RhoA-floxed mice (RhoAfl/fl: C57BL/6 background), in which exon 3 of the Rhoa gene was flanked by loxP sites, were generated and used in our previous study (46 (link)). The mice were then mated with C57BL/6 mice expressing Cre recombinase under the control of the α-myosin heavy chain promoter (Myh6-Cre; Jackson Laboratory) to generate cardiomyocyte-specific RhoA cKO mice. In the Myh6-Cre mice, Cre exerts its recombination activity specifically in cardiomyocytes but not in other tissues such as the liver, lung, skeletal muscle, and spleen (47 (link)), and the recombinase functions from embryonic day 9.5 (48 (link)). Mice harboring RhoAfl/fl alleles alone were used as controls. The mice were housed in specific pathogen-free conditions at the Research Centre for Animal Life Science of Shiga University of Medical Science. All animal protocols were in accordance with institutional guidelines, including Animal Research Reporting of In Vivo Experiments (ARRIVE) guidelines, and were approved by the Animal Care and Use Committee of Shiga University of Medical Science (No. 2020-9-8).
Myh6 cre
Manufactured by Jackson ImmunoResearch
Sourced in United States
Myh6-Cre is a Cre recombinase transgene that is expressed under the control of the myosin heavy chain 6 (Myh6) promoter. This promoter drives expression specifically in cardiomyocytes.
Automatically generated - may contain errors
Lab products found in correlation
Myh6 mercremer, by Jackson ImmunoResearch (1 mentions)
Nkx2.5 cre, by Jackson ImmunoResearch (1 mentions)
Smad4fl fl mice, by Jackson ImmunoResearch (1 mentions)
Mercremer, by Jackson ImmunoResearch (1 mentions)
P53flox, by Jackson ImmunoResearch (1 mentions)
Alb cre, by Jackson ImmunoResearch (1 mentions)
Ckm cre, by Jackson ImmunoResearch (1 mentions)
Adipoq cre, by Jackson ImmunoResearch (1 mentions)
9 protocols using myh6 cre
1
Cardiomyocyte-Specific RhoA Knockout Mice
2
Genetically Engineered Mice for TrkB.T1 and BDNF
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TrkB.T1 knockout and conditional mutant mice were generated as described previously (Dorsey et al., 2006 (link)). BDNF-HA mice (Yang et al., 2009 (link)) were a gift of B. Hempstead (Cornell University, New York, NY). BDNF conditional (Rios et al., 2001 (link)) mutants as well as Myh6-cre (Agah et al., 1997 (link)) and Cadherin5-cre (Alva et al., 2006 (link)) transgenic mice were obtained from the Jackson Laboratory. The Rosa26floxedLacZ mouse (strain 003474; The Jackson Laboratory) was used as a Cre reporter strain to test the tissue/cellular expression pattern of cre transgenic mice. Animals were bred in a specific, pathogen-free facility with food and water ad libitum. All experimental procedures followed the National Institutes of Health guidelines for animal care and use and were approved by the National Cancer Institute at Frederick Animal Care and Use Committee.
3
Cardiomyocyte-Specific QKI Knockout Mice
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Animal studies were approved by the Institutional Animal Care and Use Committee of the University of Amsterdam and carried out in compliance with the guidelines of this institution and the Directive 2010/63/EU of the European Parliament. Animal husbandry was performed by the Animal Research Institute AMC.
Cardiomyocyte-specific knock-out mice of Qki were generated by crossing the previously generated Qki-floxed mice13 (link) with the conditional Myh6-Cre (Jackson Laboratory stock #011038) and with the tamoxifen-inducible Myh6-MerCreMer (Jackson Laboratory stock #005657)22 (link) in C57BL/6N background. In all experiments, mice had a single copy of the Cre or the MerCreMer (MCM) recombinase allele. Males and females were included in the experiments.
For inducing MerCreMer recombinase activity, a tamoxifen solution (2.5 mg/mL tamoxifen in 10% ethanol, 90% sunflower oil) was injected intraperitoneally for 4 consecutive days (total dose: 100 mg tamoxifen/kg mouse) in 12–17-week-old mice (n per group: 5 ciQKI WT, 6 ciQKI HET, and 9 ciQKI KO).
Echocardiography and electrocardiogram (ECG) recordings were performed as indicated in theSupplemental Methods .
Cardiomyocyte-specific knock-out mice of Qki were generated by crossing the previously generated Qki-floxed mice13 (link) with the conditional Myh6-Cre (Jackson Laboratory stock #011038) and with the tamoxifen-inducible Myh6-MerCreMer (Jackson Laboratory stock #005657)22 (link) in C57BL/6N background. In all experiments, mice had a single copy of the Cre or the MerCreMer (MCM) recombinase allele. Males and females were included in the experiments.
For inducing MerCreMer recombinase activity, a tamoxifen solution (2.5 mg/mL tamoxifen in 10% ethanol, 90% sunflower oil) was injected intraperitoneally for 4 consecutive days (total dose: 100 mg tamoxifen/kg mouse) in 12–17-week-old mice (n per group: 5 ciQKI WT, 6 ciQKI HET, and 9 ciQKI KO).
Echocardiography and electrocardiogram (ECG) recordings were performed as indicated in the
4
Transgenic Mouse Strains for Genetic Studies
5
Generation of Cardiomyocyte-Specific SMAD4 Knockout Mice
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To achieve conditional deletion of SMAD4 specifically in CM, SMAD4fl/fl mice (Stock No. 017462, The Jackson Laboratory, Bar Harbor, Maine) were crossed with mice carrying the MerCreMer (MCM) transgene driven by the alpha-myosin heavy chain promoter (Myh6-Cre+/+) (Stock No. 005657, The Jackson Laboratory). Further details of generation and characterization of the CM-specific SMAD4 knockout (KO) mice are described in the Results section. The Institutional Animal Care and Use Committee of Vanderbilt University Medical Center approved all animal procedures and treatments used in this study (protocol #M1700133-00).
6
Targeted Cardiac Proteomic Analysis
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Animals were housed in pathogen‐free animal facility at the University of Pittsburgh with ad libitum access to food and water. The Mybpc3−/− mice used in the present study were generated previously.4 (link) Briefly, mice with a knockout first tm1a allele of the Mybpc3 gene (Mybpc3tm1a) in C57BL/6J background were crossed with an ACTB:Flp deleter line to create a conditional Mybpc3 allele (Mybpc3tm1c) and then crossed with a CMV:Cre line to generate the germline null allele of Mybpc3−/−. Cardiomyocyte deletion of p53 was accomplished by crossing Mybpc3−/− with p53flox (Jackson 008462) and Myh6Cre+/− (Jackson 011038) to generate Mybpc3−/−/p53 fl/flMyh6Cre+/− animals. The transgenic mouse lines expressing human wild‐type troponin T2, cardiac type (TNNT2WT), or mutant cardiac troponin T (TNNT2I79N)9 (link) (kindly provided by Bjorn Knollmann, Vanderbilt University) were crossed into a C57BL/6J genetic background for a minimum of 6 generations before analysis. Investigators were blinded to animal genotyping and/or treatment at time of data collection, and no animals were excluded from analysis. The sample size (n) included per group was stated in each figure legend.
7
Generation and Characterization of Ptpmt1 Conditional Mice
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Ptpmt1fl/+ mice with the C57Bl/6 background were generated in our previous study (Yu et al., 2013 (link)). Ckm-Cre+ (Brüning et al., 1998 (link)) (Stock# 006475), Myh6-Cre+ (Agah et al., 1997 (link)) (Stock# 011038), Alb-Cre+ (Postic et al., 1999 (link)) (Stock# 003574), and Adipoq-Cre+ (Eguchi et al., 2011 (link)) (Stock# 010803) mice with the C57BL/6 background were purchased from the Jackson Laboratory. To avoid potential side effects of Cre, Ptpmt1+/+/Cre+ were used as controls for Ptpmt1fl/fl/Cre+ and the Cre transgene was hemizygous in both mouse types. In initial pilot experiments, we examined Ptpmt1+/+/Cre+ and no defects were observed in these animals. Mice were kept under specific pathogen-free conditions in Case Western Reserve University Animal Resources Center and Emory University Division of Animal Resources (Protocol # PROTO201700884). Mice of the same age, sex, and genotype were randomly grouped for subsequent analyses (investigators were not blinded). All animal procedures complied with the NIH Guidelines for the Care and Use of Laboratory Animals and were approved by the Institutional Animal Care and Use Committee.
8
Studying Vsig4 Knockout Mice
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cGAS-/- (Stock No. 026554) Sting-flox (Stock No. 031670), iDTR (Stock No. 007900; Cre-inducible expression of diphtheria toxin receptor), Myh6-Cre (Stock No. 011038), Clec4f-Cre (Stock No. 033296) mice were received from the Jackson Laboratory. Vsig4-/- mice (C57BL/6J-Vsig4em1Smoc) were received from Shanghai model organisms. Vsig4 wild-type (WT) mice were produced by crossing Vsig4 heterozygous mice together. Ageing mice used in these studies were 100-108 wks old, and young mice were 8-12 wks old. To block Vsig4 function, young Myh6Cre+Stingf/f male mice were injected with purified Vsig4 antibodies before gut mEV treatment. through tail vein injection. All mice were maintained on a 12/12 hr light-dark cycle. All animal procedures were performed in accordance with the University of California, San Diego Research Guidelines for the Care and Use of Laboratory Animals, and all animals were randomly assigned to cohorts when used.
9
Cardiomyocyte-specific Afadin Knockout
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Conditional Knockout Mice C57BL/6 mice with homozygous floxed exon 2 of the afadin gene were crossed with mice expressing Cre recombinase under the control of the α-myosin heavy chain gene promoter (Myh6-Cre; Jackson Laboratory, Bar Harbor, ME, USA). This was performed to create afadin cKO with selective afadin deletion in cardiomyocytes. 18, (link)19 Mice harboring afadin-floxed alleles alone were used as controls.
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