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Swi/snf complex

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https://www.readbyqxmd.com/read/28807921/candida-albicans-swi-snf-and-mediator-complexes-differentially-regulate-mrr1-induced-mdr1-expression-and-fluconazole-resistance
#1
Zhongle Liu, Lawrence C Myers
Long-term azole treatment of patients with chronic Candida albicans infections can lead to drug resistance. Gain-of-function (GOF) mutations in the transcription factor Mrr1 and the consequent transcriptional activation of MDR1, a drug efflux coding gene, is a common pathway by which this human fungal pathogen acquires fluconazole resistance. This work elucidates the previously unknown downstream transcription mechanisms utilized by hyperactive Mrr1. We've identified the Swi/Snf chromatin remodeling complex as a key co-activator for Mrr1, which is required to maintain basal and induced 'open' chromatin, and Mrr1 occupancy, at the MDR1 promoter...
August 14, 2017: Antimicrobial Agents and Chemotherapy
https://www.readbyqxmd.com/read/28768829/the-saga-complex-together-with-transcription-factors-and-the-endocytic-protein-rvs167p-coordinate-the-reprofiling-of-gene-expression-in-response-to-changes-in-sterol-composition-in-saccharomyces-cerevisiae
#2
Gisèle Dewhurst-Maridor, Daniel Abegg, Fabrice P A David, Jacques Rougemont, Cameron C Scott, Alexander Adibekian, Howard Riezman
Changes in cellular sterol species and concentrations can have profound effects on the transcriptional profile. In yeast, mutants defective in sterol biosynthesis show a wide range of changes in transcription, including a co-induction of anaerobic genes and ergosterol biosynthesis genes, biosynthesis of basic amino acids, and several stress genes. However the mechanisms underlying these changes are unknown. We identified mutations in the SAGA complex, a co-activator of transcription, which abrogate the ability to carry out most of these sterol-dependent transcriptional changes...
August 2, 2017: Molecular Biology of the Cell
https://www.readbyqxmd.com/read/28754838/the-chromatin-remodeling-bap-complex-limits-tumor-promoting-activity-of-the-hippo-pathway-effector-yki-to-prevent-neoplastic-transformation-in-drosophila-epithelia
#3
Shilin Song, Héctor Herranz, Stephen M Cohen
SWI/SNF chromatin remodeling complexes are mutated in many human cancers. In this report we make use of a Drosophila genetic model for epithelial tumor formation to explore the tumor suppressive role of SWI/SNF complex proteins. Members of the BAP complex exhibit tumor suppressor activity in tissue overexpressing the Yorkie (Yki) proto-oncogene, but not in tissue overexpressing EGFR. The BAP complex has been reported to serve as a Yki-binding cofactor to support Yki target expression. However, we observed that depletion of BAP leads to ectopic expression of Yki targets both autonomously and non-autonomously, suggesting additional indirect effects...
July 28, 2017: Disease Models & Mechanisms
https://www.readbyqxmd.com/read/28741798/novel-orally-bioavailable-ezh1-2-dual-inhibitors-with-greater-antitumor-efficacy-than-an-ezh2-selective-inhibitor
#4
Daisuke Honma, Osamu Kanno, Jun Watanabe, Junzo Kinoshita, Makoto Hirasawa, Emi Nosaka, Machiko Shiroishi, Takeshi Takizawa, Isao Yasumatsu, Takao Horiuchi, Akira Nakao, Keisuke Suzuki, Tomonori Yamasaki, Katsuyoshi Nakajima, Miho Hayakawa, Takanori Yamazaki, Ajay Singh Yadav, Nobuaki Adachi
Polycomb repressive complex 2 (PRC2) methylates histone H3 lysine 27 and represses gene expression to regulate cell proliferation and differentiation. Enhancer of zeste homolog 2 (EZH2) or its close homolog EZH1 functions as a catalytic subunit of PRC2, so there are two PRC2 complexes containing either EZH2 or EZH1. Tumorigenic functions of EZH2 and its synthetic lethality with some subunits of SWItch/Sucrose Non-Fermentable (SWI/SNF) chromatin remodeling complexes have been observed. However, little is known about the function of EZH1 in tumorigenesis...
July 25, 2017: Cancer Science
https://www.readbyqxmd.com/read/28739803/chromatin-remodeling-swi-snf-complex-regulates-coenzyme-q6-synthesis-and-a-metabolic-shift-to-respiration-in-yeast
#5
Agape M Awad, Srivats Venkataramanan, Anish Nag, Anoop Raj Galivanche, Michelle C Bradley, Lauren Neves, Stephen Douglass, Catherine F Clarke, Tracy L Johnson
Despite its relatively streamlined genome, there are many important examples of regulated RNA splicing in Saccharomyces cerevisiae Here we report a role for the chromatin remodeler SWI/SNF in respiration, partially via the regulation of splicing. We find that a nutrient-dependent decrease in Snf2 leads to an increase in splicing of the PTC7 transcript. The spliced PTC7 transcript encodes a mitochondrial phosphatase regulator of biosynthesis of coenzyme Q6 (ubiquinone, or CoQ6), a mitochondrial redox-active lipid essential for electron and proton transport in respiration, and increased splicing of PTC7 increases CoQ6 levels...
July 24, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28737768/arid1a-mutated-ovarian-cancers-depend-on-hdac6%C3%A2-activity
#6
Benjamin G Bitler, Shuai Wu, Pyoung Hwa Park, Yang Hai, Katherine M Aird, Yemin Wang, Yali Zhai, Andrew V Kossenkov, Ana Vara-Ailor, Frank J Rauscher Iii, Weiping Zou, David W Speicher, David G Huntsman, Jose R Conejo-Garcia, Kathleen R Cho, David W Christianson, Rugang Zhang
ARID1A, encoding a subunit of the SWI/SNF chromatin-remodelling complex, is the most frequently mutated epigenetic regulator across all human cancers. ARID1A and TP53 mutations are typically mutually exclusive. Therapeutic approaches that correlate with this genetic characteristic remain to be explored. Here, we show that HDAC6 activity is essential in ARID1A-mutated ovarian cancers. Inhibition of HDAC6 activity using a clinically applicable small-molecule inhibitor significantly improved the survival of mice bearing ARID1A-mutated tumours...
August 2017: Nature Cell Biology
https://www.readbyqxmd.com/read/28737171/brg1-swi-snf-dependent-regulation-of-the-wt1-transcriptional-landscape-mediates-epicardial-activity-during-heart-development-and-disease
#7
Joaquim Miguel Vieira, Sara Howard, Cristina Villa Del Campo, Sveva Bollini, Karina N Dubé, Megan Masters, Damien N Barnette, Mala Rohling, Xin Sun, Laura E Hankins, Daria Gavriouchkina, Ruth Williams, Daniel Metzger, Pierre Chambon, Tatjana Sauka-Spengler, Benjamin Davies, Paul R Riley
Epicardium-derived cells (EPDCs) contribute cardiovascular cell types during development and in adulthood respond to Thymosin β4 (Tβ4) and myocardial infarction (MI) by reactivating a fetal gene programme to promote neovascularization and cardiomyogenesis. The mechanism for epicardial gene (re-)activation remains elusive. Here we reveal that BRG1, the essential ATPase subunit of the SWI/SNF chromatin-remodelling complex, is required for expression of Wilms' tumour 1 (Wt1), fetal EPDC activation and subsequent differentiation into coronary smooth muscle, and restores Wt1 activity upon MI...
July 24, 2017: Nature Communications
https://www.readbyqxmd.com/read/28731042/molecular-alterations-of-coexisting-thyroid-papillary-carcinoma-and-anaplastic-carcinoma-identification-of-tert-mutation-as-an-independent-risk-factor-for-transformation
#8
Naoki Oishi, Tetsuo Kondo, Aya Ebina, Yukiko Sato, Junko Akaishi, Rumi Hino, Noriko Yamamoto, Kunio Mochizuki, Tadao Nakazawa, Hiroshi Yokomichi, Koichi Ito, Yuichi Ishikawa, Ryohei Katoh
Thyroid papillary carcinoma is the most common endocrine neoplasm and generally carries a favorable prognosis. However, a small subset of papillary carcinomas transforms into anaplastic carcinoma, an undifferentiated cancer with a dismal prognosis. Recent studies using next-generation sequencing revealed the genomic landscape of papillary carcinoma and anaplastic carcinoma. However, risk factors for anaplastic transformation in papillary carcinoma remain obscure. In the present study, we investigated molecular alterations of papillary carcinoma and anaplastic carcinoma components in 27 tumors in which anaplastic carcinoma coexisted with antecedent papillary carcinoma...
July 21, 2017: Modern Pathology: An Official Journal of the United States and Canadian Academy of Pathology, Inc
https://www.readbyqxmd.com/read/28716950/analysis-of-small-critical-regions-of-swi1-conferring-prion-formation-maintenance-and-transmission
#9
Stephanie Valtierra, Zhiqiang Du, Liming Li
Saccharomyces cerevisiae contains several prion elements, which are epigenetically transmitted as self-perpetuating protein conformations. One such prion is [SWI(+) ], whose protein determinant is Swi1, a subunit of the SWI/SNF chromatin-remodeling complex. We previously reported that [SWI(+) ] formation results in a partial loss-of-function phenotype of poor growth in non-glucose media and abolishment of multicellularity. We also showed that the first 38 amino acids of Swi1 propagated [SWI(+)]. We show here that a region as small as the first 32 amino acids of Swi1 (Swi11-32) can decorate [SWI(+)] aggregation and stably maintain and transmit [SWI(+)] independently of full-length Swi1...
July 17, 2017: Molecular and Cellular Biology
https://www.readbyqxmd.com/read/28716731/arid1a-represses-hepatocellular-carcinoma-cell-proliferation-and-migration-through-lncrna-mvih
#10
Sheng Cheng, Lan Wang, Chuan-Huai Deng, Shi-Chun Du, Ze-Guang Han
ARID1A, encoding the BAF250a subunit of SWI/SNF complex, has a high mutation frequency in numerous types of cancer. LncRNAs, a type of non-coding RNAs longer than 200 nucleotides, have been reported to interplay with SWI/SNF complex during cancer progression. However, whether the interaction between ARID1A and lncRNA affects hepatocellular carcinoma (HCC) still needs to be investigated. Here, we reveal that ARID1A interacts with lncRNA MVIH through some region(s) or domain(s) including ARID domain and C-terminal ARID1A protein binding domain...
July 14, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28716547/cellular-senescence-regulated-by-swi-snf-complex-subunits-through-p53-p21-and-p16-prb-pathway
#11
Ling He, Ying Chen, Jianguo Feng, Weichao Sun, Shun Li, Mengting Ou, Liling Tang
SWI/SNF complex is an evolutionarily well-conserved chromatin-remodeling complex, which is implicated in the nucleosomes removing or sliding, impacting on the DNA repair, replication and genes expression regulation. The SWI/SNF complex consists up to 12 protein subunits. The catalytic subunits are BRG1 or BRM, which are exclusive ATPase subunits. BRG1 has been reported to play an important role in cellular senescence. However, The function of non-catalytic subunits involved in cellular senescence is rarely investigated...
July 15, 2017: International Journal of Biochemistry & Cell Biology
https://www.readbyqxmd.com/read/28714904/brd9-inhibition-alone-or-in-combination-with-cytostatic-compounds-as-a-therapeutic-approach-in-rhabdoid-tumors
#12
Katja F Krämer, Natalia Moreno, Michael C Frühwald, Kornelius Kerl
Rhabdoid tumors (RT) are malignant neoplasms of early childhood. Despite intensive therapy, survival is poor and new treatment approaches are required. The only recurrent mutations in these tumors affect SMARCB1 and less commonly SMARCA4, both subunits of the chromatin remodeling complex SWItch/Sucrose Non-Fermentable (SWI/SNF). Loss of these two core subunits alters the function of the SWI/SNF complex, resulting in tumor development. We hypothesized that inhibition of aberrant SWI/SNF function by selective blockade of the BRD9 subunit of the SWI/SNF complex would reduce tumor cell proliferation...
July 16, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28707666/-identification-of-proteins-associated-with-transcription-factors-hoxa9-and-e2a-pbx1-by-tandem-affinity-purification
#13
E A Shestakova, M Boutin, S Bourassa, E Bonneil, J J Bijl
Chimeric transcription factor E2A-PBX1 induces the development of acute lymphoblastic B-cell leukemia in children. Using a transgenic mouse model, we previously demonstrated that homeobox (HOX) gene HOXA9 genetically interact with E2A-PBX1 gene in the development of B-cell leukemia in mice. HOXA9 itself is a potent oncogene resulting in myeloid leukemia when overexpressed, which is strongly accelerated by its collaborator Meis1. HOX, PBX1 and MEIS1 proteins have been shown to form hetero dimeric or trimeric complexes in different combinations...
May 2017: Molekuliarnaia Biologiia
https://www.readbyqxmd.com/read/28700662/brg1-promotes-hepatocarcinogenesis-by-regulating-proliferation-and-invasiveness
#14
Benedikt Kaufmann, Baocai Wang, Suyang Zhong, Melanie Laschinger, Pranali Patil, Miao Lu, Volker Assfalg, Zhangjun Cheng, Helmut Friess, Norbert Hüser, Guido von Figura, Daniel Hartmann
The chromatin remodeler complex SWI/SNF plays an important role in physiological and pathological processes. Brahma related gene 1(BRG1), a catalytic subunit of the SWI/SNF complex, is known to be mutated in hepatocellular carcinoma (HCC). However, its role in HCC remains unclear. Here, we investigate the role of BRG1 on cell growth and invasiveness as well as its effect on the expression of putative target genes. Expression of BRG1 was examined in human liver tissue samples and in HCC cell lines. In addition, BRG1 was silenced in human HCC cell lines to analyse cell growth and invasiveness by growth curves, colony formation assay, invasion assay and the expression of putative target genes...
2017: PloS One
https://www.readbyqxmd.com/read/28692045/impact-of-histone-demethylase-kdm3a-dependent-ap-1-transactivity-on-hepatotumorigenesis-induced-by-pi3k-activation
#15
T Nakatsuka, K Tateishi, Y Kudo, K Yamamoto, H Nakagawa, H Fujiwara, R Takahashi, K Miyabayashi, Y Asaoka, Y Tanaka, H Ijichi, Y Hirata, M Otsuka, M Kato, J Sakai, M Tachibana, H Aburatani, Y Shinkai, K Koike
Epigenetic gene regulation linked to oncogenic pathways is an important focus of cancer research. KDM3A, a histone H3 lysine 9 (H3K9) demethylase, is known to have a pro-tumorigenic function. Here, we showed that KDM3A contributes to liver tumor formation through the phosphatidylinositol 3-kinase (PI3K) pathway, which is often activated in hepatocellular carcinoma. Loss of Kdm3a attenuated tumor formation in Pik3ca transgenic (Tg) mouse livers. Transcriptome analysis of pre-cancerous liver tissues revealed that the expression of activator protein 1 (AP-1) target genes was induced by PI3K activation, but blunted upon Kdm3a ablation...
July 10, 2017: Oncogene
https://www.readbyqxmd.com/read/28691782/a-novel-microduplication-of-arid1b-clinical-genetic-and-proteomic-findings
#16
Catarina M Seabra, Nicholas Szoko, Serkan Erdin, Ashok Ragavendran, Alexei Stortchevoi, Patrícia Maciel, Kathleen Lundberg, Daniela Schlatzer, Janice Smith, Michael E Talkowski, James F Gusella, Marvin R Natowicz
Genetic alterations of ARID1B have been recently recognized as one of the most common mendelian causes of intellectual disability and are associated with both syndromic and non-syndromic phenotypes. The ARID1B protein, a subunit of the chromatin remodeling complex SWI/SNF-A, is involved in the regulation of transcription and multiple downstream cellular processes. We report here the clinical, genetic, and proteomic phenotypes of an individual with a unique apparent de novo mutation of ARID1B due to an intragenic duplication...
September 2017: American Journal of Medical Genetics. Part A
https://www.readbyqxmd.com/read/28688083/the-swi-snf-chromatin-remodeling-factors-baf60a-b-and-c-in-nutrient-signaling-and-metabolic-control
#17
REVIEW
Ruo-Ran Wang, Ran Pan, Wenjing Zhang, Junfen Fu, Jiandie D Lin, Zhuo-Xian Meng
Metabolic syndrome has become a global epidemic that adversely affects human health. Both genetic and environmental factors contribute to the pathogenesis of metabolic disorders; however, the mechanisms that integrate these cues to regulate metabolic physiology and the development of metabolic disorders remain incompletely defined. Emerging evidence suggests that SWI/SNF chromatin-remodeling complexes are critical for directing metabolic reprogramming and adaptation in response to nutritional and other physiological signals...
July 7, 2017: Protein & Cell
https://www.readbyqxmd.com/read/28683324/doc1-dependent-recruitment-of-nurd-reveals-antagonism-with-swi-snf-during-epithelial-mesenchymal-transition-in-oral-cancer-cells
#18
Adone Mohd-Sarip, Miriam Teeuwssen, Alice G Bot, Maria J De Herdt, Stefan M Willems, Robert J Baatenburg de Jong, Leendert H J Looijenga, Diana Zatreanu, Karel Bezstarosti, Job van Riet, Edwin Oole, Wilfred F J van Ijcken, Harmen J G van de Werken, Jeroen A Demmers, Riccardo Fodde, C Peter Verrijzer
The Nucleosome Remodeling and Deacetylase (NURD) complex is a key regulator of cell differentiation that has also been implicated in tumorigenesis. Loss of the NURD subunit Deleted in Oral Cancer 1 (DOC1) is associated with human oral squamous cell carcinomas (OSCCs). Here, we show that restoration of DOC1 expression in OSCC cells leads to a reversal of epithelial-mesenchymal transition (EMT). This is caused by the DOC1-dependent targeting of NURD to repress key transcriptional regulators of EMT. NURD recruitment drives extensive epigenetic reprogramming, including eviction of the SWI/SNF remodeler, formation of inaccessible chromatin, H3K27 deacetylation, and binding of PRC2 and KDM1A, followed by H3K27 methylation and H3K4 demethylation...
July 5, 2017: Cell Reports
https://www.readbyqxmd.com/read/28665819/targeting-ezh2-in-cancer-therapy
#19
Makoto Yamagishi, Kaoru Uchimaru
PURPOSE OF REVIEW: The present review introduces recent outstanding progress pertaining to Enhancer of zeste homolog 2 (EZH2), especially regarding its mode of action as a master regulator of chromatin, and provides molecular-based evidence for targeting EZH2 in cancer therapy. We discuss the active development of small molecules targeting the enzymatic activity of EZH2/polycomb repressive complex 2 (PRC2). RECENT FINDINGS: Genetic, transcriptional, and posttranscriptional dysregulation of EZH2 is frequently observed in many cancer types...
July 13, 2017: Current Opinion in Oncology
https://www.readbyqxmd.com/read/28642448/combined-brd4-and-cdk9-inhibition-as-a-new-therapeutic-approach-in-malignant-rhabdoid-tumors
#20
Natalia Moreno, Till Holsten, Julius Mertins, Annabelle Zhogbi, Pascal Johann, Marcel Kool, Michael Meisterernst, Kornelius Kerl
Rhabdoid tumors are caused by the deletion of SMARCB1, whose protein encodes the SMARCB1 subunit of the chromatin remodeling complex SWI/SNF that is involved in global chromatin organization and gene expression control. Simultaneously inhibiting the main players involved in the deregulated transcription machinery is a promising option for preventing exaggerated tumor cell proliferation and survival as it may bypass compensatory mechanisms. In support of this hypothesis, we report efficient impairment of cellular proliferation and strong induction of cell death elicited by inhibition of bromodomain protein BRD4 and transcription kinase CDK9 using small molecular compounds...
June 21, 2017: Oncotarget
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