Tom Cooper Lab



Cooper Lab Members Indicated in Bold


Nitschke, L. & Cooper, T. A. (2024) Combinatorial effects of ion channel mis-splicing as a cause of myopathy in myotonic dystrophy. J. Clin. Invest. 134. Pubmed.

Penna, M. S., Hu, R.-C., Rodney, G. G. and Cooper, T. A. (2023) The role of Limch1 alternative splicing in skeletal muscle function. Life Sci Alliance 6, e202201868. Pubmed.

Lucas, L. and Cooper, T.A. (2023 Insights into cell-specific functions of microtubules in skeletal muscle development and homeostasis. International Journal of Molecular Sciences. Pubmed.

Nitschke, L., Hu, R-C, Miller, A.N., Lucas, L. and Cooper, T.A. (2023) Alternative splicing mediates the compensatory upregulation of MBNL2 upon MBNL1 loss-of-function. Nucl. Acids Res. 10.1093/nar/gkac1219. Online ahead of print. Pubmed.

Peterson, J. and Cooper, T.A. (2022) Clinical and molecular insights into gastrointestinal dysfunction in myotonic dystrophy types 1 & 2. International Journal of Molecular Sciences 23, 14779. Pubmed.

Rao, A.N., Campbell, H.W., Guan, X, Word, T.A., Wehrens, X.H.T, Xia, Z. and Cooper, T.A. (2021) Reversible cardiac disease features in an inducible CUG-repeat RNA expressing mouse model of myotonic dystrophy. J. Clin. Invest. Insight. 8, 143465. Pubmed.

Johnson, S. and Cooper, T.A. (2021) Overlapping mechanisms of lncRNA and expanded microsatellite RNA. Wiley Interdiscip Rev. RNA. 12, e1634. Pubmed.

Rao, A.N., Campbell, H.W., Guan, X, Word, T.A., Wehrens, X.H.T, Xia, Z. and Cooper, T.A. (2021) Reversible cardiac disease features in an inducible CUG-repeat RNA expressing mouse model of myotonic dystrophy. J. Clin. Invest. Insight. 8, 143465. Pubmed.

Johnson, S. and Cooper, T.A. (2021) Overlapping mechanisms of lncRNA and expanded microsatellite RNA. Wiley Interdiscip Rev. RNA. 12, e1634. Pubmed.

Misra, C., Bangru, S., Lin, F., Lam, k., Koenig, S.N., Lubbers, E.R., Hedhli, J., Murphy, N.P., Parker, D.J., Dobrucki, L.W., Cooper, T.A., Tajkhorshid, E., Mohler, P.J., and Kalsotra, A. (2020) Overexpression of a non-muscle RBFOX2 isoform triggers cardiac conduction defects in myotonic dystrophy. Dev. Cell 52., 748-763. Pubmed.

Cox, D.C., Xiangnan, G., Xia, Z., and Cooper, T.A. (2020) Increased nuclear but not cytoplasmic activities of CELF1 protein leads to muscle wasting. Hum. Mol. Genet. 29, 1729-1744. Pubmed.

Sharp, L., Cox, D.C. and Cooper, T.A. (2019) Endurance exercise leads to beneficial effects in a mouse model of myotonic dystrophy type 1. Muscle and Nerve 60, 779–789. Pubmed.

Pang, P.D., Alsina, K.M., Cao, S., Koushik, A.B., Wehrens, X.H.T., Cooper, T.A. (2018) CRISPR-mediated expression of the fetal Scn5a isoform in adult mice causes conduction defects and arrhythmias. J. Amer. Heart Assoc. 19, e010393. Pubmed.

Blue, R.E, Koushik, A., Engels, N.E., Cooper, T.A., Giudice, J. (2018) Using CRISPR/Cas9 to modulate endogenous alternative splicing of trafficking genes during mouse development. Int J Biochem Cell Biol. 105, 134-143. Pubmed.

Payer, L., Steranka, J., Ardeljan, D., Walker, J., Fitzgerald, K., Calabresi, P., Cooper, T.A. Burns, K. (2018) Alu insertion variants alter mRNA splicing. Nucl. Acids Res. 47, 421-431. Pubmed.

Singh, R.K., Kolonin, A.M., Fiorotto, M.L. and Cooper, T. A. (2018) Rbfox splicing factors maintain skeletal muscle mass by regulating calpain3 and proteostasis. Cell Reports. 24, 197-208. Pubmed

Morriss, G.R., Rajapakshe, K., Huang, S., Coarfa, C. and Cooper, T.A. (2018) Mechanisms of skeletal muscle wasting in a mouse model for myotonic dystrophy type 1. 27, 2789-2804. Pubmed

Brinegar, A.E., Zheng, X., Loehr J.A., Li, W., Rodney G.G., and Cooper T.A. (2017) Extensive alternative splicing transitions during postnatal skeletal muscle development are required for calcium handling functions. eLife 6:e27192. Pubmed

Manning, K.S., Rao, A.N., Castro, M. and Cooper, T.A. (2017) BNANC gapmers revert splicing defects and reduce RNA foci with low toxicity in myotonic dystrophy cell models. ACS Chem Biol. 12, 2503-2509. Pubmed

Rao, AN. and Cooper, T.A. (2017) A Therapeutic Double Whammy: Transcriptional or Post-transcriptional Suppression of Microsatellite Repeat Toxicity by Cas9. Mol. Cell 68:473–475. Pubmed

Sharpe, J. J. and Cooper, T. A. Unexpected consequences: exon skipping caused by CRISPR-generated mutations. Genome Biol. 18, 109 (2017). Pubmed

Morriss, G. R. and Cooper, T. A. (2017) Protein sequestration as a normal function of long noncoding RNAs and a pathogenic mechanism of RNAs containing nucleotide repeat expansions. Hum. Genet. doi:10.1007/s00439-017-1807-6. Pubmed

Manning, K.S. and Cooper, T.A. (2017) The roles of RNA processing in translating genotype to phenotype. Nature Reviews Mol. Cell. Biology 18, 102-114. Pubmed

Giudice J., Loehr J.A., Rodney G.G., and Cooper T.A. (2016) Alternative splicing of four trafficking genes regulates myofiber structure and skeletal muscle physiology. Cell Reports 17, 1923-1933. Pubmed

Giudice, J., Xia, Z., Li, W. & Cooper, T.A. Neonatal cardiac dysfunction and transcriptome changes caused by the absence of Celf1. Sci. Rep. 6, 35550 (2016). Pubmed

Cox, D.C. and Cooper, T.A. (2016) Non-canonical RAN Translation of CGG Repeats Has Canonical Requirements. Mol. Cell 62, 155-156. Pubmed

Brinegar, A.E. and Cooper, T.A. (2016) Roles for RNA-binding proteins in development and disease. Brain Research. 1647, 1-8. Pubmed

Jaiswal, M., Haelterman, N.A., Sandoval, H., Xiong, B., Donti, T., Kalsotra, A., Yamamoto, S., Cooper, T.A., Graham, B. and Bellen, H.J. (2015) Impaired mitochondrial energy production causes light induced photoreceptor degeneration independent of oxidative stress. PLoS Biology 13, e1002197. Pubmed

Hsu, T.Y.-T., Simon, L.M., Neill, N., Marcotte, R., Sayad, A., Bland, C.S., Echeverria, G.V., Sun,T., Kurley, S.J., Tyagi, S., Karlin, K.L., Dominguez-Vidaña, R., Hartman, J.D., Renwick, A. Scorsone, K., Bernardi, R.J., Skinner, S.O., Jain, A., Orellana, M., Lagisetti, C., Golding, I., Jung, S.Y., Neilson, J.R., Zhang, X., Cooper, T.A., Webb, T.R., Neel, B.G., Shaw, C.A., Westbrook, T.F. (2015) The spliceosome is a therapeutic vulnerability in MYC-driven cancer. Nature 525, 384-388. Pubmed

Wang, E.T., Ward, A.J., Giudice, J., Treacy, D., Wang, T.T., Housman, D.E., Cooper, T.A., Burge, C.B. (2015) Antagonistic regulation of mRNA expression and splicing by CELF and MBNL proteins. Genome Research 25, 858-871. Pubmed

Gennarino, V.A., Singh, R.K., White, J.J., De Maio, A., Han, K., Kim, J-Y., Jafar-Nejad, P., di Ronza, A., Kang, H., Sayegh, L.S., Cooper, T.A., Orr, H.T., Sillitoe, R.V., and Zoghbi, H.Y. (2015) Pumilio1 haploinsufficiency leads to SCA1-like neurodegeneration by increasing wild-type ataxin1 levels. Cell 160, 1087-1098. Pubmed

Pedrotti, S., Giudice, J., Dagnino-Acosta, A., Knoblauch, M., Singh, R.K., Hanna, A., Mo, Q., Hicks, J., Hamilton, S.L., Cooper, T.A. (2015) The RNA-binding protein Rbfox1 regulates splicing required for skeletal muscle structure and function Human Molecular Genetics 24, 2360-2374. Pubmed

Xia, Z., Donehower, L.A., Cooper, T.A., Neilson, J.R., Wheeler, D.A., Wagner, E.J., Li, W. (2014) Dynamic analysis of alternative polyadenylation from RNA-seq (DaPars) reveals landscape of 3' UTR usage across seven tumor types. Nature Communications 5, 3603. Pubmed

Singh, R.K., Zheng, X., Bland, C.S., Kalsotra, A., Scavuzzo, M.A., Curk, T., Ule, J., Li, W. and Cooper, T. A. (2014) Rbfox2-coordinated alternative splicing of Mef2d and Rock2 controls myoblast fusion during myogenesis. Mol. Cell 55, 592-603. Pubmed

Giudice, J., Zheng, X., Wang, E.T., Scavuzzo, M.A., Ward, A.J., Kalsotra, A., Wei, W, Wehrens, X.H.T., Burge, C.B., Li, W. and Cooper, T.A. (2014) Alternative splicing regulates vesicular trafficking genes in cardiomyocytes during postnatal heart development. Nature Communications 5, 3603. Pubmed

Giudice, J. and Cooper, T. A. (2014) RNA binding proteins in heart development. Adv Exp Med Biol. 825, 389-429. Pubmed

Pedrotti, S. and Cooper, T.A. (2014) (Mis)-splicing in disease. J. Pathology 233,1-3. Pubmed

Kalsotra, A., Singh, R.K., Gurha, P., Ward, A.J., Creighton, C. and Cooper, T.A. (2014) The Mef2 transcription network is disrupted in myotonic dystrophy heart tissue dramatically altering miRNA and mRNA expression Cell Reports 6, 336-345. Pubmed

Echeverria, G.V. and Cooper, T.A. (2014) Muscleblind-like 1 activities insulin receptor exon 11 inclusion by enhancing U2AF65 binding and splicing of the upstream intron. Nucleic Acids Res. 42, 1893-1903. Pubmed

Gao, Z. and Cooper, T.A. (2013) Re-expression of PKM2 in type 1 myofibers correlates with altered glucose metabolism dystrophy. Proc Natl Acad Sci U.S.A. 110, 13570-13575. Pubmed

Cooper, T.A. (2014) In vivo SELEX strategies, In R.K. Hartmann, A. Bindereif, A. Schon, and E. Westhof (ed.).Handbook of RNA Biochemistry, Second Edition. Wiley-VCH Verlag GmbH and Co, Weinheim.

Gao, Z. and Cooper, T.A. (2012) Antisense oligonucleotides: rising stars in eliminating RNA toxicity in myotonic dystrophy. Human Gene Therapy 24, 499-507. Pubmed

Cooper, T.A. (2012) Implications of widespread covalent modification of mRNA. Circulation Research (Commentary) 111, 1491-1493.

Lee, J.E., Bennett, C.F., and Cooper, T.A. (2012) RNase H-mediated degradation of toxic RNA in myotonic dystrophy type 1. Proc. Nat’l Acad. Sci. 109, 4221-4226. Pubmed

Echeverria, G. V., and Cooper, T.A. (2012) RNA-binding proteins in microsatellite expansion disorders: mediators of RNA toxicity. Brain Research 1462, 100-111. Pubmed

Singh, R., and Cooper, T.A. (2012) Pre-mRNA splicing in disease and therapeutics. Trends in Molecular Medicine 18, 472-482. Pubmed

Gomes-Pereira, M., and Cooper, T.A., Gourdon, G. (2011) Myotonic dystrophy mouse models: towards rational therapy development. Trends in Molecular Medicine 17, 506-517. Pubmed

Cooper, T.A. (2011) Regulating mRNA complexity in the mammalian brain. Nature Genetics 43, 618-619. (News and Views) Pubmed

Kalsotra, A., and Cooper, T.A. (2011) Functional consequences of developmentally regulated alternative splicing Nature Rev. Genet. 12, 715-729. Pubmed

Grammatikakis, I. Goo, Y.H., Echeverria, G.V., and Cooper, T.A. (2011) Identification of MBNL1 and MBNL3 domains required for alternative splicing activation and repression. Nucl. Acids Res. 39, 2769-2780. Pubmed

Orengo, J.P., Ward, A.J., and Cooper, T.A. (2011) Alternative splicing misregulation secondary to skeletal muscle regeneration. Annals Neurology 69, 681-690. Pubmed

Meerbrey, K.L., Hu, G., Kessler, J.D., Roarty, K., Li, M.Z., Fang, J.E., Herschkowitz, J.I., Burrows, A.E., Ciccia, A., Sun, T., Schmitt, E.M., Bernardi, R.J., Fu, X., Bland, C.S., Cooper, T.A., Schiff, R., Rosen, J.M., Westbrook, T.F., Elledge, S.J. (2011) The pINDUCER lentiviral toolkit for inducible RNA interference in vitro and in vivo. Proc Natl Acad Sci U S A. 108, 3665-3670. Pubmed

Bland, C.S., Wang, E.T., Vu, A., David, M.P., Castle, J.C., Johnson, J.M., Burge, C.B., and Cooper, T.A. (2010) Global regulation of alternative splicing during myogenic differentiation. Nucl. Acids Res. 38, 7651-7654. Pubmed

Ward, A.J., Rimer, M., Killian, J.M., Dowling, J.J. and Cooper, T.A. (2010)CUGBP1 overexpression in mouse skeletal muscle reproduces features of myotonic dystrophy type 1.Hum Mol Genet. 19, 3614-3622 Pubmed

Kalsotra, A., Wang, K., Li, P.F., and Cooper, T.A. (2010) MicroRNAs coordinate an alternative splicing network during mouse postnatal heart development. Genes Dev. 24, 653-658. Pubmed

Koshelev M., Sarma S, Price RE, Wehrens XH, and Cooper, T.A. (2010) Heart-specific overexpression of CUGBP1 reproduces functional and molecular abnormalities of myotonic dystrophy type 1. Hum Mol Genet. 19, 1066-1075. Pubmed

Ward, A.J. and Cooper, T.A. (2010) The pathobiology of splicing. J Pathol. 220, 152-163. Pubmed

Lee, J.E. and Cooper, T.A. (2009) Pathogenic Mechanisms of Myotonic Dystrophy. Biochem Soc Trans. 37, 1281-1286. Pubmed

Cooper, T.A. (2009) Chemical reversal of the RNA gain of function in myotonic dystrophy. Proc Natl Acad Sci USA. 106, 18433-18434. Pubmed

Wang, G.S., Kuyumcu-Martinez, M.N., Sarma, S, Mathur, N., Wehrens, X.H., Cooper, T.A. (2009) PKC inhibition ameliorates the cardiac phenotype in a mouse model of myotonic dystrophy type 1. J Clin Invest. 119, 3797-3806. Pubmed

Cooper, T.A. (2009) Neutralizing toxic RNA. Science 325, 272-327. Pubmed

Cooper, T.A., Wan, L., and Dreyfuss, G. RNA and disease. (2009) Cell 136, 777–793. Pubmed

Goo, Y.H. and Cooper, T.A. (2009) CUGBP2 directly interacts with U2 17S snRNP components and promotes U2 snRNA binding to cardiac troponin T pre-mRNA. Nucleic Acids Res. 37, 4275-4286. Pubmed

Kalsotra, A., Tran, D., Ward, A., Xiao, X., Burge, C.B., Castle, J.M., Johnson, J.C., and Cooper, T.A.(2008) A conserved program of regulated alternative splicing during vertebrate heart development . Proc. Nat'l Acad. Sci. 105, 20333-20338. PubMed

Castle, J.C., Zhang, C., Shah, J.K, Kulkarni, A.V., Kalsotra, A., Cooper, T.A ., and Johnson, J.M. (2008) Differential expression of 24,426 human alternative splicing events and predicted cis-regulation in 48 tissues and cell lines. Nat. Genet. 40, 1416-1425. PubMed

Orengo, J.P., Chambon, P., Metzger, D., Mosier, D.R., Snipes, G.J. and Cooper, T.A. (2008) Expanded CTG repeats within the DMPK 3¹ UTR causes severe skeletal muscle wasting in an inducible mouse model for myotonic dystrophy. Proc. Nat¹l Acad. Sci. 105, 2646-2651. PubMed

Kuyumcu-Martinez, N.M., Wang, G.S., and Cooper, T.A. (2007) Increased steady state levels of CUG-BP1 in Myotonic Dystrophy 1 are due to PKC-mediated hyper-phosphorylation. Mol. Cell 28, 68-78. PubMed

Wang, G.S., Kearney, D.L., De Biasi, M., Taffet, G.E., and Cooper, T.A. (2007) Elevation of RNA-binding protein CUGBP1 is an early event in an inducible heart-specific mouse model of myotonic dystrophy. J. Clin. Invest. 117, 2802-2811. PubMed

Orengo, J.P. and Cooper, T.A. (2007) Alternative splicing in disease in Alternative splicing in the post-genomic era, B.R. Graveley and B. Blencowe, ed. Landes publishing; pp. 212-223.

Chapple , J.P., Anthony, K., Martin, T.R., Cooper, J.D. , Cooper, T.A., and Gallo, J-M. (2007) Expression, localization and Tau Exon 10 splicing activity of the brain RNA-binding protein TNRC4. Hum. Mol. Gen. 16, 2760-2769. PubMed

Dhaenens , C.M., Schraen-Maschke , S., Vingtdeux , V. , Vanbrussel, E., Leroy, O., Delplanque, J., Tran , H., Delacourte, A., Vermersch, P. , Gruffat, H., Sergeant, A , Mahadevan, M., Ishiura, S. , Buée, L: , Cooper, T.A. , Caillet-Boudin, M.L., Charlet-Berguerand, N. , Sablonnière, B. , and Sergeant, N. Altered splicing of Tau and MBNL1 by long expanded CUG repeats in Myotonic Dystrophy of Type I brain: new insights in DM1 pathophysiology. Experimental Neurology 210, 467-478.

Wang, G.S. and Cooper T.A. (2007) Splicing in disease: disruption of the splicing code and the decoding machinery. Nature Rev. Genet. 8, 749-761. PubMed

Cooper, T.A. (2007) Regulation of chloride ion conductance during skeletal muscle development and in disease. Amer. J. Physiol: Cell Physiology 292, C1245-1247. PubMed

Bland, C.S. and Cooper, T.A. (2007) Micromanaging alternative splicing during muscle differentiation Dev Cell 12, 171-17. PubMed

Cooper, T.A. (2006) A reversal of fortune for myotonic dystrophy? N Engl J Med. 355, 1825-1827. PubMed

Ranum L.P. and Cooper, T.A. (2006) RNA-mediated neuromuscular disorders. Ann. Rev. Neuroscience, 29, 259-277. PubMed

Orengo, J., Bundman, D., and Cooper, T.A. (2006) A bichromatic fluorescent reporter for cell-based screens of alternative splicing Nucl. Acids Res. 34, e148. PubMed

Singh, G, N. and Cooper, T.A. (2006) A minigene reporter for identification and analysis of cis elements and trans factors affecting pre-mRNA splicing.(2006) BioTechniques 41,177-181. PubMed

de Haro, M., Al-Ramahi, I,, De Gouyon, B., Ukani, L., Rosa, A., Faustino, N.A., Ashizawa, T.,Cooper, T.A. and Botas, J. (2006) MBNL1 and CUGBP1 modify expanded CUG-induced toxicity in a Drosophila model of Myotonic Dystrophy Type 1. Hum. Mol. Gen. 15, 2138-2145. PubMed

Thornton, C.A., Swanson, M.S., and Cooper, T.A. (2006) The RNA-mediated disease process in myotonic dystrophy. In Genetic Instabilities and Hereditary Neurological Diseases (Second Edition). T. Ashizawa and R.D. Wells (Eds.). p. 37-54.

Kuyumcu-Martinez, N.M. and Cooper, T.A. (2006) Mis-regulation of alternative splicing causes pathogenesis in myotonic dystrophy. Progress in Molecular and Subcellular Biology 44, 133-159. PubMed

Cooper, T.A. (2005) Use of minigene systems to dissect alternative splicing elements. Methods 37, 331-340. PubMed

Ladd, A.N., Taffet, G.E., Hartley, C., Kearney, D.L. and Cooper, T.A. (2005) Cardiac-specific repression of CELF activity disrupts alternative splicing and causes cardiomyopathy. Mol. Cell. Biol. 25, 6267-6278. PubMed

Leroy, O., Wang, J., Maurage, C.A., Parent, M., Cooper, T., Buee, L., Sergeant, N., Andreadis, A., Caillet-Boudin, M.L. (2006) Brain-specific change in alternative splicing of Tau exon 6 in myotonic dystrophy type 1. Biochim Biophys Acta. 1762, 460-467. Pubmed

Han, J. and Cooper, T.A. (2005) Characterization of CELF splicing activation and repression domains in vivo Nucl. Acids Res. 33, 2769-2780. PubMed

Ho, T., Bundman, D., Armstrong, D.L., and Cooper, T.A. (2005) Transgenic mice expressing CUG-BP1 reproduce the myotonic dystrophy pattern of splicing. Hum. Mol. Genet. 14, 1539-1547. PubMed

Ladd, A.L. Stenberg, M.G., Swanson, M.S., and Cooper, T.A. (2005) A dynamic balance between activation and repression regulates pre-mRNA alternative splicing during heart development. Dev. Dyn. 233, 783-793. PubMed

Ho, T., Savkur, R.S., Poulos, M., Mancini., M.M., Swanson, M.S., and Cooper, T.A. (2005) Co-localization of muscleblind with RNA foci is separable from mis-regulation of alternative splicing in myotonic dystrophy J. Cell Science 118, 2923-2933. PubMed

Cooper, T.A. (2005) Alternative splicing regulation impacts heart development. Cell 120, 1-2. PubMed

Cooper, T. A. (2005) In vivo SELEX strategies, p. 840-852. In R. K. Hartmann, A. Bindereif, A. Schon, and E. Westhof (ed.), Handbook of RNA Biochemistry, vol. 2. Wiley-VCH Verlag GmbH and Co, Weinheim.

Faustino, N.A. and Cooper, T.A. (2005) Identification of putative new splicing targets for ETR-3 using its SELEX sequences. Mol. Cell. Biol. 25, 879-887. PubMed

Ladd, A.N. and Cooper, T.A. (2004) Nuclear-cytoplasmic localization of the RNA binding protein ETR-3 is controlled by multiple localization elements. J. Cell Science 117, 3519-3529. PubMed

Ho, T., Charlet-B., N., Poulos, M., Singh, G., Swanson, M.S., and Cooper, T.A. (2004) Muscleblind proteins regulate alternative splicing. EMBO J. 23, 3103-3112. PubMed

Singh, G., Charlet-B., N., Han, J., and Cooper, T.A. (2004) ETR-3 and CELF4 protein domains required for RNA binding and splicing activity in vivo. Nucl. Acids Res. 32, 1232-1241. PubMed

Ladd, A.N., Nguyen, N.H. Malhotra, K. and Cooper, T.A. (2004) CELF6, a member of the CELF family of RNA binding proteins, regulates MSE-dependent alternative splicing. J. Biol. Chem. 279,17756-17764. PubMed

Savkur, R.S., Philips, A.V., Cooper, T.A., Dalton, J.C., Moseley, M.L., Ranum, L.P.W., Day, J.W. (2004) Insulin receptor splicing alteration in myotonic dystrophy type 2. Am. J. Hum. Genet. 74:1309-1313. PubMed

Faustino, N.A. and Cooper, T.A. (2003) RNA splicing and human disease. Genes Dev. 17, 419-437. PubMed

Gromak, N., Matlin, A.J., Cooper, T.A., and Smith, C.W.J. (2003) Antagonistic regulation of alpha-actinin alternative splicing by CELF proteins and polypyrimidine tract binding protein. RNA 9, 443-456. PubMed

Ladd, A.N., Cooper, T.A. (2002) Finding signals that regulate alternative splicing in the post-genomic era. Genome Biology 3, 8.1-8.16. PubMed

Timchenko LT, Tapscott SJ, Cooper TA, Monckton DG. (2002) Myotonic dystrophy: discussion of molecular basis. Adv Exp Med Biol. 516, 27-45. PubMed

Charlet-B., Singh, G, N., Philips, A.V., Grice, E.A., and Cooper, T.A (2002). Loss of the muscle-specific chloride channel in type 1 myotonic dystrophy due to misregulated alternative splicing. Mol. Cell 10, 45-53. PubMed

Charlet-B., Singh, G, N., Logan, P.E., and Cooper, T.A. (2002) Dynamic antagonism between CELF proteins and PTB regulate splicing of a muscle-specific exon in both muscle and nonmuscle cells. Mol. Cell 9, 649-658. PubMed

Cooper, T.A. (2001) Highlights of alternative splicing regulation session: yes, no, maybe--a history of paradigm shifts. Science STKE. Oct 23;2001(105):PE35. PubMed

Savkur, R., Philips, A.V., and Cooper, T.A. (2001) Aberrant regulation of insulin receptor alternative splicing is associated with insulin resistance in myotonic dystrophy. Nat Gen. 29, 40-47. PubMed

Stickeler, E., Fraser, S.D., Honig, A., Chen, A.L., Berget, S.M. and Cooper, T.A. (2001) The RNA binding protein YB-1 recognizes A/C-rich exon enhancers and stimulates splicing of the CD44 alternative exon v4. EMBO J. 20, 3821-3830. PubMed

Ladd, A.N., Charlet-B., N., and Cooper, T.A. (2001) The CELF family of RNA binding proteins is implicated in cell-specific and developmentally regulated alternative splicing Mol. Cell. Biol. 21,1285-1296. PubMed

Ryan, K.J., Charlet-B., N., and Cooper, T.A. (2000) Binding of PurH to a muscle-specific splicing enhancer correlates with exon inclusion in vivo. J. Biol. Chem. 275, 20618-20626. PubMed

Philips, A.V. and Cooper, T.A. (2000) RNA and human disease. Cell. Mol. Life Sci. 57, 235-249. PubMed

Stark, J.M., Cooper, T.A., Roth M.B. (1999) The relative strengths of SR protein-mediated associations of alternative and constitutive exons can influence alternative splicing. J. Biol. Chem., 274, 29838-29842. PubMed

Cooper, T.A. (1999) Strategies for defining pre-mRNA cis elements that regulate cell specific splicing in "RNA-Protein Interactions", Susan R. Haynes, Ed.; Methods in Molecular Biology Series, John M. Walker, Ed., (Humana Press), vol. 118, 391-403. PubMed

Cooper, T.A. (1999) In vivo SELEX in vertebrate cells in "RNA-Protein Interactions", Susan R. Haynes, Ed.; Methods in Molecular Biology Series, John M. Walker, Ed., (Humana Press), vol 118, 405-417. PubMed

Stoss, O., Cooper, T.A., and Stamm, S. (1999) Alternative splicing determines the intracellular localization of the muscle specific nucleolar proteins NOP30-1 and NOP30-2. J. Biol.Chem. 274, 10951-10962. PubMed

Cooper, T.A. (1998) Muscle-specific splicing of a heterologous exon mediated by a single muscle-specific splicing enhancer from the cardiac troponin T gene. Mol. Cell. Biol. 18, 4519-4525. PubMed

Philips, A.V., Timchenko, L.T., and Cooper, T.A. (1998) Disruption of splicing regulated by a CUG-binding protein in myotonic dystrophy. Science 280, 737-741. PubMed

Elrick, L.L., Humphrey, M.B., Cooper, T.A., and Berget, S.M. (1998) A short sequence within two purine-rich enhancers determines 5' splice site specificity. Mol. Cell. Biol. 18, 343-352. PubMed

Cooper, T.A. and Mattox, W. (1997) The regulation of splice site selection and its role in human disease. Amer. J. Hum. Gen. 61, 259-266.

Coulter, L., Landree, M., and Cooper, T.A. (1997) Identification of a new class of exonic splicing enhancers by in vivo selection. Mol. Cell. Biol. 17, 2143-2150. PubMed

Ryan, K.J. and Cooper, T.A. (1996) Muscle-specific splicing enhancers regulate inclusion of the cardiac troponin T alternative exon in embryonic skeletal muscle. Mol. Cell. Biol. 16, 4014-4023. PubMed

Ramchatesingh, J., Zahler, A.M., Neugebauer, K.M., Roth, M.B. and Cooper, T.A. (1995) A subset of SR proteins activates splicing of the cardiac troponin T alternative exon by direct interactions with an exonic enhancer. Mol. Cell. Biol. 15, 4898-4907. PubMed

Humphrey, M.B., Bryan, J., Cooper, T.A., Berget, S.M. (1995) A 32 nucleotide exon splicing enhancer regulates usage of competing 5' splice sites in a differential internal exon. Mol. Cell. Biol. 15, 3979-3988. PubMed

Lee, A.B. and Cooper, T.A. (1995) An improved direct PCR screen of bacterial colonies: wooden toothpicks inhibit PCR amplification. BioTechniques 18, 225-226.

Xu, R., Teng, J., and Cooper, T.A. (1993). The cardiac troponin T alternative exon contains a novel purine-rich positive splicing element. Mol. Cell. Biol. 13, 3660-3674. PubMed

Cooper, T.A. (1992). In vitro splicing of cardiac troponin T precursors: exon mutations disrupt splicing of the upstream intron. J. Biol. Chem. 267, 5330-5338. PubMed