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Swi/snf complex

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https://www.readbyqxmd.com/read/28303890/baf60b-mediated-atm-p53-activation-blocks-cell-identity-conversion-by-sensing-chromatin-opening
#1
Shuyi Ji, Linying Zhu, Yimeng Gao, Xiaoran Zhang, Yupeng Yan, Jin Cen, Rongxia Li, Rong Zeng, Lujian Liao, Chunhui Hou, Yawei Gao, Shaorong Gao, Gang Wei, Lijian Hui
Lineage conversion by expression of lineage-specific transcription factors is a process of epigenetic remodeling that has low efficiency. The mechanism by which a cell resists lineage conversion is largely unknown. Using hepatic-specific transcription factors Foxa3, Hnf1α and Gata4 (3TF) to induce hepatic conversion in mouse fibroblasts, we showed that 3TF induced strong activation of the ATM-p53 pathway, which led to proliferation arrest and cell death, and it further prevented hepatic conversion. Notably, ATM activation, independent of DNA damage, responded to chromatin opening during hepatic conversion...
March 17, 2017: Cell Research
https://www.readbyqxmd.com/read/28297605/identifying-cell-cycle-modulators-that-selectively-target-arid1a-deficiency-using-high-throughput-image-based-screening
#2
Lihong Zhang, Jianfeng Shen, Yuping Yin, Yang Peng, Lulu Wang, Hui-Ju Hsieh, Qian Shen, Powel H Brown, Kaixiong Tao, Ivan P Uray, Guang Peng
ARID1A, a component of the chromatin remodeling complex SWI/SNF, is an evolutionarily conserved complex that uses the energy of adenosine triphosphate hydrolysis to remodel chromatin structure and functions as a master regulator of gene transcription. Recent genomic studies have revealed that ARID1A is one of the most frequently mutated genes in human cancers. However, therapeutic approaches that selectively target ARID1A-mutant tumors are not yet clinically available. Our previous study showed that ARID1A facilitates chromatin response and cell cycle checkpoint activation after DNA damage...
March 1, 2017: SLAS Discov
https://www.readbyqxmd.com/read/28292935/selective-killing-of-smarca2-and-smarca4-deficient-small-cell-carcinoma-of-the-ovary-hypercalcemic-type-cells-by-inhibition-of-ezh2-in-vitro-and-in-vivo-preclinical-models
#3
Elayne Chan-Penebre, Kelli Armstrong, Allison Drew, Alexandra R Grassian, Igor Feldman, Sarah K Knutson, Kristy Kuplast-Barr, Maria Roche, John Campbell, Peter Ho, Robert A Copeland, Richard Chesworth, Jesse J Smith, Heike Keilhack, Scott A Ribich
The SWI/SNF complex is a major regulator of gene expression and is increasingly thought to play an important role in human cancer, as evidenced by the high frequency of subunit mutations across virtually all cancer types. We previously reported that in preclinical models, malignant rhabdoid tumors, which are deficient in the SWI/SNF core component INI1 (SMARCB1), are selectively killed by inhibitors of the H3K27 histone methyltransferase EZH2. Given the demonstrated antagonistic activities of the SWI/SNF complex and the EZH2-containing PRC2 complex, we investigated whether additional cancers with SWI/SNF mutations are sensitive to selective EZH2 inhibition...
March 14, 2017: Molecular Cancer Therapeutics
https://www.readbyqxmd.com/read/28291122/smarcb1-ini-1-deficient-sinonasal-carcinoma-a-series-of-39-cases-expanding-the-morphologic-and-clinicopathologic-spectrum-of-a-recently-described-entity
#4
Abbas Agaimy, Arndt Hartmann, Cristina R Antonescu, Simion I Chiosea, Samir K El-Mofty, Helene Geddert, Heinrich Iro, James S Lewis, Bruno Märkl, Stacey E Mills, Marc-Oliver Riener, Thomas Robertson, Ann Sandison, Sabine Semrau, Roderick H W Simpson, Edward Stelow, William H Westra, Justin A Bishop
To more fully characterize the clinical and pathologic spectrum of a recently described tumor entity of the sinonasal tract characterized by loss of nuclear expression of SMARCB1 (INI1), we analyzed 39 SMARCB1-deficient sinonasal carcinomas collected from multiple medical centers. The tumors affected 23 males and 16 females with an age range of 19 to 89 years (median, 52). All patients presented with locally advanced disease (T3, n=5; T4, n=27) involving the sinuses (mainly ethmoid) with variable involvement of the nasal cavity...
April 2017: American Journal of Surgical Pathology
https://www.readbyqxmd.com/read/28289221/gentamicin-b1-is-a-minor-gentamicin-component-with-major-nonsense-mutation-suppression-activity
#5
Alireza Baradaran-Heravi, Jürgen Niesser, Aruna D Balgi, Kunho Choi, Carla Zimmerman, Andrew P South, Hilary J Anderson, Natalie C Strynadka, Marcel B Bally, Michel Roberge
Nonsense mutations underlie about 10% of rare genetic disease cases. They introduce a premature termination codon (PTC) and prevent the formation of full-length protein. Pharmaceutical gentamicin, a mixture of several related aminoglycosides, is a frequently used antibiotic in humans that can induce PTC readthrough and suppress nonsense mutations at high concentrations. However, testing of gentamicin in clinical trials has shown that safe doses of this drug produce weak and variable readthrough activity that is insufficient for use as therapy...
March 13, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28262751/the-swi-snf-chromatin-remodelling-complex-is-required-for-maintenance-of-lineage-specific-enhancers
#6
Burak H Alver, Kimberly H Kim, Ping Lu, Xiaofeng Wang, Haley E Manchester, Weishan Wang, Jeffrey R Haswell, Peter J Park, Charles W M Roberts
Genes encoding subunits of SWI/SNF (BAF) chromatin remodelling complexes are collectively altered in over 20% of human malignancies, but the mechanisms by which these complexes alter chromatin to modulate transcription and cell fate are poorly understood. Utilizing mouse embryonic fibroblast and cancer cell line models, here we show via ChIP-seq and biochemical assays that SWI/SNF complexes are preferentially targeted to distal lineage specific enhancers and interact with p300 to modulate histone H3 lysine 27 acetylation...
March 6, 2017: Nature Communications
https://www.readbyqxmd.com/read/28256572/clinicopathological-and-molecular-characterization-of-smarca4-deficient-thoracic-sarcomas-with-comparison-to-potentially-related-entities
#7
Akihiko Yoshida, Eisuke Kobayashi, Takashi Kubo, Makoto Kodaira, Toru Motoi, Noriko Motoi, Kan Yonemori, Yuichiro Ohe, Shun-Ichi Watanabe, Akira Kawai, Takashi Kohno, Hiroshi Kishimoto, Hitoshi Ichikawa, Nobuyoshi Hiraoka
A growing number of studies suggest critical tumor suppressor roles of the SWI/SNF chromatin remodeling complex in a variety of human cancers. The recent discovery of SMARCA4-deficient thoracic sarcomas has added to the list of tumor groups with the SMARCA4 inactivating mutation. To better characterize these tumors and establish their nosological status, we undertook a clinicopathological and molecular analysis of 12 SMARCA4-deficient thoracic sarcomas and compared them with three potentially related disease entities...
March 3, 2017: Modern Pathology: An Official Journal of the United States and Canadian Academy of Pathology, Inc
https://www.readbyqxmd.com/read/28253716/arid1a-gene-knockdown-promotes-neuroblastoma-migration-and-invasion
#8
C Li, Z Xu, Z Zhao, Q An, L Wang, Y Yu, D Piao
Neuroblastoma is the most common extracranial solid tumor in childhood which often acquires drug resistance and becomes aggressive phenotypes. The high-risk patients suffer from high mortality due to the limitation of the treatment strategies. ARID1A (AT-rich interactive domain-containing protein 1A), a subunit of SWI/SNF complexes, is considered as a tumor suppressor in many cancers. The aim of the present study was to investigate the effect of ARID1A on migration and invasion in neuroblastoma cells. The shRNA targeting ARID1A was designed and delivered into SK-N-SH cells to knock down ARID1A expression...
March 3, 2017: Neoplasma
https://www.readbyqxmd.com/read/28253434/a-general-non-radioactive-atpase-assay-for-chromatin-remodeling-complexes
#9
Benjamin Z Stanton, Courtney Hodges, Gerald R Crabtree, Keji Zhao
Chromatin remodeling complexes couple the energy released from ATP hydrolysis to facilitate transcription, recombination, and repair mechanisms essential for a wide variety of biologic responses. While recombinant expression of the regulatory subunits of these enzymes is possible, measuring catalytic (ATPase) activity of the intact complexes recovered from normal or mutant cells is critical for understanding their mechanisms. SWI/SNF-like remodeling complexes can be megadaltons in size and include many regulatory subunits, making reconstitution of purified subunits challenging for recapitulating in vivo function...
March 2, 2017: Current Protocols in Chemical Biology
https://www.readbyqxmd.com/read/28249160/loss-of-snf5-induces-formation-of-an-aberrant-swi-snf-complex
#10
Payel Sen, Jie Luo, Arjan Hada, Solomon G Hailu, Mekonnen Lemma Dechassa, Jim Persinger, Sandipan Brahma, Somnath Paul, Jeff Ranish, Blaine Bartholomew
The SWI/SNF chromatin remodeling complex is highly conserved from yeast to human, and aberrant SWI/SNF complexes contribute to human disease. The Snf5/SMARCB1/INI1 subunit of SWI/SNF is a tumor suppressor frequently lost in pediatric rhabdoid cancers. We examined the effects of Snf5 loss on the composition, nucleosome binding, recruitment, and remodeling activities of yeast SWI/SNF. The Snf5 subunit is shown by crosslinking-mass spectrometry (CX-MS) and subunit deletion analysis to interact with the ATPase domain of Snf2 and to form a submodule consisting of Snf5, Swp82, and Taf14...
February 28, 2017: Cell Reports
https://www.readbyqxmd.com/read/28249159/composition-and-function-of-mutant-swi-snf-complexes
#11
Arnob Dutta, Mihaela Sardiu, Madelaine Gogol, Joshua Gilmore, Daoyong Zhang, Laurence Florens, Susan M Abmayr, Michael P Washburn, Jerry L Workman
The 12-subunit Swi/Snf chromatin remodeling complex is conserved from yeast to humans. It functions to alter nucleosome positions by either sliding nucleosomes on DNA or evicting histones. Interestingly, 20% of all human cancers carry mutations in subunits of the Swi/Snf complex. Many of these mutations cause protein instability and loss, resulting in partial Swi/Snf complexes. Although several studies have shown that histone acetylation and activator-dependent recruitment of Swi/Snf regulate its function, it is less well understood how subunits regulate stability and function of the complex...
February 28, 2017: Cell Reports
https://www.readbyqxmd.com/read/28249153/deciphering-subunit-specific-functions-within-swi-snf-complexes
#12
Amanda L Hughes, Tom Owen-Hughes
In this issue of Cell Reports, Sen et al. and Dutta et al. reveal the modularity of the yeast SWI/SNF chromatin remodeling complex and show that loss of different subunits leads to distinct consequences for gene expression.
February 28, 2017: Cell Reports
https://www.readbyqxmd.com/read/28238438/arid2-modulates-dna-damage-response-in-human-hepatocellular-carcinoma-cells
#13
Atsushi Oba, Shu Shimada, Yoshimitsu Akiyama, Taketo Nishikawaji, Kaoru Mogushi, Hiromitsu Ito, Satoshi Matsumura, Arihiro Aihara, Yusuke Mitsunori, Daisuke Ban, Takanori Ochiai, Atsushi Kudo, Hiroshi Asahara, Atsushi Kaida, Masahiko Miura, Minoru Tanabe, Shinji Tanaka
BACKGROUND & AIMS: Recent genomic studies have identified frequent mutations of AT-rich interactive domain 2 (ARID2) in hepatocellular carcinoma (HCC), but it is not still understood how ARID2 exhibits tumor suppressor activities. METHODS: We established the ARID2 knockout human HCC cell lines by using CRISPR/Cas9 system, and investigated the gene expression profiles and biological functions. RESULTS: Bioinformatic analysis indicated that UV-response genes were negatively regulated in the ARID2 knockout cells, and they were sensitized to UV irradiation...
February 23, 2017: Journal of Hepatology
https://www.readbyqxmd.com/read/28228591/the-swi-snf-chromatin-regulator-brg1-modulates-the-transcriptional-regulatory-activity-of-the-ebv-dna-polymerase-processivity-factor-bmrf1
#14
Mei-Tzu Su, Ya-Ting Wang, Yen-Ju Chen, Su-Fang Lin, Ching-Hwa Tsai, Mei-Ru Chen
During lytic phase of Epstein-Barr virus (EBV), binding of the transactivator Zta to the origin of lytic replication (oriLyt) and the BHLF1 transcript, forming a stable RNA-DNA hybrid, are required to initiate viral DNA replication. EBV-encoded viral DNA replication proteins form complexes to amplify viral DNA. BMRF1, the viral DNA polymerase accessory factor, is essential for lytic DNA replication and also known as a transcriptional regulator of the expression of BHLF1 and BALF2 (ssDNA-binding protein). In order to determine systematically how BMRF1 regulates viral transcription, a BMRF1 knockout bacmid was generated to analyze viral gene expression using a viral DNA microarray...
February 22, 2017: Journal of Virology
https://www.readbyqxmd.com/read/28212646/linking-long-non-coding-rnas-and-swi-snf-complexes-to-chromatin-remodeling-in-cancer
#15
REVIEW
Yanyan Tang, Jinpeng Wang, Yu Lian, Chunmei Fan, Ping Zhang, Yingfen Wu, Xiayu Li, Fang Xiong, Xiaoling Li, Guiyuan Li, Wei Xiong, Zhaoyang Zeng
Chromatin remodeling controls gene expression and signaling pathway activation, and aberrant chromatin structure and gene dysregulation are primary characteristics of human cancer progression. Recent reports have shown that long non-coding RNAs (lncRNAs) are tightly associated with chromatin remodeling. In this review, we focused on important chromatin remodelers called the switching defective/sucrose nonfermenting (SWI/SNF) complexes, which use the energy of ATP hydrolysis to control gene transcription by altering chromatin structure...
February 17, 2017: Molecular Cancer
https://www.readbyqxmd.com/read/28209126/a-meta-analysis-reveals-complex-regulatory-properties-at-taf14-repressed-genes
#16
Josipa Nemet, Nikolina Vidan, Mary Sopta
BACKGROUND: Regulation of gene transcription in response to stress is central to a cell's ability to cope with environmental challenges. Taf14 is a YEATS domain protein in S.cerevisiae that physically associates with several transcriptionally relevant multisubunit complexes including the general transcription factors TFIID and TFIIF and the chromatin-modifying complexes SWI/SNF, INO80, RSC and NuA3. TAF14 deletion strains are sensitive to a variety of stresses suggesting that it plays a role in the transcriptional stress response...
February 16, 2017: BMC Genomics
https://www.readbyqxmd.com/read/28202515/systematic-in-vivo-inactivation-of-chromatin-regulating-enzymes-identifies-setd2-as-a-potent-tumor-suppressor-in-lung-adenocarcinoma
#17
David M Walter, Olivia S Venancio, Elizabeth L Buza, John W Tobias, Charuhas Deshpande, A Andrea Gudiel, Caroline Kim-Kiselak, Michelle Cicchini, Travis J Yates, David M Feldser
Chromatin modifying genes are frequently mutated in human lung adenocarcinoma, but the functional impact of these mutations on disease initiation and progression is not well understood. Using a CRISPR-based approach, we systematically inactivated three of the most commonly mutated chromatin regulatory genes in two KrasG12D-driven mouse models of lung adenocarcinoma to characterize the impact of their loss. Targeted inactivation of SWI/SNF nucleosome remodeling complex members Smarca4 (Brg1) or Arid1a had complex effects on lung adenocarcinoma initiation and progression...
February 15, 2017: Cancer Research
https://www.readbyqxmd.com/read/28188921/mediator-swi-snf-and-saga-complexes-regulate-yap8-dependent-transcriptional-activation-of-acr2-in-response-to-arsenate
#18
Regina Andrade Menezes, Catarina Pimentel, Ana Rita Courelas Silva, Catarina Amaral, Jawad Merhej, Frédéric Devaux, Claudina Rodrigues-Pousada
Response to arsenic stress in Saccharomyces cerevisiae is orchestrated by the regulatory protein Yap8, which mediates transcriptional activation of ACR2 and ACR3. This study contributes to the state of art knowledge of the molecular mechanisms underlying yeast stress response to arsenate as it provides the genetic and biochemical evidences that Yap8, through cysteine residues 132, 137, and 274, is the sensor of presence of arsenate in the cytosol. Moreover, it is here reported for the first time the essential role of the Mediator complex in the transcriptional activation of ACR2 by Yap8...
February 7, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28176137/smarca4-deficient-sinonasal-carcinoma
#19
Abbas Agaimy, Wilko Weichert
The term "sinonasal undifferentiated carcinoma (SNUC)" has been coined in 1986 for a highly aggressive sinonasal tract epithelial neoplasm showing distinctive morphology, but lacking any specific line of differentiation. Recent developments resulted in a dynamic splitting of new entities traditionally included in the spectrum of SNUC. Sinonasal NUT-midline carcinoma, adamantinoma-like Ewing family tumors and most recently, SMARCB1(INI1)-deficient sinonasal carcinoma are the main entities defined by specific genetic aberrations...
February 7, 2017: Head and Neck Pathology
https://www.readbyqxmd.com/read/28167502/a-genetic-interaction-analysis-identifies-cancer-drivers-that-modify-egfr-dependency
#20
Sida Liao, Teresa Davoli, Yumei Leng, Mamie Z Li, Qikai Xu, Stephen J Elledge
A large number of cancer drivers have been identified through tumor sequencing efforts, but how they interact and the degree to which they can substitute for each other have not been systematically explored. To comprehensively investigate how cancer drivers genetically interact, we searched for modifiers of epidermal growth factor receptor (EGFR) dependency by performing CRISPR, shRNA, and expression screens in a non-small cell lung cancer (NSCLC) model. We elucidated a broad spectrum of tumor suppressor genes (TSGs) and oncogenes (OGs) that can genetically modify proliferation and survival of cancer cells when EGFR signaling is altered...
January 15, 2017: Genes & Development
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