Alb cre mice

Manufactured by Jackson ImmunoResearch

Sourced in Montenegro, United States, Switzerland

Alb-Cre mice are a transgenic mouse model that expresses Cre recombinase under the control of the albumin (Alb) promoter. This model allows for the conditional deletion or modification of targeted genes in hepatocytes, the primary cell type of the liver.

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37 protocols using alb cre mice

Generation of Arid1a Liver-Specific Knockout Mice

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Alb-Cre mice were obtained from Jackson Laboratory ( Sacramento, CA) and Arid1a^flox/flox mice were kindly provided by Bin Zhou's laboratory (Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, Shanghai, China), Arid1a liver-specific knockout mice were generated by crossing Alb-Cre mice with Arid1a^flox/flox mice. Primers for validation of genotypes are listed in Table 2. All mice were male in a C57BL/6 background and all animal experiments were performed under the approval of the Institutional Animal Care and Use Committee.Table 2

Primers for mouse genotyping

Primer	Sequence
Arid1a-flox	F: 5'-ATCCTGTGTACAGAACTTAAGC-3'
Arid1a-flox	R: 5'-CTTTCCCATTACTCTTTCCTGC-3'
Alb-cre	F: 5'-GAAGCAGAAGCTTAGGAAGATGG-3'
Alb-cre	R: 5'-TTGGCCCCTTACCATAACTG-3'

Zhang F.K., Ni Q.Z., Wang K., Cao H.J., Guan D.X., Zhang E.B., Ma N., Wang Y.K., Zheng Q.W., Xu S., Zhu B., Chen T.W., Xia J., Qiu X.S., Ding X.F., Jiang H., Qiu L., Wang X., Chen W., Cheng S.Q., Xie D, & Li J.J. (2022). Targeting USP9X–AMPK Axis in ARID1A-Deficient Hepatocellular Carcinoma. Cellular and Molecular Gastroenterology and Hepatology, 14(1), 101-127.

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Liver-Specific Fasn Knockout Mice

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Fasn^fl/fl mice in C57BL/6 background were described previously.19 (link)
AlbCre mice in C57BL/6 background20 (link) were obtained from the Jackson Laboratory (Bar Harbor, Maine, USA). Fasn^fl/fl mice were crossed with AlbCre mice to eventually generate liver-specific Fasn knockout mice (Fasn^LKO mice). The physiological phenotype of Fasn^LKO mice has been extensively characterised.21 (link) Both male and female mice were used in the study, and no sex-dependent differences were detected. Hydrodynamic transfection was performed as described.22 (link) Mice were monitored weekly, euthanised and liver tissues collected when they developed large abdominal masses or by 40–50 weeks postinjection. The detailed mouse experiment data are available in online supplementary table S1. All mice were housed, fed and monitored in accordance with protocols approved by the Committee for Animal Research at the University of California, San Francisco.

Che L., Chi W., Qiao Y., Zhang J., Song X., Liu Y., Li L., Jia J., Pilo M.G., Wang J., Cigliano A., Ma Z., Kuang W., Tang Z., Zhang Z., Shui G., Ribback S., Dombrowski F., Evert M., Pascale R.M., Cossu C., Pes G.M., Osborne T.F., Calvisi D.F., Chen X, & Chen L. (2019). Cholesterol biosynthesis supports the growth of hepatocarcinoma lesions depleted of fatty acid synthase in mice and humans. Gut, 69(1), 177-186.

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Hepatocyte-specific Deletion of G9a

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Floxed G9a (G9a^flox/flox) mice were generated as described previously^{10 (link),46 (link)} and Alb-Cre mice were purchased from The Jackson Laboratory^{47 (link)}. Mice were maintained in a temperature- and light-controlled facility, and permitted ad libitum regular chow diet and autoclaved water. All mice were backcrossed with the C57BL/6 strain and the male progeny were analyzed. All the experiments were performed in accordance with protocols approved by the Animal Ethics Committee of the University of Tokyo.
HCC was induced as previously described^{23 (link)}. 15-day-old WT and G9a^ΔHep mice were injected intraperitoneally (i.p.) with DEN (Sigma, St. Louis, MO, USA) (25 mg/kg) alone or in combination with 22 weekly injections of CCl₄ (Wako, Osaka, Japan) (0.5 ml/kg i.p., dissolved in corn oil). To evaluate acute effects of G9a in damaged hepatocytes, 8-week-old WT and G9a^ΔHep mice were treated with DEN (100 mg/kg i.p.) and sacrificed 48 h after DEN administration. In vivo G9a inhibitor treatment was performed as previously described^{48 (link)}. WT mice were injected i.p. with G9a inhibitor UNC0642 (5 mg/kg) for 10 days before and after DEN administration. Randomization or blinding of animal experiments were not possible.

Nakatsuka T., Tateishi K., Kato H., Fujiwara H., Yamamoto K., Kudo Y., Nakagawa H., Tanaka Y., Ijichi H., Ikenoue T., Ishizawa T., Hasegawa K., Tachibana M., Shinkai Y, & Koike K. (2021). Inhibition of histone methyltransferase G9a attenuates liver cancer initiation by sensitizing DNA-damaged hepatocytes to p53-induced apoptosis. Cell Death & Disease, 12(1), 99.

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Transgenic Mouse Model for Liver Cancer

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Male Alb‐Cre/BRAFV600E transgenic (5–13 wk of age), and age‐matched control BRAFV600E and C57BL/6 mice (Charles River Japan) were used in this study. Alb‐Cre/BRAFV600E transgenic and control BRAFV600E mice were generated by in vitro fertilization using homozygous male BRAFV600E mice [B6.129P2(Cg)‐Braftm1Mmcm>/J; Jackson] and heterozygous female Alb‐Cre mice (Jackson) as described previously.8 The male litters were genotyped to separate the Alb‐Cre/BRAFV600E transgenic and control BRAFV600E mice with and without the Alb‐Cre gene. Some of the Alb‐Cre/BRAFV600E transgenic and control BRAFV600E mice were given aspirin (Asp) at a daily dose of 5 μg/g body weight by oral intubation from 4 to 8 wk after birth. Hepatic tumors were induced by neonatal treatment with 5 μg/g body weight of DEN on day 15 after birth in male B6C3F1 mice (Charles River Japan), and the tumor samples were collected at 8‐12 mo of age. The mice were housed in plastic cages with sterilized wood chips and given a standard chow diet (CMF, Oriental Yeast) and sterilized water ad libitum. The mouse breeding room was kept at 25°C with a 12 h light and 12 h dark cycle. All procedures performed on mice were approved by the Asahikawa Medical University Animal Experiment Committee following the guidelines for the humane care and protection of animals.

Tanaka H., Horioka K., Yamamoto M., Asari M., Okuda K., Yamazaki K., Shimizu K, & Ogawa K. (2019). Overproduction of thrombopoietin by BRAFV600E‐mutated mouse hepatocytes and contribution of thrombopoietin to hepatocarcinogenesis. Cancer Science, 110(9), 2748-2759.

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Genetic Mouse Models for Metabolic Research

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C57BL/6J mice and alb Cre⁺ mice were purchased from The Jackson Laboratory. Sort1-KO mice were a gift from Carlos Morales (McGill University, Montreal, Canada). Sort1^fl/fl mice were a gift from Merck. All mice were housed 3–5 mice per cage in a climate controlled room with a 12:12-light/dark cycle with ad libitum access to regular chow diet. Where specifically noted in the text, animals were fed HFD ad libitum containing 45% kcal of fat (D12451, Research Diets) for a duration of 12 weeks. In some experiments, mice were injected with 0.05, 0.5, or 1 μg per gram of body weight of tunicamycin. Experiments were performed on 8– to 22-week-old male mice. Mice were assigned to experimental groups based on weight matching. Mice were euthanized by cervical dislocation after isoflurane inhalation.

Conlon D.M., Schneider C.V., Ko Y.A., Rodrigues A., Guo K., Hand N.J, & Rader D.J. (2022). Sortilin restricts secretion of apolipoprotein B-100 by hepatocytes under stressed but not basal conditions. The Journal of Clinical Investigation, 132(6), e144334.

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Mouse Strain Generation and Validation

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Prkci^f/f and Alb-Cre mice were previously described (Nakanishi et al., 2018 (link); Umemura et al., 2016 ). Alb-Cre mice were purchased from Jackson Laboratories. Nfe2l2^−/− mice were kindly provided by Dr. Michael Karin, Ph.D. (Todoric et al., 2017 (link)). All these mouse strains were generated in a C57BL/6 background. NSG mice were purchased from the animal core at SBP Medical Discovery Institute. All mice were born and maintained under pathogen-free conditions. Animal handling and experimental procedures were approved by the Institutional Animal Care and Use Committee at SBP Medical Discovery Institute.

Kudo Y., Sugimoto M., Arias E., Kasashima H., Cordes T., Linares J.F., Duran A., Nakanishi Y., Nakanishi N., L’Hermitte A., Campos A., Senni N., Rooslid T., Roberts L.R., Maria Cuervo A., Metallo C.M., Karin M., Diaz-Meco M.T, & Moscat J. (2020). PKCλ/ι loss induces autophagy, oxidative phosphorylation, and NRF2 to promote liver cancer progression. Cancer cell, 38(2), 247-262.e11.

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Generating Liver-Specific SIRT2 Knockout Mice

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The liver-specific SIRT2-KO mice were produced by crossing SIRT2^flox/flox mice obtained from Johan Auwerxd Laboratory (Switzerland)^{47 (link)} and Alb-Cre mice purchased from Jackson Laboratory (USA) in a C57BL/6 background. Recombinant AAV8 constructs expressing targeted mouse SIRT2, SIRT2-H187A, LCN2, C/EBPβ, or mutated C/EBPβ (K101R and K102R) under the control of TBG promoter were generated by Sunbio Techservice Inc. (Shanghai, China). A noncoding plasmid carrying only the TBG promoter was used to produce control vector particles. All animals received care in compliance with protocols approved by the Institutional Animal Use and Care Committee of Shanghai Jiaotong University School of Medicine.

Zhang Y., Long X., Ruan X., Wei Q., Zhang L., Wo L., Huang D., Lin L., Wang D., Xia L., Zhao Q., Liu J., Zhao Q, & He M. (2021). SIRT2-mediated deacetylation and deubiquitination of C/EBPβ prevents ethanol-induced liver injury. Cell Discovery, 7, 93.

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Liver-specific Sirt1 and Bmal1 Knockout in Mice

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All animal procedures were in accordance with guidelines of the Institutional Animal Care and Use Committee at Northwestern University. Mouse protocols approved in this study include IS00003543, IS00007712, IS00001143 and IS00000601. Mice were housed at 23–25 °C in the Center for Comparative Medicine at Northwestern University and maintained under 12:12 h light/dark cycles at 40–60% humidity with ad libitum access to regular chow and water unless otherwise indicated. C57BL/6J mice were purchased from Jackson Laboratories. Sirt1^fx/fx mice harbouring LoxP sites surrounding exon 4 of Sirt1 were from S. Imai (Washington University, St. Louis). Alb-Cre mice were purchased from Jackson Laboratories. For liver-specific Sirt1 knockout studies, Alb-Cre; Sirt1^fx/fx mice were used for western blotting and ChIP-Seq, whereas Sirt1^fx/fx mice retro-orbitally injected with AAV8–TBG-iCre were used for transcriptomic, metabolomic and physiological studies. For inducible liver-specific Bmal1 knockout studies, mice harbouring LoxP sites surrounding exon 8 were retro-orbitally injected with AAV8–TBG-iCre. Male mice, 4–6 months old, were used in all experiments, except for studies monitoring fasted body temperature which were performed in 4–6-month-old female mice.

Levine D.C., Kuo H.Y., Hong H.K., Cedernaes J., Hepler C., Wright A.G., Sommars M.A., Kobayashi Y., Marcheva B., Gao P., Ilkayeva O.R., Omura C., Ramsey K.M., Newgard C.B., Barish G.D., Peek C.B., Chandel N.S., Mrksich M, & Bass J. (2021). NADH inhibition of SIRT1 links energy state to transcription during time-restricted feeding. Nature Metabolism, 3(12), 1621-1632.

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Liver-Specific G9a Knockout Mice

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G9a Liv-KO mice (G9a fl/fl, Alb-cre/+) and wild-type littermates (G9a fl/fl, Alb-cre/-) were generated by crossing G9a floxed mice (Tachibana et al. 2007 (link)) with Alb-cre mice (Stock # 003574, Jackson Laboratory). Mice were fed rodent chow and allowed water and feed ad libitum. Liver and blood samples were collected from adult (10-week old) male G9a Liv-KO mice and the wild-type littermates (N=6 per group). Liver tissues were snap frozen in liquid nitrogen upon collection and stored at −80 ºC until use. For LPS study, adult (10-week old) male G9a Liv-KO mice and the wild-type littermates (N=6 per group) were sacrificed to collect liver and blood samples 16 h after ip injection of LPS (L3012, Sigma) 5 mg/kg (in saline). Core body temperature (rectal temperature) was measured 16 h after LPS treatment before tissue collection using a digital thermometer. To prepare serum samples, the clotted blood samples were centrifuged at 8000 rpm for 10 min and the resultant supernatants were stored at −80 ºC until use. All animals received humane care and all animal procedures in this study were approved by the Institutional Animal Care and Use Committee (IACUC) of the SUNY Upstate Medical University.

Lu H., Lei X, & Zhang Q. (2018). Liver-specific knockout of histone methyltransferase G9a impairs liver maturation and dysregulates inflammatory, cytoprotective, and drug-processing genes. Xenobiotica; the fate of foreign compounds in biological systems, 49(6), 740-752.

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Genetically Engineered Mice for Liver Research

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C57BL/6J wild-type (WT) and Opn^−/− (B6.Cg-Spp1^tm1Blh/J) mice were obtained from the Jackson Laboratory (Bar Harbor, Maine, USA). Opn^+/− mice were intercrossed and littermates were used in all experiments. The Opn transgenic mice overexpressing OPN in hepatocytes (Opn^Hep Tg) under the serum amyloid-P component promoter were donated by Dr Mochida (Saitama Medical University, Saitama, Japan).10 (link) These mice were crossbred for 10 generations with the same strain and stock number of C57BL/6J WT listed above. The Hmgb1^fl/fl mice were donated by Dr Billiar (University of Pittsburgh, Pittsburgh, Pennsylvania, USA). In these mice, the Hmgb1^loxP allele was created by inserting loxP sites within introns 1 and 2 flanking exon 2 of Hmgb1.11 (link) The Hmgb1^fl/fl mice were bred with Alb.Cre mice (the Jackson Laboratory) to generate hepatocyte-specific Hmgb1^fl/flAlb.Cre mice (abbreviated as Hmgb1^ΔHep). All animals received humane care according to the criteria outlined in the ‘Guide for the Care and Use of Laboratory Animals’ prepared by the National Academy of Sciences and published by the National Institutes of Health.

Arriazu E., Ge X., Leung T.M., Magdaleno F., Lopategi A., Lu Y., Kitamura N., Urtasun R., Theise N., Antoine D.J, & Nieto N. (2016). Signalling via the osteopontin and high mobility group box-1 axis drives the fibrogenic response to liver injury. Gut, 66(6), 1123-1137.

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