The E3 ubiquitin ligase HectD3 attenuates cardiac hypertrophy and inflammation in mice

[1]  P. Hines.  From development to disease , 2021 .

[2]  Martin Eisenacher,et al.  The PRIDE database and related tools and resources in 2019: improving support for quantification data , 2018, Nucleic Acids Res..

[3]  R. Arena,et al.  Usefulness of Canakinumab to Improve Exercise Capacity in Patients With Long-Term Systolic Heart Failure and Elevated C-Reactive Protein. , 2018, The American journal of cardiology.

[4]  D. Stetson,et al.  SUMO2 and SUMO3 redundantly prevent a noncanonical type I interferon response , 2018, Proceedings of the National Academy of Sciences.

[5]  J. Stamler,et al.  Distinct roles of resident and nonresident macrophages in nonischemic cardiomyopathy , 2018, Proceedings of the National Academy of Sciences.

[6]  Sumanth D. Prabhu,et al.  CCR2+ Monocyte-Derived Infiltrating Macrophages Are Required for Adverse Cardiac Remodeling During Pressure Overload , 2018, JACC. Basic to translational science.

[7]  H. Katus,et al.  Protocol for Efficient Generation and Characterization of Adeno-Associated Viral Vectors. , 2017, Human gene therapy methods.

[8]  O. Ritter,et al.  Sumoylation-independent activation of Calcineurin-NFAT-signaling via SUMO2 mediates cardiomyocyte hypertrophy , 2016, Scientific Reports.

[9]  Daniel G. Anderson,et al.  Proliferation and Recruitment Contribute to Myocardial Macrophage Expansion in Chronic Heart Failure. , 2016, Circulation research.

[10]  R. Lüllmann-Rauch,et al.  Dyrk1a regulates the cardiomyocyte cell cycle via D-cyclin-dependent Rb/E2f-signalling. , 2016, Cardiovascular research.

[11]  Thomas Braun,et al.  The Ubiquitin-Like SUMO System and Heart Function: From Development to Disease. , 2016, Circulation research.

[12]  R. Lüllmann-Rauch,et al.  Myozap Deficiency Promotes Adverse Cardiac Remodeling via Differential Regulation of Mitogen-activated Protein Kinase/Serum-response Factor and β-Catenin/GSK-3β Protein Signaling* , 2015, The Journal of Biological Chemistry.

[13]  S. Nisole,et al.  Small Ubiquitin-like Modifier Alters IFN Response , 2015, The Journal of Immunology.

[14]  E. Y. Kim,et al.  Involvement of activated SUMO-2 conjugation in cardiomyopathy. , 2015, Biochimica et biophysica acta.

[15]  D. Mann.  Innate immunity and the failing heart: the cytokine hypothesis revisited. , 2015, Circulation research.

[16]  Steven L Salzberg,et al.  HISAT: a fast spliced aligner with low memory requirements , 2015, Nature Methods.

[17]  W. Paschen,et al.  SUMO proteomics to decipher the SUMO‐modified proteome regulated by various diseases , 2015, Proteomics.

[18]  Jennifer E Van Eyk,et al.  Posttranslational modifications of lysine and evolving role in heart pathologies—Recent developments , 2015, Proteomics.

[19]  Alyssa C. Frazee,et al.  Ballgown bridges the gap between transcriptome assembly and expression analysis , 2015, Nature Biotechnology.

[20]  S. Salzberg,et al.  StringTie enables improved reconstruction of a transcriptome from RNA-seq reads , 2015, Nature Biotechnology.

[21]  Lan Lin,et al.  rMATS: Robust and flexible detection of differential alternative splicing from replicate RNA-Seq data , 2014, Proceedings of the National Academy of Sciences.

[22]  A. Hoeft,et al.  Ly6Clow and Not Ly6Chigh Macrophages Accumulate First in the Heart in a Model of Murine Pressure-Overload , 2014, PloS one.

[23]  R. Hajjar,et al.  The role of SUMO-1 in cardiac oxidative stress and hypertrophy. , 2014, Antioxidants & redox signaling.

[24]  A. Nordheim,et al.  Rapid and highly efficient inducible cardiac gene knockout in adult mice using AAV-mediated expression of Cre recombinase. , 2014, Cardiovascular research.

[25]  Joanna Wesoly,et al.  Data Mining of Atherosclerotic Plaque Transcriptomes Predicts STAT1-Dependent Inflammatory Signal Integration in Vascular Disease , 2014, International journal of molecular sciences.

[26]  L. Leinwand,et al.  Pregnancy as a cardiac stress model. , 2014, Cardiovascular research.

[27]  N. Frey,et al.  Dysbindin is a potent inducer of RhoA–SRF-mediated cardiomyocyte hypertrophy , 2013, The Journal of cell biology.

[28]  C. Chiang,et al.  Sumoylation in gene regulation, human disease, and therapeutic action , 2013, F1000prime reports.

[29]  J. Satoh,et al.  A Comprehensive Profile of ChIP-Seq-Based STAT1 Target Genes Suggests the Complexity of STAT1-Mediated Gene Regulatory Mechanisms , 2013, Gene regulation and systems biology.

[30]  J. Kocher,et al.  CPAT: Coding-Potential Assessment Tool using an alignment-free logistic regression model , 2013, Nucleic acids research.

[31]  J. Molkentin,et al.  Signaling effectors underlying pathologic growth and remodeling of the heart. , 2013, The Journal of clinical investigation.

[32]  O. Silvennoinen,et al.  Structure-function analysis indicates that sumoylation modulates DNA-binding activity of STAT1 , 2012, BMC Biochemistry.

[33]  Juliana O. Odetunde,et al.  Coronary Artery Remodeling in a Model of Left Ventricular Pressure Overload Is Influenced by Platelets and Inflammatory Cells , 2012, PloS one.

[34]  P. Kanellakis,et al.  A pro-fibrotic role for interleukin-4 in cardiac pressure overload. , 2012, Cardiovascular research.

[35]  J. Molkentin,et al.  Interaction Between NF&kgr;B and NFAT Coordinates Cardiac Hypertrophy and Pathological Remodeling , 2012, Circulation research.

[36]  R. Knight,et al.  STAT transcription in the ischemic heart , 2012, JAK-STAT.

[37]  M. Laakso,et al.  Low-grade inflammation and the phenotypic expression of myocardial fibrosis in hypertrophic cardiomyopathy , 2012, Heart.

[38]  R. Knight,et al.  STAT1 deficiency in the heart protects against myocardial infarction by enhancing autophagy , 2012, Journal of cellular and molecular medicine.

[39]  D. Torella,et al.  Physiological cardiac remodelling in response to endurance exercise training: cellular and molecular mechanisms , 2011, Heart.

[40]  J. Bujnicki,et al.  STAT1 as a novel therapeutical target in pro-atherogenic signal integration of IFNγ, TLR4 and IL-6 in vascular disease. , 2011, Cytokine & growth factor reviews.

[41]  Marcel Martin.  Cutadapt removes adapter sequences from high-throughput sequencing reads , 2011 .

[42]  K. Sarge,et al.  SUMO and its role in human diseases. , 2011, International review of cell and molecular biology.

[43]  Lionel B Ivashkiv,et al.  Cross-regulation of signaling pathways by interferon-gamma: implications for immune responses and autoimmune diseases. , 2009, Immunity.

[44]  S. Subramaniam,et al.  Chemoattractant Signaling between Tumor Cells and Macrophages Regulates Cancer Cell Migration, Metastasis and Neovascularization , 2009, PloS one.

[45]  H. Katus,et al.  DYRK1A Is a Novel Negative Regulator of Cardiomyocyte Hypertrophy* , 2009, The Journal of Biological Chemistry.

[46]  E. Heinzle,et al.  A 2D reversed-phase × ion-pair reversed-phase HPLC-MALDI TOF/TOF-MS approach for shotgun proteome analysis , 2009, Analytical and bioanalytical chemistry.

[47]  N. Frangogiannis,et al.  Characterization of the inflammatory and fibrotic response in a mouse model of cardiac pressure overload , 2009, Histochemistry and Cell Biology.

[48]  R. Bohle,et al.  AP-1 and STAT-1 decoy oligodeoxynucleotides attenuate transplant vasculopathy in rat cardiac allografts. , 2008, Cardiovascular research.

[49]  B. Williams,et al.  Mapping and quantifying mammalian transcriptomes by RNA-Seq , 2008, Nature Methods.

[50]  D. Willis.  A decade on , 2008, Journal of intellectual disabilities : JOID.

[51]  Hugo A. Katus,et al.  Gene Expression Pattern in Biomechanically Stretched Cardiomyocytes: Evidence for a Stretch-Specific Gene Program , 2008, Hypertension.

[52]  F. Melchior,et al.  Concepts in sumoylation: a decade on , 2007, Nature Reviews Molecular Cell Biology.

[53]  C. Fielding,et al.  Classic interleukin-6 receptor signaling and interleukin-6 trans-signaling differentially control angiotensin II-dependent hypertension, cardiac signal transducer and activator of transcription-3 activation, and vascular hypertrophy in vivo. , 2007, The American journal of pathology.

[54]  J. Molkentin,et al.  Regulation of cardiac hypertrophy by intracellular signalling pathways , 2006, Nature Reviews Molecular Cell Biology.

[55]  O. Silvennoinen,et al.  SUMO-1 conjugation selectively modulates STAT1-mediated gene responses. , 2005, Blood.

[56]  S. Sindel,et al.  An Association Between Inflammatory State and Left Ventricular Hypertrophy in Hemodialysis Patients , 2005, Renal failure.

[57]  L. Ivashkiv,et al.  IFN-gamma-primed macrophages exhibit increased CCR2-dependent migration and altered IFN-gamma responses mediated by Stat1. , 2005, Journal of immunology.

[58]  C. D. dos Remedios,et al.  Activation of signal transducer and activator of transcription (STAT) pathways in failing human hearts. , 2003, Cardiovascular research.

[59]  Wenzheng Zhang,et al.  Signal transducers and activators of transcription 3 (STAT3) inhibits transcription of the inducible nitric oxide synthase gene by interacting with nuclear factor kappaB. , 2002, The Biochemical journal.

[60]  R. Knight,et al.  Ischemia-induced STAT-1 Expression and Activation Play a Critical Role in Cardiomyocyte Apoptosis* , 2000, The Journal of Biological Chemistry.

[61]  Jeffrey Robbins,et al.  A Calcineurin-Dependent Transcriptional Pathway for Cardiac Hypertrophy , 1998, Cell.

[62]  D. Levy,et al.  Targeted Disruption of the Mouse Stat1 Gene Results in Compromised Innate Immunity to Viral Disease , 1996, Cell.

[63]  J. Darnell,et al.  Interferon activation of the transcription factor Stat91 involves dimerization through SH2-phosphotyrosyl peptide interactions , 1994, Cell.

[64]  J. Darnell,et al.  A single phosphotyrosine residue of Stat91 required for gene activation by interferon-gamma. , 1993, Science.