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SETDB1

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https://www.readbyqxmd.com/read/29774127/paf1-complex-interactions-with-setdb1-mediate-promoter-h3k9-methylation-and-transcriptional-repression-of-hoxa9-and-meis1-in-acute-myeloid-leukemia
#1
James Ropa, Nirmalya Saha, Zhiling Chen, Justin Serio, Wei Chen, Dattatreya Mellacheruvu, Lili Zhao, Venkatesha Basrur, Alexey I Nesvizhskii, Andrew G Muntean
The Polymerase Associated Factor 1 complex (PAF1c) is an epigenetic co-modifying complex that directly contacts RNA polymerase II (RNAPII) and several epigenetic regulating proteins. Mutations, overexpression and loss of expression of subunits of the PAF1c are observed in various forms of cancer suggesting proper regulation is needed for cellular development. However, the biochemical interactions with the PAF1c that allow dynamic gene regulation are unclear. We and others have shown that the PAF1c makes a direct interaction with MLL fusion proteins, which are potent oncogenic drivers of acute myeloid leukemia (AML)...
April 24, 2018: Oncotarget
https://www.readbyqxmd.com/read/29740006/identification-of-target-genes-regulated-by-the-drosophila-histone-methyltransferase-eggless-reveals-a-role-of-decapentaplegic-in-apoptotic-signaling
#2
Igojo Kang, Yourim Choi, Sueun Jung, Jae Yun Lim, Dooyoung Lee, Sumeet Gupta, Woongjoon Moon, Chanseok Shin
Epigenetic gene regulation is essential for developmental processes. Eggless (Egg), the Drosophila orthologue of the mammalian histone methyltransferase, SETDB1, is known to be involved in the survival and differentiation of germline stem cells and piRNA cluster transcription during Drosophila oogenesis; however the detailed mechanisms remain to be determined. Here, using high-throughput RNA sequencing, we investigated target genes regulated by Egg in an unbiased manner. We show that Egg plays diverse roles in particular piRNA pathway gene expression, some long non-coding RNA expression, apoptosis-related gene regulation, and Decapentaplegic (Dpp) signaling during Drosophila oogenesis...
May 8, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29739365/histone-methyltransferase-setdb1-promotes-cells-proliferation-and-migration-by-interacting-withtiam1-in-hepatocellular-carcinoma
#3
Yuqin Zhang, Jing Huang, Qisheng Li, Keli Chen, Yonghao Liang, Zetao Zhan, Feng Ye, Wen Ni, Longhua Chen, Yi Ding
BACKGROUND: SETDB1 is a histone H3K9 methyltransferase, which plays a significant role in the occurrence and progression of tumors. Previous studies have confirmed that T-lymphom invasion and metastasis gene (Tiam1) is a protein associated with the metastasis of hepatocellular carcinoma (HCC); however, we have not yet been successful in elucidating the specific mechanism of HCC. METHODS: Yeast two-hybrid test was conducted to screen proteins that interacted with Tiam1 gene...
May 8, 2018: BMC Cancer
https://www.readbyqxmd.com/read/29728365/a-crispr-knockout-screen-identifies-setdb1-target-retroelement-silencing-factors-in-embryonic-stem-cells
#4
Kei Fukuda, Akihiko Okuda, Kosuke Yusa, Yoichi Shinkai
In mouse embryonic stem cells (mESCs), expression of provirus and endogenous retroelements is epigenetically repressed. Although many cellular factors involved in retroelement silencing have been identified, the complete molecular mechanism remains elusive. In this study, we performed a genome-wide CRISPR screen to advance our understanding of retroelement silencing in mESCs. The Moloney murine leukemia virus (MLV)-based retroviral vector MSCV-GFP, which is repressed by the SETDB1/KAP1 pathway in mESCs was used as a reporter provirus and we identified more than 80 genes involved in this process...
May 4, 2018: Genome Research
https://www.readbyqxmd.com/read/29703894/a-somatic-role-for-the-histone-methyltransferase-setdb1-in-endogenous-retrovirus-silencing
#5
Masaki Kato, Keiko Takemoto, Yoichi Shinkai
Subsets of endogenous retroviruses (ERVs) are derepressed in mouse embryonic stem cells (mESCs) deficient for Setdb1, which catalyzes histone H3 lysine 9 trimethylation (H3K9me3). Most of those ERVs, including IAPs, remain silent if Setdb1 is deleted in differentiated embryonic cells; however they are derepressed when deficient for Dnmt1, suggesting that Setdb1 is dispensable for ERV silencing in somatic cells. However, H3K9me3 enrichment on ERVs is maintained in differentiated cells and is mostly diminished in mouse embryonic fibroblasts (MEFs) lacking Setdb1...
April 27, 2018: Nature Communications
https://www.readbyqxmd.com/read/29558503/retraction-setdb1-is-involved-in-postembryonic-dna-methylation-and-gene-silencing-in-drosophila
#6
(no author information available yet)
No abstract text is available yet for this article.
2018: PloS One
https://www.readbyqxmd.com/read/29536689/-transcription-factors-analysis-of-subchondral-bone-in-early-experimental-osteoarthritis-based-on-gene-expression-profiles
#7
Rong-Kai Zhang, Guo-Wei Li, Dong Jiang, Da-Wei Zhang, Bing Yu, Lu-Kun Yang
OBJECTIVE: To identify the master transcription factors (TF) that might be responsible for the gene expression alteration of OA. METHODS: Raw expression data for rat OA model(GSE30322) was downloaded from NCBI GEO database. Microarray data analysis for rat and human was carried out separately using functions from limma packagein R, gene expression was considered as significantly changed between conditions if adjusted P -value<0.05 and the absolute value of fold change>=2...
February 25, 2018: Zhongguo Gu Shang, China Journal of Orthopaedics and Traumatology
https://www.readbyqxmd.com/read/29492189/distinct-histone-modifications-denote-early-stress-induced-drug-tolerance-in-cancer
#8
Abdullah Al Emran, Diego M Marzese, Dinoop Ravindran Menon, Mitchell S Stark, Joachim Torrano, Heinz Hammerlindl, Gao Zhang, Patricia Brafford, Matthew P Salomon, Nellie Nelson, Sabrina Hammerlindl, Deepesh Gupta, Gordon B Mills, Yiling Lu, Richard A Sturm, Keith Flaherty, Dave S B Hoon, Brian Gabrielli, Meenhard Herlyn, Helmut Schaider
Besides somatic mutations or drug efflux, epigenetic reprogramming can lead to acquired drug resistance. We recently have identified early stress-induced multi-drug tolerant cancer cells termed induced drug-tolerant cells (IDTCs). Here, IDTCs were generated using different types of cancer cell lines; melanoma, lung, breast and colon cancer. A common loss of the H3K4me3 and H3K27me3 and gain of H3K9me3 mark was observed as a significant response to drug exposure or nutrient starvation in IDTCs. These epigenetic changes were reversible upon drug holidays...
February 2, 2018: Oncotarget
https://www.readbyqxmd.com/read/29449904/expression-profiling-of-chromatin-modifying-enzymes-and-global-dna-methylation-in-cd4-t-cells-from-patients-with-chronic-hiv-infection-at-different-hiv-control-and-progression-states
#9
Roberta Nicoleta Bogoi, Alicia de Pablo, Eulalia Valencia, Luz Martín-Carbonero, Victoria Moreno, Helem Haydee Vilchez-Rueda, Victor Asensi, Rosa Rodriguez, Victor Toledano, Berta Rodés
Background: Integration of human immunodeficiency virus type 1 (HIV-1) into the host genome causes global disruption of the chromatin environment. The abundance level of various chromatin-modifying enzymes produces these alterations and affects both the provirus and cellular gene expression. Here, we investigated potential changes in enzyme expression and global DNA methylation in chronically infected individuals with HIV-1 and compared these changes with non-HIV infected individuals...
2018: Clinical Epigenetics
https://www.readbyqxmd.com/read/29351814/setdb1-prevents-tet2-dependent-activation-of-iap-retroelements-in-na%C3%A3-ve-embryonic-stem-cells
#10
Özgen Deniz, Lorenzo de la Rica, Kevin C L Cheng, Dominik Spensberger, Miguel R Branco
BACKGROUND: Endogenous retroviruses (ERVs), which are responsible for 10% of spontaneous mouse mutations, are kept under control via several epigenetic mechanisms. The H3K9 histone methyltransferase SETDB1 is essential for ERV repression in embryonic stem cells (ESCs), with DNA methylation also playing an important role. It has been suggested that SETDB1 protects ERVs from TET-dependent DNA demethylation, but the relevance of this mechanism for ERV expression remains unclear. Moreover, previous studies have been performed in primed ESCs, which are not epigenetically or transcriptionally representative of preimplantation embryos...
January 19, 2018: Genome Biology
https://www.readbyqxmd.com/read/29339137/oxygen-induced-alterations-in-the-expression-of-chromatin-modifying-enzymes-and-the-transcriptional-regulation-of-imprinted-genes
#11
William M Skiles, Avery Kester, Jane H Pryor, Mark E Westhusin, Michael C Golding, Charles R Long
Embryo culture and assisted reproductive technologies have been associated with a disproportionately high number of epigenetic abnormalities in the resulting offspring. However, the mechanisms by which these techniques influence the epigenome remain poorly defined. In this study, we evaluated the capacity of oxygen concentration to influence the transcriptional control of a selection of key enzymes regulating chromatin structure. In mouse embryonic stem cells, oxygen concentrations modulated the transcriptional regulation of the TET family of enzymes, as well as the de novo methyltransferase Dnmt3a...
June 2018: Gene Expression Patterns: GEP
https://www.readbyqxmd.com/read/29234025/h3k14ac-is-linked-to-methylation-of-h3k9-by-the-triple-tudor-domain-of-setdb1
#12
Renata Z Jurkowska, Su Qin, Goran Kungulovski, Wolfram Tempel, Yanli Liu, Pavel Bashtrykov, Judith Stiefelmaier, Tomasz P Jurkowski, Srikanth Kudithipudi, Sara Weirich, Raluca Tamas, Hong Wu, Ludmila Dombrovski, Peter Loppnau, Richard Reinhardt, Jinrong Min, Albert Jeltsch
SETDB1 is an essential H3K9 methyltransferase involved in silencing of retroviruses and gene regulation. We show here that its triple Tudor domain (3TD) specifically binds to doubly modified histone H3 containing K14 acetylation and K9 methylation. Crystal structures of 3TD in complex with H3K14ac/K9me peptides reveal that peptide binding and K14ac recognition occurs at the interface between Tudor domains (TD) TD2 and TD3. Structural and biochemical data demonstrate a pocket switch mechanism in histone code reading, because K9me1 or K9me2 is preferentially recognized by the aromatic cage of TD3, while K9me3 selectively binds to TD2...
December 12, 2017: Nature Communications
https://www.readbyqxmd.com/read/29233829/smad3-mediated-recruitment-of-the-methyltransferase-setdb1-eset-controls-snail1-expression-and-epithelial-mesenchymal-transition
#13
Dan Du, Yoko Katsuno, Dominique Meyer, Erine H Budi, Si-Han Chen, Hartmut Koeppen, Hongjun Wang, Rosemary J Akhurst, Rik Derynck
During epithelial-mesenchymal transition (EMT), reprogramming of gene expression is accompanied by histone modifications. Whether EMT-promoting signaling directs functional changes in histone methylation has not been established. We show here that the histone lysine methyltransferase SETDB1 represses EMT and that, during TGF-β-induced EMT, cells attenuate SETDB1 expression to relieve this inhibition. SETDB1 also controls stem cell generation, cancer cell motility, invasion, metastatic dissemination, as well as sensitivity to certain cancer drugs...
January 2018: EMBO Reports
https://www.readbyqxmd.com/read/29228278/zinc-finger-protein-274-regulates-imprinted-expression-of-transcripts-in-prader-willi-syndrome-neurons
#14
Maéva Langouët, Heather R Glatt-Deeley, Michael S Chung, Clémence M Dupont-Thibert, Elodie Mathieux, Erin C Banda, Christopher E Stoddard, Leann Crandall, Marc Lalande
Prader-Willi syndrome (PWS) is characterized by neonatal hypotonia, developmental delay and hyperphagia/obesity and is caused by the absence of paternal contribution to chromosome 15q11-q13. Using induced pluripotent stem cell (iPSC) models of PWS, we previously discovered an epigenetic complex that is comprised of the zinc-finger protein ZNF274 and the SET domain bifurcated 1 (SETDB1) histone H3 lysine 9 (H3K9) methyltransferase and that silences the maternal alleles at the PWS locus. Here, we have knocked out ZNF274 and rescued the expression of silent maternal alleles in neurons derived from PWS iPSC lines, without affecting DNA methylation at the PWS-Imprinting Center (PWS-IC)...
February 1, 2018: Human Molecular Genetics
https://www.readbyqxmd.com/read/29158805/histone-methyltransferase-setdb1-promotes-the-progression-of-colorectal-cancer-by-inhibiting-the-expression-of-tp53
#15
Keli Chen, Fengjiao Zhang, Jie Ding, Yonghao Liang, Zetao Zhan, Yizhi Zhan, Long-Hua Chen, Yi Ding
SETDB1 is a novel histone methyltransferase associated with the functional tri-methylation of histone H3K9. Although aberrant high expression of SETDB1 was experimentally obversed in a variety of solid tumors, its underlying mechanisms in human carcinogenesis are not well known. In this study, we investigated the expression of SETDB1 in a large cohort of colorectal cancer (CRC) samples and cell lines for the first time. Our findings showed that SETDB1 was highly expressed in majority CRC tissues and cell lines; moreover, up-regulation of SETDB1 was negatively correlated with the survival rate of CRC patients...
2017: Journal of Cancer
https://www.readbyqxmd.com/read/29151149/impact-of-xist-rna-on-chromatin-modifications-and-transcriptional-silencing-maintenance-at-different-stages-of-imprinted-x-chromosome-inactivation-in-vole-microtus-levis
#16
Alexander I Shevchenko, Elena V Grigor'eva, Sergey P Medvedev, Irina S Zakharova, Elena V Dementyeva, Eugeny A Elisaphenko, Anastasia A Malakhova, Sophia V Pavlova, Suren M Zakian
In vole Microtus levis, cells of preimplantation embryo and extraembryonic tissues undergo imprinted X chromosome inactivation (iXCI) which is triggered by a long non-coding nuclear RNA, Xist. At early stages of iXCI, chromatin of vole inactive X chromosome is enriched with the HP1 heterochromatin-specific protein, trimethylated H3K9 and H4K20 attributable to constitutive heterochromatin. In the study, using vole trophoblast stem (TS) cells as a model of iXCI, we further investigated chromatin of the inactive X chromosome of M...
March 2018: Chromosoma
https://www.readbyqxmd.com/read/29109980/the-abundance-of-metabolites-related-to-protein-methylation-correlates-with-the-metastatic-capacity-of-human-melanoma-xenografts
#17
Xiaolei Shi, Alpaslan Tasdogan, Fang Huang, Zeping Hu, Sean J Morrison, Ralph J DeBerardinis
Metabolic reprogramming is a major factor in transformation, and particular metabolic phenotypes correlate with oncogenotype, tumor progression, and metastasis. By profiling metabolites in 17 patient-derived xenograft melanoma models, we identified durable metabolomic signatures that correlate with biological features of the tumors. BRAF mutant tumors had metabolomic and metabolic flux features of enhanced glycolysis compared to BRAF wild-type tumors. Tumors that metastasized efficiently from their primary sites had elevated levels of metabolites related to protein methylation, including trimethyllysine (TML)...
November 2017: Science Advances
https://www.readbyqxmd.com/read/29108991/setdb1-mediated-fosb-regulation-via-erk2-is-associated-with-an-increase-in-cell-invasiveness-during-anticancer-drug-treatment-of-a549-human-lung-cancer-cells
#18
Han-Heom Na, Keun-Cheol Kim
We have determined a functional link to the inverse expression of SETDB1 and FosB following anticancer drug treatment. Doxorubicin treatment caused decreased SETDB1 expression and FosB overexpression both at the mRNA and protein levels. The decreased HMTase activity of SETDB1 coincided with altered occupancy across the promoter region of the FosB gene. SETDB1 overexpression decreased the luciferase reporter activity containing the FosB promoter region, but siSETDB1 increased the luciferase reporter activity, suggesting that SETDB1 directly and negatively regulated FosB expression...
January 1, 2018: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/29066607/cancer-cells-on-your-histone-marks-get-setdb1-silence-retrotransposons-and-go
#19
Luisa Robbez-Masson, Christopher H C Tie, Helen M Rowe
Cancer cells thrive on genetic and epigenetic changes that confer a selective advantage but also need strategies to avoid immune recognition. In this issue, Cuellar et al. (2017. J. Cell Biol https://doi.org/10.1083/jcb.201612160) find that the histone methyltransferase SETDB1 enables acute myeloid leukemia cells to evade sensing of retrotransposons by innate immune receptors.
November 6, 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/28981838/an-efficient-method-for-generation-of-bi-allelic-null-mutant-mouse-embryonic-stem-cells-and-its-application-for-investigating-epigenetic-modifiers
#20
Cynthia L Fisher, Hendrik Marks, Lily Ting-Yin Cho, Robert Andrews, Sam Wormald, Thomas Carroll, Vivek Iyer, Peri Tate, Barry Rosen, Hendrik G Stunnenberg, Amanda G Fisher, William C Skarnes
Mouse embryonic stem (ES) cells are a popular model system to study biological processes, though uncovering recessive phenotypes requires inactivating both alleles. Building upon resources from the International Knockout Mouse Consortium (IKMC), we developed a targeting vector for second allele inactivation in conditional-ready IKMC 'knockout-first' ES cell lines. We applied our technology to several epigenetic regulators, recovering bi-allelic targeted clones with a high efficiency of 60% and used Flp recombinase to restore expression in two null cell lines to demonstrate how our system confirms causality through mutant phenotype reversion...
December 1, 2017: Nucleic Acids Research
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