Relevant bibliographies by topics / Complexe SWItch/Sucrose Non-Fermentable

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  2. Dissertations / Theses

Academic literature on the topic 'Complexe SWItch/Sucrose Non-Fermentable'

Author: Grafiati
Published: 16 November 2024
Last updated: 31 July 2025

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Journal articles on the topic "Complexe SWItch/Sucrose Non-Fermentable"

1

Choi, Sung Kyung, Myoung Jun Kim, and Jueng Soo You. "SMARCB1 Acts as a Quiescent Gatekeeper for Cell Cycle and Immune Response in Human Cells." International Journal of Molecular Sciences 21, no. 11 (2020): 3969. http://dx.doi.org/10.3390/ijms21113969.

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Switch/sucrose non-fermentable (SWI/SNF)-related matrix-associated actin-dependent regulator of chromatin (SMARC) subfamily B member 1 (SMARCB1) is a core subunit of the switch/sucrose non-fermentable (SWI/SNF) complex, one of the adenosine triphosphate (ATP)-dependent chromatin remodeler complexes. The unique role of SMARCB1 has been reported in various cellular contexts. Here, we focused on the general role of the ubiquitous expression of SMARCB1 in a normal cell state. We selected ARPE19 (human primary retinal pigment epithelium) and IMR90 (from human fetal lung fibroblasts) cell lines as t
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Nguyen, Thinh T., Joanne G. A. Savory, Travis Brooke-Bisschop, et al. "Cdx2 Regulates Gene Expression through Recruitment of Brg1-associated Switch-Sucrose Non-fermentable (SWI-SNF) Chromatin Remodeling Activity." Journal of Biological Chemistry 292, no. 8 (2017): 3389–99. http://dx.doi.org/10.1074/jbc.m116.752774.

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The packaging of genomic DNA into nucleosomes creates a barrier to transcription that can be relieved through ATP-dependent chromatin remodeling via complexes such as the switch-sucrose non-fermentable (SWI-SNF) chromatin remodeling complex. The SWI-SNF complex remodels chromatin via conformational or positional changes of nucleosomes, thereby altering the access of transcriptional machinery to target genes. The SWI-SNF complex has limited ability to bind to sequence-specific elements, and, therefore, its recruitment to target loci is believed to require interaction with DNA-associated transcr
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3

Liu, Hongyu, Yang Zhao, Guizhen Zhao, Yongjie Deng, Y. Eugene Chen, and Jifeng Zhang. "SWI/SNF Complex in Vascular Smooth Muscle Cells and Its Implications in Cardiovascular Pathologies." Cells 13, no. 2 (2024): 168. http://dx.doi.org/10.3390/cells13020168.

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Mature vascular smooth muscle cells (VSMC) exhibit a remarkable degree of plasticity, a characteristic that has intrigued cardiovascular researchers for decades. Recently, it has become increasingly evident that the chromatin remodeler SWItch/Sucrose Non-Fermentable (SWI/SNF) complex plays a pivotal role in orchestrating chromatin conformation, which is critical for gene regulation. In this review, we provide a summary of research related to the involvement of the SWI/SNF complexes in VSMC and cardiovascular diseases (CVD), integrating these discoveries into the current landscape of epigenetic
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Rembiałkowska, Nina, Katarzyna Rekiel, Piotr Urbanowicz, et al. "Epigenetic Dysregulation in Cancer: Implications for Gene Expression and DNA Repair-Associated Pathways." International Journal of Molecular Sciences 26, no. 13 (2025): 6531. https://doi.org/10.3390/ijms26136531.

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Epigenetic modifications are heritable, reversible alterations that causally reshape chromatin architecture and thereby influence DNA repair without changing nucleotide sequence. DNA methylation, histone modifications and non-coding RNAs profoundly influence DNA repair mechanisms and genomic stability. Aberrant epigenetic patterns in cancer compromise DNA damage recognition and repair, therefore impairing homologous recombination (HR), non-homologous end joining (NHEJ), and base excision repair (BER) by suppressing key repair genes and lowering access to repair sites. Then it is dissected how
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Del Savio, Elisa, and Roberta Maestro. "Beyond SMARCB1 Loss: Recent Insights into the Pathobiology of Epithelioid Sarcoma." Cells 11, no. 17 (2022): 2626. http://dx.doi.org/10.3390/cells11172626.

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Epithelioid sarcoma (ES) is a very rare and aggressive mesenchymal tumor of unclear origin and uncertain lineage characterized by a prevalent epithelioid morphology. The only recurrent genetic alteration reported in ES as yet is the functional inactivation of SMARCB1 (SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily B member 1), a key component of the SWI/SNF (SWItch/Sucrose Non-Fermentable) chromatin remodeling complexes. How SMARCB1 deficiency dictates the clinicopathological characteristics of ES and what other molecular defects concur to its malignant prog
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Wanior, Marek, Andreas Krämer, Stefan Knapp, and Andreas C. Joerger. "Exploiting vulnerabilities of SWI/SNF chromatin remodelling complexes for cancer therapy." Oncogene 40, no. 21 (2021): 3637–54. http://dx.doi.org/10.1038/s41388-021-01781-x.

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AbstractMulti-subunit ATPase-dependent chromatin remodelling complexes SWI/SNF (switch/sucrose non-fermentable) are fundamental epigenetic regulators of gene transcription. Functional genomic studies revealed a remarkable mutation prevalence of SWI/SNF-encoding genes in 20–25% of all human cancers, frequently driving oncogenic programmes. Some SWI/SNF-mutant cancers are hypersensitive to perturbations in other SWI/SNF subunits, regulatory proteins and distinct biological pathways, often resulting in sustained anticancer effects and synthetic lethal interactions. Exploiting these vulnerabilitie
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7

Soto-Castillo, Juan José, Lucía Llavata-Marti, Roser Fort-Culillas, et al. "SWI/SNF Complex Alterations in Tumors with Rhabdoid Features: Novel Therapeutic Approaches and Opportunities for Adoptive Cell Therapy." International Journal of Molecular Sciences 24, no. 13 (2023): 11143. http://dx.doi.org/10.3390/ijms241311143.

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The SWItch/Sucrose Non-Fermentable (SWI/SNF) chromatin-remodeling complex is one of the most remarkably altered epigenetic regulators in cancer. Pathogenic mutations in genes encoding SWI/SNF-related proteins have been recently described in many solid tumors, including rare and aggressive malignancies with rhabdoid features with no standard therapies in advanced or metastatic settings. In recent years, clinical trials with targeted drugs aimed at restoring its function have shown discouraging results. However, preclinical data have found an association between these epigenetic alterations and
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8

Hasan, Nesrin, and Nita Ahuja. "The Emerging Roles of ATP-Dependent Chromatin Remodeling Complexes in Pancreatic Cancer." Cancers 11, no. 12 (2019): 1859. http://dx.doi.org/10.3390/cancers11121859.

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Pancreatic cancer is an aggressive cancer with low survival rates. Genetic and epigenetic dysregulation has been associated with the initiation and progression of pancreatic tumors. Multiple studies have pointed to the involvement of aberrant chromatin modifications in driving tumor behavior. ATP-dependent chromatin remodeling complexes regulate chromatin structure and have critical roles in stem cell maintenance, development, and cancer. Frequent mutations and chromosomal aberrations in the genes associated with subunits of the ATP-dependent chromatin remodeling complexes have been detected i
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Collingwood, TN, FD Urnov, and AP Wolffe. "Nuclear receptors: coactivators, corepressors and chromatin remodeling in the control of transcription." Journal of Molecular Endocrinology 23, no. 3 (1999): 255–75. http://dx.doi.org/10.1677/jme.0.0230255.

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A contemporary view of hormone action at the transcriptional level requires knowledge of the transcription factors including the hormone receptor that may bind to promoters or enhancers, together with the chromosomal context within which these regulatory proteins function. Nuclear receptors provide the best examples of transcriptional control through the targeted recruitment of large protein complexes that modify chromosomal components and reversibly stabilize or destabilize chromatin. Ligand-dependent recruitment of transcriptional coactivators destabilizes chromatin by mechanisms including h
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Padilla-Benavides, Teresita, Pablo Reyes-Gutierrez, and Anthony N. Imbalzano. "Regulation of the Mammalian SWI/SNF Family of Chromatin Remodeling Enzymes by Phosphorylation during Myogenesis." Biology 9, no. 7 (2020): 152. http://dx.doi.org/10.3390/biology9070152.

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Myogenesis is the biological process by which skeletal muscle tissue forms. Regulation of myogenesis involves a variety of conventional, epigenetic, and epigenomic mechanisms that control chromatin remodeling, DNA methylation, histone modification, and activation of transcription factors. Chromatin remodeling enzymes utilize ATP hydrolysis to alter nucleosome structure and/or positioning. The mammalian SWItch/Sucrose Non-Fermentable (mSWI/SNF) family of chromatin remodeling enzymes is essential for myogenesis. Here we review diverse and novel mechanisms of regulation of mSWI/SNF enzymes by kin
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Dissertations / Theses on the topic "Complexe SWItch/Sucrose Non-Fermentable"

1

Bretones, Santamarina Jorge. "Integrated multiomic analysis, synthetic lethality inference and network pharmacology to identify SWI/SNF subunit-specific pathway alterations and targetable vulnerabilities." Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASL049.

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De nos jours, la communauté scientifique s'accorde sur la nécessité de diagnostics et de thérapies personnalisés pour les patients atteints de cancer, conçus par des études translationnelles combinant approches expérimentales et statistiques. Les défis actuels incluent la validation de modèles expérimentaux précliniques et leur profilage multi-omiques, ainsi que la conception de méthodes bioinformatiques et mathématiques dédiées pour identifier les combinaisons de médicaments optimales pour chaque patient.Cette thèse a visé à concevoir de telles approches statistiques pour analyser différents
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