Gotowe bibliografie tematyczne / SWItch/Sucrose Non-Fermentable complex

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Gotowa bibliografia na temat „SWItch/Sucrose Non-Fermentable complex”

Autor: Grafiati

Data publikacji: 16 listopada 2024

Data aktualizacji: 31 lipca 2025

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Artykuły w czasopismach na temat "SWItch/Sucrose Non-Fermentable complex"

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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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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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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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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Cruz-Tapia, Roberto Onner, Ana María Cano-Valdez, Abelardo Meneses-García, et al. "Switch/Sucrose Non-Fermentable (SWI/SNF) Complex—Partial Loss in Sinonasal Squamous Cell Carcinoma: A High-Grade Morphology Impact and Progression." Current Issues in Molecular Biology 46, no. 11 (2024): 12183–95. http://dx.doi.org/10.3390/cimb46110723.

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Sinonasal carcinomas are aggressive neoplasms that present a high morbidity and mortality rate with an unfavorable prognosis. This group of tumors exhibits morphological and genetic diversity. Genetic and epigenetic alterations in these neoplasms are the current targets for diagnosis and treatment. The most common type of cancer originating in the sinonasal tract is sinonasal squamous cell carcinomas (SNSCCs), which present different histological patterns and variable histological aggressiveness. A significant number of alterations have been reported in sinonasal tumors, including deficiencies

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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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Wu, Shuai, Nail Fatkhutdinov, Leah Rosin, et al. "ARID1A spatially partitions interphase chromosomes." Science Advances 5, no. 5 (2019): eaaw5294. http://dx.doi.org/10.1126/sciadv.aaw5294.

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ARID1A, a subunit of the SWItch/Sucrose Non-Fermentable (SWI/SNF) chromatin-remodeling complex, localizes to both promoters and enhancers to influence transcription. However, the role of ARID1A in higher-order spatial chromosome partitioning and genome organization is unknown. Here, we show that ARID1A spatially partitions interphase chromosomes and regulates higher-order genome organization. The SWI/SNF complex interacts with condensin II, and they display significant colocalizations at enhancers. ARID1A knockout drives the redistribution of condensin II preferentially at enhancers, which pos

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El Hadidy and Uversky. "Intrinsic Disorder of the BAF Complex: Roles in Chromatin Remodeling and Disease Development." International Journal of Molecular Sciences 20, no. 21 (2019): 5260. http://dx.doi.org/10.3390/ijms20215260.

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The two-meter-long DNA is compressed into chromatin in the nucleus of every cell, which serves as a significant barrier to transcription. Therefore, for processes such as replication and transcription to occur, the highly compacted chromatin must be relaxed, and the processes required for chromatin reorganization for the aim of replication or transcription are controlled by ATP-dependent nucleosome remodelers. One of the most highly studied remodelers of this kind is the BRG1- or BRM-associated factor complex (BAF complex, also known as SWItch/sucrose non-fermentable (SWI/SNF) complex), which

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Li, Jing Jing, and Cheok Soon Lee. "The Role of the AT-Rich Interaction Domain 1A Gene (ARID1A) in Human Carcinogenesis." Genes 15, no. 1 (2023): 5. http://dx.doi.org/10.3390/genes15010005.

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The switch/sucrose non-fermentable (SWI/SNF) (SWI/SNF) complex uses energy from ATP hydrolysis to mobilise nucleosomes on chromatin. Components of SWI/SNF are mutated in 20% of all human cancers, of which mutations in AT-rich binding domain protein 1A (ARID1A) are the most common. ARID1A is mutated in nearly half of ovarian clear cell carcinoma and around one-third of endometrial and ovarian carcinomas of the endometrioid type. This review will examine in detail the molecular functions of ARID1A, including its role in cell cycle control, enhancer regulation, and the prevention of telomerase ac

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Ngo, Carine, and Sophie Postel-Vinay. "Immunotherapy for SMARCB1-Deficient Sarcomas: Current Evidence and Future Developments." Biomedicines 10, no. 3 (2022): 650. http://dx.doi.org/10.3390/biomedicines10030650.

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Mutations in subunits of the SWItch Sucrose Non-Fermentable (SWI/SNF) complex occur in 20% of all human tumors. Among these, the core subunit SMARCB1 is the most frequently mutated, and SMARCB1 loss represents a founder driver event in several malignancies, such as malignant rhabdoid tumors (MRT), epithelioid sarcoma, poorly differentiated chordoma, and renal medullary carcinoma (RMC). Intriguingly, SMARCB1-deficient pediatric MRT and RMC have recently been reported to be immunogenic, despite their very simple genome and low tumor mutational burden. Responses to immune checkpoint inhibitors ha

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Rozprawy doktorskie na temat "SWItch/Sucrose Non-Fermentable complex"

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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