Ldlr b6.129s7 ldlrtm1her j

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The Ldlr−/−;B6.129S7‐Ldlrtm1Her/J mouse is a genetically modified strain that lacks the low-density lipoprotein receptor (LDLR) gene. This model is commonly used in research related to lipid metabolism and cardiovascular disease.

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Apoe b6.129p2 apoetm1unc j, by Jackson ImmunoResearch (2 mentions) C57bl 6j, by Jackson ImmunoResearch (1 mentions) B6 sjl ptprca pepcb boyj, by Jackson ImmunoResearch (1 mentions) Wild type c57bl 6j, by Jackson ImmunoResearch (1 mentions) B6.129p2 apoetm1unc, by Jackson ImmunoResearch (1 mentions) C57bl 6 mice, by Jackson ImmunoResearch (1 mentions) B6 cg tg tcratcrb 425cbn j ot 2, by Jackson ImmunoResearch (1 mentions) C57bl 6j wt, by Jackson ImmunoResearch (1 mentions)

9 protocols using ldlr b6.129s7 ldlrtm1her j

Genetically Modified C57BL/6J Mice

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C57BL/6J.AlbCre⁺Cc1^fl/fl mice were generated, as described,⁽¹⁷⁾ and backcrossed >6 times with Ldlr^−/−;B6.129S7‐Ldlrtm1Her/J (JAX#002207; Jackson Laboratory, Bar Harbor, ME). Offspring were genotyped by polymerase chain reaction (PCR) analysis of ear DNA, using Ceacam1‐specific primers (Supporting Fig. S1). We used homozygotes with the wild‐type Ceacam1 allele with AlbCre (Ldlr^−/−AlbCre⁺Cc1^+/+ or Alb⁺Cc1^+/+) or without AlbCre (Ldlr^−/−AlbCre^–Cc1^+/+ or Alb^–Cc1^+/+) and homozygotes with the Ceacam1‐floxed allele with AlbCre (Ldlr^−/−AlbCre⁺Cc1^fl/fl or Alb⁺Cc1^fl/fl) or without AlbCre (Ldlr^−/−AlbCre^–Cc1^fl/fl or Alb^–Cc1^fl/fl); all homozygotes from the same breeding were used to mitigate potential confounding effects of floxing and introducing AlbCre.

Ghadieh H.E., Abu Helal R., Muturi H.T., Issa D.D., Russo L., Abdallah S.L., Najjar J.A., Benencia F., Vazquez G., Li W, & Najjar S.M. (2020). Loss of Hepatic Carcinoembryonic Antigen‐Related Cell Adhesion Molecule 1 Links Nonalcoholic Steatohepatitis to Atherosclerosis. Hepatology Communications, 4(11), 1591-1609.

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Characterizing Aortic Pathogenesis in Mice

Cited 2 times

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Procedures for handling mice were approved by the Washington University and Sanford-Burnham institutional animal care and use committees. LDLR^−/−B6.129S7-Ldlrtm1Her/J (19 (link)) and SM22-CreTg(Tagln-cre)1Her/J (15 (link)) mice were obtained from The Jackson Laboratory. Msx1(fl/fl);Msx2(fl/fl) mice have been described (20 (link)) and were bred onto the LDLR^−/− background. Experimental SM22-Cre;Msx1(fl/fl);Msx2(fl/fl);LDLR^−/−, SM22-Cre;Msx2(fl/fl);LDLR^−/−, and Msx1(fl/fl);Msx2(fl/fl);LDLR^−/− control animals were obtained through the breeding scheme outlined in Fig. 1. At 5–10 weeks of age, animals were weighed. Male sibling cohorts (n = 4–13 per genotype as indicated) of Msx1(fl/fl);Msx2(fl/fl);LDLR^−/− and SM22-Cre;Msx1(fl/fl);Msx2(fl/fl);LDLR^−/− mice with equivalent starting weights were challenged with high-fat western diet (HFD) (TD88137; Teklad Lab Animal Diets; Harlan) for 2 months. At the end of the dietary challenge, thoracic aortas were harvested, weighed, and extracted for calcium, collagen, or total RNA, implementing methods previously detailed (9 (link),21 (link)).

Cheng S.L., Behrmann A., Shao J.S., Ramachandran B., Krchma K., Bello Arredondo Y., Kovacs A., Mead M., Maxson R, & Towler D.A. (2014). Targeted Reduction of Vascular Msx1 and Msx2 Mitigates Arteriosclerotic Calcification and Aortic Stiffness in LDLR-Deficient Mice Fed Diabetogenic Diets. Diabetes, 63(12), 4326-4337.

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Aging and Diet Effects in Grx1 Mice

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LDLR^-/- (B6.129S7-Ldlr^tm1Her/J, stock number 002207) and C57BL/6 J (stock number 000664) were obtained from Jackson Laboratory. Grx1^-/- mice were kindly provided by Dr. Yvonne Janssen-Heininger, University of Vermont, with kind permission from Dr. Ye-Shih Ho, Wayne State University. The mice were backcrossed into the C57BL/6 J genetic background for more than 10 generations. All mice were maintained in colony cages on a 12-h light/12-h dark cycle and fed a normal mouse laboratory diet unless otherwise stated. For the aging study, C57BL/6 J (wild-type; 5 males and 5 females) and Grx1^-/- mice (6 males and 5 females) were fed chow diet (5.5% fat wt/wt, Prolab® RMH 3000 5P00, LabDiet) for 18 months. Body weights and fasting glucose levels were measured every 4 weeks. For the bone marrow (BM) transplantation experiments, 4 weeks after the transplantation, male and female BM-recipient mice were switched to a high-calorie diet (HCD; 21% milk fat wt/wt and 0.2% cholesterol wt/wt. diet no. F55440, Bio-Serv) for 6 or 20 weeks. Body weights were measured weekly and fasting blood glucose every 3 weeks using a glucometer. All studies were performed in accordance with the guidelines and regulations of and with the approval of the Institutional Animal Care and Use Committees.

Ahn Y.J., Wang L., Tavakoli S., Nguyen H.N., Short J.D, & Asmis R. (2022). Glutaredoxin 1 controls monocyte reprogramming during nutrient stress and protects mice against obesity and atherosclerosis in a sex-specific manner. Nature Communications, 13, 790.

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Ldlr Knockout Mouse Model

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All animal studies were approved by the University of British Columbia animal ethics committee. Male Ldlr knock-out (Ldlr-/-;B6;129S7-Ldlr^tm1Her/J) and genetic background control mice, body weight 25–30 grams, 10–16 weeks old, were purchased from Jackson Labs (Bar Harbor, ME).

Topchiy E., Cirstea M., Kong H.J., Boyd J.H., Wang Y., Russell J.A, & Walley K.R. (2016). Lipopolysaccharide Is Cleared from the Circulation by Hepatocytes via the Low Density Lipoprotein Receptor. PLoS ONE, 11(5), e0155030.

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Mouse Breeding and Housing for Research

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Wild type C57BL/6J (#000664),
Apoe^−/−(B6.129P2-Apoe^tm1Unc/J,
#002052), Tet2^−/−(B6(Cg)-Tet2^tm1.2Rao/J,
#023359), Ldlr^−/−(B6.129S7-Ldlr^tm1Her/J,
#002207), and CD45.1 mice
(B6.SJL-Ptprc^aPepc^b/BoyJ, #002014) were
purchased from The Jackson Laboratory (Bar Harbor, ME, USA). For all
experiments, littermates of the same sex were randomly assigned to
experimental groups. Mice were group-housed on a 12:12hrs light:dark cycle
at 22°C with access to standard mouse chow or diet and water
ad libitum. The study protocols were approved and
reviewed by the Institutional Animal Care and Use Committee (IACUC) at
Massachusetts General Hospital (Boston, MA, USA) and all animal experiments
were performed in compliance with relevant regulatory standards.

Heyde A., Rohde D., McAlpine C.S., Zhang S., Hoyer F.F., Gerold J.M., Cheek D., Iwamoto Y., Schloss M.J., Vandoorne K., Iborra-Egea O., Muñoz-Guijosa C., Bayes-Genis A., Reiter J.G., Craig M., Swirski F.K., Nahrendorf M., Nowak M.A, & Naxerova K. (2021). Increased stem cell proliferation in atherosclerosis accelerates clonal hematopoiesis. Cell, 184(5), 1348-1361.e22.

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Atherosclerosis Induction in Hyperlipidemic Mice

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All animal handling and experimental procedures were approved by the Institutional Animal Care and Use Committee at the University of North Carolina – Chapel Hill (IACUC ID: 18–303). 4–6-week-old male ApoE^−/− mice (B6.129P2-Apoetm1Unc, stock number: 002052), LDLr^−/− (B6.129S7-Ldlrtm1Her/J, stock number: 002207) and C57Bl/6 mice (stock number: 000664) were purchased from Jackson laboratory. C57Bl/6 mice were fed standard chow. Mice were allowed ad libitum access to food and water throughout the study. After 1 week acclimation in the Division of Comparative Medicine (DCM) facility, ApoE^−/− and LDLr^−/− were placed on a western high-fat diet containing 40% fat, 17% protein, 43% carbohydrate by kcal and 0.15% cholesterol by weight (RD Western Diet, catalog number: D12079Bi). apoE^−/− and LDLr^−/− mice were fed with the high-fat diet over the course of 8–15 weeks. Mice underwent experimental procedures and were sacrificed when they were approximately either 13–15 weeks old or 20–22 weeks old.

Maiocchi S., Cartaya A., Thai S., Akerman A, & Bahnson E. (2022). 2021 Biomaterials Science Emerging Investigators Issue: Antioxidant Response Activating nanoParticles (ARAPas) localize to atherosclerotic plaque and locally activate the Nrf2 pathway. Biomaterials science, 10(5), 1231-1247.

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Generating Genetically Modified Mice

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C57BL/6J-Tg Itgax-cre,-EGFP 4097Ach/J (CD11c-Cre-GFP; Stock # 007567) and B6.129S7-Ldlr^tm1Her/J (Ldlr^−/−; Stock # 002207) mice were originally obtained from the Jackson Laboratory (Bar Harbor, ME). Mice homozygous for the Fcgr2b^fl alleles were generously gifted from Jeffery V. Ravetch (The Rockefeller University, New York City, NY) and bred with CD11c-Cre⁺ mice to obtain CD11c-Cre⁺Fcgr2b^fl/fl mice and CD11c-Cre^- mice as determined by PCR. (Please see Major Resources Table in the Supplemental Material). All mice were subsequently housed and maintained at Vanderbilt University. Procedures were approved by the Vanderbilt University Institutional Animal Care and Use Committee.

Marvin J., Rhoads J.P, & Major A.S. (2019). FcγRIIb on CD11c+ cells modulates serum cholesterol and triglyceride levels and differentially affects atherosclerosis in male and female Ldlr−/− mice. Atherosclerosis, 285, 108-119.

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Genetic and Dietary Modulation of Aortic Stiffness

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Female B6.129S7-Ldlr^tm1Her/J −/− (Ldlr−/−) (Jackson Laboratory, stock #002207) were bred with male Eln+/− mice^{22 (link)}. Males at the F3 – F6 generation were used because previous data on blood pressure and aortic stiffness in Eln+/− mice were obtained for males^{19 (link)}. Genotypes included in the study are: Eln+/+Ldlr−/−, Eln+/−Ldlr−/−, Eln+/+Ldlr+/+, Eln+/−Ldlr+/+. After weaning at three weeks of age, mice were provided with normal diet (ND) or WD (AIN-76A, Purina Test Labs) for 16 weeks. All protocols were approved by the Institutional Animal Care and Use Committee.

Maedeker J.A., Stoka K.V., Bhayani S.A., Gardner W.S., Bennett L., Procknow J.D., Staiculescu M.C., Walji T.A., Craft C.S, & Wagenseil J.E. (2016). Hypertension and decreased aortic compliance due to reduced elastin amounts do not increase atherosclerotic plaque accumulation in Ldlr−/− mice. Atherosclerosis, 249, 22-29.

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Genetic Knockout Mouse Models

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C57Bl/6J (WT), B6.SJL-PtprcaPepcb/BoyJ (CD45.1⁺), B6.129P2(SJL)-Myd88tm1.1Defr/J (Myd88^−/−), B10.129S2(B6)-Ighmtm1Cgn/J (µMT), B6.Cg-Tg(TcraTcrb)425Cbn/J (OT-II), B6.129S7-Ldlrtm1Her/J (Ldlr^−/−) and B6.129P2-Apoetm1Unc/J (Apoe^−/−) were purchased from The Jackson Laboratory (Bar Harbor, ME). GM-CSF-deficient mice (Csf2^−/−) were kindly provided by Dr. Randy Seeley, University of Cincinnati, USA. GM-CSF-receptor deficient mice (Csf2rb^−/−) were kindly provided by Dr. Jeffrey Whitsett, Cincinnati Children’s Hospital Medical Center, USA. All protocols are approved by the Animal Review Committee at Massachusetts General Hospital.

Hilgendorf I., Theurl I., Gerhardt L.M., Robbins C.S., Weber G.F., Gonen A., Iwamoto Y., Degousee N., Holderried T.A., Winter C., Zirlik A., Lin H.Y., Sukhova G.K., Butany J., Rubin B.B., Witztum J.L., Libby P., Nahrendorf M., Weissleder R, & Swirski F.K. (2014). Innate Response Activator B Cells Aggravate Atherosclerosis by Stimulating TH1 Adaptive Immunity. Circulation, 129(16), 1677-1687.

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