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| The alpha-MHC-MerCreMer transgene has the mouse Myh6 promoter (myosin, heavy polypeptide 6, cardiac muscle, alpha; alpha-MHC) directing expression of a tamoxifen-inducible Cre recombinase (MerCreMer) to juvenile and adult cardiac myocytes. When alpha-MHC-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 alpha-MHC-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 . | |||||||||||||||||||
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Description
Strain Information
Former Names B6;129-Tg(Myh6-cre/Esr1)1Jmk/J (Changed: 30-MAR-10 ) B6129-Tg(Myh6-cre/Esr1)1Jmk/J (Changed: 21-JUL-09 ) B6129-Tg(Myh6-cre/Esr1)1Jmk (Changed: 13-MAR-06 ) Type Mutant Stock; Transgenic; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Mating System Homozygote x Homozygote (Female x Male) 17-MAR-06 Species laboratory mouse Generation +N1F12 (25-MAR-11)
Generation DefinitionsDonating Investigator Jeffery D. Molkentin, Children's Hospital Medical Center Description
The alpha-MHC-MerCreMer transgene has the mouse Myh6 promoter (myosin, heavy polypeptide 6, cardiac muscle, alpha; alpha-MHC) directing expression of a tamoxifen-inducible Cre recombinase (MerCreMer) to juvenile and adult cardiac myocytes. Mice homozygous for the alpha-MHC-MerCreMer transgene are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. 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. Insertion of this transgene and its protein show no changes in echocardiography, heart mass or pathology, or hypertrophy marker genes compared to nontransgenic littermates. Of note, the MerCreMer double fusion protein has substantially greater Cre recombinase activity with less promiscuity compared with the CreMer single fusion protein. When alpha-MHC-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 alpha-MHC-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 .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.
Development
The alpha-MHC-MerCreMer transgene was designed with the mouse Myh6 promoter (myosin, heavy polypeptide 6, cardiac muscle, alpha; alpha-MHC) upstream of the MerCreMer protein. 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 alpha-MHC-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. alpha-MHC-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. Upon arrival, mutant mice were bred with B6129SF1/J mice (Stock No. 101043) to establish the colony. Mutant mice were then bred together to generate a homozygous colony.
Control Information
| Control | ||
|---|---|---|
| 101045 B6129SF2/J | (approximate) | |
| Considerations for Choosing Controls | ||
Related Strains
Strains carrying Tg(Myh6-cre/Esr1*)1Jmk allele
005657 B6.FVB(129)-Tg(Myh6-cre/Esr1*)1Jmk/J View Strains carrying Tg(Myh6-cre/Esr1*)1Jmk (1 strain)
Additional Web Information
Introduction to Cre-lox technology
Phenotype
Phenotype Information
This mouse can be used to support research in many areas including:
cre relatedCardiovascular Research
Heart Abnormalities
Developmental Biology Research
Internal/Organ Defects
heart
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: Cre-lox System
Tissue/Cell Markers: Cre-lox System
Research Tools
Cre-lox System
Genetics Research
Mutagenesis and Transgenesis
Mutagenesis and Transgenesis: Cre-lox System
Genes & Alleles
Gene & Allele Information provided by MGI
| Allele Symbol | Tg(Myh6-cre/Esr1*)1Jmk | ||
|---|---|---|---|
| Allele Name | transgene insertion 1, Jeffery D Molkentin | ||
| Allele Type | Transgenic (Cre/Flp) | ||
| Common Name(s) | MCM; MerCreMer; Tg(Myh6-cre/Esr1)1Jmk; alpha-MHC-MerCreMer; alphaMHC-Cre-Mer-Cre; mER-CRE-mER; mer; | ||
| Mutation Made By | Jeffery Molkentin, Children's Hospital Medical Center | ||
| Strain of Origin | FVB | ||
| 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 | ||
| Expressed Gene | cre, cre recombinase, bacteriophage P1 | ||
| Cre recombinase is an enzyme derived from the bacteriophage P1 that specifically recognizes loxP sites. Cre has been shown to effectively mediate the excision of DNA located between loxP sites. After the excision event, the DNA ends recombine leaving a single loxP site in place of the intervening sequence. | |||
| Promoter | Myh6, myosin, heavy polypeptide 6, cardiac muscle, alpha, murine, murine | ||
| Gene Symbol and Name | Tg(Myh6-cre/Esr1*)1Jmk, transgene insertion 1, Jeffery D Molkentin | ||
| Chromosome | UN | ||
| Gene Common Name(s) | MCM; MerCreMer; Tg(Myh6-cre/Esr1)1Jmk; alpha-MHC-MerCreMer; alphaMHC-Cre-Mer-Cre; mer; | ||
| Driver Note | Myh6 | ||
| Inducible Note | induced by tamoxifen | ||
| 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. [MGI Ref ID J:82027] | ||
Genotyping
Genotyping Information
Genotyping Protocols
Generic Cre Quantitative PCR, QPCR
Generic Cre, Standard PCR
Tg(cre/Esr1), Standard PCR
Helpful Links
Genotyping resources and troubleshooting
References
References provided by MGI
Selected Reference(s)
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: 11440973] [MGI Ref ID J:82027]
Additional References
Tg(Myh6-cre/Esr1*)1Jmk relatedAgarwal 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: 20634485] [MGI Ref ID 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: 20364083] [MGI Ref ID 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: 22326846] [MGI Ref ID J:183806]
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: 19328205] [MGI Ref ID 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: 19894134] [MGI Ref ID J:159266]
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: 21220308] [MGI Ref ID 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: 22326951] [MGI Ref ID 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: 19632177] [MGI Ref ID J:157327]
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: 20852327] [MGI Ref ID 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: 22589547] [MGI Ref ID J:188370]
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: 21223971] [MGI Ref ID J:171016]
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: 16738313] [MGI Ref ID J:109612]
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: 21507952] [MGI Ref ID 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: 20071776] [MGI Ref ID J:156680]
Di RM; Feng QT; Chang Z; Luan Q; Zhang YY; Huang J; Li XL; Yang ZZ. 2010. PDK1 plays a critical role in regulating cardiac function in mice and human. Chin Med J (Engl) 123(17):2358-63. [PubMed: 21034549] [MGI Ref ID J:168636]
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: 22504483] [MGI Ref ID J:183926]
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: 20167673] [MGI Ref ID 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: 20864565] [MGI Ref ID J:185900]
Gaborit N; Sakuma R; Wylie JN; Kim KH; Zhang SS; Hui CC; Bruneau BG. 2012. Cooperative and antagonistic roles for Irx3 and Irx5 in cardiac morphogenesis and postnatal physiology. Development 139(21):4007-19. [PubMed: 22992950] [MGI Ref ID J:189007]
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: 18391012] [MGI Ref ID J:137268]
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: 22133878] [MGI Ref ID J:184413]
Hall ME; Smith G; Hall JE; Stec DE. 2011. Systolic dysfunction in cardiac-specific ligand-inducible MerCreMer transgenic mice. Am J Physiol Heart Circ Physiol 301(1):H253-60. [PubMed: 21536850] [MGI Ref ID J:173254]
Herrmann S; Stieber J; Stockl G; Hofmann F; Ludwig A. 2007. HCN4 provides a 'depolarization reserve' and is not required for heart rate acceleration in mice. EMBO J 26(21):4423-32. [PubMed: 17914461] [MGI Ref ID J:139560]
Horstkotte J; Perisic T; Schneider M; Lange P; Schroeder M; Kiermayer C; Hinkel R; Ziegler T; Mandal PK; David R; Schulz S; Schmitt S; Widder J; Sinowatz F; Becker BF; Bauersachs J; Naebauer M; Franz WM; Jeremias I; Brielmeier M; Zischka H; Conrad M; Kupatt C. 2011. Mitochondrial thioredoxin reductase is essential for early postischemic myocardial protection. Circulation 124(25):2892-902. [PubMed: 22144571] [MGI Ref ID J:193792]
Huang J; Min Lu M; Cheng L; Yuan LJ; Zhu X; Stout AL; Chen M; Li J; Parmacek MS. 2009. Myocardin is required for cardiomyocyte survival and maintenance of heart function. Proc Natl Acad Sci U S A 106(44):18734-9. [PubMed: 19850880] [MGI Ref ID J:154666]
Ichikawa Y; Bayeva M; Ghanefar M; Potini V; Sun L; Mutharasan RK; Wu R; Khechaduri A; Jairaj Naik T; Ardehali H. 2012. Disruption of ATP-binding cassette B8 in mice leads to cardiomyopathy through a decrease in mitochondrial iron export. Proc Natl Acad Sci U S A 109(11):4152-7. [PubMed: 22375032] [MGI Ref ID J:182234]
Ito K; Akazawa H; Tamagawa M; Furukawa K; Ogawa W; Yasuda N; Kudo Y; Liao CH; Yamamoto R; Sato T; Molkentin JD; Kasuga M; Noda T; Nakaya H; Komuro I. 2009. PDK1 coordinates survival pathways and beta-adrenergic response in the heart. Proc Natl Acad Sci U S A 106(21):8689-94. [PubMed: 19429709] [MGI Ref ID J:150014]
Iversen PO; Andersson KB; Finsen AV; Sjaastad I; von Lueder TG; Sejersted OM; Attramadal H; Christensen G. 2010. Separate mechanisms cause anemia in ischemic vs. nonischemic murine heart failure. Am J Physiol Regul Integr Comp Physiol 298(3):R808-14. [PubMed: 20032264] [MGI Ref ID J:159263]
Kalsotra A; Wang K; Li PF; Cooper TA. 2010. MicroRNAs coordinate an alternative splicing network during mouse postnatal heart development. Genes Dev 24(7):653-8. [PubMed: 20299448] [MGI Ref ID J:158730]
Kim BE; Turski ML; Nose Y; Casad M; Rockman HA; Thiele DJ. 2010. Cardiac copper deficiency activates a systemic signaling mechanism that communicates with the copper acquisition and storage organs. Cell Metab 11(5):353-63. [PubMed: 20444417] [MGI Ref ID J:160929]
Koitabashi N; Bedja D; Zaiman AL; Pinto YM; Zhang M; Gabrielson KL; Takimoto E; Kass DA. 2009. Avoidance of transient cardiomyopathy in cardiomyocyte-targeted tamoxifen-induced MerCreMer gene deletion models. Circ Res 105(1):12-5. [PubMed: 19520971] [MGI Ref ID J:164749]
Koitabashi N; Danner T; Zaiman AL; Pinto YM; Rowell J; Mankowski J; Zhang D; Nakamura T; Takimoto E; Kass DA. 2011. Pivotal role of cardiomyocyte TGF-beta signaling in the murine pathological response to sustained pressure overload. J Clin Invest 121(6):2301-12. [PubMed: 21537080] [MGI Ref ID J:173921]
Kostetskii I; Li J; Xiong Y; Zhou R; Ferrari VA; Patel VV; Molkentin JD; Radice GL. 2005. Induced deletion of the N-cadherin gene in the heart leads to dissolution of the intercalated disc structure. Circ Res 96(3):346-54. [PubMed: 15662031] [MGI Ref ID J:98828]
Kratsios P; Catela C; Salimova E; Huth M; Berno V; Rosenthal N; Mourkioti F. 2010. Distinct roles for cell-autonomous Notch signaling in cardiomyocytes of the embryonic and adult heart. Circ Res 106(3):559-72. [PubMed: 20007915] [MGI Ref ID J:170885]
Lavine KJ; Kovacs A; Ornitz DM. 2008. Hedgehog signaling is critical for maintenance of the adult coronary vasculature in mice. J Clin Invest 118(7):2404-14. [PubMed: 18568073] [MGI Ref ID J:137685]
Lavine KJ; White AC; Park C; Smith CS; Choi K; Long F; Hui CC; Ornitz DM. 2006. Fibroblast growth factor signals regulate a wave of Hedgehog activation that is essential for coronary vascular development. Genes Dev 20(12):1651-66. [PubMed: 16778080] [MGI Ref ID J:109722]
Li J; Levin MD; Xiong Y; Petrenko N; Patel VV; Radice GL. 2008. N-cadherin haploinsufficiency affects cardiac gap junctions and arrhythmic susceptibility. J Mol Cell Cardiol 44(3):597-606. [PubMed: 18201716] [MGI Ref ID J:133753]
Li J; Patel VV; Kostetskii I; Xiong Y; Chu AF; Jacobson JT; Yu C; Morley GE; Molkentin JD; Radice GL. 2005. Cardiac-specific loss of N-cadherin leads to alteration in connexins with conduction slowing and arrhythmogenesis. Circ Res 97(5):474-81. [PubMed: 16100040] [MGI Ref ID J:112334]
Li J; Swope D; Raess N; Cheng L; Muller EJ; Radice GL. 2011. Cardiac tissue-restricted deletion of plakoglobin results in progressive cardiomyopathy and activation of {beta}-catenin signaling. Mol Cell Biol 31(6):1134-44. [PubMed: 21245375] [MGI Ref ID J:170618]
Li R; Wu Y; Manso AM; Gu Y; Liao P; Israeli S; Yajima T; Nguyen U; Huang MS; Dalton ND; Peterson KL; Ross RS. 2012. beta1 integrin gene excision in the adult murine cardiac myocyte causes defective mechanical and signaling responses. Am J Pathol 180(3):952-62. [PubMed: 22248583] [MGI Ref ID J:181934]
Li Y; Yin R; Liu J; Wang P; Wu S; Luo J; Zhelyabovska O; Yang Q. 2009. Peroxisome proliferator-activated receptor delta regulates mitofusin 2 expression in the heart. J Mol Cell Cardiol 46(6):876-82. [PubMed: 19265701] [MGI Ref ID J:157147]
Lin X; Yang X; Li Q; Ma Y; Cui S; He D; Lin X; Schwartz RJ; Chang J. 2012. Protein tyrosine phosphatase-like A regulates myoblast proliferation and differentiation through MyoG and the cell cycling signaling pathway. Mol Cell Biol 32(2):297-308. [PubMed: 22106411] [MGI Ref ID J:183657]
Lisewski U; Shi Y; Wrackmeyer U; Fischer R; Chen C; Schirdewan A; Juttner R; Rathjen F; Poller W; Radke MH; Gotthardt M. 2008. The tight junction protein CAR regulates cardiac conduction and cell-cell communication. J Exp Med 205(10):2369-79. [PubMed: 18794341] [MGI Ref ID J:140109]
Loffredo FS; Steinhauser ML; Gannon J; Lee RT. 2011. Bone marrow-derived cell therapy stimulates endogenous cardiomyocyte progenitors and promotes cardiac repair. Cell Stem Cell 8(4):389-98. [PubMed: 21474103] [MGI Ref ID J:171357]
Louch WE; Hougen K; Mork HK; Swift F; Aronsen JM; Sjaastad I; Reims HM; Roald B; Andersson KB; Christensen G; Sejersted OM. 2010. Sodium accumulation promotes diastolic dysfunction in end-stage heart failure following Serca2 knockout. J Physiol 588(Pt 3):465-78. [PubMed: 20008467] [MGI Ref ID J:159265]
Lu Z; Jiang YP; Wang W; Xu XH; Mathias RT; Entcheva E; Ballou LM; Cohen IS; Lin RZ. 2009. Loss of cardiac phosphoinositide 3-kinase p110 alpha results in contractile dysfunction. Circulation 120(4):318-25. [PubMed: 19597047] [MGI Ref ID J:166421]
Lu Z; Wu CY; Jiang YP; Ballou LM; Clausen C; Cohen IS; Lin RZ. 2012. Suppression of Phosphoinositide 3-Kinase Signaling and Alteration of Multiple Ion Currents in Drug-Induced Long QT Syndrome. Sci Transl Med 4(131):131ra50. [PubMed: 22539774] [MGI Ref ID J:183985]
Makino A; Suarez J; Wang H; Belke DD; Scott BT; Dillmann WH. 2009. Thyroid hormone receptor-beta is associated with coronary angiogenesis during pathological cardiac hypertrophy. Endocrinology 150(4):2008-15. [PubMed: 19074585] [MGI Ref ID J:158077]
McGaffin KR; Witham WG; Yester KA; Romano LC; O'Doherty RM; McTiernan CF; O'Donnell CP. 2011. Cardiac-specific leptin receptor deletion exacerbates ischaemic heart failure in mice. Cardiovasc Res 89(1):60-71. [PubMed: 20833647] [MGI Ref ID J:167785]
Meissner M; Weissgerber P; Londono JE; Prenen J; Link S; Ruppenthal S; Molkentin JD; Lipp P; Nilius B; Freichel M; Flockerzi V. 2011. Moderate Calcium Channel Dysfunction in Adult Mice with Inducible Cardiomyocyte-specific Excision of the cacnb2 Gene. J Biol Chem 286(18):15875-82. [PubMed: 21357697] [MGI Ref ID J:172090]
Moellendorf S; Kessels C; Peiseler L; Raupach A; Jacoby C; Vogt N; Lindecke A; Koch L; Bruning J; Heger J; Kohrer K; Godecke A. 2012. IGF-IR signaling attenuates the age-related decline of diastolic cardiac function. Am J Physiol Endocrinol Metab 303(2):E213-22. [PubMed: 22589390] [MGI Ref ID J:187250]
Moga MA; Nakamura T; Robbins J. 2008. Genetic approaches for changing the heart and dissecting complex syndromes. J Mol Cell Cardiol 45(2):148-55. [PubMed: 18601931] [MGI Ref ID J:139282]
Moshal KS; Kumar M; Tyagi N; Mishra PK; Metreveli N; Rodriguez WE; Tyagi SC. 2009. Restoration of contractility in hyperhomocysteinemia by cardiac-specific deletion of NMDA-R1. Am J Physiol Heart Circ Physiol 296(3):H887-92. [PubMed: 19181966] [MGI Ref ID J:146860]
Nakai A; Yamaguchi O; Takeda T; Higuchi Y; Hikoso S; Taniike M; Omiya S; Mizote I; Matsumura Y; Asahi M; Nishida K; Hori M; Mizushima N; Otsu K. 2007. The role of autophagy in cardiomyocytes in the basal state and in response to hemodynamic stress. Nat Med 13(5):619-24. [PubMed: 17450150] [MGI Ref ID J:121778]
Parlakian A; Charvet C; Escoubet B; Mericskay M; Molkentin JD; Gary-Bobo G; De Windt LJ; Ludosky MA; Paulin D; Daegelen D; Tuil D; Li Z. 2005. Temporally controlled onset of dilated cardiomyopathy through disruption of the SRF gene in adult heart. Circulation 112(19):2930-9. [PubMed: 16260633] [MGI Ref ID J:135043]
Peng J; Raddatz K; Molkentin JD; Wu Y; Labeit S; Granzier H; Gotthardt M. 2007. Cardiac hypertrophy and reduced contractility in hearts deficient in the titin kinase region. Circulation 115(6):743-51. [PubMed: 17261657] [MGI Ref ID J:132331]
Petrich BG; Molkentin JD; Wang Y. 2003. Temporal activation of c-Jun N-terminal kinase in adult transgenic heart via cre-loxP-mediated DNA recombination. FASEB J 17(6):749-51. [PubMed: 12594183] [MGI Ref ID J:128410]
Poomvanicha M; Wegener JW; Blaich A; Fischer S; Domes K; Moosmang S; Hofmann F. 2011. Facilitation and Ca2+-dependent inactivation are modified by mutation of the Ca(v)1.2 channel IQ motif. J Biol Chem 286(30):26702-7. [PubMed: 21665954] [MGI Ref ID J:175463]
Porrello ER; Mahmoud AI; Simpson E; Johnson BA; Grinsfelder D; Canseco D; Mammen PP; Rothermel BA; Olson EN; Sadek HA. 2013. Regulation of neonatal and adult mammalian heart regeneration by the miR-15 family. Proc Natl Acad Sci U S A 110(1):187-92. [PubMed: 23248315] [MGI Ref ID J:192621]
Qian J; Ling S; Castillo AC; Long B; Birnbaum Y; Ye Y. 2012. Regulation of phosphatase and tensin homolog on chromosome 10 in response to hypoxia. Am J Physiol Heart Circ Physiol 302(9):H1806-17. [PubMed: 22367504] [MGI Ref ID J:186577]
Raake PW; Vinge LE; Gao E; Boucher M; Rengo G; Chen X; DeGeorge BR Jr; Matkovich S; Houser SR; Most P; Eckhart AD; Dorn GW 2nd; Koch WJ. 2008. G protein-coupled receptor kinase 2 ablation in cardiac myocytes before or after myocardial infarction prevents heart failure. Circ Res 103(4):413-22. [PubMed: 18635825] [MGI Ref ID J:152649]
Rosati B; Yan Q; Lee MS; Liou SR; Ingalls B; Foell J; Kamp TJ; McKinnon D. 2011. Robust L-type calcium current expression following heterozygous knockout of the Cav1.2 gene in adult mouse heart. J Physiol 589(Pt 13):3275-88. [PubMed: 21521762] [MGI Ref ID J:189406]
Ruan H; Li J; Ren S; Gao J; Li G; Kim R; Wu H; Wang Y. 2009. Inducible and cardiac specific PTEN inactivation protects ischemia/reperfusion injury. J Mol Cell Cardiol 46(2):193-200. [PubMed: 19038262] [MGI Ref ID J:149180]
Ruan H; Mitchell S; Vainoriene M; Lou Q; Xie LH; Ren S; Goldhaber JI; Wang Y. 2007. Gi alpha 1-mediated cardiac electrophysiological remodeling and arrhythmia in hypertrophic cardiomyopathy. Circulation 116(6):596-605. [PubMed: 17646583] [MGI Ref ID J:139853]
Sano M; Minamino T; Toko H; Miyauchi H; Orimo M; Qin Y; Akazawa H; Tateno K; Kayama Y; Harada M; Shimizu I; Asahara T; Hamada H; Tomita S; Molkentin JD; Zou Y; Komuro I. 2007. p53-induced inhibition of Hif-1 causes cardiac dysfunction during pressure overload. Nature 446(7134):444-8. [PubMed: 17334357] [MGI Ref ID J:120332]
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Smith S; Witkowski A; Moghul A; Yoshinaga Y; Nefedov M; de Jong P; Feng D; Fong L; Tu Y; Hu Y; Young SG; Pham T; Cheung C; Katzman SM; Brand MD; Quinlan CL; Fens M; Kuypers F; Misquitta S; Griffey SM; Tran S; Gharib A; Knudsen J; Hannibal-Bach HK; Wang G; Larkin S; Thweatt J; Pasta S. 2012. Compromised mitochondrial fatty acid synthesis in transgenic mice results in defective protein lipoylation and energy disequilibrium. PLoS One 7(10):e47196. [PubMed: 23077570] [MGI Ref ID J:192213]
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Health & husbandry
Health & Colony Maintenance Information
Animal Health Reports
Room Number AX12
Colony Maintenance
Breeding & Husbandry When maintaining a live colony, these mice may be bred as homozygotes. Mating System Homozygote x Homozygote (Female x Male) 17-MAR-06 Diet Information LabDiet® 5K52/5K67
Pricing and Purchasing
Pricing, Supply Level & Notes, Controls
| Pricing for USA, Canada and Mexico shipping destinations |
|
Live Mice
Price per mouse (US dollars $) Gender Genotypes Provided Individual Mouse $232.00 Female or Male Homozygous for Tg(Myh6-cre/Esr1*)1Jmk
Price per Pair (US dollars $) Pair Genotype $464.00 Homozygous for Tg(Myh6-cre/Esr1*)1Jmk x Homozygous for Tg(Myh6-cre/Esr1*)1Jmk Standard Supply
Repository-Live. Repository-Live represents an exclusive set of over 1500 unique mouse models maintained at The Jackson Laboratory to support a vast array of research areas. The breeding colonies for Repository Strains provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. Repository-live orders are treated as custom orders. Within 2 business days, we respond to each availability inquiry or order with various delivery options. Repository Strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping.
| Pricing for International shipping destinations |
|
Live Mice
Price per mouse (US dollars $) Gender Genotypes Provided Individual Mouse $301.60 Female or Male Homozygous for Tg(Myh6-cre/Esr1*)1Jmk
Price per Pair (US dollars $) Pair Genotype $603.20 Homozygous for Tg(Myh6-cre/Esr1*)1Jmk x Homozygous for Tg(Myh6-cre/Esr1*)1Jmk Standard Supply
Repository-Live. Repository-Live represents an exclusive set of over 1500 unique mouse models maintained at The Jackson Laboratory to support a vast array of research areas. The breeding colonies for Repository Strains provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. Repository-live orders are treated as custom orders. Within 2 business days, we respond to each availability inquiry or order with various delivery options. Repository Strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping.
|
|
|
Standard Supply
Repository-Live. Repository-Live represents an exclusive set of over 1500 unique mouse models maintained at The Jackson Laboratory to support a vast array of research areas. The breeding colonies for Repository Strains provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. Repository-live orders are treated as custom orders. Within 2 business days, we respond to each availability inquiry or order with various delivery options. Repository Strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping.
General Supply Notes
- Genomic DNA is available for this strain from the Mouse DNA Resource.
Control Information
| Control | ||
|---|---|---|
| 101045 B6129SF2/J | (approximate) | |
| Considerations for Choosing Controls | ||
| Control Pricing Information for Genetically Engineered Mutant Strains. | ||
Payment Terms and Conditions
Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.
See Terms of Use tab for General Terms and Conditions
The Jackson Laboratory's Genotype Promise
The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.Ordering Information
JAX® Mice
Surgical and Preconditioning Services
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Tel: 1-800-422-6423 or 1-207-288-5845
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Terms of Use
Terms of Use
General Terms and Conditions
For Licensing and Use Restrictions view the link(s) below:
- Mice are subject to US Patent 6040430.
- Use of MICE by companies or for-profit entities requires a license prior to shipping.
Contact information
General inquiries regarding Terms of UseContracts Administration
| phone: | 207-288-6470 |
| fax: | 207-288-6655 |
JAX® Mice, Products & Services Conditions of Use
"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "RECIPIENT" means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.No Warranty
MICE, PRODUCTS AND SERVICES ARE PROVIDED “AS IS”. JACKSON EXTENDS NO WARRANTIES OF ANY KIND, EITHER EXPRESS, IMPLIED, OR STATUTORY, WITH RESPECT TO MICE, PRODUCTS OR SERVICES, INCLUDING ANY IMPLIED WARRANTY OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE, OR ANY WARRANTY OF NON-INFRINGEMENT OF ANY PATENT, TRADEMARK, OR OTHER INTELLECTUAL PROPERTY RIGHTS.
In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.
No Liability
In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. Unless prohibited by law, in purchasing or receiving MICE, PRODUCTS or services from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.
MICE and PRODUCTS are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.
The foregoing represents the General Terms and Conditions applicable to JACKSON’s MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and services by JACKSON, and by its licensees and distributors.
Acceptance of delivery of MICE, PRODUCTS or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or services by JACKSON.