Literatura académica sobre el tema "MuscleBlind Like (MBNL)"
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Artículos de revistas sobre el tema "MuscleBlind Like (MBNL)"
Bargiela, Ariadna, Maria Sabater-Arcis, Jorge Espinosa-Espinosa, Miren Zulaica, Adolfo Lopez de Munain y 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, n.º 50 (21 de noviembre de 2019): 25203–13. http://dx.doi.org/10.1073/pnas.1820297116.
Texto completoVoss, Dillon, Anthony Sloan, Eli Bar y 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 (noviembre de 2020): ii223—ii224. http://dx.doi.org/10.1093/neuonc/noaa215.936.
Texto completoOverby, 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, n.º 4 (31 de marzo de 2023): 1118. http://dx.doi.org/10.3390/pharmaceutics15041118.
Texto completoYadava, Ramesh S., Mahua Mandal y Mani S. Mahadevan. "Studying the Effect of MBNL1 and MBNL2 Loss in Skeletal Muscle Regeneration". International Journal of Molecular Sciences 25, n.º 5 (26 de febrero de 2024): 2687. http://dx.doi.org/10.3390/ijms25052687.
Texto completoGonzález, Àlex L., Daniel Fernández-Remacha, José Ignacio Borrell, Jordi Teixidó y Roger Estrada-Tejedor. "Cognate RNA-Binding Modes by the Alternative-Splicing Regulator MBNL1 Inferred from Molecular Dynamics". International Journal of Molecular Sciences 23, n.º 24 (18 de diciembre de 2022): 16147. http://dx.doi.org/10.3390/ijms232416147.
Texto completoVerbeeren, Jens, Joana Teixeira y 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, n.º 12 (22 de diciembre de 2023): e1011109. http://dx.doi.org/10.1371/journal.pgen.1011109.
Texto completoTerenzi, Fulvia y Andrea N. Ladd. "Conserved developmental alternative splicing of muscleblind-like (MBNL) transcripts regulates MBNL localization and activity". RNA Biology 7, n.º 1 (enero de 2010): 43–55. http://dx.doi.org/10.4161/rna.7.1.10401.
Texto completoLópez-Martínez, Andrea, Patricia Soblechero-Martín, Laura de-la-Puente-Ovejero, Gisela Nogales-Gadea y Virginia Arechavala-Gomeza. "An Overview of Alternative Splicing Defects Implicated in Myotonic Dystrophy Type I". Genes 11, n.º 9 (22 de septiembre de 2020): 1109. http://dx.doi.org/10.3390/genes11091109.
Texto completoSznajder, Łukasz J. y Maurice S. Swanson. "Short Tandem Repeat Expansions and RNA-Mediated Pathogenesis in Myotonic Dystrophy". International Journal of Molecular Sciences 20, n.º 13 (9 de julio de 2019): 3365. http://dx.doi.org/10.3390/ijms20133365.
Texto completoTanner, Matthew K., Zhenzhi Tang y Charles A. Thornton. "Targeted splice sequencing reveals RNA toxicity and therapeutic response in myotonic dystrophy". Nucleic Acids Research 49, n.º 4 (27 de enero de 2021): 2240–54. http://dx.doi.org/10.1093/nar/gkab022.
Texto completoTesis sobre el tema "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.
Texto completoVergnol, 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.
Texto completoFour 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
Capítulos de libros sobre el tema "MuscleBlind Like (MBNL)"
Moreno, Nerea, Irene González-Martínez, Rubén Artero y Estefanía Cerro-Herreros. "Rapid Determination of MBNL1 Protein Levels by Quantitative Dot Blot for the Evaluation of Antisense Oligonucleotides in Myotonic Dystrophy Myoblasts". En Methods in Molecular Biology, 207–15. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2010-6_13.
Texto completo