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Gotowe bibliografie tematyczne / MuscleBlind Like (MBNL)

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Gotowa bibliografia na temat „MuscleBlind Like (MBNL)”

Autor: Grafiati

Data publikacji: 14 grudnia 2024

Data aktualizacji: 31 lipca 2025

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Artykuły w czasopismach na temat "MuscleBlind Like (MBNL)"

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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 (2019): 25203–13. http://dx.doi.org/10.1073/pnas.1820297116.

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Myotonic dystrophy type 1 (DM1) is a life-threatening and chronically debilitating neuromuscular disease caused by the expansion of a CTG trinucleotide repeat in the 3′ UTR of the DMPK gene. The mutant RNA forms insoluble structures capable of sequestering RNA binding proteins of the Muscleblind-like (MBNL) family, which ultimately leads to phenotypes. In this work, we demonstrate that treatment with the antiautophagic drug chloroquine was sufficient to up-regulate MBNL1 and 2 proteins in Drosophila and mouse (HSALR) models and patient-derived myoblasts. Extra Muscleblind was functional at the

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Voss, 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 (2020): ii223—ii224. http://dx.doi.org/10.1093/neuonc/noaa215.936.

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Abstract Muscleblind-like-proteins (MBNL) belong to a family of tissue-specific RNA metabolism-regulators that control pre-messenger RNA-splicing (AS). Inactivation of MBNL causes an adult-to-fetal AS transition, resulting in the development of myotonic dystrophy. We have previously shown that the aggressive brain cancer, glioblastoma (GBM), maintains stem-like features (GSC) through hypoxia-induced responses. Accordingly, we hypothesized that the hypoxia-induced responses in GBM might also include MBNL-based AS to promote tumor progression. When cultured in hypoxia, GSCs rapidly export MBNL1

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Gabel, Austin M., Edie I. Crosse, Andrea E. Belleville, et al. "Muscleblind-like proteins are novel modulators of the tumor-immune microenvironment." PLOS One 20, no. 4 (2025): e0321148. https://doi.org/10.1371/journal.pone.0321148.

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Exploiting the immune system to eradicate cancer cells is an area of intense clinical study. However, the mechanisms that shape the tumor-immune microenvironment are incompletely understood. Here, we identify Muscleblind-like (MBNL) proteins as novel modulators of the tumor-immune microenvironment across diverse cancers. We demonstrate that loss of tumor MBNL expression results in an attenuated response to interferon gamma and reduced tumor antigen presentation in melanoma, breast cancer, and colorectal cancer cells. Parallel experiments in a syngeneic mouse melanoma model revealed that MBNL l

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Overby, Sarah, Estefanía Cerro-Herreros, Jorge Espinosa-Espinosa, 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 (2023): 1118. http://dx.doi.org/10.3390/pharmaceutics15041118.

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The symptoms of Myotonic Dystrophy Type 1 (DM1) are multi-systemic and life-threatening. The neuromuscular disorder is rooted in a non-coding CTG microsatellite expansion in the DM1 protein kinase (DMPK) gene that, upon transcription, physically sequesters the Muscleblind-like (MBNL) family of splicing regulator proteins. The high-affinity binding occurring between the proteins and the repetitions disallow MBNL proteins from performing their post-transcriptional splicing regulation leading to downstream molecular effects directly related to disease symptoms such as myotonia and muscle weakness

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Yadava, 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 (2024): 2687. http://dx.doi.org/10.3390/ijms25052687.

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Loss of function of members of the muscleblind-like (MBNL) family of RNA binding proteins has been shown to play a key role in the spliceopathy of RNA toxicity in myotonic dystrophy type 1 (DM1), the most common muscular dystrophy affecting adults and children. MBNL1 and MBNL2 are the most abundantly expressed members in skeletal muscle. A key aspect of DM1 is poor muscle regeneration and repair, leading to dystrophy. We used a BaCl2-induced damage model of muscle injury to study regeneration and effects on skeletal muscle satellite cells (MuSCs) in Mbnl1∆E3/∆E3 and Mbnl2∆E2/∆E2 knockout mice.

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González, 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 (2022): 16147. http://dx.doi.org/10.3390/ijms232416147.

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The muscleblind-like protein family (MBNL) plays a prominent role in the regulation of alternative splicing. Consequently, the loss of MBNL function resulting from sequestration by RNA hairpins triggers the development of a neuromuscular disease called myotonic dystrophy (DM). Despite the sequence and structural similarities between the four zinc-finger domains that form MBNL1, recent studies have revealed that the four binding domains have differentiated splicing activity. The dynamic behaviors of MBNL1 ZnFs were simulated using conventional molecular dynamics (cMD) and steered molecular dyna

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Verbeeren, 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 (2023): e1011109. http://dx.doi.org/10.1371/journal.pgen.1011109.

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The Muscleblind-like (MBNL) family is a highly conserved set of RNA-binding proteins (RBPs) that regulate RNA metabolism during the differentiation of various animal tissues. Functional insufficiency of MBNL affects muscle and central nervous system development, and contributes to the myotonic dystrophies (DM), a set of incurable multisystemic disorders. Studies on the regulation of MBNL genes are essential to provide insight into the gene regulatory networks controlled by MBNL proteins and to understand how dysregulation within these networks causes disease. In this study, we demonstrate the

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Terenzi, Fulvia, and Andrea N. Ladd. "Conserved developmental alternative splicing of muscleblind-like (MBNL) transcripts regulates MBNL localization and activity." RNA Biology 7, no. 1 (2010): 43–55. http://dx.doi.org/10.4161/rna.7.1.10401.

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López-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 (2020): 1109. http://dx.doi.org/10.3390/genes11091109.

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Myotonic dystrophy type I (DM1) is the most common form of adult muscular dystrophy, caused by expansion of a CTG triplet repeat in the 3′ untranslated region (3′UTR) of the myotonic dystrophy protein kinase (DMPK) gene. The pathological CTG repeats result in protein trapping by expanded transcripts, a decreased DMPK translation and the disruption of the chromatin structure, affecting neighboring genes expression. The muscleblind-like (MBNL) and CUG-BP and ETR-3-like factors (CELF) are two families of tissue-specific regulators of developmentally programmed alternative splicing that act as ant

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Sznajder, 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 (2019): 3365. http://dx.doi.org/10.3390/ijms20133365.

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Short tandem repeat (STR) or microsatellite, expansions underlie more than 50 hereditary neurological, neuromuscular and other diseases, including myotonic dystrophy types 1 (DM1) and 2 (DM2). Current disease models for DM1 and DM2 propose a common pathomechanism, whereby the transcription of mutant DMPK (DM1) and CNBP (DM2) genes results in the synthesis of CUG and CCUG repeat expansion (CUGexp, CCUGexp) RNAs, respectively. These CUGexp and CCUGexp RNAs are toxic since they promote the assembly of ribonucleoprotein (RNP) complexes or RNA foci, leading to sequestration of Muscleblind-like (MBN

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Rozprawy doktorskie na temat "MuscleBlind Like (MBNL)"

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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.

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Vergnol, 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.

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Quatre protéines CaVβ (CaVβ1 à CaVβ4) sont connues comme des sous-unités régulatrices des canaux Ca2+ dépendants du voltage (Voltage-gated Ca2+ Channels, VGCC), chacune ayant des profils d'expression spécifiques selon leur fonction. Bien qu'elles soient principalement reconnues pour leur rôle dans la régulation des VGCC, les protéines CaVβ peuvent également agir indépendamment de ces canaux, en tant que régulateurs de l'expression génique. Parmi ces protéines, CaVβ1 est exprimée dans le muscle squelettique sous différentes isoformes. L'isoforme adulte constitutive, CaVβ1D, est localisée au niv

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Części książek na temat "MuscleBlind Like (MBNL)"

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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. Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2010-6_13.

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AbstractWestern blot assays are not adequate for high-throughput screening of protein expression because it is an expensive and time-consuming technique. Here we demonstrate that quantitative dot blots in plate format are a better option to determine the absolute contents of a given protein in less than 48 h. The method was optimized for the detection of the Muscleblind-like 1 protein in patient-derived myoblasts treated with a collection of more than 100 experimental oligonucleotides.

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