Academic literature on the topic 'MuscleBlind Like (MBNL)'
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Journal articles on the topic "MuscleBlind Like (MBNL)"
Bargiela, Ariadna, Maria Sabater-Arcis, Jorge Espinosa-Espinosa, Miren Zulaica, Adolfo Lopez de Munain, and Ruben Artero. "Increased Muscleblind levels by chloroquine treatment improve myotonic dystrophy type 1 phenotypes in in vitro and in vivo models." Proceedings of the National Academy of Sciences 116, no. 50 (November 21, 2019): 25203–13. http://dx.doi.org/10.1073/pnas.1820297116.
Full textVoss, Dillon, Anthony Sloan, Eli Bar, and Eli Bar. "TAMI-49. THE ALTERNATIVE SPLICING FACTOR MBNL1 INHIBITS GLIOBLASTOMA TUMOR INITIATION AND PROGRESSION BY REDUCING HYPOXIA-INDUCED STEMNESS." Neuro-Oncology 22, Supplement_2 (November 2020): ii223—ii224. http://dx.doi.org/10.1093/neuonc/noaa215.936.
Full textOverby, Sarah, Estefanía Cerro-Herreros, Jorge Espinosa-Espinosa, Irene González-Martínez, Nerea Moreno, Juan Fernández-Costa, Jordina Balaguer-Trias, et al. "BlockmiR AONs as Site-Specific Therapeutic MBNL Modulation in Myotonic Dystrophy 2D and 3D Muscle Cells and HSALR Mice." Pharmaceutics 15, no. 4 (March 31, 2023): 1118. http://dx.doi.org/10.3390/pharmaceutics15041118.
Full textYadava, Ramesh S., Mahua Mandal, and Mani S. Mahadevan. "Studying the Effect of MBNL1 and MBNL2 Loss in Skeletal Muscle Regeneration." International Journal of Molecular Sciences 25, no. 5 (February 26, 2024): 2687. http://dx.doi.org/10.3390/ijms25052687.
Full textGonzález, Àlex L., Daniel Fernández-Remacha, José Ignacio Borrell, Jordi Teixidó, and Roger Estrada-Tejedor. "Cognate RNA-Binding Modes by the Alternative-Splicing Regulator MBNL1 Inferred from Molecular Dynamics." International Journal of Molecular Sciences 23, no. 24 (December 18, 2022): 16147. http://dx.doi.org/10.3390/ijms232416147.
Full textVerbeeren, Jens, Joana Teixeira, and Susana M. D. A. Garcia. "The Muscleblind-like protein MBL-1 regulates microRNA expression in Caenorhabditis elegans through an evolutionarily conserved autoregulatory mechanism." PLOS Genetics 19, no. 12 (December 22, 2023): e1011109. http://dx.doi.org/10.1371/journal.pgen.1011109.
Full textTerenzi, Fulvia, and Andrea N. Ladd. "Conserved developmental alternative splicing of muscleblind-like (MBNL) transcripts regulates MBNL localization and activity." RNA Biology 7, no. 1 (January 2010): 43–55. http://dx.doi.org/10.4161/rna.7.1.10401.
Full textLópez-Martínez, Andrea, Patricia Soblechero-Martín, Laura de-la-Puente-Ovejero, Gisela Nogales-Gadea, and Virginia Arechavala-Gomeza. "An Overview of Alternative Splicing Defects Implicated in Myotonic Dystrophy Type I." Genes 11, no. 9 (September 22, 2020): 1109. http://dx.doi.org/10.3390/genes11091109.
Full textSznajder, Łukasz J., and Maurice S. Swanson. "Short Tandem Repeat Expansions and RNA-Mediated Pathogenesis in Myotonic Dystrophy." International Journal of Molecular Sciences 20, no. 13 (July 9, 2019): 3365. http://dx.doi.org/10.3390/ijms20133365.
Full textTanner, Matthew K., Zhenzhi Tang, and Charles A. Thornton. "Targeted splice sequencing reveals RNA toxicity and therapeutic response in myotonic dystrophy." Nucleic Acids Research 49, no. 4 (January 27, 2021): 2240–54. http://dx.doi.org/10.1093/nar/gkab022.
Full textDissertations / Theses on the topic "MuscleBlind Like (MBNL)"
Fleming, Victoria Amber. "Complex Regulation Of Neurofibromatosis Type I Exon 23a Inclusion By The CUG-BP AND ETR-3-LIKE Factors (CELF) And Muscleblind-Like (MBNL) Proteins." Case Western Reserve University School of Graduate Studies / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=case1333490345.
Full textVergnol, Amélie. "Les isoformes CaVβ1 : rôle dans la formation de la jonction neuromusculaire et implication dans la physiopathologie de la Dystrophie Myotonique de type 1." Electronic Thesis or Diss., Sorbonne université, 2024. http://www.theses.fr/2024SORUS305.
Full textFour CaVβ proteins (CaVβ1 to CaVβ4) are described as regulatory subunit of Voltage-gated Ca2+ channel (VGCC), each exhibiting specific expression pattern in excitable cells based on their function. While primarily recognized for their role in VGCC regulation, CaVβ proteins also function independently of channels, acting as regulators of gene expression. Among these, CaVβ1 is expressed in skeletal muscle as different isoforms. The adult constitutive isoform, CaVβ1D, is located at the sarcolemma and more specifically at the triad, where it plays a crucial role in regulating CaV1 to control Excitation-Contraction Coupling (ECC) mechanism, essential for muscle contraction.In this thesis, we further explored the less studied CaVβ1 isoforms, with a particular focus on embryonic/perinatal variants, including the previously described CaVβ1E. We investigated their roles in the neuromuscular and muscular systems. Indeed, CaVβ1 proteins have been showed as essential for NeuroMuscular Junction (NMJ) development, though the involvement of specific isoform remains unclear. Our investigation assessed the role of CaVβ1 isoforms at different stages of NMJ formation and maturation/maintenance. Additionally, given the deregulation of CaVβ1 in Myotonic Dystrophy Type 1 (DM1), we explored its functional role in this muscular pathological context.First, we identified CaVβ1A as another isoform expressed during embryogenesis and perinatal stages. Our findings revealed that CaVβ1 isoforms expressions are regulated by the differential activation of promoters during development: a promoter1 in exon 1 drives CaVβ1A/E expressions, while a promoter2 in exon 2B controls CaVβ1D expression. Interestingly, nerve damage in adult muscle triggers a shift toward the promoter1 activation and leading to the re-expression of CaVβ1A/E transcripts. Furthermore, we found that CaVβ1 embryonic/perinatal isoforms are critical for proper in vitro pre-patterning of myotubes and that their postnatal expressions influences NMJ maturation/maintenance. In the pathological context of DM1, we observed the increased expression of CaVβ1A/E, which appears to mitigate myotonia symptoms. In addition, we found that the modulation of their expression is linked with MBNL proteins, which are central in the pathophysiology of DM1. In conclusion, this thesis work has clarified knowledge of the various CaVβ1 isoforms in skeletal muscle and provides new insights into their role in two independent contexts of NMJ development and DM1 pathophysiology. Understanding CaVβ1 protein regulation in skeletal muscle is essential to decipher muscle homeostasis mechanisms and potentially identify new therapeutic targets to face muscular disorders
Book chapters on the topic "MuscleBlind Like (MBNL)"
Moreno, Nerea, Irene González-Martínez, Rubén Artero, and Estefanía Cerro-Herreros. "Rapid Determination of MBNL1 Protein Levels by Quantitative Dot Blot for the Evaluation of Antisense Oligonucleotides in Myotonic Dystrophy Myoblasts." In Methods in Molecular Biology, 207–15. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2010-6_13.
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