A1cf

Summary

Gene Symbol: A1cf
Description: APOBEC1 complementation factor
Alias: 1810073H04Rik, ACF64, ACF65, ASP, Acf, MCM, MerCreMer, Tg(Myh6-cre/Esr1*)1Jmk, mer, APOBEC1 complementation factor, APOBEC-1 stimulating protein, APOBEC1-stimulating protein, Tg(Myh6-cre/Esr1)1Jmk, alpha-MHC-MerCreMer, alphaMHC-Cre-Mer-Cre, apobec-1 complementation factor
Species: mouse
Products:     A1cf

Top Publications

  1. Nakai A, Yamaguchi O, Takeda T, Higuchi Y, Hikoso S, Taniike M, et al. The role of autophagy in cardiomyocytes in the basal state and in response to hemodynamic stress. Nat Med. 2007;13:619-24 pubmed
  2. Andersson K, Birkeland J, Finsen A, Louch W, Sjaastad I, Wang Y, et al. Moderate heart dysfunction in mice with inducible cardiomyocyte-specific excision of the Serca2 gene. J Mol Cell Cardiol. 2009;47:180-7 pubmed publisher
    ..Our data demonstrate that SR-independent Ca(2+) transport mechanisms temporarily can prevent major cardiac dysfunction despite a major reduction of SERCA2 in cardiomyocytes. ..
  3. Hall M, Smith G, Hall J, Stec D. Systolic dysfunction in cardiac-specific ligand-inducible MerCreMer transgenic mice. Am J Physiol Heart Circ Physiol. 2011;301:H253-60 pubmed publisher
    ..To circumvent this limitation, a widely used inducible cardiac-specific model, Myh6-MerCreMer (Cre), using tamoxifen (TAM) to activate Cre has been developed...
  4. Bround M, Asghari P, Wambolt R, Bohunek L, Smits C, Philit M, et al. Cardiac ryanodine receptors control heart rate and rhythmicity in adult mice. Cardiovasc Res. 2012;96:372-80 pubmed publisher
    ..Given that RYR2 levels can be reduced in pathological conditions, including heart failure and diabetic cardiomyopathy, we predict that RYR2 loss contributes to disease-associated bradycardia, arrhythmia, and sudden death. ..
  5. Lu Z, Jiang Y, Wang W, Xu X, Mathias R, Entcheva E, et al. Loss of cardiac phosphoinositide 3-kinase p110 alpha results in contractile dysfunction. Circulation. 2009;120:318-25 pubmed publisher
    ..PI3K p110alpha but not p110beta regulates the LTCC in cardiac myocytes. Decreased signaling to p110alpha reduces the number of LTCCs on the cell surface and thus attenuates I(Ca,L) and contractility. ..
  6. Raake P, Vinge L, Gao E, Boucher M, Rengo G, Chen X, et al. G protein-coupled receptor kinase 2 ablation in cardiac myocytes before or after myocardial infarction prevents heart failure. Circ Res. 2008;103:413-22 pubmed publisher
    ..but was ablated after birth (alphaMHC-Cre x GRK2 fl/fl) or only after administration of tamoxifen (alphaMHC-MerCreMer x GRK2 fl/fl) and examined the consequences of GRK2 ablation before and after surgical coronary artery ligation ..
  7. van Oort R, Garbino A, Wang W, Dixit S, Landstrom A, Gaur N, et al. Disrupted junctional membrane complexes and hyperactive ryanodine receptors after acute junctophilin knockdown in mice. Circulation. 2011;123:979-88 pubmed publisher
    ..Thus, our novel approach of cardiac-specific short hairpin RNA-mediated knockdown of junctophilin-2 has uncovered a critical role for junctophilin in intracellular Ca2+ release in the heart. ..
  8. Andersson K, Winer L, Mørk H, Molkentin J, Jaisser F. Tamoxifen administration routes and dosage for inducible Cre-mediated gene disruption in mouse hearts. Transgenic Res. 2010;19:715-25 pubmed publisher
    ..Fusion of mutant estrogen receptor ligand-binding domains to Cre recombinase (Cre-ER(T), MerCreMer) combined with cardiac-directed gene expression has been used to generate several cardiac-specific tamoxifen-..
  9. Wang D, Patel V, Ricciotti E, Zhou R, Levin M, Gao E, et al. Cardiomyocyte cyclooxygenase-2 influences cardiac rhythm and function. Proc Natl Acad Sci U S A. 2009;106:7548-52 pubmed publisher
    ..The COX-2 gene was floxed and crossed into merCremer mice under the alpha-myosin heavy-chain promoter...

More Information

Publications95

  1. Li J, Patel V, Kostetskii I, Xiong Y, Chu A, Jacobson J, et al. Cardiac-specific loss of N-cadherin leads to alteration in connexins with conduction slowing and arrhythmogenesis. Circ Res. 2005;97:474-81 pubmed
    ..Our data suggest that perturbation of the N-cadherin/catenin complex in heart disease may be an underlying cause, leading to the establishment of the arrythmogenic substrate by destabilizing gap junctions at the cell surface. ..
  2. Battiprolu P, Hojayev B, Jiang N, Wang Z, Luo X, Iglewski M, et al. Metabolic stress-induced activation of FoxO1 triggers diabetic cardiomyopathy in mice. J Clin Invest. 2012;122:1109-18 pubmed publisher
    ..Together, these data suggest that activation of FoxO1 is an important mediator of diabetic cardiomyopathy and is a promising therapeutic target for the disease. ..
  3. Bharadwaj K, Hiyama Y, Hu Y, Huggins L, Ramakrishnan R, Abumrad N, et al. 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. 2010;285:37976-86 pubmed publisher
    ..Endogenously labeled mouse chylomicrons were produced by tamoxifen treatment of ?-actin-MerCreMer/LpL(flox/flox) mice. Induced loss of LpL increased TG levels >10-fold and reduced HDL by >50%...
  4. Louch W, Hougen K, Mørk H, Swift F, Aronsen J, Sjaastad I, et al. Sodium accumulation promotes diastolic dysfunction in end-stage heart failure following Serca2 knockout. J Physiol. 2010;588:465-78 pubmed publisher
    ..Our observations indicate that if cytosolic Na(+) gain is prevented, up-regulated Ca(2+) extrusion mechanisms can maintain near-normal diastolic function in the absence of SERCA2. ..
  5. Koitabashi N, Bedja D, Zaiman A, Pinto Y, Zhang M, Gabrielson K, et al. Avoidance of transient cardiomyopathy in cardiomyocyte-targeted tamoxifen-induced MerCreMer gene deletion models. Circ Res. 2009;105:12-5 pubmed publisher
    Cardiac myocyte targeted MerCreMer transgenic mice expressing tamoxifen-inducible Cre driven by the alpha-myosin heavy chain promoter are increasingly used to control gene expression in the adult heart...
  6. Touvron M, Escoubet B, Mericskay M, Angelini A, Lamotte L, Santini M, et al. Locally expressed IGF1 propeptide improves mouse heart function in induced dilated cardiomyopathy by blocking myocardial fibrosis and SRF-dependent CTGF induction. Dis Model Mech. 2012;5:481-91 pubmed publisher
    ..Locally acting mIGF1 efficiently protects the myocardium from these adverse processes, and might thus represent a therapeutic avenue to counter DCM. ..
  7. Loffredo F, Steinhauser M, Gannon J, Lee R. Bone marrow-derived cell therapy stimulates endogenous cardiomyocyte progenitors and promotes cardiac repair. Cell Stem Cell. 2011;8:389-98 pubmed publisher
    ..Therapy with c-kit(+) cells but not mesenchymal stem cells improved cardiac function. These findings suggest that stimulation of endogenous cardiogenic progenitor activity is a critical mechanism of cardiac cell therapy. ..
  8. Noh H, Okajima K, Molkentin J, Homma S, Homma S, Goldberg I. Acute lipoprotein lipase deletion in adult mice leads to dyslipidemia and cardiac dysfunction. Am J Physiol Endocrinol Metab. 2006;291:E755-60 pubmed
    ..Cardiac specific loss of LPL in 8-wk-old mice was produced by a 2-wk tamoxifen treatment of MerCreMer (MCM)/Lpl(flox/flox) mice...
  9. Stokke M, Hougen K, Sjaastad I, Louch W, Briston S, Enger U, et al. Reduced SERCA2 abundance decreases the propensity for Ca2+ wave development in ventricular myocytes. Cardiovasc Res. 2010;86:63-71 pubmed publisher
    ..SERCA2 knockout [Serca2(flox/flox) Tg(alphaMHC-MerCreMer); KO] mice allowing inducible cardiomyocyte-specific disruption of the Serca2 gene in adult mice were compared ..
  10. Swift F, Franzini Armstrong C, Øyehaug L, Enger U, Andersson K, Christensen G, et al. Extreme sarcoplasmic reticulum volume loss and compensatory T-tubule remodeling after Serca2 knockout. Proc Natl Acad Sci U S A. 2012;109:3997-4001 pubmed publisher
    ..T-tubule proliferation occurs without loss of the original ordered transverse orientation and thus constitutes the basis for compensation of the declining SR function without structural disarrangement...
  11. Sohal D, Nghiem M, Crackower M, Witt S, Kimball T, Tymitz K, et al. Temporally regulated and tissue-specific gene manipulations in the adult and embryonic heart using a tamoxifen-inducible Cre protein. Circ Res. 2001;89:20-5 pubmed
    ..a tamoxifen-inducible Cre recombinase protein fused to two mutant estrogen-receptor ligand-binding domains (MerCreMer) under the control of the alpha-myosin heavy chain promoter...
  12. Parlakian A, Charvet C, Escoubet B, Mericskay M, Molkentin J, Gary Bobo G, et al. Temporally controlled onset of dilated cardiomyopathy through disruption of the SRF gene in adult heart. Circulation. 2005;112:2930-9 pubmed
    ..These cardiac-specific SRF-deficient mice have the morphological and clinical features of acquired dilated cardiomyopathy in humans and may therefore be used as an inducible model of this disorder. ..
  13. Bround M, Wambolt R, Luciani D, Kulpa J, Rodrigues B, Brownsey R, et al. Cardiomyocyte ATP production, metabolic flexibility, and survival require calcium flux through cardiac ryanodine receptors in vivo. J Biol Chem. 2013;288:18975-86 pubmed publisher
    ..RYR2-mediated Ca(2+) fluxes are therefore proximal controllers of mitochondrial Ca(2+), ATP levels, and a cascade of transcription factors controlling metabolism and survival. ..
  14. Bersell K, Arab S, Haring B, Kuhn B. Neuregulin1/ErbB4 signaling induces cardiomyocyte proliferation and repair of heart injury. Cell. 2009;138:257-70 pubmed publisher
    ..Undifferentiated progenitor cells did not contribute to NRG1-induced cardiomyocyte proliferation. Thus, increasing the activity of the NRG1/ErbB4 signaling pathway may provide a molecular strategy to promote myocardial regeneration. ..
  15. Ichikawa Y, Bayeva M, Ghanefar M, Potini V, Sun L, Mutharasan R, et al. 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. 2012;109:4152-7 pubmed publisher
    ..In summary, this report provides characterization of a protein involved in mitochondrial iron export. ..
  16. Peng J, Raddatz K, Molkentin J, Wu Y, Labeit S, Granzier H, et al. Cardiac hypertrophy and reduced contractility in hearts deficient in the titin kinase region. Circulation. 2007;115:743-51 pubmed
    ..These novel functions of titin might provide a rationale for future therapeutic approaches to attenuate or reverse symptoms of heart failure. ..
  17. Kalume F, Westenbroek R, Cheah C, Yu F, Oakley J, Scheuer T, et al. Sudden unexpected death in a mouse model of Dravet syndrome. J Clin Invest. 2013;123:1798-808 pubmed publisher
    ..These results have important implications for prevention of SUDEP in DS patients. ..
  18. Wang W, Landstrom A, Wang Q, Munro M, Beavers D, Ackerman M, et al. Reduced junctional Na+/Ca2+-exchanger activity contributes to sarcoplasmic reticulum Ca2+ leak in junctophilin-2-deficient mice. Am J Physiol Heart Circ Physiol. 2014;307:H1317-26 pubmed publisher
    ..Cardiac myocytes isolated from tamoxifen-inducible conditional knockdown mice of JPH2 (MCM-shJPH2) were subjected to confocal Ca(2+) imaging...
  19. Chang H, Wu R, Shang M, Sato T, Chen C, Shapiro J, et al. Reduction in mitochondrial iron alleviates cardiac damage during injury. EMBO Mol Med. 2016;8:247-67 pubmed publisher
    ..Overall, our findings suggest that mitochondrial iron contributes to cardiac ischemic damage, and may be a novel therapeutic target against ischemic heart disease. ..
  20. Yamaguchi T, Suzuki T, Sato T, Takahashi A, Watanabe H, Kadowaki A, et al. The CCR4-NOT deadenylase complex controls Atg7-dependent cell death and heart function. Sci Signal. 2018;11: pubmed publisher
    ..Thus, mRNA deadenylation mediated by the CCR4-NOT complex is crucial to prevent Atg7-induced cell death and heart failure, suggesting a role for mRNA deadenylation in targeting autophagy genes to maintain normal cardiac homeostasis. ..
  21. Hamdi H, Boitard S, Planat Bénard V, Pouly J, Neamatalla H, Joanne P, et al. Efficacy of epicardially delivered adipose stroma cell sheets in dilated cardiomyopathy. Cardiovasc Res. 2013;99:640-7 pubmed publisher
    ..These protective effects were also accompanied by a reduction of myocardial fibrosis. These results strongly suggest the functional relevance of epicardially delivered cell-seeded biomaterials to non-ischaemic heart failure. ..
  22. Paul D, Grevengoed T, Pascual F, Ellis J, Willis M, Coleman R. Deficiency of cardiac Acyl-CoA synthetase-1 induces diastolic dysfunction, but pathologic hypertrophy is reversed by rapamycin. Biochim Biophys Acta. 2014;1841:880-7 pubmed publisher
    ..These data indicate that Acsl1-deficiency causes diastolic dysfunction and that mTOR activation is linked to the development of cardiac hypertrophy in Acsl1(H-/-) mice. ..
  23. Wu S, Kao C, Wang L, Creighton C, Yang J, Donti T, et al. Increased COUP-TFII expression in adult hearts induces mitochondrial dysfunction resulting in heart failure. Nat Commun. 2015;6:8245 pubmed publisher
  24. Bull M, Methawasin M, Strom J, Nair P, Hutchinson K, Granzier H. Alternative Splicing of Titin Restores Diastolic Function in an HFpEF-Like Genetic Murine Model (Ttn?IAjxn). Circ Res. 2016;119:764-72 pubmed publisher
    ..No effective therapies exists for treating this pervasive syndrome; therefore, our data on RBM20 inhibition are clinically significant. ..
  25. Choi Y, de Mattos A, Shao D, Li T, Nabben M, Kim M, et al. Preservation of myocardial fatty acid oxidation prevents diastolic dysfunction in mice subjected to angiotensin II infusion. J Mol Cell Cardiol. 2016;100:64-71 pubmed publisher
    ..20mg/kg/day for 5days) was sufficient to delete ACC2 protein and increase cardiac FAO by 50% in ACC2 flox/flox-MerCreMer+ mice (iKO). After 4weeks of AngII (1...
  26. Eckle T, Hartmann K, Bonney S, Reithel S, Mittelbronn M, Walker L, et al. Adora2b-elicited Per2 stabilization promotes a HIF-dependent metabolic switch crucial for myocardial adaptation to ischemia. Nat Med. 2012;18:774-82 pubmed publisher
  27. Thomas R, Roberts D, Kubli D, Lee Y, Quinsay M, Owens J, et al. Loss of MCL-1 leads to impaired autophagy and rapid development of heart failure. Genes Dev. 2013;27:1365-77 pubmed publisher
    ..These data demonstrate that MCL-1 is essential for mitochondrial homeostasis and induction of autophagy in the heart. This study also raises concerns about potential cardiotoxicity for chemotherapeutics that target MCL-1. ..
  28. Kwong J, Davis J, Baines C, Sargent M, Karch J, Wang X, et al. Genetic deletion of the mitochondrial phosphate carrier desensitizes the mitochondrial permeability transition pore and causes cardiomyopathy. Cell Death Differ. 2014;21:1209-17 pubmed publisher
    ..In addition, mice lacking Slc25a3 in the heart serve as a novel model of metabolic, mitochondrial-driven cardiomyopathy. ..
  29. da Costa Martins P, Bourajjaj M, Gladka M, Kortland M, van Oort R, Pinto Y, et al. Conditional dicer gene deletion in the postnatal myocardium provokes spontaneous cardiac remodeling. Circulation. 2008;118:1567-76 pubmed publisher
    ..Overall, these results indicate that modifications in miRNA biogenesis affect both juvenile and adult myocardial morphology and function. ..
  30. Ruan H, Li J, Ren S, Gao J, Li G, Kim R, et al. Inducible and cardiac specific PTEN inactivation protects ischemia/reperfusion injury. J Mol Cell Cardiol. 2009;46:193-200 pubmed publisher
    ..Inhibiting PTEN may serve as a potential approach to exert cardiac protection against ischemia reperfusion injury. ..
  31. Cheng L, Yung A, Covarrubias M, Radice G. Cortactin is required for N-cadherin regulation of Kv1.5 channel function. J Biol Chem. 2011;286:20478-89 pubmed publisher
    ..These data suggest that in addition to gap junction remodeling, aberrant Kv1.5 channel function contributes to the arrhythmogenic phenotype in N-cad CKO mice. ..
  32. Biesemann N, Mendler L, Wietelmann A, Hermann S, Schäfers M, Kruger M, et al. Myostatin regulates energy homeostasis in the heart and prevents heart failure. Circ Res. 2014;115:296-310 pubmed publisher
    ..Our results uncover an important role of myostatin in the heart for maintaining cardiac energy homeostasis and preventing cardiac hypertrophy. ..
  33. Okada H, Lai N, Kawaraguchi Y, Liao P, Copps J, Sugano Y, et al. Integrins protect cardiomyocytes from ischemia/reperfusion injury. J Clin Invest. 2013;123:4294-308 pubmed publisher
    ..These data suggest that ?7?1D integrin modifies Ca2+ regulatory pathways and offers a means to protect the myocardium from ischemic injury. ..
  34. Ji Y, Zhang P, Zhang X, Zhao Y, Deng K, Jiang X, et al. The ubiquitin E3 ligase TRAF6 exacerbates pathological cardiac hypertrophy via TAK1-dependent signalling. Nat Commun. 2016;7:11267 pubmed publisher
    ..Taken together, we define TRAF6 as an essential molecular switch leading to cardiac hypertrophy in a TAK1-dependent manner. ..
  35. Cao D, Jiang N, Blagg A, Johnstone J, Gondalia R, Oh M, et al. Mechanical unloading activates FoxO3 to trigger Bnip3-dependent cardiomyocyte atrophy. J Am Heart Assoc. 2013;2:e000016 pubmed publisher
    ..transgenic mice harboring a cardiomyocyte-specific constitutively active FoxO3 mutant (caFoxO3(flox);?MHC-Mer-Cre-Mer)...
  36. Wang P, Liu J, Li Y, Wu S, Luo J, Yang H, et al. Peroxisome proliferator-activated receptor {delta} is an essential transcriptional regulator for mitochondrial protection and biogenesis in adult heart. Circ Res. 2010;106:911-9 pubmed publisher
    ..PPARdelta is an essential regulator of cardiac mitochondrial protection and biogenesis and PPARdelta activation can be a potential therapeutic target for cardiac disorders. ..
  37. CHEN P, Patel J, Powers P, Fitzsimons D, Moss R. Dissociation of structural and functional phenotypes in cardiac myosin-binding protein C conditional knockout mice. Circulation. 2012;126:1194-205 pubmed publisher
  38. Blaich A, Pahlavan S, Tian Q, Oberhofer M, Poomvanicha M, Lenhardt P, et al. 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. 2012;287:22616-25 pubmed publisher
    ..2(L2) allele by tamoxifen-induced cardiac-specific activation of the MerCreMer Cre recombinase...
  39. Streicher J, Ren S, Herschman H, Wang Y. MAPK-activated protein kinase-2 in cardiac hypertrophy and cyclooxygenase-2 regulation in heart. Circ Res. 2010;106:1434-43 pubmed publisher
    ..p38 activity in adult myocytes can contribute to pathological hypertrophy and remodeling in adult heart and that MK2 is an important downstream molecule responsible for specific features of p38-induced cardiac pathology. ..
  40. Bakker M, Boink G, Boukens B, Verkerk A, van den Boogaard M, den Haan A, et al. T-box transcription factor TBX3 reprogrammes mature cardiac myocytes into pacemaker-like cells. Cardiovasc Res. 2012;94:439-49 pubmed publisher
  41. Xie Z, Su W, Liu S, Zhao G, Esser K, Schroder E, et al. Smooth-muscle BMAL1 participates in blood pressure circadian rhythm regulation. J Clin Invest. 2015;125:324-36 pubmed publisher
  42. Villa del Campo C, Clavería C, Sierra R, Torres M. Cell competition promotes phenotypically silent cardiomyocyte replacement in the mammalian heart. Cell Rep. 2014;8:1741-1751 pubmed publisher
    ..These results show that the capacity for cell competition in mammals is not restricted to stem cell populations and suggest that stimulated cell competition has potential as a cardiomyocyte-replacement strategy. ..
  43. Kritzer M, Li J, Passariello C, Gayanilo M, Thakur H, Dayan J, et al. The scaffold protein muscle A-kinase anchoring protein ? orchestrates cardiac myocyte hypertrophic signaling required for the development of heart failure. Circ Heart Fail. 2014;7:663-72 pubmed publisher
  44. Quick A, Wang Q, Philippen L, Barreto Torres G, Chiang D, Beavers D, et al. SPEG (Striated Muscle Preferentially Expressed Protein Kinase) Is Essential for Cardiac Function by Regulating Junctional Membrane Complex Activity. Circ Res. 2017;120:110-119 pubmed publisher
    ..A novel cardiac myocyte-specific Speg conditional knockout (MCM-Spegfl/fl) model revealed that adult-onset SPEG deficiency results in heart failure (HF)...
  45. Goonasekera S, Hammer K, Auger Messier M, Bodi I, Chen X, Zhang H, et al. Decreased cardiac L-type Ca²? channel activity induces hypertrophy and heart failure in mice. J Clin Invest. 2012;122:280-90 pubmed publisher
    ..This state results in calcineurin/nuclear factor of activated T cells signaling that promotes hypertrophy and disease. ..
  46. Turski M, Brady D, Kim H, Kim B, Nose Y, Counter C, et al. A novel role for copper in Ras/mitogen-activated protein kinase signaling. Mol Cell Biol. 2012;32:1284-95 pubmed publisher
    ..These results demonstrate a role for Ctr1 and Cu in activating a pathway well known to play a key role in normal physiology and in cancer. ..
  47. Ericsson M, Andersson K, Amundsen B, Torp S, Sjaastad I, Christensen G, et al. High-intensity exercise training in mice with cardiomyocyte-specific disruption of Serca2. J Appl Physiol (1985). 2010;108:1311-20 pubmed publisher
    ..Nevertheless, SERCA2 KO mice were able to maintain maximal running speed in response to exercise training despite a large decrease in VO2max. ..
  48. Wu W, Hu Y, Li J, Zhu W, Ha T, Que L, et al. Silencing of Pellino1 improves post-infarct cardiac dysfunction and attenuates left ventricular remodelling in mice. Cardiovasc Res. 2014;102:46-55 pubmed publisher
    ..Our data demonstrate that Pellino1 plays an important role in the pathogenesis of MI. Targeting Pellino1 may ameliorate cardiac dysfunction and remodelling following MI. ..
  49. Li J, Li C, Liang D, Lv F, Yuan T, The E, et al. LRP6 acts as a scaffold protein in cardiac gap junction assembly. Nat Commun. 2016;7:11775 pubmed publisher
    ..These findings uncover a distinct role of LRP6 as a platform for intracellular protein trafficking. ..
  50. Watson L, Facundo H, Ngoh G, Ameen M, Brainard R, Lemma K, et al. O-linked ?-N-acetylglucosamine transferase is indispensable in the failing heart. Proc Natl Acad Sci U S A. 2010;107:17797-802 pubmed publisher
    ..These data provide keen insights into the pathophysiology of the failing heart and illuminate a previously unrecognized point of integration between metabolism and cardiac function in the failing heart. ..
  51. Galloway C, Ashton J, Sparks J, Mooney R, Smith H. Metabolic regulation of APOBEC-1 complementation factor trafficking in mouse models of obesity and its positive correlation with the expression of ApoB protein in hepatocytes. Biochim Biophys Acta. 2010;1802:976-85 pubmed publisher
    APOBEC-1 Complementation Factor (ACF) is an RNA-binding protein that interacts with apoB mRNA to support RNA editing. ACF traffics between the cytoplasm and nucleus...
  52. Schreiber R, Diwoky C, Schoiswohl G, Feiler U, Wongsiriroj N, Abdellatif M, et al. Cold-Induced Thermogenesis Depends on ATGL-Mediated Lipolysis in Cardiac Muscle, but Not Brown Adipose Tissue. Cell Metab. 2017;26:753-763.e7 pubmed publisher
    ..We conclude that functional NST requires adequate substrate supply and cardiac function, but does not depend on ATGL-mediated lipolysis in BAT. ..
  53. Tomar D, Dong Z, Shanmughapriya S, Koch D, Thomas T, Hoffman N, et al. MCUR1 Is a Scaffold Factor for the MCU Complex Function and Promotes Mitochondrial Bioenergetics. Cell Rep. 2016;15:1673-85 pubmed publisher
    ..These studies establish the existence of a MCU complex that assembles at the mitochondrial integral membrane and regulates Ca(2+)-dependent mitochondrial metabolism. ..
  54. Sileikyte J, Blachly Dyson E, Sewell R, Carpi A, Menabò R, Di Lisa F, et al. Regulation of the mitochondrial permeability transition pore by the outer membrane does not involve the peripheral benzodiazepine receptor (Translocator Protein of 18 kDa (TSPO)). J Biol Chem. 2014;289:13769-81 pubmed publisher
    ..These results call into question a wide variety of studies implicating TSPO in a number of pathological processes through its actions on the PTP. ..
  55. Zhong W, Mao S, Tobis S, Angelis E, Jordan M, Roos K, et al. Hypertrophic growth in cardiac myocytes is mediated by Myc through a Cyclin D2-dependent pathway. EMBO J. 2006;25:3869-79 pubmed
    ..These data suggest that Myc is required for a normal hypertrophic response and that its growth-promoting effects are also mediated through a CycD2-dependent pathway. ..
  56. Woulfe K, Gao E, Lal H, Harris D, Fan Q, Vagnozzi R, et al. Glycogen synthase kinase-3beta regulates post-myocardial infarction remodeling and stress-induced cardiomyocyte proliferation in vivo. Circ Res. 2010;106:1635-45 pubmed publisher
    ..These studies suggest that inhibition of GSK-3beta could be a strategy to both prevent remodeling and to promote cardiac regeneration in pathological states. ..
  57. Xiao R, Sun Y, Ding J, Lin S, Rose D, Rosenfeld M, et al. Splicing regulator SC35 is essential for genomic stability and cell proliferation during mammalian organogenesis. Mol Cell Biol. 2007;27:5393-402 pubmed
    ..These findings reveal the involvement of SC35 in specific pathways in regulating cell proliferation and genomic stability during mammalian organogenesis and suggest its potential function in tumorigenesis. ..
  58. Bao M, Zhang X, Li L, Cai Z, Liu X, Wan N, et al. Cardioprotective role of growth/differentiation factor 1 in post-infarction left ventricular remodelling and dysfunction. J Pathol. 2015;236:360-72 pubmed publisher
    ..Thus, GDF1 may serve as a valuable therapeutic target for the treatment of MI. ..
  59. Li L, Chen Y, Doan J, Murray J, Molkentin J, Liu Q. Transforming growth factor β-activated kinase 1 signaling pathway critically regulates myocardial survival and remodeling. Circulation. 2014;130:2162-72 pubmed publisher
    ..These results indicate that TAK1 functions as a key survival factor in the heart by directly antagonizing necroptosis, which is critical for the maintenance of myocardial homeostasis and the prevention of adverse myocardial remodeling. ..
  60. Wu C, Jia Z, Wang W, Ballou L, Jiang Y, Chen B, et al. PI3Ks maintain the structural integrity of T-tubules in cardiac myocytes. PLoS ONE. 2011;6:e24404 pubmed publisher
    ..These results could have important medical implications because several PI3K inhibitors that target both isoforms are being used to treat cancer patients in clinical trials. ..
  61. Porrello E, Mahmoud A, Simpson E, Johnson B, Grinsfelder D, Canseco D, et al. Regulation of neonatal and adult mammalian heart regeneration by the miR-15 family. Proc Natl Acad Sci U S A. 2013;110:187-92 pubmed publisher
    ..We conclude that the neonatal mammalian heart can regenerate after myocardial infarction through proliferation of preexisting cardiomyocytes and that the miR-15 family contributes to postnatal loss of cardiac regenerative capacity. ..
  62. Roy S, Banerjee J, Gnyawali S, Khanna S, He G, Pfeiffer D, et al. Suppression of Induced microRNA-15b Prevents Rapid Loss of Cardiac Function in a Dicer Depleted Model of Cardiac Dysfunction. PLoS ONE. 2013;8:e66789 pubmed publisher
    ..Anti-miRNA based suppression of inducible miRNA-15b can prevent rapid loss of cardiac function in a Dicer-depleted adult heart and can be a key approach worthy of therapeutic consideration. ..
  63. Huang J, Min Lu M, Cheng L, Yuan L, Zhu X, Stout A, et al. Myocardin is required for cardiomyocyte survival and maintenance of heart function. Proc Natl Acad Sci U S A. 2009;106:18734-9 pubmed publisher
    ..Conversely, proapoptotic factors are induced and activated in myocardin-deficient hearts. We conclude that the transcriptional coactivator myocardin is required for maintenance of heart function and ultimately cardiomyocyte survival. ..
  64. Ichikawa Y, Ghanefar M, Bayeva M, Wu R, Khechaduri A, Naga Prasad S, et al. Cardiotoxicity of doxorubicin is mediated through mitochondrial iron accumulation. J Clin Invest. 2014;124:617-30 pubmed publisher
    ..These results suggest that the cardiotoxic effects of doxorubicin develop from mitochondrial iron accumulation and that reducing mitochondrial iron levels protects against doxorubicin-induced cardiomyopathy. ..
  65. Wang W, Barnabei M, Asp M, Heinis F, Arden E, Davis J, et al. Noncanonical EF-hand motif strategically delays Ca2+ buffering to enhance cardiac performance. Nat Med. 2013;19:305-12 pubmed publisher
    ..Strategic design of new EF-hand motif domains to modulate intracellular Ca(2+) signaling could benefit many biological systems with abnormal Ca(2+) handling, including the diseased heart. ..
  66. Herrmann S, Stieber J, Stöckl G, Hofmann F, Ludwig A. HCN4 provides a 'depolarization reserve' and is not required for heart rate acceleration in mice. EMBO J. 2007;26:4423-32 pubmed
  67. Tane S, Okayama H, Ikenishi A, Amemiya Y, Nakayama K, Takeuchi T. Two inhibitory systems and CKIs regulate cell cycle exit of mammalian cardiomyocytes after birth. Biochem Biophys Res Commun. 2015;466:147-54 pubmed publisher
  68. Fassett J, Xu X, Kwak D, Wang H, Liu X, Hu X, et al. Microtubule Actin Cross-linking Factor 1 regulates cardiomyocyte microtubule distribution and adaptation to hemodynamic overload. PLoS ONE. 2013;8:e73887 pubmed publisher
    ..Together, these data identify for the first time, a role for MACF1 in cardiomyocyte microtubule distribution and in adaptation to hemodynamic overload. ..
  69. Koitabashi N, Danner T, Zaiman A, Pinto Y, Rowell J, Mankowski J, et al. Pivotal role of cardiomyocyte TGF-? signaling in the murine pathological response to sustained pressure overload. J Clin Invest. 2011;121:2301-12 pubmed publisher
    ..Thus, myocyte targeting is required to modulate TGF-? in hearts subjected to pressure overload, with noncanonical pathways predominantly affecting the maladaptive hypertrophy/dysfunction. ..
  70. Mak T, Hauck L, Grothe D, Billia F. p53 regulates the cardiac transcriptome. Proc Natl Acad Sci U S A. 2017;114:2331-2336 pubmed publisher
    ..The complex contributions of p53 define a biological paradigm for the p53 regulator network in the heart under physiological conditions. ..
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