Connection

THOMAS COOPER to Animals

This is a "connection" page, showing publications THOMAS COOPER has written about Animals.
Connection Strength

1.421
  1. MBNL overexpression rescues cardiac phenotypes in a myotonic dystrophy type 1 heart mouse model. J Clin Invest. 2025 Feb 11; 135(7).
    View in: PubMed
    Score: 0.055
  2. Rescue of Scn5a mis-splicing does not improve the structural and functional heart defects of a DM1 heart mouse model. Hum Mol Genet. 2024 10 07; 33(20):1789-1799.
    View in: PubMed
    Score: 0.054
  3. The role of Limch1 alternative splicing in skeletal muscle function. Life Sci Alliance. 2023 06; 6(6).
    View in: PubMed
    Score: 0.048
  4. Alternative splicing mediates the compensatory upregulation of MBNL2 upon MBNL1 loss-of-function. Nucleic Acids Res. 2023 02 22; 51(3):1245-1259.
    View in: PubMed
    Score: 0.048
  5. Increased nuclear but not cytoplasmic activities of CELF1 protein leads to muscle wasting. Hum Mol Genet. 2020 06 27; 29(10):1729-1744.
    View in: PubMed
    Score: 0.040
  6. Endurance exercise leads to beneficial molecular and physiological effects in a mouse model of myotonic dystrophy type 1. Muscle Nerve. 2019 12; 60(6):779-789.
    View in: PubMed
    Score: 0.038
  7. CRISPR -Mediated Expression of the Fetal Scn5a Isoform in Adult Mice Causes Conduction Defects and Arrhythmias. J Am Heart Assoc. 2018 10 02; 7(19):e010393.
    View in: PubMed
    Score: 0.035
  8. Mechanisms of skeletal muscle wasting in a mouse model for myotonic dystrophy type 1. Hum Mol Genet. 2018 08 15; 27(16):2789-2804.
    View in: PubMed
    Score: 0.035
  9. Rbfox-Splicing Factors Maintain Skeletal Muscle Mass by Regulating Calpain3 and Proteostasis. Cell Rep. 2018 07 03; 24(1):197-208.
    View in: PubMed
    Score: 0.035
  10. A Therapeutic Double Whammy: Transcriptional or Post-transcriptional Suppression of Microsatellite Repeat Toxicity by Cas9. Mol Cell. 2017 11 02; 68(3):473-475.
    View in: PubMed
    Score: 0.033
  11. Extensive alternative splicing transitions during postnatal skeletal muscle development are required for calcium handling functions. Elife. 2017 08 11; 6.
    View in: PubMed
    Score: 0.033
  12. Alternative Splicing of Four Trafficking Genes Regulates Myofiber Structure and Skeletal Muscle Physiology. Cell Rep. 2016 11 15; 17(8):1923-1933.
    View in: PubMed
    Score: 0.031
  13. Neonatal cardiac dysfunction and transcriptome changes caused by the absence of Celf1. Sci Rep. 2016 10 19; 6:35550.
    View in: PubMed
    Score: 0.031
  14. Roles for RNA-binding proteins in development and disease. Brain Res. 2016 09 15; 1647:1-8.
    View in: PubMed
    Score: 0.030
  15. Rbfox2-coordinated alternative splicing of Mef2d and Rock2 controls myoblast fusion during myogenesis. Mol Cell. 2014 Aug 21; 55(4):592-603.
    View in: PubMed
    Score: 0.027
  16. Alternative splicing regulates vesicular trafficking genes in cardiomyocytes during postnatal heart development. Nat Commun. 2014 Apr 22; 5:3603.
    View in: PubMed
    Score: 0.026
  17. The Mef2 transcription network is disrupted in myotonic dystrophy heart tissue, dramatically altering miRNA and mRNA expression. Cell Rep. 2014 Jan 30; 6(2):336-45.
    View in: PubMed
    Score: 0.026
  18. RNA-binding proteins in heart development. Adv Exp Med Biol. 2014; 825:389-429.
    View in: PubMed
    Score: 0.026
  19. Reexpression of pyruvate kinase M2 in type 1 myofibers correlates with altered glucose metabolism in myotonic dystrophy. Proc Natl Acad Sci U S A. 2013 Aug 13; 110(33):13570-5.
    View in: PubMed
    Score: 0.025
  20. Antisense oligonucleotides: rising stars in eliminating RNA toxicity in myotonic dystrophy. Hum Gene Ther. 2013 May; 24(5):499-507.
    View in: PubMed
    Score: 0.024
  21. Pre-mRNA splicing in disease and therapeutics. Trends Mol Med. 2012 Aug; 18(8):472-82.
    View in: PubMed
    Score: 0.023
  22. RNase H-mediated degradation of toxic RNA in myotonic dystrophy type 1. Proc Natl Acad Sci U S A. 2012 Mar 13; 109(11):4221-6.
    View in: PubMed
    Score: 0.022
  23. RNA-binding proteins in microsatellite expansion disorders: mediators of RNA toxicity. Brain Res. 2012 Jun 26; 1462:100-11.
    View in: PubMed
    Score: 0.022
  24. Functional consequences of developmentally regulated alternative splicing. Nat Rev Genet. 2011 Sep 16; 12(10):715-29.
    View in: PubMed
    Score: 0.022
  25. Alternative splicing dysregulation secondary to skeletal muscle regeneration. Ann Neurol. 2011 Apr; 69(4):681-90.
    View in: PubMed
    Score: 0.021
  26. Identification of MBNL1 and MBNL3 domains required for splicing activation and repression. Nucleic Acids Res. 2011 Apr; 39(7):2769-80.
    View in: PubMed
    Score: 0.021
  27. Global regulation of alternative splicing during myogenic differentiation. Nucleic Acids Res. 2010 Nov; 38(21):7651-64.
    View in: PubMed
    Score: 0.020
  28. CUGBP1 overexpression in mouse skeletal muscle reproduces features of myotonic dystrophy type 1. Hum Mol Genet. 2010 Sep 15; 19(18):3614-22.
    View in: PubMed
    Score: 0.020
  29. MicroRNAs coordinate an alternative splicing network during mouse postnatal heart development. Genes Dev. 2010 Apr 01; 24(7):653-8.
    View in: PubMed
    Score: 0.020
  30. Heart-specific overexpression of CUGBP1 reproduces functional and molecular abnormalities of myotonic dystrophy type 1. Hum Mol Genet. 2010 Mar 15; 19(6):1066-75.
    View in: PubMed
    Score: 0.019
  31. Pathogenic mechanisms of myotonic dystrophy. Biochem Soc Trans. 2009 Dec; 37(Pt 6):1281-6.
    View in: PubMed
    Score: 0.019
  32. PKC inhibition ameliorates the cardiac phenotype in a mouse model of myotonic dystrophy type 1. J Clin Invest. 2009 Dec; 119(12):3797-806.
    View in: PubMed
    Score: 0.019
  33. Chemical reversal of the RNA gain of function in myotonic dystrophy. Proc Natl Acad Sci U S A. 2009 Nov 03; 106(44):18433-4.
    View in: PubMed
    Score: 0.019
  34. Molecular biology. Neutralizing toxic RNA. Science. 2009 Jul 17; 325(5938):272-3.
    View in: PubMed
    Score: 0.019
  35. CUGBP2 directly interacts with U2 17S snRNP components and promotes U2 snRNA binding to cardiac troponin T pre-mRNA. Nucleic Acids Res. 2009 Jul; 37(13):4275-86.
    View in: PubMed
    Score: 0.019
  36. A postnatal switch of CELF and MBNL proteins reprograms alternative splicing in the developing heart. Proc Natl Acad Sci U S A. 2008 Dec 23; 105(51):20333-8.
    View in: PubMed
    Score: 0.018
  37. Expanded CTG repeats within the DMPK 3' UTR causes severe skeletal muscle wasting in an inducible mouse model for myotonic dystrophy. Proc Natl Acad Sci U S A. 2008 Feb 19; 105(7):2646-51.
    View in: PubMed
    Score: 0.017
  38. Increased steady-state levels of CUGBP1 in myotonic dystrophy 1 are due to PKC-mediated hyperphosphorylation. Mol Cell. 2007 Oct 12; 28(1):68-78.
    View in: PubMed
    Score: 0.017
  39. Elevation of RNA-binding protein CUGBP1 is an early event in an inducible heart-specific mouse model of myotonic dystrophy. J Clin Invest. 2007 Oct; 117(10):2802-11.
    View in: PubMed
    Score: 0.017
  40. Micromanaging alternative splicing during muscle differentiation. Dev Cell. 2007 Feb; 12(2):171-2.
    View in: PubMed
    Score: 0.016
  41. Alternative splicing in disease. Adv Exp Med Biol. 2007; 623:212-23.
    View in: PubMed
    Score: 0.016
  42. A bichromatic fluorescent reporter for cell-based screens of alternative splicing. Nucleic Acids Res. 2006; 34(22):e148.
    View in: PubMed
    Score: 0.016
  43. A reversal of misfortune for myotonic dystrophy? N Engl J Med. 2006 Oct 26; 355(17):1825-7.
    View in: PubMed
    Score: 0.016
  44. Minigene reporter for identification and analysis of cis elements and trans factors affecting pre-mRNA splicing. Biotechniques. 2006 Aug; 41(2):177-81.
    View in: PubMed
    Score: 0.015
  45. Misregulation of alternative splicing causes pathogenesis in myotonic dystrophy. Prog Mol Subcell Biol. 2006; 44:133-59.
    View in: PubMed
    Score: 0.015
  46. Use of minigene systems to dissect alternative splicing elements. Methods. 2005 Dec; 37(4):331-40.
    View in: PubMed
    Score: 0.015
  47. Dynamic balance between activation and repression regulates pre-mRNA alternative splicing during heart development. Dev Dyn. 2005 Jul; 233(3):783-93.
    View in: PubMed
    Score: 0.014
  48. Cardiac tissue-specific repression of CELF activity disrupts alternative splicing and causes cardiomyopathy. Mol Cell Biol. 2005 Jul; 25(14):6267-78.
    View in: PubMed
    Score: 0.014
  49. Identification of CELF splicing activation and repression domains in vivo. Nucleic Acids Res. 2005; 33(9):2769-80.
    View in: PubMed
    Score: 0.014
  50. Transgenic mice expressing CUG-BP1 reproduce splicing mis-regulation observed in myotonic dystrophy. Hum Mol Genet. 2005 Jun 01; 14(11):1539-47.
    View in: PubMed
    Score: 0.014
  51. Muscleblind proteins regulate alternative splicing. EMBO J. 2004 Aug 04; 23(15):3103-12.
    View in: PubMed
    Score: 0.013
  52. Multiple domains control the subcellular localization and activity of ETR-3, a regulator of nuclear and cytoplasmic RNA processing events. J Cell Sci. 2004 Jul 15; 117(Pt 16):3519-29.
    View in: PubMed
    Score: 0.013
  53. ETR-3 and CELF4 protein domains required for RNA binding and splicing activity in vivo. Nucleic Acids Res. 2004; 32(3):1232-41.
    View in: PubMed
    Score: 0.013
  54. Finding signals that regulate alternative splicing in the post-genomic era. Genome Biol. 2002 Oct 23; 3(11):reviews0008.
    View in: PubMed
    Score: 0.012
  55. Dynamic antagonism between ETR-3 and PTB regulates cell type-specific alternative splicing. Mol Cell. 2002 Mar; 9(3):649-58.
    View in: PubMed
    Score: 0.011
  56. Highlights of alternative splicing regulation session: yes, no, maybe--a history of paradigm shifts. Sci STKE. 2001 Oct 23; 2001(105):pe35.
    View in: PubMed
    Score: 0.011
  57. The CELF family of RNA binding proteins is implicated in cell-specific and developmentally regulated alternative splicing. Mol Cell Biol. 2001 Feb; 21(4):1285-96.
    View in: PubMed
    Score: 0.010
  58. Binding of PurH to a muscle-specific splicing enhancer functionally correlates with exon inclusion in vivo. J Biol Chem. 2000 Jul 07; 275(27):20618-26.
    View in: PubMed
    Score: 0.010
  59. Modulation of alternative splicing of trafficking genes by genome editing reveals functional consequences in muscle biology. Int J Biochem Cell Biol. 2018 12; 105:134-143.
    View in: PubMed
    Score: 0.009
  60. Muscle-specific splicing of a heterologous exon mediated by a single muscle-specific splicing enhancer from the cardiac troponin T gene. Mol Cell Biol. 1998 Aug; 18(8):4519-25.
    View in: PubMed
    Score: 0.009
  61. Identification of a new class of exonic splicing enhancers by in vivo selection. Mol Cell Biol. 1997 Apr; 17(4):2143-50.
    View in: PubMed
    Score: 0.008
  62. Muscle-specific splicing enhancers regulate inclusion of the cardiac troponin T alternative exon in embryonic skeletal muscle. Mol Cell Biol. 1996 Aug; 16(8):4014-23.
    View in: PubMed
    Score: 0.008
  63. The spliceosome is a therapeutic vulnerability in MYC-driven cancer. Nature. 2015 Sep 17; 525(7569):384-8.
    View in: PubMed
    Score: 0.007
  64. Impaired Mitochondrial Energy Production Causes Light-Induced Photoreceptor Degeneration Independent of Oxidative Stress. PLoS Biol. 2015 Jul; 13(7):e1002197.
    View in: PubMed
    Score: 0.007
  65. Antagonistic regulation of mRNA expression and splicing by CELF and MBNL proteins. Genome Res. 2015 Jun; 25(6):858-71.
    View in: PubMed
    Score: 0.007
  66. Pumilio1 haploinsufficiency leads to SCA1-like neurodegeneration by increasing wild-type Ataxin1 levels. Cell. 2015 Mar 12; 160(6):1087-98.
    View in: PubMed
    Score: 0.007
  67. The cardiac troponin T alternative exon contains a novel purine-rich positive splicing element. Mol Cell Biol. 1993 Jun; 13(6):3660-74.
    View in: PubMed
    Score: 0.006
  68. In vitro splicing of cardiac troponin T precursors. Exon mutations disrupt splicing of the upstream intron. J Biol Chem. 1992 Mar 15; 267(8):5330-8.
    View in: PubMed
    Score: 0.006
  69. The pINDUCER lentiviral toolkit for inducible RNA interference in vitro and in vivo. Proc Natl Acad Sci U S A. 2011 Mar 01; 108(9):3665-70.
    View in: PubMed
    Score: 0.005
  70. Overexpression of MBNL1 fetal isoforms and modified splicing of Tau in the DM1 brain: two individual consequences of CUG trinucleotide repeats. Exp Neurol. 2008 Apr; 210(2):467-78.
    View in: PubMed
    Score: 0.004
  71. MBNL1 and CUGBP1 modify expanded CUG-induced toxicity in a Drosophila model of myotonic dystrophy type 1. Hum Mol Genet. 2006 Jul 01; 15(13):2138-45.
    View in: PubMed
    Score: 0.004
  72. Myotonic dystrophy: discussion of molecular basis. Adv Exp Med Biol. 2002; 516:27-45.
    View in: PubMed
    Score: 0.003
  73. A short sequence within two purine-rich enhancers determines 5' splice site specificity. Mol Cell Biol. 1998 Jan; 18(1):343-52.
    View in: PubMed
    Score: 0.002
Connection Strength

The connection strength for concepts is the sum of the scores for each matching publication.

Publication scores are based on many factors, including how long ago they were written and whether the person is a first or senior author.