JAX
Mouse Strain Datasheet - 005657
B6.FVB(129)-A1cfTg(Myh6-cre/Esr1*)1Jmk/J
Also Known As: αMHC-MerCreMer
The alpha-MHC-MerCreMer (αMHC-MerCreMer) transgene has the mouse cardiac-specific alpha-myosin heavy chain promoter (αMHC or alpha-MHC; Myh6) directing expression of a tamoxifen-inducible Cre recombinase (MerCreMer) to juvenile and adult cardiac myocytes. These αMHC-MerCreMer transgenic mice allow the creation of bitransgenic mice for Cre-lox studies of temporally regulated deletion of loxP-flanked targeted genes in cardiac tissues/cells.
Donating Investigator
IMR Colony, The Jackson Laboratory
Genetic overview
| Genetic Background | Generation |
|---|---|
|
N10F13
|
A1cfTg(Myh6-cre/Esr1*)1Jmk
| Allele Type |
|---|
| Transgenic (Inducible, Null/Knockout, Recombinase-expressing) |
Research Applications
- Cardiovascular Research
- Developmental Biology Research
- Internal/Organ Research
- Research Tools
Detailed Description
The alpha;MHC-MerCreMer transgene has the mouse cardiac-specific alpha-myosin heavy chain promoter (αMHC or alpha-MHC; Myh6) directing expression of a tamoxifen-inducible Cre recombinase (MerCreMer) to juvenile and adult cardiac myocytes. Mice homozygous for the αMHC-MerCreMer transgene are viable and fertile prior to tamoxifen administration. Cre recombinase expression in heart tissue is confirmed by western blot. Southern blot confirmed heart cell-specificity compared to brain, kidney, lung, liver and skeletal muscle.
The MerCreMer double fusion protein has substantially greater Cre recombinase activity with less promiscuity compared with the CreMer single fusion protein. When αMHC-MerCreMer transgenic mice are bred with mice containing loxP-flanked sequences, tamoxifen-inducible Cre-mediated recombination is expected to result in deletion of the floxed sequences in heart cells of the offspring. These αMHC-MerCreMer transgenic mice allow the creation of double mutant/bitransgenic animals for Cre-lox studies of temporally regulated deletion of loxP-flanked targeted genes in cardiac tissues/cells.
View cre expression characterization.
A 2013 publication reported that αMHC-MerCreMer transgenic mice given multi-dose tamoxifen injections develop heart defects (Lexow et al. 2013 Dis Model Mech; PMID:23929940). Specifically, those defects were decreased cardiac function, focal fibrosis (left ventricle, septum and right ventricle), focal cell infiltration into the myocardium, significantly elevated proinflammatory markers (IL1β, IL6, TNFα, IFNγ and Ccl2) and significantly elevated cardiac remodeling markers (ANF, BNP and Col3A1). Importantly, a single tamoxifen injection (40 mg tamoxifen/kg body weight) resulted in the same uniform recombination in cardiomyocyte fibers without the cardiomyopathological effects. Therefore, it is strongly recommended that the most appropriate induction method for each model be determined prior to extensive experimentation, and the optimal dose of tamoxifen be adjusted to the lowest concentration required for achieving sufficient recombination. Please refer to Lexow et al. 2013 for a detailed discussion.
A 2016 publication extensively characterized the transgene insertion site (Harkins and Whitton 2016 Transgenic Res; PMID:27165291) using the C57BL/6-congenic αMHC-MerCreMer strain (Stock No. 005657, which was derived from Stock No. 005650). Their study revealed the insertion site on chromosome 19 was accompanied by a 19.5 kbp deletion of genomic DNA (chr19:31,852,891-31,872,392 bp). The deleted region spans a portion of the A1cf locus (including the promoter, exon 1 and part of intron 1), as well as several computer-predicted regulatory sites. This deletion eradicates A1cf protein expression in the expected gene-dosage fashion: hepatic A1CF protein levels were highest in non-carriers (C57BL/6J), intermediate in hemizygotes and undetectable in homozygotes. Importantly, in the tissue expressing MerCreMer (heart), no A1CF protein was detected in non-carriers (C57BL/6J), hemizygotes or homozygotes. To mitigate any effects of A1CF-deficiency, researchers should distinguish the zygosity of the αMHC-MerCreMer mice most suitable for their experiment.
Harkins and Whitton 2016 also described the transgene components and sequence rearrangements; these aspects are more fully reviewed in the strain development section. Regarding expression, these additional elements have not been reported to have any adverse effects on the cell specificity of transgene expression nor the efficacy of tamoxifen-inducible Cre recombinase activity.
The MerCreMer double fusion protein consists of Cre recombinase flanked on each end with a mutated murine estrogen receptor (mer) ligand binding domain (amino acids 281-599, G525R); which does not bind its natural ligand (17β-estradiol) at physiological concentrations but will bind the synthetic estrogen receptor ligands 4-hydroxytamoxifen (OHT or tamoxifen) and, with lesser sensitivity, ICI 182780. Restricted to the cytoplasm, MerCreMer can only gain access to the nuclear compartment after exposure to tamoxifen. To counteract the mixed estrogen agonist effects of tamoxifen injections, which can result in late fetal abortions in pregnant mice, progesterone may be coadministered.
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. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
Development
The alpha-MHC-MerCreMer (αMHC-MerCreMer) transgene was designed with the mouse Myh6 promoter (myosin, heavy polypeptide 6, cardiac muscle, alpha; alpha-MHC) upstream of the MerCreMer protein (see additional information below). The MerCreMer double fusion protein has a Cre recombinase cDNA sequence flanked on each end with a mutated murine estrogen receptor (mer) ligand binding domain (amino acids 281-599, G525R); thus rendering cre expression tamoxifen-inducible yet estrogen-insensitive. The αMHC-MerCreMer transgene was microinjected into FVB/N embryos. These embryos were implanted into pseudopregnant FVB/N females. Mice from founder line 1 demonstrated robust MerCreMer protein expression (107 kDa) in the juvenile and adult heart. αMHC-MerCreMer mice from line 1 were backcrossed to mice with a (B6 x 129/Sv)F1 genetic background for 15 generations prior to arrival at The Jackson Laboratory Repository (as Stock No. 005650). Upon arrival, some mice were backcrossed to C57BL/6J inbred mice (Stock No. 000664) for several generations to generate this congenic strain (Stock No. 005657). As of July 2011, the colony has been backcrossed onto C57BL/6J for at least nine generations.
Additional information: a 2016 publication extensively characterized the transgene insertion site (Harkins and Whitton 2016 Transgenic Res; PMID:27165291) using the C57BL/6-congenic αMHC-MerCreMer strain (Stock No. 005657). Their study revealed:
(i) the original transgene was designed with MerCreMer followed by a 60 bp multiple cloning site (MCS) and then ~480 bp sequence from the human growth hormone transcriptional terminator (HGHt)
(ii) several regions of transgenic sequence are rearranged/duplicated/inverted adjacent to both sides of the original transgene (additional details below)
(iii) the transgene insertion on chromosome 19 concomitantly caused a 19.5 kbp deletion of chromosome 19 DNA (chr19:31,852,891-31,872,392 bp) that spans a portion of the APOBEC1 complementation factor locus (A1cf; including the promoter, exon 1 and part of intron 1), as well as several computer-predicted regulatory sites.
Regarding (ii): a number of upstream transgene rearrangements and duplications were identified, but not fully characterized as these additional elements have not been reported to have any adverse effects on the cell specificity of transgene expression nor the efficacy of tamoxifen-inducible Cre recombinase activity. In the region downstream of the first HGHt sequence, they identified (from 5' to 3') a DraI-containing MCS, a complex set of short duplicated/inverted regions from the αMHC promoter sequence (RptsProm - composed of five rearranged promoter tracts that varied in length [from 70-142 bp]; one in direct orientation, and the remainder inverted), another duplication encompassing the latter 321 bp of Mer (RptMer), an EcoRV-containing MCS, a duplicated copy of HGHt (RptHGHt), another different MCS and a short 60 bp repeat from Mer (that constitutes the 3' terminus of the inserted transgene).
Expression Data
| Expressed Gene | cre, cre recombinase, bacteriophage P1 |
|---|---|
| Site of Expression | tamoxifen inducible (yet estrogen insensitive) Cre recombinase protein fused to two mutant estrogen-receptor ligand-binding domains (MerCreMer); expression in developing and adult heart |
Control Suggestions
Selected References
- Sohal DS; Nghiem M; Crackower MA; Witt SA; Kimball TR; Tymitz KM; Penninger JM; Molkentin JD. 2001. Temporally regulated and tissue-specific gene manipulations in the adult and embryonic heart using a tamoxifen-inducible Cre protein. Circ Res 89(1):20-5. PubMed: 11440973MGI: J:82027
A1cfTg(Myh6-cre/Esr1*)1Jmk
Allele Symbol: A1cfTg(Myh6-cre/Esr1*)1Jmk
| Allele Name | transgene insertion 1, Jeffery D Molkentin |
|---|---|
| Allele Type | Transgenic (Inducible, Null/Knockout, Recombinase-expressing) |
| Allele Synonym(s) | CM-MCM; MCM; MerCreMer; Myh6-MerCreMer; Tg(Myh6-cre/Esr1)1Jmk; alpha-MHC-MerCreMer; alphaMHC-Cre-Mer-Cre; mER-CRE-mER; mer |
| Gene Symbol and Name | A1cf, APOBEC1 complementation factor |
| Gene Synonym(s) | 1810073H04Rik; 1810073H04Rik; A1cft; ACF; ACF64; ACF65; APOBEC1CF; ASP; Acf; Apobec-1; RIKEN cDNA 1810073H04 gene; Tg(Myh6-cre/Esr1)1Jmk; Tg(Myh6-cre/Esr1*)1Jmk; apobec-1 complementation factor; transgene insertion 1, Jeffery D Molkentin |
| Promoter | Myh6, myosin, heavy polypeptide 6, cardiac muscle, alpha, murine, murine |
| Expressed Gene | cre, cre recombinase, bacteriophage P1 |
| Site of Expression | tamoxifen inducible (yet estrogen insensitive) Cre recombinase protein fused to two mutant estrogen-receptor ligand-binding domains (MerCreMer); expression in developing and adult heart |
| Strain of Origin | FVB/N |
| Chromosome | 19 |
| Molecular Note | This transgene expresses a cre recombinase/ mutant estrogen receptor ligand binding domain fusion protein under the control of a mouse cardiac-specific alpha-myosin heavy chain promoter. Expression was detected in the juvenile and adult heart, but the protein is inactive until induced with tamoxifen. Integration of the transgene in to Chr. 19 deleted a 19,500 bp fragment including the promoter, exon 1, and part of intron 1 of the A1cf gene. Western analysis of liver from homozygous transgenic mice does not detect A1cf protein. |
| Mutations Made By | Jeffery Molkentin, Cincinnati Children's Hospital |
Disease Terms
Research Areas By Genotype
This mouse can be used to support research in many areas including:
- Cardiovascular Research
- Heart Abnormalities
- Developmental Biology Research
- Internal/Organ Defects
- heart
- Internal/Organ Defects
- Internal/Organ Research
- Heart Abnormalities
- Research Tools
- Cardiovascular Research
- Cre-lox System
- Cre-lox System
- Cre Recombinase Expression
- Cre Recombinase Expression: Inducible
- Developmental Biology Research
- Cre-lox System
- Genetics Research
- Mutagenesis and Transgenesis
- Mutagenesis and Transgenesis: Cre-lox System
- Tissue/Cell Markers
- Tissue/Cell Markers: Cre-lox System
- Cardiovascular Research
Genotype: cre related
- Research Tools
- Cre-lox System
- Genetics Research
- Mutagenesis and Transgenesis
- Mutagenesis and Transgenesis: Cre-lox System
References
- Sohal DS; Nghiem M; Crackower MA; Witt SA; Kimball TR; Tymitz KM; Penninger JM; Molkentin JD. 2001. Temporally regulated and tissue-specific gene manipulations in the adult and embryonic heart using a tamoxifen-inducible Cre protein. Circ Res 89(1):20-5. PubMed: 11440973MGI: J:82027
Additional - A1cfTg(Myh6-cre/Esr1*)1Jmk related
- Agarwal U; Ghalayini W; Dong F; Weber K; Zou YR; Rabbany SY; Rafii S; Penn MS. 2010. Role of cardiac myocyte CXCR4 expression in development and left ventricular remodeling after acute myocardial infarction. Circ Res 107(5):667-76. PubMed: 20634485MGI: J:175028
- Ahuja P; Zhao P; Angelis E; Ruan H; Korge P; Olson A; Wang Y; Jin ES; Jeffrey FM; Portman M; Maclellan WR. 2010. Myc controls transcriptional regulation of cardiac metabolism and mitochondrial biogenesis in response to pathological stress in mice. J Clin Invest 120(5):1494-505. PubMed: 20364083MGI: J:161484
- Ali R; Huang Y; Maher SE; Kim RW; Giordano FJ; Tellides G; Geirsson A. 2012. miR-1 mediated suppression of Sorcin regulates myocardial contractility through modulation of Ca2+ signaling. J Mol Cell Cardiol 52(5):1027-37. PubMed: 22326846MGI: J:183806
- Ali S; Ussher JR; Baggio LL; Kabir MG; Charron MJ; Ilkayeva O; Newgard CB; Drucker DJ. 2015. Cardiomyocyte glucagon receptor signaling modulates outcomes in mice with experimental myocardial infarction. Mol Metab 4(2):132-43. PubMed: 25685700MGI: J:220981
- Ali SR; Hippenmeyer S; Saadat LV; Luo L; Weissman IL; Ardehali R. 2014. Existing cardiomyocytes generate cardiomyocytes at a low rate after birth in mice. Proc Natl Acad Sci U S A 111(24):8850-5. PubMed: 24876275MGI: J:211645
- Althof N; Harkins S; Kemball CC; Flynn CT; Alirezaei M; Whitton JL. 2014. In vivo ablation of type I interferon receptor from cardiomyocytes delays coxsackieviral clearance and accelerates myocardial disease. J Virol 88(9):5087-99. PubMed: 24574394MGI: J:214430
- Andersson KB; Birkeland JA; Finsen AV; Louch WE; Sjaastad I; Wang Y; Chen J; Molkentin JD; Chien KR; Sejersted OM; Christensen G. 2009. Moderate heart dysfunction in mice with inducible cardiomyocyte-specific excision of the Serca2 gene. J Mol Cell Cardiol 47(2):180-7. PubMed: 19328205MGI: J:157143
- Andersson KB; Winer LH; Mork HK; Molkentin JD; Jaisser F. 2009. Tamoxifen administration routes and dosage for inducible Cre-mediated gene disruption in mouse hearts. Transgenic Res :. PubMed: 19894134MGI: J:159266
- Bakker ML; Boink GJ; Boukens BJ; Verkerk AO; van den Boogaard M; den Haan AD; Hoogaars WM; Buermans HP; de Bakker JM; Seppen J; Tan HL; Moorman AF; 't Hoen PA; Christoffels VM. 2012. T-box transcription factor TBX3 reprogrammes mature cardiac myocytes into pacemaker-like cells. Cardiovasc Res 94(3):439-49. PubMed: 22419669MGI: J:200811
- Bao MW; Zhang XJ; Li L; Cai Z; Liu X; Wan N; Hu G; Wan F; Zhang R; Zhu X; Xia H; Li H. 2015. Cardioprotective role of growth/differentiation factor 1 in post-infarction left ventricular remodelling and dysfunction. J Pathol 236(3):360-72. PubMed: 25726944MGI: J:222749
- Baruscotti M; Bucchi A; Viscomi C; Mandelli G; Consalez G; Gnecchi-Rusconi T; Montano N; Casali KR; Micheloni S; Barbuti A; Difrancesco D. 2011. Deep bradycardia and heart block caused by inducible cardiac-specific knockout of the pacemaker channel gene Hcn4. Proc Natl Acad Sci U S A 108(4):1705-10. PubMed: 21220308MGI: J:168248
- Battiprolu PK; Hojayev B; Jiang N; Wang ZV; Luo X; Iglewski M; Shelton JM; Gerard RD; Rothermel BA; Gillette TG; Lavandero S; Hill JA. 2012. Metabolic stress-induced activation of FoxO1 triggers diabetic cardiomyopathy in mice. J Clin Invest 122(3):1109-18. PubMed: 22326951MGI: J:184484
- Bersell K; Arab S; Haring B; Kuhn B. 2009. Neuregulin1/ErbB4 signaling induces cardiomyocyte proliferation and repair of heart injury. Cell 138(2):257-70. PubMed: 19632177MGI: J:157327
- Bersell K; Choudhury S; Mollova M; Polizzotti BD; Ganapathy B; Walsh S; Wadugu B; Arab S; Kuhn B. 2013. Moderate and high amounts of tamoxifen in alpha-MHC-MerCreMer mice induce a DNA damage response, leading to heart failure and death. Dis Model Mech 6(6):1459-69. PubMed: 23929941MGI: J:200993
- Bharadwaj KG; Hiyama Y; Hu Y; Huggins LA; Ramakrishnan R; Abumrad NA; Shulman GI; Blaner WS; Goldberg IJ. 2010. Chylomicron- and VLDL-derived lipids enter the heart through different pathways: in vivo evidence for receptor- and non-receptor-mediated fatty acid uptake. J Biol Chem 285(49):37976-86. PubMed: 20852327MGI: J:167341
- Blaich A; Pahlavan S; Tian Q; Oberhofer M; Poomvanicha M; Lenhardt P; Domes K; Wegener JW; Moosmang S; Ruppenthal S; Scholz A; Lipp P; Hofmann F. 2012. Mutation of the calmodulin binding motif IQ of the L-type Ca(v)1.2 Ca2+ channel to EQ induces dilated cardiomyopathy and death. J Biol Chem 287(27):22616-25. PubMed: 22589547MGI: J:188370
- Boardman NT; Aronsen JM; Louch WE; Sjaastad I; Willoch F; Christensen G; Sejersted O; Aasum E. 2014. Impaired left ventricular mechanical and energetic function in mice after cardiomyocyte-specific excision of Serca2. Am J Physiol Heart Circ Physiol 306(7):H1018-24. PubMed: 24486508MGI: J:210089
- Bolli R; Stein AB; Guo Y; Wang OL; Rokosh G; Dawn B; Molkentin JD; Sanganalmath SK; Zhu Y; Xuan YT. 2011. A murine model of inducible, cardiac-specific deletion of STAT3: its use to determine the role of STAT3 in the upregulation of cardioprotective proteins by ischemic preconditioning. J Mol Cell Cardiol 50(4):589-97. PubMed: 21223971MGI: J:171016
- Bround MJ; Asghari P; Wambolt RB; Bohunek L; Smits C; Philit M; Kieffer TJ; Lakatta EG; Boheler KR; Moore ED; Allard MF; Johnson JD. 2012. Cardiac ryanodine receptors control heart rate and rhythmicity in adult mice. Cardiovasc Res 96(3):372-80. PubMed: 22869620MGI: J:210083
- Bround MJ; Wambolt R; Cen H; Asghari P; Albu RF; Han J; McAfee D; Pourrier M; Scott NE; Bohunek L; Kulpa JE; Chen SR; Fedida D; Brownsey RW; Borchers CH; Foster LJ; Mayor T; Moore ED; Allard MF; Johnson JD. 2016. Cardiac Ryanodine Receptor (Ryr2)-mediated Calcium Signals Specifically Promote Glucose Oxidation via Pyruvate Dehydrogenase. J Biol Chem 291(45):23490-23505. PubMed: 27621312MGI: J:237376
- Bround MJ; Wambolt R; Luciani DS; Kulpa JE; Rodrigues B; Brownsey RW; Allard MF; Johnson JD. 2013. Cardiomyocyte ATP production, metabolic flexibility, and survival require calcium flux through cardiac ryanodine receptors in vivo. J Biol Chem 288(26):18975-86. PubMed: 23678000MGI: J:199652
- Bull M; Methawasin M; Strom J; Nair P; Hutchinson K; Granzier H. 2016. Alternative Splicing of Titin Restores Diastolic Function in an HFpEF-Like Genetic Murine Model (TtnDeltaIAjxn). Circ Res 119(6):764-72. PubMed: 27470639MGI: J:237829
- Cao DJ; Jiang N; Blagg A; Johnstone JL; Gondalia R; Oh M; Luo X; Yang KC; Shelton JM; Rothermel BA; Gillette TG; Dorn GW; Hill JA. 2013. Mechanical unloading activates FoxO3 to trigger Bnip3-dependent cardiomyocyte atrophy. J Am Heart Assoc 2(2):e000016. PubMed: 23568341MGI: J:196679
- Chang HC; Wu R; Shang M; Sato T; Chen C; Shapiro JS; Liu T; Thakur A; Sawicki KT; Prasad SV; Ardehali H. 2016. Reduction in mitochondrial iron alleviates cardiac damage during injury. EMBO Mol Med 8(3):247-67. PubMed: 26896449MGI: J:229593
- Chen J; Huang ZP; Seok HY; Ding J; Kataoka M; Zhang Z; Hu X; Wang G; Lin Z; Wang S; Pu WT; Liao R; Wang DZ. 2013. mir-17-92 cluster is required for and sufficient to induce cardiomyocyte proliferation in postnatal and adult hearts. Circ Res 112(12):1557-66. PubMed: 23575307MGI: J:213298
- Chen PP; Patel JR; Powers PA; Fitzsimons DP; Moss RL. 2012. Dissociation of structural and functional phenotypes in cardiac myosin-binding protein C conditional knockout mice. Circulation 126(10):1194-205. PubMed: 22829020MGI: J:202199
- Chen WY; Hong J; Gannon J; Kakkar R; Lee RT. 2015. Myocardial pressure overload induces systemic inflammation through endothelial cell IL-33. Proc Natl Acad Sci U S A 112(23):7249-54. PubMed: 25941360MGI: J:222767
- Chen X; Shevtsov SP; Hsich E; Cui L; Haq S; Aronovitz M; Kerkela R; Molkentin JD; Liao R; Salomon RN; Patten R; Force T. 2006. The beta-catenin/T-cell factor/lymphocyte enhancer factor signaling pathway is required for normal and stress-induced cardiac hypertrophy. Mol Cell Biol 26(12):4462-73. PubMed: 16738313MGI: J:109612
- Chen Y; Decker KF; Zheng D; Matkovich SJ; Jia L; Dorn GW 2nd. 2013. A nucleus-targeted alternately spliced Nix/Bnip3L protein isoform modifies nuclear factor kappaB (NFkappaB)-mediated cardiac transcription. J Biol Chem 288(22):15455-65. PubMed: 23603904MGI: J:199612
- Chen Y; Liu Y; Dorn GW 2nd. 2011. Mitochondrial fusion is essential for organelle function and cardiac homeostasis. Circ Res 109(12):1327-31. PubMed: 22052916MGI: J:192714
- Cheng L; Yung A; Covarrubias M; Radice GL. 2011. Cortactin Is Required for N-cadherin Regulation of Kv1.5 Channel Function. J Biol Chem 286(23):20478-89. PubMed: 21507952MGI: J:173489
- Chintalgattu V; Ai D; Langley RR; Zhang J; Bankson JA; Shih TL; Reddy AK; Coombes KR; Daher IN; Pati S; Patel SS; Pocius JS; Taffet GE; Buja LM; Entman ML; Khakoo AY. 2010. Cardiomyocyte PDGFR-beta signaling is an essential component of the mouse cardiac response to load-induced stress. J Clin Invest 120(2):472-84. PubMed: 20071776MGI: J:156680
- Coleman JL; Brennan K; Ngo T; Balaji P; Graham RM; Smith NJ. 2015. Rapid Knockout and Reporter Mouse Line Generation and Breeding Colony Establishment Using EUCOMM Conditional-Ready Embryonic Stem Cells: A Case Study. Front Endocrinol (Lausanne) 6:105. PubMed: 26175717MGI: J:236578
- Deng KQ; Wang A; Ji YX; Zhang XJ; Fang J; Zhang Y; Zhang P; Jiang X; Gao L; Zhu XY; Zhao Y; Gao L; Yang Q; Zhu XH; Wei X; Pu J; Li H. 2016. Suppressor of IKKvarepsilon is an essential negative regulator of pathological cardiac hypertrophy. Nat Commun 7:11432. PubMed: 27249321MGI: J:239911
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- Diaz-Trelles R; Scimia MC; Bushway P; Tran D; Monosov A; Monosov E; Peterson K; Rentschler S; Cabrales P; Ruiz-Lozano P; Mercola M. 2016. Notch-independent RBPJ controls angiogenesis in the adult heart. Nat Commun 7:12088. PubMed: 27357444MGI: J:240788
- Dirkx E; Gladka MM; Philippen LE; Armand AS; Kinet V; Leptidis S; El Azzouzi H; Salic K; Bourajjaj M; da Silva GJ; Olieslagers S; van der Nagel R; de Weger R; Bitsch N; Kisters N; Seyen S; Morikawa Y; Chanoine C; Heymans S; Volders PG; Thum T; Dimmeler S; Cserjesi P; Eschenhagen T; da Costa Martins PA; De Windt LJ. 2013. Nfat and miR-25 cooperate to reactivate the transcription factor Hand2 in heart failure. Nat Cell Biol 15(11):1282-93. PubMed: 24161931MGI: J:208305
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- Eckle T; Hartmann K; Bonney S; Reithel S; Mittelbronn M; Walker LA; Lowes BD; Han J; Borchers CH; Buttrick PM; Kominsky DJ; Colgan SP; Eltzschig HK. 2012. Adora2b-elicited Per2 stabilization promotes a HIF-dependent metabolic switch crucial for myocardial adaptation to ischemia. Nat Med 18(5):774-82. PubMed: 22504483MGI: J:183926
- Enomoto D; Obana M; Miyawaki A; Maeda M; Nakayama H; Fujio Y. 2015. Cardiac-specific ablation of the STAT3 gene in the subacute phase of myocardial infarction exacerbated cardiac remodeling. Am J Physiol Heart Circ Physiol 309(3):H471-80. PubMed: 26055795MGI: J:226366
- Ericsson M; Andersson KB; Amundsen BH; Torp SH; Sjaastad I; Christensen G; Sejersted OM; Ellingsen O. 2010. High-intensity exercise training in mice with cardiomyocyte-specific disruption of Serca2. J Appl Physiol 108(5):1311-20. PubMed: 20167673MGI: J:185849
- Ericsson M; Sjaland C; Andersson KB; Sjaastad I; Christensen G; Sejersted OM; Ellingsen O. 2010. Exercise training before cardiac-specific Serca2 disruption attenuates the decline in cardiac function in mice. J Appl Physiol 109(6):1749-55. PubMed: 20864565MGI: J:185900
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- Fassett JT; Xu X; Kwak D; Wang H; Liu X; Hu X; Bache RJ; Chen Y. 2013. Microtubule Actin Cross-linking Factor 1 regulates cardiomyocyte microtubule distribution and adaptation to hemodynamic overload. PLoS One 8(9):e73887. PubMed: 24086300MGI: J:206484
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- Georges R; Nemer G; Morin M; Lefebvre C; Nemer M. 2008. Distinct expression and function of alternatively spliced Tbx5 isoforms in cell growth and differentiation. Mol Cell Biol 28(12):4052-67. PubMed: 18391012MGI: J:137268
- Gong G; Song M; Csordas G; Kelly DP; Matkovich SJ; Dorn GW 2nd. 2015. Parkin-mediated mitophagy directs perinatal cardiac metabolic maturation in mice. Science 350(6265):aad2459. PubMed: 26785495MGI: J:229454
- Gonzalez-Valdes I; Hidalgo I; Bujarrabal A; Lara-Pezzi E; Padron-Barthe L; Garcia-Pavia P; Gomez P; Redondo JM; Ruiz-Cabello JM; Jimenez-Borreguero LJ; Enriquez JA; de la Pompa JL; Hidalgo A; Gonzalez S. 2015. Bmi1 limits dilated cardiomyopathy and heart failure by inhibiting cardiac senescence. Nat Commun 6:6473. PubMed: 25751743MGI: J:221894
- Goonasekera SA; Hammer K; Auger-Messier M; Bodi I; Chen X; Zhang H; Reiken S; Elrod JW; Correll RN; York AJ; Sargent MA; Hofmann F; Moosmang S; Marks AR; Houser SR; Bers DM; Molkentin JD. 2012. Decreased cardiac L-type Ca(2)(+) channel activity induces hypertrophy and heart failure in mice. J Clin Invest 122(1):280-90. PubMed: 22133878MGI: J:184413
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