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SWI/SNF

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https://www.readbyqxmd.com/read/28938122/genome-regulation-by-polycomb-and-trithorax-70-years-and-counting
#1
REVIEW
Bernd Schuettengruber, Henri-Marc Bourbon, Luciano Di Croce, Giacomo Cavalli
Polycomb (PcG) and Trithorax (TrxG) group proteins are evolutionarily conserved chromatin-modifying factors originally identified as part of an epigenetic cellular memory system that maintains repressed or active gene expression states. Recently, they have been shown to globally control a plethora of cellular processes. This functional diversity is achieved by their ability to regulate chromatin at multiple levels, ranging from modifying local chromatin structure to orchestrating the three-dimensional organization of the genome...
September 21, 2017: Cell
https://www.readbyqxmd.com/read/28924147/tumor-suppression-via-inhibition-of-swi-snf-complex-dependent-nf-%C3%AE%C2%BAb-activation
#2
Kazuyoshi Kobayashi, Hiroaki Hiramatsu, Shinya Nakamura, Kyousuke Kobayashi, Takeshi Haraguchi, Hideo Iba
The transcription factor NF-κB is constitutively activated in many epithelial tumors but few NF-κB inhibitors are suitable for cancer therapy because of its broad biological effects. We previously reported that the d4-family proteins (DPF1, DPF2, DPF3a/b) function as adaptor proteins linking NF-κB with the SWI/SNF complex. Here, using epithelial tumor cell lines, A549 and HeLaS3, we demonstrate that exogenous expression of the highly-conserved N-terminal 84-amino acid region (designated "CT1") of either DPF2 or DPF3a/b has stronger inhibitory effects on anchorage-independent growth than the single knockdown of any d4-family protein...
September 18, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28901494/molecular-mechanisms-of-pathogenesis-in-hepatocellular-carcinoma-revealed-by-rna%C3%A2-sequencing
#3
Yao Liu, Zhe Yang, Feng Du, Qiao Yang, Jie Hou, Xiaohong Yan, Yi Geng, Yaning Zhao, Hua Wang
The present study aimed to explore the underlying molecular mechanisms of hepatocellular carcinoma (HCC). RNA‑sequencing profiles GSM629264 and GSM629265, from the GSE25599 data set, were downloaded from the Gene Expression Omnibus database and processed by quality evaluation. GSM629264 and GSM629265 were from HCC and adjacent non‑cancerous tissues, respectively. TopHat software was used for alignment analysis, followed by the detection of novel splicing sites. In addition, the Cufflinks software package was used to analyze gene expressions, and the Cuffdiff program was used to screen for differently expressed genes (DEGs) and differentially expressed splicing variants...
September 11, 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28899659/brg1-promotes-vegf-a-expression-and-angiogenesis-in-human-colorectal-cancer-cells
#4
Jingqin Lan, Haijie Li, Xuelai Luo, Junbo Hu, Guihua Wang
Angiogenesis plays an important role in tumor growth and progression in solid tumors. Vascular endothelial growth factor (VEGF) is one of the most critical and specific factors that stimulate both physiological and pathological angiogenesis. Here, we report a novel role of BRG1, the core subunit of SWI/SNF family complexes, in angiogenesis. In this study, we demonstrate that BRG1 is overexpressed in colorectal cancer and decreased expression of BRG1 not only blocks cell proliferation but remarkably inhibits the ability of HUVECs to form capillary-like structures...
September 9, 2017: Experimental Cell Research
https://www.readbyqxmd.com/read/28892201/two-brm-promoter-polymorphisms-predict-poor-survival-in-patients-with-hepatocellular-carcinoma
#5
Ivan Pasic, Kit Man Wong, Jonghun John Lee, Osvaldo Espin-Garcia, Yonathan Brhane, Dangxiao Cheng, Zhuo Chen, Devalben Patel, Catherine Brown, Roxana Bucur, David Reisman, Jennifer J Knox, Wei Xu, Rayjean J Hung, Geoffrey Guo, Sean P Cleary
BACKGROUND: Polymorphisms in the promoter of the BRM gene, a critical subunit of the chromatin remodeling SWI/SNF complex, have previously been implicated in risk and prognosis in Caucasian-predominant lung, head and neck, esophageal, and pancreatic cancers, and in hepatocellular cancers in Asians. We investigated the role of these polymorphisms in hepatocellular carcinoma (HCC) risk and prognosis. METHODS: HCC cases were recruited in a comprehensive cancer centre while the matched controls were recruited from family practice units from the same catchment area...
September 11, 2017: Molecular Carcinogenesis
https://www.readbyqxmd.com/read/28885261/epigenetic-alterations-in-bone-and-soft-tissue-tumors
#6
John Wojcik, Kumarasen Cooper
Human malignancies are driven by heritable alterations that lead to unchecked cellular proliferation, invasive growth and distant spread. Heritable changes can arise from changes in DNA sequence, or, alternatively, through altered gene expression rooted in epigenetic mechanisms. In recent years, high-throughput sequencing of tumor genomes has revealed a central role for mutations in epigenetic regulatory complexes in oncogenic processes. Through interactions with or direct modifications of chromatin, these proteins help control the accessibility of genes, and thus the transcriptional profile of a cell...
September 6, 2017: Advances in Anatomic Pathology
https://www.readbyqxmd.com/read/28884947/confirmation-of-an-arid2-defect-in-swi-snf-related-intellectual-disability
#7
Ruben Van Paemel, Pauline De Bruyne, Saskia van der Straaten, Marleen D'hondt, Urlien Fränkel, Annelies Dheedene, Björn Menten, Bert Callewaert
We present a 4-year-old girl with delayed neuromotor development, short stature of prenatal onset, and specific behavioral and craniofacial features harboring an intragenic deletion in the ARID2 gene. The phenotype confirmed the major features of the recently described ARID2-related intellectual disability syndrome. However, our patient showed overlapping features with Nicolaides-Baraitser syndrome and Coffin-Siris syndrome, providing further arguments to reclassify these disorders as "SWI/SNF-related intellectual disability syndromes...
September 8, 2017: American Journal of Medical Genetics. Part A
https://www.readbyqxmd.com/read/28868352/swi-snf-tumor-suppressor-gene-pbrm1-baf180-in-human-clear-cell-kidney-cancer
#8
Amrita M Nargund, Hatice U Osmanbeyoglu, Emily H Cheng, James J Hsieh
Mutations within chromatin modulating protein complexes have dominated the novel cancer gene landscape. However, little is known about how individual aberrations contribute to cancer formation. A novel Pbrm1 kidney cancer mouse model examining the role of Pbrm1 provides much needed clue concerning how SWI/SNF complexes might function as tumor suppressors.
2017: Molecular & Cellular Oncology
https://www.readbyqxmd.com/read/28868154/smarcd1-regulates-senescence-associated-lipid-accumulation-in-hepatocytes
#9
Chisato Inoue, Chong Zhao, Yumi Tsuduki, Miyako Udono, Lixiang Wang, Masatoshi Nomura, Yoshinori Katakura
Previously, we have identified 16 senescence-associated genes by a subtractive proteomic analysis using presenescent and senescent human fibroblast cells, TIG-1. The aim of this study was to clarify the role of SMARCD1, one of the identified genes, also known as BAF60a, in hepatic senescence. SMARCD1 is a member of the SWI/SNF chromatin remodeling complex family, and regulates the transcription of target genes through the alterations of chromatin structure. We demonstrated that the reduced expression of SMARCD1 triggers cellular senescence and induces the accumulation of lipids, suggesting that SMARCD1 acts as a mediator in these processes...
2017: NPJ Aging and Mechanisms of Disease
https://www.readbyqxmd.com/read/28865954/comparative-expression-profiling-of-atrad5b-and-atndl1-hints-towards-a-role-in-g-protein-mediated-signaling
#10
Nisha Khatri, Swati Singh, Nasmeen Hakim, Yashwanti Mudgil
Arabidopsis AtRAD5B encodes for a putative helicase of the class SWItch/Sucrose Non-Fermentable (SWI/SNF) ATPases. We identified AtRAD5B as an interactor of N-MYC DOWNREGULATED-LIKE1 (AtNDL1) in a yeast two-hybrid screen. AtNDL1 is a G protein signaling component which regulates auxin transport and gradients together with GTP binding protein beta 1 (AGB1). Auxin gradients are known to recruit SWI/SNF remodeling complexes to the chromatin and regulate expression of genes involved in flower and leaf formation...
September 1, 2017: Gene Expression Patterns: GEP
https://www.readbyqxmd.com/read/28863077/undifferentiated-endometrial-carcinomas-show-frequent-loss-of-core-switch-sucrose-nonfermentable-complex-proteins
#11
Martin Köbel, Lien N Hoang, Basile Tessier-Cloutier, Bo Meng, Robert A Soslow, Colin J R Stewart, Cheng-Han Lee
Undifferentiated endometrial carcinoma is an aggressive type of endometrial carcinoma that typically presents with advanced stage disease and rapid clinical progression. In contrast to dedifferentiated endometrial carcinoma, undifferentiated carcinoma lacks a concurrent differentiated (typically low-grade endometrioid) carcinoma component, though the undifferentiated component of dedifferentiated carcinoma is similar histologically and immunophenotypically to pure undifferentiated carcinoma. We recently identified 3 mutually exclusive mechanisms of switch/sucrose nonfermentable (SWI/SNF) complex inactivation (BRG1 inactivation, INI1 inactivation or ARID1A/ARID1B co-inactivation) that are associated with histologic dedifferentiation in the majority of dedifferentiated endometrial carcinoma...
August 31, 2017: American Journal of Surgical Pathology
https://www.readbyqxmd.com/read/28844864/the-short-isoform-of-brd4-promotes-hiv-1-latency-by-engaging-repressive-swi-snf-chromatin-remodeling-complexes
#12
Ryan J Conrad, Parinaz Fozouni, Sean Thomas, Hendrik Sy, Qiang Zhang, Ming-Ming Zhou, Melanie Ott
BET proteins commonly activate cellular gene expression, yet inhibiting their recruitment paradoxically reactivates latent HIV-1 transcription. Here we identify the short isoform of BET family member BRD4 (BRD4S) as a corepressor of HIV-1 transcription. We found that BRD4S was enriched in chromatin fractions of latently infected T cells, and it was more rapidly displaced from chromatin upon BET inhibition than the long isoform. BET inhibition induced marked nucleosome remodeling at the latent HIV-1 promoter, which was dependent on the activity of BRG1-associated factors (BAF), an SWI/SNF chromatin-remodeling complex with known repressive functions in HIV-1 transcription...
September 21, 2017: Molecular Cell
https://www.readbyqxmd.com/read/28842672/downregulation-of-parp1-transcription-by-promoter-associated-e2f4-rbl2-hdac1-brm-complex-contributes-to-repression-of-pluripotency-stem-cell-factors-in-human-monocytes
#13
Wiśnik Ewelina, Płoszaj Tomasz, Robaszkiewicz Agnieszka
Differentiation of certain cell types is followed by a downregulation of PARP1 expression. We show that the reduction in the abundance of PARP1 in hematopoietic progenitor cells and monocytes is tightly controlled by the cell cycle. The differentiation-associated cell cycle exit induces E2F1 replacement with E2F4 at the PARP1 promoter and the assembly of an E2F4-RBL2-HDAC1-BRM(SWI/SNF) repressor complex which deacetylates nucleosomes and compacts chromatin. In G1 arrested cells, PARP1 transcription is reduced by the recruitment of E2F1-RB1-HDAC1-EZH2(PRC2)-BRM/BRG1(SWI/SNF), which additionally trimethylates H3K27 and causes an even higher increase in nucleosome density...
August 25, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28810143/genomic-evolution-of-breast-cancer-metastasis-and-relapse
#14
Lucy R Yates, Stian Knappskog, David Wedge, James H R Farmery, Santiago Gonzalez, Inigo Martincorena, Ludmil B Alexandrov, Peter Van Loo, Hans Kristian Haugland, Peer Kaare Lilleng, Gunes Gundem, Moritz Gerstung, Elli Pappaemmanuil, Patrycja Gazinska, Shriram G Bhosle, David Jones, Keiran Raine, Laura Mudie, Calli Latimer, Elinor Sawyer, Christine Desmedt, Christos Sotiriou, Michael R Stratton, Anieta M Sieuwerts, Andy G Lynch, John W Martens, Andrea L Richardson, Andrew Tutt, Per Eystein Lønning, Peter J Campbell
Patterns of genomic evolution between primary and metastatic breast cancer have not been studied in large numbers, despite patients with metastatic breast cancer having dismal survival. We sequenced whole genomes or a panel of 365 genes on 299 samples from 170 patients with locally relapsed or metastatic breast cancer. Several lines of analysis indicate that clones seeding metastasis or relapse disseminate late from primary tumors, but continue to acquire mutations, mostly accessing the same mutational processes active in the primary tumor...
August 14, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28807921/candida-albicans-swi-snf-and-mediator-complexes-differentially-regulate-mrr1-induced-mdr1-expression-and-fluconazole-resistance
#15
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
#16
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/28767641/iswi-chromatin-remodellers-sense-nucleosome-modifications-to-determine-substrate-preference
#17
Geoffrey P Dann, Glen P Liszczak, John D Bagert, Manuel M Müller, Uyen T T Nguyen, Felix Wojcik, Zachary Z Brown, Jeffrey Bos, Tatyana Panchenko, Rasmus Pihl, Samuel B Pollock, Katharine L Diehl, C David Allis, Tom W Muir
ATP-dependent chromatin remodellers regulate access to genetic information by controlling nucleosome positions in vivo. However, the mechanism by which remodellers discriminate between different nucleosome substrates is poorly understood. Many chromatin remodelling proteins possess conserved protein domains that interact with nucleosomal features. Here we used a quantitative high-throughput approach, based on the use of a DNA-barcoded mononucleosome library, to profile the biochemical activity of human ISWI family remodellers in response to a diverse set of nucleosome modifications...
August 31, 2017: Nature
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
#18
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/28753627/nuclear-cytoplasmic-transport-defects-in-bbs6-underlie-congenital-heart-disease-through-perturbation-of-a-chromatin-remodeling-protein
#19
Charles Anthony Scott, Autumn N Marsden, Michael R Rebagliati, Qihong Zhang, Xitiz Chamling, Charles C Searby, Lisa M Baye, Val C Sheffield, Diane C Slusarski
Mutations in BBS6 cause two clinically distinct syndromes, Bardet-Biedl syndrome (BBS), a syndrome caused by defects in cilia transport and function, as well as McKusick-Kaufman syndrome, a genetic disorder characterized by congenital heart defects. Congenital heart defects are rare in BBS, and McKusick-Kaufman syndrome patients do not develop retinitis pigmentosa. Therefore, the McKusick-Kaufman syndrome allele may highlight cellular functions of BBS6 distinct from the presently understood functions in the cilia...
July 2017: PLoS Genetics
https://www.readbyqxmd.com/read/28741798/novel-orally-bioavailable-ezh1-2-dual-inhibitors-with-greater-antitumor-efficacy-than-an-ezh2-selective-inhibitor
#20
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
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