Connection

THOMAS COOPER to RNA-Binding Proteins

This is a "connection" page, showing publications THOMAS COOPER has written about RNA-Binding Proteins.
Connection Strength

8.948
  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: 0.713
  2. 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: 0.622
  3. Protein sequestration as a normal function of long noncoding RNAs and a pathogenic mechanism of RNAs containing nucleotide repeat expansions. Hum Genet. 2017 09; 136(9):1247-1263.
    View in: PubMed
    Score: 0.417
  4. Roles for RNA-binding proteins in development and disease. Brain Res. 2016 09 15; 1647:1-8.
    View in: PubMed
    Score: 0.384
  5. 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: 0.344
  6. RNA-binding proteins in heart development. Adv Exp Med Biol. 2014; 825:389-429.
    View in: PubMed
    Score: 0.330
  7. Muscleblind-like 1 activates insulin receptor exon 11 inclusion by enhancing U2AF65 binding and splicing of the upstream intron. Nucleic Acids Res. 2014 Feb; 42(3):1893-903.
    View in: PubMed
    Score: 0.326
  8. RNA-binding proteins in microsatellite expansion disorders: mediators of RNA toxicity. Brain Res. 2012 Jun 26; 1462:100-11.
    View in: PubMed
    Score: 0.290
  9. 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: 0.266
  10. 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: 0.259
  11. 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: 0.250
  12. 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: 0.240
  13. 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: 0.233
  14. 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: 0.215
  15. 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: 0.214
  16. A reversal of misfortune for myotonic dystrophy? N Engl J Med. 2006 Oct 26; 355(17):1825-7.
    View in: PubMed
    Score: 0.201
  17. 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: 0.183
  18. Colocalization of muscleblind with RNA foci is separable from mis-regulation of alternative splicing in myotonic dystrophy. J Cell Sci. 2005 Jul 01; 118(Pt 13):2923-33.
    View in: PubMed
    Score: 0.183
  19. Identification of CELF splicing activation and repression domains in vivo. Nucleic Acids Res. 2005; 33(9):2769-80.
    View in: PubMed
    Score: 0.181
  20. 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: 0.181
  21. Identification of putative new splicing targets for ETR-3 using sequences identified by systematic evolution of ligands by exponential enrichment. Mol Cell Biol. 2005 Feb; 25(3):879-87.
    View in: PubMed
    Score: 0.178
  22. Muscleblind proteins regulate alternative splicing. EMBO J. 2004 Aug 04; 23(15):3103-12.
    View in: PubMed
    Score: 0.171
  23. 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: 0.171
  24. 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: 0.167
  25. CELF6, a member of the CELF family of RNA-binding proteins, regulates muscle-specific splicing enhancer-dependent alternative splicing. J Biol Chem. 2004 Apr 23; 279(17):17756-64.
    View in: PubMed
    Score: 0.166
  26. Clinical and Molecular Insights into Gastrointestinal Dysfunction in Myotonic Dystrophy Types 1 & 2. Int J Mol Sci. 2022 Nov 26; 23(23).
    View in: PubMed
    Score: 0.153
  27. 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: 0.145
  28. The RNA binding protein YB-1 binds A/C-rich exon enhancers and stimulates splicing of the CD44 alternative exon v4. EMBO J. 2001 Jul 16; 20(14):3821-30.
    View in: PubMed
    Score: 0.139
  29. 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: 0.135
  30. 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: 0.114
  31. Disruption of splicing regulated by a CUG-binding protein in myotonic dystrophy. Science. 1998 May 01; 280(5364):737-41.
    View in: PubMed
    Score: 0.111
  32. A subset of SR proteins activates splicing of the cardiac troponin T alternative exon by direct interactions with an exonic enhancer. Mol Cell Biol. 1995 Sep; 15(9):4898-907.
    View in: PubMed
    Score: 0.093
  33. Antagonistic regulation of mRNA expression and splicing by CELF and MBNL proteins. Genome Res. 2015 Jun; 25(6):858-71.
    View in: PubMed
    Score: 0.090
  34. 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: 0.090
  35. Dynamic analyses of alternative polyadenylation from RNA-seq reveal a 3'-UTR landscape across seven tumour types. Nat Commun. 2014 Nov 20; 5:5274.
    View in: PubMed
    Score: 0.088
  36. Alternative splicing regulates vesicular trafficking genes in cardiomyocytes during postnatal heart development. Nat Commun. 2014 Apr 22; 5:3603.
    View in: PubMed
    Score: 0.084
  37. Alternative splicing dysregulation secondary to skeletal muscle regeneration. Ann Neurol. 2011 Apr; 69(4):681-90.
    View in: PubMed
    Score: 0.068
  38. Global regulation of alternative splicing during myogenic differentiation. Nucleic Acids Res. 2010 Nov; 38(21):7651-64.
    View in: PubMed
    Score: 0.065
  39. MicroRNAs coordinate an alternative splicing network during mouse postnatal heart development. Genes Dev. 2010 Apr 01; 24(7):653-8.
    View in: PubMed
    Score: 0.063
  40. Pathogenic mechanisms of myotonic dystrophy. Biochem Soc Trans. 2009 Dec; 37(Pt 6):1281-6.
    View in: PubMed
    Score: 0.062
  41. 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: 0.062
  42. 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: 0.062
  43. Molecular biology. Neutralizing toxic RNA. Science. 2009 Jul 17; 325(5938):272-3.
    View in: PubMed
    Score: 0.061
  44. 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: 0.055
  45. 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: 0.054
  46. 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: 0.049
  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: 0.046
  48. Alternative splicing regulation impacts heart development. Cell. 2005 Jan 14; 120(1):1-2.
    View in: PubMed
    Score: 0.044
  49. 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: 0.032
  50. The relative strengths of SR protein-mediated associations of alternative and constitutive exons can influence alternative splicing. J Biol Chem. 1999 Oct 15; 274(42):29838-42.
    View in: PubMed
    Score: 0.031
  51. The regulation of splice-site selection, and its role in human disease. Am J Hum Genet. 1997 Aug; 61(2):259-66.
    View in: PubMed
    Score: 0.026
  52. Impaired Mitochondrial Energy Production Causes Light-Induced Photoreceptor Degeneration Independent of Oxidative Stress. PLoS Biol. 2015 Jul; 13(7):e1002197.
    View in: PubMed
    Score: 0.023
  53. Myotonic dystrophy: discussion of molecular basis. Adv Exp Med Biol. 2002; 516:27-45.
    View in: PubMed
    Score: 0.009
  54. Alternative splicing determines the intracellular localization of the novel nuclear protein Nop30 and its interaction with the splicing factor SRp30c. J Biol Chem. 1999 Apr 16; 274(16):10951-62.
    View in: PubMed
    Score: 0.007
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.