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https://www.readbyqxmd.com/read/28877962/toward-the-human-cellular-micrornaome
#1
Matthew N McCall, Min-Sik Kim, Mohammed Adil, Arun H Patil, Yin Lu, Christopher J Mitchell, Pamela Leal-Rojas, Jinchong Xu, Manoj Kumar, Valina L Dawson, Ted M Dawson, Alexander S Baras, Avi Z Rosenberg, Dan E Arking, Kathleen H Burns, Akhilesh Pandey, Marc K Halushka
MicroRNAs are short RNAs that serve as regulators of gene expression and are essential components of normal development as well as modulators of disease. MicroRNAs generally act cell-autonomously, and thus their localization to specific cell types is needed to guide our understanding of microRNA activity. Current tissue-level data have caused considerable confusion, and comprehensive cell-level data do not yet exist. Here, we establish the landscape of human cell-specific microRNA expression. This project evaluated 8 billion small RNA-seq reads from 46 primary cell types, 42 cancer or immortalized cell lines, and 26 tissues...
September 6, 2017: Genome Research
https://www.readbyqxmd.com/read/28838216/bet-inhibitors-a-novel-epigenetic-approach
#2
D B Doroshow, J P Eder, P M LoRusso
Epigenetics has been defined as 'the structural adaptation of chromosomal regions so as to register, signal or perpetuate altered activity states.' Currently, several classes of anticancer drugs function at the epigenetic level, including inhibitors of DNA methyltransferase, histone deacetylase (HDAC), lysine-specific demethylase 1, zeste homolog 2, and bromodomain and extra-terminal motif (BET) proteins.BET proteins have multiple functions, including the initiation and elongation of transcription and cell cycle regulation...
August 1, 2017: Annals of Oncology: Official Journal of the European Society for Medical Oncology
https://www.readbyqxmd.com/read/28710101/superenhancers-drive-neuroblastoma-differentiation-states
#3
(no author information available yet)
Superenhancer-associated transcriptional networks promote neuroblastoma heterogeneity.
July 14, 2017: Cancer Discovery
https://www.readbyqxmd.com/read/28687569/bet-degradation-is-more-effective-than-competitive-inhibition-in-t-all
#4
(no author information available yet)
The BET degrader dBET6 induces global BRD4 depletion, whereas JQ1 preferentially affects superenhancers.
July 7, 2017: Cancer Discovery
https://www.readbyqxmd.com/read/28587674/navise-superenhancer-navigator-integrating-epigenomics-signal-algebra
#5
Alex M Ascensión, Mikel Arrospide-Elgarresta, Ander Izeta, Marcos J Araúzo-Bravo
BACKGROUND: Superenhancers are crucial structural genomic elements determining cell fate, and they are also involved in the determination of several diseases, such as cancer or neurodegeneration. Although there are pipelines which use independent pieces of software to predict the presence of superenhancers from genome-wide chromatin marks or DNA-interaction protein binding sites, there is not yet an integrated software tool that processes automatically algebra combinations of raw data sequencing into a comprehensive final annotated report of predicted superenhancers...
June 6, 2017: BMC Bioinformatics
https://www.readbyqxmd.com/read/28490839/higher-order-chromatin-regulation-of-inflammatory-gene-expression
#6
REVIEW
Jin-Wen Xu, Shuang Ling, Jun Liu
Whether it is caused by viruses and bacteria infection, or low-grade chronic inflammation of atherosclerosis and cellular senescence, the transcription factor (TF) NF-κB plays a central role in the inducible expression of inflammatory genes. Accumulated evidence has indicated that the chromatin environment is the main determinant of TF binding in gene expression regulation, including the stimulus-responsive NF-κB. Dynamic changes in intra- and interchromosomes are the key regulatory mechanisms promoting the binding of TFs...
2017: Mediators of Inflammation
https://www.readbyqxmd.com/read/28359147/functional-enhancers-as-master-regulators-of-tissue-specific-gene-regulation-and-cancer-development
#7
REVIEW
Je Yeong Ko, Sumin Oh, Kyung Hyun Yoo
Tissue-specific transcription is critical for normal development, and abnormalities causing undesirable gene expression may lead to diseases such as cancer. Such highly organized transcription is controlled by enhancers with specific DNA sequences recognized by transcription factors. Enhancers are associated with chromatin modifications that are distinct epigenetic features in a tissue-specific manner. Recently, super-enhancers comprising enhancer clusters co-occupied by lineage-specific factors have been identified in diverse cell types such as adipocytes, hair follicle stem cells, and mammary epithelial cells...
March 2017: Molecules and Cells
https://www.readbyqxmd.com/read/28115742/mef2c-transcription-factor-is-associated-with-the-genetic-and-epigenetic-risk-architecture-of-schizophrenia-and-improves-cognition-in-mice
#8
A C Mitchell, B Javidfar, V Pothula, D Ibi, E Y Shen, C J Peter, L K Bicks, T Fehr, Y Jiang, K J Brennand, R L Neve, J Gonzalez-Maeso, S Akbarian
Large-scale consortia mapping the genomic risk architectures of schizophrenia provide vast amounts of molecular information, with largely unexplored therapeutic potential. We harnessed publically available information from the Psychiatric Genomics Consortium, and report myocyte enhancer factor 2C (MEF2C) motif enrichment in sequences surrounding the top scoring single-nucleotide polymorphisms within risk loci contributing by individual small effect to disease heritability. Chromatin profiling at base-pair resolution in neuronal nucleosomes extracted from prefrontal cortex of 34 subjects, including 17 cases diagnosed with schizophrenia, revealed MEF2C motif enrichment within cis-regulatory sequences, including neuron-specific promoters and superenhancers, affected by histone H3K4 hypermethylation in disease cases...
January 24, 2017: Molecular Psychiatry
https://www.readbyqxmd.com/read/28062474/smarcb1-mutations-disrupt-enhancer-activity-in-rhabdoid-tumors
#9
(no author information available yet)
Loss of the SWI/SNF subunit SMARCB1 disrupts enhancer activation but retains superenhancer activity.
January 6, 2017: Cancer Discovery
https://www.readbyqxmd.com/read/27807035/nucleoporin-mediated-regulation-of-cell-identity-genes
#10
Arkaitz Ibarra, Chris Benner, Swati Tyagi, Jonah Cool, Martin W Hetzer
The organization of the genome in the three-dimensional space of the nucleus is coupled with cell type-specific gene expression. However, how nuclear architecture influences transcription that governs cell identity remains unknown. Here, we show that nuclear pore complex (NPC) components Nup93 and Nup153 bind superenhancers (SE), regulatory structures that drive the expression of key genes that specify cell identity. We found that nucleoporin-associated SEs localize preferentially to the nuclear periphery, and absence of Nup153 and Nup93 results in dramatic transcriptional changes of SE-associated genes...
October 15, 2016: Genes & Development
https://www.readbyqxmd.com/read/27664237/superenhancer-reprogramming-drives-a-b-cell-epithelial-transition-and-high-risk-leukemia
#11
Yeguang Hu, Zhihong Zhang, Mariko Kashiwagi, Toshimi Yoshida, Ila Joshi, Nilamani Jena, Rajesh Somasundaram, Akinola Olumide Emmanuel, Mikael Sigvardsson, Julien Fitamant, Nabeel El-Bardeesy, Fotini Gounari, Richard A Van Etten, Katia Georgopoulos
IKAROS is required for the differentiation of highly proliferative pre-B-cell precursors, and loss of IKAROS function indicates poor prognosis in precursor B-cell acute lymphoblastic leukemia (B-ALL). Here we show that IKAROS regulates this developmental stage by positive and negative regulation of superenhancers with distinct lineage affiliations. IKAROS defines superenhancers at pre-B-cell differentiation genes together with B-cell master regulators such as PAX5, EBF1, and IRF4 but is required for a highly permissive chromatin environment, a function that cannot be compensated for by the other transcription factors...
September 1, 2016: Genes & Development
https://www.readbyqxmd.com/read/27340176/ino80-governs-superenhancer-mediated-oncogenic-transcription-and-tumor-growth-in-melanoma
#12
Bingying Zhou, Li Wang, Shu Zhang, Brian D Bennett, Fan He, Yan Zhang, Chengliang Xiong, Leng Han, Lixia Diao, Pishun Li, David C Fargo, Adrienne D Cox, Guang Hu
Superenhancers (SEs) are large genomic regions with a high density of enhancer marks. In cancer, SEs are found near oncogenes and dictate cancer gene expression. However, how oncogenic SEs are regulated remains poorly understood. Here, we show that INO80, a chromatin remodeling complex, is required for SE-mediated oncogenic transcription and tumor growth in melanoma. The expression of Ino80, the SWI/SNF ATPase, is elevated in melanoma cells and patient melanomas compared with normal melanocytes and benign nevi...
June 15, 2016: Genes & Development
https://www.readbyqxmd.com/read/27294782/functional-interdependence-of-brd4-and-dot1l-in-mll-leukemia
#13
Omer Gilan, Enid Y N Lam, Isabelle Becher, Dave Lugo, Ester Cannizzaro, Gerard Joberty, Aoife Ward, Meike Wiese, Chun Yew Fong, Sarah Ftouni, Dean Tyler, Kym Stanley, Laura MacPherson, Chen-Fang Weng, Yih-Chih Chan, Margherita Ghisi, David Smil, Christopher Carpenter, Peter Brown, Neil Garton, Marnie E Blewitt, Andrew J Bannister, Tony Kouzarides, Brian J P Huntly, Ricky W Johnstone, Gerard Drewes, Sarah-Jane Dawson, Cheryl H Arrowsmith, Paola Grandi, Rab K Prinjha, Mark A Dawson
Targeted therapies against disruptor of telomeric silencing 1-like (DOT1L) and bromodomain-containing protein 4 (BRD4) are currently being evaluated in clinical trials. However, the mechanisms by which BRD4 and DOT1L regulate leukemogenic transcription programs remain unclear. Using quantitative proteomics, chemoproteomics and biochemical fractionation, we found that native BRD4 and DOT1L exist in separate protein complexes. Genetic disruption or small-molecule inhibition of BRD4 and DOT1L showed marked synergistic activity against MLL leukemia cell lines, primary human leukemia cells and mouse leukemia models...
July 2016: Nature Structural & Molecular Biology
https://www.readbyqxmd.com/read/27135981/oncogenic-notch-signaling-in-t-cell-and-b-cell-lymphoproliferative-disorders
#14
Mark Y Chiang, Vedran Radojcic, Ivan Maillard
PURPOSE OF REVIEW: This article highlights recent discoveries about Notch activation and its oncogenic functions in lymphoid malignancies, and discusses the therapeutic potential of Notch inhibition. RECENT FINDINGS: NOTCH mutations arise in a broad spectrum of lymphoid malignancies and are increasingly scrutinized as putative therapeutic targets. In T-cell acute lymphoblastic leukemia (T-ALL), NOTCH1 mutations affect the extracellular negative regulatory region and lead to constitutive Notch activation, although mutated receptors remain sensitive to Notch ligands...
July 2016: Current Opinion in Hematology
https://www.readbyqxmd.com/read/27111282/chromatin-immunoprecipitation-from-fixed-clinical-tissues-reveals-tumor-specific-enhancer-profiles
#15
Paloma Cejas, Lewyn Li, Nicholas K O'Neill, Melissa Duarte, Prakash Rao, Michaela Bowden, Chensheng W Zhou, Marta Mendiola, Emilio Burgos, Jaime Feliu, Juan Moreno-Rubio, Héctor Guadalajara, Víctor Moreno, Damián García-Olmo, Joaquim Bellmunt, Stephanie Mullane, Michelle Hirsch, Christopher J Sweeney, Andrea Richardson, X Shirley Liu, Myles Brown, Ramesh A Shivdasani, Henry W Long
Extensive cross-linking introduced during routine tissue fixation of clinical pathology specimens severely hampers chromatin immunoprecipitation followed by next-generation sequencing (ChIP-seq) analysis from archived tissue samples. This limits the ability to study the epigenomes of valuable, clinically annotated tissue resources. Here we describe fixed-tissue chromatin immunoprecipitation sequencing (FiT-seq), a method that enables reliable extraction of soluble chromatin from formalin-fixed paraffin-embedded (FFPE) tissue samples for accurate detection of histone marks...
June 2016: Nature Medicine
https://www.readbyqxmd.com/read/26752646/ccat1-is-an-enhancer-templated-rna-that-predicts-bet-sensitivity-in-colorectal-cancer
#16
Mark L McCleland, Kathryn Mesh, Edward Lorenzana, Vivek S Chopra, Ehud Segal, Colin Watanabe, Benjamin Haley, Oleg Mayba, Murat Yaylaoglu, Florian Gnad, Ron Firestein
Colon tumors arise in a stepwise fashion from either discrete genetic perturbations or epigenetic dysregulation. To uncover the key epigenetic regulators that drive colon cancer growth, we used a CRISPR loss-of-function screen and identified a number of essential genes, including the bromodomain and extraterminal (BET) protein BRD4. We found that BRD4 is critical for colon cancer proliferation, and its knockdown led to differentiation effects in vivo. JQ1, a BET inhibitor, preferentially reduced growth in a subset of epigenetically dysregulated colon cancers characterized by the CpG island methylator phenotype (CIMP)...
February 2016: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/26472909/suboptimization-of-developmental-enhancers
#17
Emma K Farley, Katrina M Olson, Wei Zhang, Alexander J Brandt, Daniel S Rokhsar, Michael S Levine
Transcriptional enhancers direct precise on-off patterns of gene expression during development. To explore the basis for this precision, we conducted a high-throughput analysis of the Otx-a enhancer, which mediates expression in the neural plate of Ciona embryos in response to fibroblast growth factor (FGF) signaling and a localized GATA determinant. We provide evidence that enhancer specificity depends on submaximal recognition motifs having reduced binding affinities ("suboptimization"). Native GATA and ETS (FGF) binding sites contain imperfect matches to consensus motifs...
October 16, 2015: Science
https://www.readbyqxmd.com/read/26471149/yap-taz-binds-to-selected-superenhancers-and-controls-pol-ii-pause-release
#18
(no author information available yet)
YAP occupies a subset of highly active enhancers and regulates RNA Pol II pause release.
December 2015: Cancer Discovery
https://www.readbyqxmd.com/read/26439301/yap-drives-growth-by-controlling-transcriptional-pause-release-from-dynamic-enhancers
#19
Giorgio G Galli, Matteo Carrara, Wei-Chien Yuan, Christian Valdes-Quezada, Basanta Gurung, Brian Pepe-Mooney, Tinghu Zhang, Geert Geeven, Nathanael S Gray, Wouter de Laat, Raffaele A Calogero, Fernando D Camargo
The Hippo/YAP signaling pathway is a crucial regulator of tissue growth, stem cell activity, and tumorigenesis. However, the mechanism by which YAP controls transcription remains to be fully elucidated. Here, we utilize global chromatin occupancy analyses to demonstrate that robust YAP binding is restricted to a relatively small number of distal regulatory elements in the genome. YAP occupancy defines a subset of enhancers and superenhancers with the highest transcriptional outputs. YAP modulates transcription from these elements predominantly by regulating promoter-proximal polymerase II (Pol II) pause release...
October 15, 2015: Molecular Cell
https://www.readbyqxmd.com/read/26054719/batf3-maintains-autoactivation-of-irf8-for-commitment-of-a-cd8%C3%AE-conventional-dc-clonogenic-progenitor
#20
Gary E Grajales-Reyes, Arifumi Iwata, Jörn Albring, Xiaodi Wu, Roxane Tussiwand, Wumesh Kc, Nicole M Kretzer, Carlos G Briseño, Vivek Durai, Prachi Bagadia, Malay Haldar, Jörg Schönheit, Frank Rosenbauer, Theresa L Murphy, Kenneth M Murphy
The transcription factors Batf3 and IRF8 are required for the development of CD8α(+) conventional dendritic cells (cDCs), but the basis for their actions has remained unclear. Here we identified two progenitor cells positive for the transcription factor Zbtb46 that separately generated CD8α(+) cDCs and CD4(+) cDCs and arose directly from the common DC progenitor (CDP). Irf8 expression in CDPs required prior autoactivation of Irf8 that was dependent on the transcription factor PU.1. Specification of the clonogenic progenitor of CD8α(+) cDCs (the pre-CD8 DC) required IRF8 but not Batf3...
July 2015: Nature Immunology
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