdh5-cre)7Mlia/J; stock number 006137 Jackson laboratory) [45 (link)], were used for immunofluorescence experiments determining PU.1 co-localization in the retina.

Dharmarajan S., Fisk D.L., Sorenson C.M., Sheibani N, & Belecky-Adams T.L. (2017). Microglia activation is essential for BMP7-mediated retinal reactive gliosis. Journal of Neuroinflammation, 14, 76.

+ Open protocol

+ Expand

Investigating Endothelial Cell-Specific AGO1 Deficiency

Check if the same lab product or an alternative is used in the 5 most similar protocols

VE-Cadherin-Cre (B6.FVB-Tg [Cdh5-cre]7 Mlia/J) and AGO1-flox mice with C57BL6 background (Ago1^tm1.1Tara/J) were purchased from the Jackson Laboratory and bred at City of Hope to generate AGO1 EC-deficient (EC-AGO1-KO) mice. EC-AGO1-KO and their WT littermates from the same breeders were housed in the same cages until subjected to metabolic phenotyping and tissue collection.
Mice (male and female) were randomized to receive irradiated high-fat high-sucrose diet (HFHS diet, D12266B, Research Diets Inc, 17% kcal protein, 32% kcal fat, 51% kcal carbohydrate) starting at 8 weeks old for 16 weeks. Mice under chow diet (D12489B, Research Diets Inc, 16.4% kcal protein, 70.8 % kcal carbohydrate, 4.6 % kcal fat) were kept under the same diet for the same duration. The diet-induced obesity model was performed with 5 batches of animals, each with 6–8 mice per genotype. Body weight was measured at the initiation of HFHS diet and subsequently every other week. Various phenotyping was performed as described in the Supplemental Methods. At the endpoints, mice were euthanized with CO₂ inhalation. Posterior subcutaneous fat pads were collected as SAT and lymph nodes were removed. The interscapular fat was isolated as BAT and epididymal adipose tissue as the WAT.

Tang X., Miao Y., Luo Y., Sriram K., Qi Z., Lin F.M., Gu Y., Lai C.H., Hsu C.Y., Peterson K.L., Keuren-Jensen K.V., Fueger P.T., Yeo G.W., Natarajan R., Zhong S, & Chen Z.B. (2020). Suppression of endothelial AGO1 promotes adipose tissue browning and improves metabolic dysfunction. Circulation, 142(4), 365-379.

+ Open protocol

+ Expand

Endothelial-specific Nek7 knockout mice

Cited 1 time

Check if the same lab product or an alternative is used in the 5 most similar protocols

Nek7 floxed mice were crossed with Cdh5-cre mice, B6.FVB-Tg(Cdh5-cre)7Mlia/J (The Jackson Laboratory), to generate endothelial cell–specific Nek7 knockout mice. After two generations, we performed genotyping and immunofluorescence for Nek7 as we have done for other mouse colonies.¹¹ (link)

Liu L., Jiang Y, & Steinle J.J. (2022). PKA and Epac1 Reduce Nek7 to Block the NLRP3 Inflammasome Proteins in the Retinal Vasculature. Investigative Ophthalmology & Visual Science, 63(1), 14.

+ Open protocol

+ Expand

About PubCompare

Our mission is to provide scientists with the largest repository of trustworthy protocols and intelligent analytical tools, thereby offering them extensive information to design robust protocols aimed at minimizing the risk of failures.

We believe that the most crucial aspect is to grant scientists access to a wide range of reliable sources and new useful tools that surpass human capabilities.

However, we trust in allowing scientists to determine how to construct their own protocols based on this information, as they are the experts in their field.

Ready to get started?

Revolutionizing how scientists
search and build protocols!