@article{Yaragatti2008, abstract = {The identification of transcriptional regulatory modules within mammalian genomes is a prerequisite to understanding the mechanisms controlling regulated gene expression. While high-throughput microarray- and sequencing-based approaches have been used to map the genomic locations of sites of nuclease hypersensitivity or target DNA sequences bound by specific protein factors, the identification of regulatory elements using functional assays, which would provide important complementary data, has been relatively rare. Here we present a method that permits the functional identification of active transcriptional regulatory modules using a simple procedure for the isolation and analysis of DNA derived from nucleosome-free regions (NFRs), the 2% of the cellular genome that contains these elements. The more than 100 new active regulatory DNAs identified in this manner from F9 cells correspond to both promoter-proximal and distal elements, and display several features predicted for endogenous transcriptional regulators, including localization within DNase-accessible chromatin and CpG islands, and proximity to expressed genes. Furthermore, comparison with published ChIP-seq data of ES-cell chromatin shows that the functional elements we identified correspond with genomic regions enriched for H3K4me3, a histone modification associated with active transcriptional regulatory elements, and that the correspondence of H3K4me3 with our promoter-distal elements is largely ES-cell specific. The majority of the distal elements exhibit enhancer activity. Importantly, these functional DNA fragments are an average 149 bp in length, greatly facilitating future applications to identify transcription factor binding sites mediating their activity. Thus, this approach provides a tool for the high-resolution identification of the functional components of active promoters and enhancers.}, added-at = {2010-01-26T20:35:53.000+0100}, author = {Yaragatti, Mahesh and Basilico, Claudio and Dailey, Lisa}, biburl = {https://www.bibsonomy.org/bibtex/2b43c7830fd9c4f46a2e8a74006711a63/denilw}, doi = {10.1101/gr.073460.107}, institution = {Department of Microbiology, New York University School of Medicine, New York, New York 10016, USA.}, interhash = {fcde3a60e9192c2cc07aee169e9286f8}, intrahash = {b43c7830fd9c4f46a2e8a74006711a63}, journal = {Genome Res}, keywords = {Animals Cell_Line Chromosome_Mapping DNA,_chemistry/isolation_/\&/_purification Deoxyribonucleases,_Type_II_Site-Specific Enhancer_Elements_(Genetics) Gene_Expression_Regulation Genomics,_methods Histones,_metabolism Mice Nucleosomes,_chemistry Polymerase_Chain_Reaction Promoter_Regions_(Genetics) Trans-Activation_(Genetics)}, month = Jun, number = 6, owner = {denilw}, pages = {930-938}, pii = {gr.073460.107}, pmid = {18441229}, timestamp = {2010-01-26T20:36:05.000+0100}, title = {Identification of active transcriptional regulatory modules by the functional assay of DNA from nucleosome-free regions.}, url = {http://dx.doi.org/10.1101/gr.073460.107}, volume = 18, year = 2008 } @article{Shannon2003, added-at = {2010-01-26T20:35:53.000+0100}, author = {Shannon, M Frances}, biburl = {https://www.bibsonomy.org/bibtex/266958e15acbc8c387ada4a6cc211a94e/denilw}, doi = {10.1038/ng0503-4}, file = {article:../papers/Transcription Factor Binding/SatB1/A nuclear address with influence.pdf:pdf}, interhash = {0e1d56af7d72c4ed15d8c5e8cb315d69}, intrahash = {66958e15acbc8c387ada4a6cc211a94e}, journal = {Nat. Genet.}, keywords = {Animals Cell_Nucleus,_genetics/metabolism Gene_Expression_Regulation Histones,_metabolism Matrix_Attachment_Region_Binding_Proteins,_genetics/metabolism Mice Models,_Genetic Nuclear_Proteins,_genetics/metabolism T-Lymphocytes,_metabolism Transcription,_Genetic}, month = May, number = 1, owner = {denilw}, pages = {4-6}, pii = {ng0503-4}, pmid = {12721542}, timestamp = {2010-01-26T20:36:03.000+0100}, title = {A nuclear address with influence.}, url = {http://dx.doi.org/10.1038/ng0503-4}, volume = 34, year = 2003 } @article{Seo2005, abstract = {Special AT-rich binding protein 1 (SATB1) originally was identified as a protein that bound to the nuclear matrix attachment regions (MARs) of the immunoglobulin heavy chain intronic enhancer. Subsequently, SATB1 was shown to repress many genes expressed in the thymus, including interleukin-2 receptor alpha, c-myc, and those encoded by mouse mammary tumor virus (MMTV), a glucocorticoid-responsive retrovirus. SATB1 binds to MARs within the MMTV provirus to repress transcription. To address the role of the nuclear matrix in SATB1-mediated repression, a series of SATB1 deletion constructs was used to determine protein localization. Wild-type SATB1 localized to the soluble nuclear, chromatin, and nuclear matrix fractions. Mutants lacking amino acids 224-278 had a greatly diminished localization to the nuclear matrix, suggesting the presence of a nuclear matrix targeting sequence (NMTS). Transient transfection experiments showed that NMTS fusions to green fluorescent protein or LexA relocalized these proteins to the nuclear matrix. Difficulties with previous assay systems prompted us to develop retroviral vectors to assess effects of different SATB1 domains on expression of MMTV proviruses or integrated reporter genes. SATB1 overexpression repressed MMTV transcription in the presence and absence of functional glucocorticoid receptor. Repression was alleviated by deletion of the NMTS, which did not affect DNA binding, or by deletion of the MAR-binding domain. Our studies indicate that both nuclear matrix association and DNA binding are required for optimal SATB1-mediated repression of the integrated MMTV promoter and may allow insulation from cellular regulatory elements.}, added-at = {2010-01-26T20:35:53.000+0100}, author = {Seo, Jin and Lozano, Mary M. and Dudley, Jaquelin P.}, biburl = {https://www.bibsonomy.org/bibtex/21ea3489288542e849046d9f1909dbebc/denilw}, doi = {10.1074/jbc.M414076200}, file = {article:/papers/Transcription Factor Binding/SatB1/{$\Nu$}clear Matrix Binding Regulates SATB1-mediated transcriptional Repression.pdf:pdf}, institution = {Institute for Cellular and Molecular Biology, The University of Texas at Austin, Austin, Texas 78712, USA.}, interhash = {83a55a030551272f829392fb6ca32a35}, intrahash = {1ea3489288542e849046d9f1909dbebc}, journal = {J Biol Chem}, keywords = {Animals Cell_Line,_Tumor Cell_Nucleus,_metabolism DNA,_chemistry DNA_Primers,_chemistry Dimerization Fibroblasts,_metabolism Gene_Deletion Genes,_Reporter Green_Fluorescent_Proteins,_metabolism Humans Interleukin-2_Receptor_alpha_Subunit Introns Jurkat_Cells Ligands Mammary_Glands,_Animal Mammary_Tumor_Virus,_Mouse,_genetics Matrix_Attachment_Region_Binding_Proteins,_metabolism/physiology Mice Microscopy,_Fluorescence Mutation Plasmids,_metabolism Polymerase_Chain_Reaction Promoter_Regions_(Genetics) Protein_Binding Protein_Structure,_Tertiary Proto-Oncogene_Proteins_c-myc,_metabolism RNA,_metabolism Rats Receptors,_Glucocorticoid,_metabolism Receptors,_Interleukin,_metabolism Recombinant_Fusion_Proteins,_chemistry Retroviridae,_genetics Ribonucleases,_metabolism Subcellular_Fractions Transcription,_Genetic Transfection}, month = Jul, number = 26, owner = {denilw}, pages = {24600-24609}, pii = {M414076200}, pmid = {15851481}, timestamp = {2010-01-26T20:36:03.000+0100}, title = {Nuclear matrix binding regulates SATB1-mediated transcriptional repression.}, url = {http://dx.doi.org/10.1074/jbc.M414076200}, volume = 280, year = 2005 } @article{Anewpathto, added-at = {2010-01-26T20:35:53.000+0100}, author = {Richon, Victoria M}, biburl = {https://www.bibsonomy.org/bibtex/24f4abcfff9ae5c2962cfe4f9efc9c814/denilw}, doi = {10.1038/nbt0608-655}, file = {article:../Cancer Epigenetics/A new path to the cancer epigenome.pdf:pdf}, institution = { Co., Inc., 33 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA. victoria_richon@merck.com}, interhash = {1d91ef02bc1335ca6fdb5f7aabd333cc}, intrahash = {4f4abcfff9ae5c2962cfe4f9efc9c814}, journal = {Nat. Biotechnol.}, keywords = {Animals Breast_Neoplasms Cell_Line Cell_Line,_Tumor Cell_Polarity Chromosome_Mapping Disease_Progression Epigenesis,_Genetic Gene_Expression_Profiling Gene_Expression_Regulation,_Neoplastic Humans Lung_Neoplasms Lymphatic_Metastasis Matrix_Attachment_Region_Binding_Proteins Mice Mice,_Nude Neoplasm_Metastasis Neoplasm_Transplantation Phenotype Prognosis RNA_Interference Tumor_Markers,_Biological}, number = 6, owner = {denilw}, pages = {655-6}, pdf = {\Cancer\A new path to the cancer epigenome.pdf}, pii = {nbt0608-655}, pmid = {18536689}, timestamp = {2010-01-26T20:36:02.000+0100}, title = {A new path to the cancer epigenome.}, url = {http://dx.doi.org/10.1038/nbt0608-655}, volume = 26, year = 2008 } @article{ANovelDNA-Bi, abstract = {The nuclear matrix attachment DNA (MAR) binding protein SATB1 is a sequence context-specific binding protein that binds in the minor groove, making virtually no contact with the DNA bases. The SATB1 binding sites consist of a special AT-rich sequence context in which one strand is well-mixed A{'}s, T{'}s, and C{'}s, excluding G{'}s (ATC sequences), which is typically found in clusters within different MARs. To determine the extent of conservation of the SATB1 gene among different species, we cloned a mouse homolog of the human STAB1 cDNA from a cDNA expression library of the mouse thymus, the tissue in which this protein is predominantly expressed. This mouse cDNA encodes a 764-amino-acid protein with a 98% homology in amino acid sequence to the human SATB1 originally cloned from testis. To characterize the DNA binding domain of this novel class of protein, we used the mouse SATB1 cDNA and delineated a 150-amino-acid polypeptide as the binding domain. This region confers full DNA binding activity, recognizes the specific sequence context, and makes direct contact with DNA at the same nucleotides as the whole protein. This DNA binding domain contains a novel DNA binding motif: when no more than 21 amino acids at either the N- or C-terminal end of the binding domain are deleted, the majority of the DNA binding activity is lost. The concomitant presence of both terminal sequences is mandatory for binding. These two terminal regions consist of hydrophilic amino acids and share homologous sequences that are different from those of any known DNA binding motifs. We propose that the DNA binding region of SATB1 extends its two terminal regions toward DNA to make direct contact with DNA.}, added-at = {2010-01-26T20:35:53.000+0100}, author = {Nakagomi, K and Kohwi, Y and Dickinson, L A and Kohwi-Shigematsu, T}, biburl = {https://www.bibsonomy.org/bibtex/27a08cbf3dda3e32ce0fbb0cc9b7c7307/denilw}, file = {article:../Motifs/A Novel DNA-Binding Motif in the Nuclear Matrix Attachment DNA-Binding Protein SATB1.pdf:pdf}, institution = {La Jolla Cancer Research Foundation, California 92037.}, interhash = {e39354f6384ab0d3c295e415f166e1e6}, intrahash = {7a08cbf3dda3e32ce0fbb0cc9b7c7307}, journal = {Mol. Cell. Biol.}, keywords = {Amino_Acid_Sequence Animals Antigens,_Nuclear Binding_Sites Cloning,_Molecular DNA,_Complementary,_genetics DNA-Binding_Proteins,_chemistry/metabolism DNA_Mutational_Analysis Deoxyribonucleoproteins,_chemistry Genes Matrix_Attachment_Region_Binding_Proteins Mice Molecular_Sequence_Data Nuclear_Matrix,_metabolism Nuclear_Proteins,_chemistry Oligodeoxyribonucleotides,_chemistry Sequence_Alignment Sequence_Deletion Sequence_Homology,_Amino_Acid Structure-Activity_Relationship TATA-Box_Binding_Protein Thymus_Gland,_chemistry Transcription_Factors,_chemistry}, month = Mar, number = 3, owner = {denilw}, pages = {1852-60}, pmid = {8114718}, timestamp = {2010-01-26T20:36:01.000+0100}, title = {A novel DNA-binding motif in the nuclear matrix attachment DNA-binding protein SATB1.}, volume = 14, year = 1994 } @article{Liu1997, abstract = {The nuclear matrix has been implicated in several cellular processes, including DNA replication, transcription, and RNA processing. In particular, transcriptional regulation is believed to be accomplished by binding of chromatin loops to the nuclear matrix and by the concentration of specific transcription factors near these matrix attachment regions (MARs). A number of MAR-binding proteins have been identified, but few have been directly linked to tissue-specific transcription. Recently, we have identified two cellular protein complexes (NBP and UBP) that bind to a region of the mouse mammary tumor virus (MMTV) long terminal repeat (LTR) previously shown to contain at least two negative regulatory elements (NREs) termed the promoter-proximal and promoter-distal NREs. These NREs are absent from MMTV strains that cause T-cell lymphomas instead of mammary carcinomas. We show here that NBP binds to a 22-bp sequence containing an imperfect inverted repeat in the promoter-proximal NRE. Previous data showed that a mutation (p924) within the inverted repeat elevated basal transcription from the MMTV promoter and destabilized the binding of NBP, but not UBP, to the proximal NRE. By using conventional and affinity methods to purify NBP from rat thymic nuclear extracts, we obtained a single major protein of 115 kDa that was identified by protease digestion and partial sequencing analysis as the nuclear matrix-binding protein special AT-rich sequence-binding protein 1 (SATB1). Antibody ablation, distamycin inhibition of binding, renaturation and competition experiments, and tissue distribution data all confirmed that the NBP complex contained SATB1. Similar types of experiments were used to show that the UBP complex contained the homeodomain protein Cux/CDP that binds the MAR of the intronic heavy-chain immunoglobulin enhancer. By using the p924 mutation within the MMTV LTR upstream of the chloramphenicol acetyltransferase gene, we generated two strains of transgenic mice that had a dramatic elevation of reporter gene expression in lymphoid tissues compared with reporter gene expression in mice expressing wild-type LTR constructs. Thus, the 924 mutation in the SATB1-binding site dramatically elevated MMTV transcription in lymphoid tissues. These results and the ability of the proximal NRE in the MMTV LTR to bind to the nuclear matrix clearly demonstrate the role of MAR-binding proteins in tissue-specific gene regulation and in MMTV-induced oncogenesis.}, added-at = {2010-01-26T20:35:53.000+0100}, author = {Liu, J. and Bramblett, D. and Zhu, Q. and Lozano, M. and Kobayashi, R. and Ross, S. R. and Dudley, J. P.}, biburl = {https://www.bibsonomy.org/bibtex/20b28ee3d638235a12d5ce4febce621dd/denilw}, file = {article:../papers/Transcription Factor Binding/SatB1/The Matrix Attachment Region-Binding Protein SATB1 Participates in Negative Regulation of Tissue-Specific Gene Expression.pdf:pdf}, institution = {Department of Microbiology and Institute for Cellular and Molecular Biology, University of Texas at Austin, 78712, USA.}, interhash = {a3135c7fc6b5c4a4b9654ae8b4b0959b}, intrahash = {0b28ee3d638235a12d5ce4febce621dd}, journal = {Mol Cell Biol}, keywords = {Amino_Acid_Sequence Animals Antiviral_Agents Cell_Line DNA-Binding_Proteins Distamycins Female Gene_Expression Homeodomain_Proteins Humans Jurkat_Cells Male Mammary_Tumor_Virus,_Mouse Matrix_Attachment_Region_Binding_Proteins Mice Mice,_Transgenic Molecular_Sequence_Data Nuclear_Proteins Rats Repressor_Proteins}, month = Sep, number = 9, owner = {denilw}, pages = {5275-5287}, pmid = {9271405}, timestamp = {2010-01-26T20:36:00.000+0100}, title = {The matrix attachment region-binding protein SATB1 participates in negative regulation of tissue-specific gene expression.}, volume = 17, year = 1997 } @article{Ko2008, abstract = {Development is a stepwise process in which multi-potent progenitor cells undergo lineage commitment, differentiation, proliferation and maturation to produce mature cells with restricted developmental potentials. This process is directed by spatiotemporally distinct gene expression programs that allow cells to stringently orchestrate intricate transcriptional activation or silencing events. In eukaryotes, chromatin structure contributes to developmental progression as a blueprint for coordinated gene expression by actively participating in the regulation of gene expression. Changes in higher order chromatin structure or covalent modification of its components are considered to be critical events in dictating lineage-specific gene expression during development. Mammalian cells utilize multi-subunit nuclear complexes to alter chromatin structure. Histone-modifying complex catalyzes covalent modifications of histone tails including acetylation, methylation, phosphorylation and ubiquitination. ATP-dependent chromatin remodeling complex, which disrupts histone-DNA contacts and induces nucleosome mobilization, requires energy from ATP hydrolysis for its catalytic activity. Here, we discuss the diverse functions of ATP-dependent chromatin remodeling complexes during mammalian development. In particular, the roles of these complexes during embryonic and hematopoietic development are reviewed in depth. In addition, pathological conditions such as tumor development that are induced by mutation of several key subunits of the chromatin remodeling complex are discussed, together with possible mechanisms that underlie tumor suppression by the complex.}, added-at = {2010-01-26T20:35:53.000+0100}, author = {Ko, Myunggon and Sohn, Dong H. and Chung, Heekyoung and Seong, Rho H.}, biburl = {https://www.bibsonomy.org/bibtex/275e043a59a50867776d7de150a7d4b4b/denilw}, doi = {10.1016/j.mrfmmm.2008.08.004}, institution = {Department of Biological Sciences, Institute of Molecular Biology and Genetics, Seoul National University, Seoul 151-742, Republic of Korea.}, interhash = {b419d4a4cd13032d38079fec9aa747e3}, intrahash = {75e043a59a50867776d7de150a7d4b4b}, journal = {Mutat Res}, keywords = {Animals Chromatin_Assembly_and_Disassembly Chromosomal_Proteins,_Non-Histone,_physiology DNA_Helicases,_physiology Embryonic_Development,_genetics Gene_Expression_Regulation Genes,_Switch,_physiology Growth_and_Development,_genetics Hematopoiesis,_genetics Humans Mice Neoplasms,_genetics Nuclear_Proteins,_physiology T-Lymphocytes,_physiology Transcription_Factors,_physiology}, month = Dec, number = {1-2}, owner = {denilw}, pages = {59-67}, pii = {S0027-5107(08)00177-2}, pmid = {18786551}, timestamp = {2010-01-26T20:36:00.000+0100}, title = {Chromatin remodeling, development and disease.}, url = {http://dx.doi.org/10.1016/j.mrfmmm.2008.08.004}, volume = 647, year = 2008 } @article{Han08, abstract = {Mechanisms underlying global changes in gene expression during tumour progression are poorly understood. SATB1 is a genome organizer that tethers multiple genomic loci and recruits chromatin-remodelling enzymes to regulate chromatin structure and gene expression. Here we show that SATB1 is expressed by aggressive breast cancer cells and its expression level has high prognostic significance (P < 0.0001), independent of lymph-node status. RNA-interference-mediated knockdown of SATB1 in highly aggressive (MDA-MB-231) cancer cells altered the expression of >1,000 genes, reversing tumorigenesis by restoring breast-like acinar polarity and inhibiting tumour growth and metastasis in vivo. Conversely, ectopic SATB1 expression in non-aggressive (SKBR3) cells led to gene expression patterns consistent with aggressive-tumour phenotypes, acquiring metastatic activity in vivo. SATB1 delineates specific epigenetic modifications at target gene loci, directly upregulating metastasis-associated genes while downregulating tumour-suppressor genes. SATB1 reprogrammes chromatin organization and the transcription profiles of breast tumours to promote growth and metastasis; this is a new mechanism of tumour progression.}, added-at = {2010-01-26T20:35:53.000+0100}, author = {Han, Hye-Jung and Russo, Jose and Kohwi, Yoshinori and Kohwi-Shigematsu, Terumi}, biburl = {https://www.bibsonomy.org/bibtex/21d2c10f3893f0364f4f5733cad8ec12c/denilw}, doi = {10.1038/nature06781}, file = {article:../Transcription Factor Binding/SatB1/SATB1 reprogrammes gene expression to promote breast tumour growth and metastasis.pdf:pdf}, institution = {Life Sciences Division, Lawrence Berkeley National Laboratory, University of California, Berkeley, California 94720, USA.}, interhash = {34baee6040568a928ab91818118af55e}, intrahash = {1d2c10f3893f0364f4f5733cad8ec12c}, journal = {Nature}, keywords = {Animals Breast_Neoplasms Cell_Line Cell_Line,_Tumor Cell_Polarity Disease_Progression Epigenesis,_Genetic Gene_Expression_Profiling Gene_Expression_Regulation,_Neoplastic Humans Lung_Neoplasms Lymphatic_Metastasis Matrix_Attachment_Region_Binding_Proteins Mice Mice,_Nude Neoplasm_Metastasis Neoplasm_Transplantation Phenotype Prognosis RNA_Interference Tumor_Markers,_Biological}, month = Mar, number = 7184, owner = {denilw}, pages = {187-93}, pdf = {C:\Users\denilw\Desktop\Steven Jones Lab\Papers\SatB1\SATB1 reprogrammes gene expression to promote breast tumour growth and metastasis.pdf}, pii = {nature06781}, pmid = {18337816}, timestamp = {2010-01-26T20:35:59.000+0100}, title = {SATB1 reprogrammes gene expression to promote breast tumour growth and metastasis.}, url = {http://dx.doi.org/10.1038/nature06781}, volume = 452, year = 2008 } @article{Davuluri2007, abstract = {The combinatorial control of gene regulatory switches involves both transcription factor (TF) complexes and associated epigenetic modifications to the chromatin template. The novel high-throughput technologies, such as Chromatin ImmunoPrecipitation ChIP-chip, have enabled genome-wide in vivo identification of TF target regulatory regions and related epigenetic modifications, which led to the view of highly dynamic TF-DNA interactions in activated or repressed promoters. Consequently, modeling and elucidating the combinatorial interaction of TFs and corresponding cis-regulatory modules in target promoters is of paramount interest. An estimated 5% of the genes in mammalian genomes code for TF proteins, and computational modeling of cis-regulatory logic would rapidly increase the pace of experimental confirmation of TF target promoters at the bench. The purpose of this chapter is to discuss the use of different bioinformatics tools for predicting the target genes of TFs of interest in mammalian genomes, and the application of these methods in the analysis of ChIP-chip experimental data. The author describes most commonly used databases and prediction programs that are available on the World Wide Web and demonstrate the use of some of these programs by an example. A list of these programs is provided along with their web Uniform Resource Locator (URLs) and guidelines for successful application are suggested.}, added-at = {2010-01-26T20:35:53.000+0100}, author = {Davuluri, Ramana V.}, biburl = {https://www.bibsonomy.org/bibtex/2a4a54589d72be458f69dd9da04ecec17/denilw}, institution = {OSU Comprehensive Cancer Center, Ohio State University, Columbus, USA.}, interhash = {de81b2209791489437c24e443a3f7813}, intrahash = {a4a54589d72be458f69dd9da04ecec17}, journal = {Methods Mol Biol}, keywords = {Animals Base_Sequence Binding_Sites,_genetics Chromatin_Immunoprecipitation,_statistics_/\&/_numerical_data Computational_Biology,_statistics_/\&/_numerical_data Computer_Simulation CpG_Islands DNA,_genetics/metabolism Databases,_Genetic Decision_Trees Epigenesis,_Genetic Humans Internet Mice Promoter_Regions_(Genetics) Transcription_Factors,_genetics/metabolism}, owner = {denilw}, pages = {129-151}, pmid = {18314581}, timestamp = {2010-01-26T20:35:57.000+0100}, title = {Bioinformatics tools for modeling transcription factor target genes and epigenetic changes.}, volume = 408, year = 2007 } @article{Cai06, abstract = {SATB1 (special AT-rich sequence binding protein 1) organizes cell type-specific nuclear architecture by anchoring specialized DNA sequences and recruiting chromatin remodeling factors to control gene transcription. We studied the role of SATB1 in regulating the coordinated expression of Il5, Il4 and Il13, located in the 200-kb T-helper 2 (T(H)2) cytokine locus on mouse chromosome 11. We show that on T(H)2 cell activation, SATB1 expression is rapidly induced to form a unique transcriptionally active chromatin structure at the cytokine locus. In this structure, chromatin is folded into numerous small loops, all anchored to SATB1 at their base. In addition, histone H3 is acetylated at Lys9 and Lys14, and the T(H)2-specific factors GATA3, STAT6 and c-Maf, the chromatin-remodeling enzyme Brg1 and RNA polymerase II are all bound across the 200-kb region. Before activation, the T(H)2 cytokine locus is already associated with GATA3 and STAT6, showing some looping, but these are insufficient to induce cytokine gene expression. Using RNA interference, we show that on cell activation, SATB1 is required not only for compacting chromatin into dense loops at the 200-kb cytokine locus but also for inducing Il4, Il5, Il13 and c-Maf expression. Thus, SATB1 is a necessary determinant for the hitherto unidentified higher-order, transcriptionally active chromatin structure that forms on T(H)2 cell activation.}, added-at = {2010-01-26T20:35:53.000+0100}, author = {Cai, Shutao and Lee, Charles C and Kohwi-Shigematsu, Terumi}, biburl = {https://www.bibsonomy.org/bibtex/2688e42c1312a37a9813e2bc9cf489b1c/denilw}, doi = {10.1038/ng1913}, file = {article:../Transcription Factor Binding/SatB1/SATB1 packages densely looped%2C transcriptionally active chromatin for coordinated expression of cytokine genes.pdf:pdf}, institution = {Lawrence Berkeley Laboratory, University of California, Berkeley, California 94720, USA.}, interhash = {d5bb3e6c8cb7f4fdb0f7545d2da94c98}, intrahash = {688e42c1312a37a9813e2bc9cf489b1c}, journal = {Nat. Genet.}, keywords = {Acetylation Animals Binding_Sites Chromatin,_chemistry/metabolism Chromatin_Immunoprecipitation,_methods Chromosomes,_chemistry Cytokines,_metabolism DNA-Binding_Proteins,_genetics/physiology DNA_Helicases,_metabolism DNA_Repair_Enzymes,_genetics GATA3_Transcription_Factor,_metabolism Gene_Expression_Regulation Histone_Acetyltransferases,_metabolism Histones,_metabolism Locus_Control_Region Lymphocyte_Activation,_physiology Matrix_Attachment_Region_Binding_Proteins,_physiology Mice Mice,_Inbred_AKR Models,_Biological Nuclear_Proteins,_metabolism Nucleic_Acid_Conformation Promoter_Regions_(Genetics) Proto-Oncogene_Proteins_c-maf,_metabolism RNA_Polymerase_II,_metabolism STAT6_Transcription_Factor,_metabolism Th2_Cells,_metabolism Transcription,_Genetic,_physiology Transcription_Factors,_metabolism}, month = Nov, number = 11, owner = {denilw}, pages = {1278-88}, pii = {ng1913}, pmid = {17057718}, timestamp = {2010-01-26T20:35:56.000+0100}, title = {SATB1 packages densely looped, transcriptionally active chromatin for coordinated expression of cytokine genes.}, url = {http://dx.doi.org/10.1038/ng1913}, volume = 38, year = 2006 } @article{Cai03, abstract = {Eukaryotic chromosomes are packaged in nuclei by many orders of folding. Little is known about how higher-order chromatin packaging might affect gene expression. SATB1 is a cell-type specific nuclear protein that recruits chromatin-remodeling factors and regulates numerous genes during thymocyte differentiation. Here we show that in thymocyte nuclei, SATB1 has a cage-like {'}network{'} distribution circumscribing heterochromatin and selectively tethers specialized DNA sequences onto its network. This was shown by fluorescence in situ hybridization on wild-type and Satb1-null thymocytes using in vivo SATB1-bound sequences as probes. Many gene loci, including that of Myc and a brain-specific gene, are anchored by the SATB1 network at specific genomic sites, and this phenomenon is precisely correlated with proper regulation of distant genes. Histone-modification analyses across a gene-enriched genomic region of 70 kb showed that acetylation of histone H3 at Lys9 and Lys14 peaks at the SATB1-binding site and extends over a region of roughly 10 kb covering genes regulated by SATB1. By contrast, in Satb1-null thymocytes, this site is marked by methylation at H3 Lys9. We propose SATB1 as a new type of gene regulator with a novel nuclear architecture, providing sites for tissue-specific organization of DNA sequences and regulating region-specific histone modification.}, added-at = {2010-01-26T20:35:53.000+0100}, author = {Cai, Shutao and Han, Hye-Jung and Kohwi-Shigematsu, Terumi}, biburl = {https://www.bibsonomy.org/bibtex/2cc43a933f4d3ee9196ea1e6e90f17849/denilw}, doi = {10.1038/ng1146}, file = {article:../SatB1/Tissue-specific nuclear architecture and gene expression regulated by SATB1.pdf:pdf}, institution = {Life Sciences Division, Lawrence Berkeley National Laboratory, 1 Cyclotron Road (84-171), University of California, Berkeley, California 94720, USA.}, interhash = {cd424773e4b2081f261db379ff257cc8}, intrahash = {cc43a933f4d3ee9196ea1e6e90f17849}, journal = {Nat. Genet.}, keywords = {Animals Binding_Sites Cell_Nucleus Chromatin DNA Gene_Expression_Regulation Genes,_myc Histones In_Situ_Hybridization,_Fluorescence Matrix_Attachment_Region_Binding_Proteins Mice Mice,_Knockout Models,_Genetic Molecular_Sequence_Data Nuclear_Proteins T-Lymphocytes Tissue_Distribution}, month = May, number = 1, owner = {denilw}, pages = {42-51}, pdf = {C:\Users\denilw\Desktop\Steven Jones Lab\Papers\SatB1\Tissue-specific nuclear architecture and gene expression regulated by SATB1.pdf}, pii = {ng1146}, pmid = {12692553}, timestamp = {2010-01-26T20:35:56.000+0100}, title = {Tissue-specific nuclear architecture and gene expression regulated by SATB1.}, url = {http://dx.doi.org/10.1038/ng1146}, volume = 34, year = 2003 } @article{Bernstein05, abstract = {We mapped histone H3 lysine 4 di- and trimethylation and lysine 9/14 acetylation across the nonrepetitive portions of human chromosomes 21 and 22 and compared patterns of lysine 4 dimethylation for several orthologous human and mouse loci. Both chromosomes show punctate sites enriched for modified histones. Sites showing trimethylation correlate with transcription starts, while those showing mainly dimethylation occur elsewhere in the vicinity of active genes. Punctate methylation patterns are also evident at the cytokine and IL-4 receptor loci. The Hox clusters present a strikingly different picture, with broad lysine 4-methylated regions that overlay multiple active genes. We suggest these regions represent active chromatin domains required for the maintenance of Hox gene expression. Methylation patterns at orthologous loci are strongly conserved between human and mouse even though many methylated sites do not show sequence conservation notably higher than background. This suggests that the DNA elements that direct the methylation represent only a small fraction of the region or lie at some distance from the site.}, added-at = {2010-01-26T20:35:53.000+0100}, author = {Bernstein, Bradley E and Kamal, Michael and Lindblad-Toh, Kerstin and Bekiranov, Stefan and Bailey, Dione K and Huebert, Dana J and McMahon, Scott and Karlsson, Elinor K and Kulbokas, Edward J and Gingeras, Thomas R and Schreiber, Stuart L and Lander, Eric S}, biburl = {https://www.bibsonomy.org/bibtex/289b2700cdaa95608fc15b6bf3eda6383/denilw}, doi = {10.1016/j.cell.2005.01.001}, file = {article:../Histone modifications/Genomic Maps and Comparative Analysis of Histone Modifications in Human and Mouse.pdf:pdf}, institution = {Howard Hughes Medical Institute, Department of Chemistry and Chemical Biology, Harvard University, 12 Oxford Street, Cambridge, MA 02138, USA. bbernst@fas.harvard.edu}, interhash = {46ac83c08b5a576a5fde6fe188916d3b}, intrahash = {89b2700cdaa95608fc15b6bf3eda6383}, journal = {Cell}, keywords = {Acetylation Animals Chromatin,_genetics/metabolism Chromosome_Mapping,_methods Chromosomes,_Human,_Pair_21,_genetics/metabolism Chromosomes,_Human,_Pair_22,_genetics/metabolism Genome Histones,_genetics/metabolism Homeodomain_Proteins,_genetics/metabolism Humans Lysine,_metabolism Methylation Mice Receptors,_Interleukin-4,_genetics}, month = Jan, number = 2, owner = {denilw}, pages = {169-81}, pii = {S0092867405000395}, pmid = {15680324}, timestamp = {2010-01-26T20:35:54.000+0100}, title = {Genomic maps and comparative analysis of histone modifications in human and mouse.}, url = {http://dx.doi.org/10.1016/j.cell.2005.01.001}, volume = 120, year = 2005 }