JDP2, a Novel Molecular Key in Heart Failure and Atrial Fibrillation?
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Jun Dimerization Protein 2 Activates Mc2r Transcriptional Activity: Role of Phosphorylation and Sumoylation
International Journal of Molecular Sciences Article Jun Dimerization Protein 2 Activates Mc2r Transcriptional Activity: Role of Phosphorylation and SUMOylation Chiung-Min Wang 1, Raymond X. Wang 1, Runhua Liu 2 and Wei-Hsiung Yang 1,* 1 Department of Biomedical Sciences, Mercer University School of Medicine, Savannah, GA 31404, USA; [email protected] (C.-M.W.); [email protected] (R.X.W.) 2 Department of Genetics and Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL 35294, USA; [email protected] * Correspondence: [email protected]; Tel.: +1-912-721-8203; Fax: +1-912-721-8268 Academic Editor: William Chi-shing Cho Received: 15 December 2016; Accepted: 26 January 2017; Published: 31 January 2017 Abstract: Jun dimerization protein 2 (JDP2), a basic leucine zipper transcription factor, is involved in numerous biological and cellular processes such as cancer development and regulation, cell-cycle regulation, skeletal muscle and osteoclast differentiation, progesterone receptor signaling, and antibacterial immunity. Though JDP2 is widely expressed in mammalian tissues, its function in gonads and adrenals (such as regulation of steroidogenesis and adrenal development) is largely unknown. Herein, we find that JDP2 mRNA and proteins are expressed in mouse adrenal gland tissues. Moreover, overexpression of JDP2 in Y1 mouse adrenocortical cancer cells increases the level of melanocortin 2 receptor (MC2R) protein. Notably, Mc2r promoter activity is activated by JDP2 in a dose-dependent manner. Next, by mapping the Mc2r promoter, we show that cAMP response elements (between −1320 and −720-bp) are mainly required for Mc2r activation by JDP2 and demonstrate that −830-bp is the major JDP2 binding site by real-time chromatin immunoprecipitation (ChIP) analysis. -
MOZ and MORF, Two Large Mystic Hats in Normal and Cancer Stem Cells
Oncogene (2007) 26, 5408–5419 & 2007 Nature Publishing Group All rights reserved 0950-9232/07 $30.00 www.nature.com/onc REVIEW MOZ and MORF, two large MYSTic HATs in normal and cancer stem cells X-J Yang and M Ullah Molecular Oncology Group, Department of Medicine, McGill University Health Center, Montre´al, Que´bec, Canada Genes of the human monocytic leukemia zinc-finger protein pattern. For cancer biology, it is thus important to MOZ (HUGO symbol, MYST3) and its paralog MORF understand the fundamental mechanisms whereby chro- (MYST4) are rearranged in chromosome translocations matin structure and function are regulated. In the associated withacute myeloid leukemia and/or benign past two decades, our knowledge about regulation in uterine leiomyomata. Both proteins have intrinsic histone this field has exploded. Known regulatory mechanisms acetyltransferase activity and are components of quartet include chromatin assembly, ATP-dependent remodeling, complexes withnoncatalytic subunits containing thebromo- covalent modification, condensin-mediated condensation, domain, plant homeodomain-linked (PHD) finger and replacement with histone variants, and association of proline-tryptophan-tryptophan-proline (PWWP)-containing noncoding RNA (reviewed by Horn and Peterson, 2002; domain, three types of structural modules characteristic of Khorasanizadeh, 2004; Li et al., 2007). Covalent chromatin regulators. Although leukemia-derived fusion pro- modification can occur at both the DNA and histone teins suchas MOZ-TIF2 promote self-renewal of leukemic levels. With histones, modifications include acetylation, stem cells, recent studies indicate that murine MOZ and phosphorylation, methylation, ubiquitination, and many MORF are important for proper development of hema- others (for reviews, see Spencer and Davie, 1999; Strahl topoietic and neurogenic progenitors, respectively, thereby and Allis, 2000; Berger, 2002; Jason et al., 2002; highlighting the importance of epigenetic integrity in Kouzarides, 2007). -
Genome-Wide Profiling of Active Enhancers in Colorectal Cancer
Genome-wide proling of active enhancers in colorectal cancer Min Wu ( [email protected] ) Wuhan University https://orcid.org/0000-0003-1372-4764 Qinglan Li Wuhan University Xiang Lin Wuhan University Ya-Li Yu Zhongnan Hospital, Wuhan University Lin Chen Wuhan University Qi-Xin Hu Wuhan University Meng Chen Zhongnan Hospital, Wuhan University Nan Cao Zhongnan Hospital, Wuhan University Chen Zhao Wuhan University Chen-Yu Wang Wuhan University Cheng-Wei Huang Wuhan University Lian-Yun Li Wuhan University Mei Ye Zhongnan Hospital, Wuhan University https://orcid.org/0000-0002-9393-3680 Article Keywords: Colorectal cancer, H3K27ac, Epigenetics, Enhancer, Transcription factors Posted Date: December 10th, 2020 DOI: https://doi.org/10.21203/rs.3.rs-119156/v1 License: This work is licensed under a Creative Commons Attribution 4.0 International License. Read Full License Genome-wide profiling of active enhancers in colorectal cancer Qing-Lan Li1, #, Xiang Lin1, #, Ya-Li Yu2, #, Lin Chen1, #, Qi-Xin Hu1, Meng Chen2, Nan Cao2, Chen Zhao1, Chen-Yu Wang1, Cheng-Wei Huang1, Lian-Yun Li1, Mei Ye2,*, Min Wu1,* 1 Frontier Science Center for Immunology and Metabolism, Hubei Key Laboratory of Cell Homeostasis, Hubei Key Laboratory of Developmentally Originated Disease, Hubei Key Laboratory of Intestinal and Colorectal Diseases, College of Life Sciences, Wuhan University, Wuhan, Hubei 430072, China 2Division of Gastroenterology, Department of Geriatrics, Hubei Clinical Centre & Key Laboratory of Intestinal and Colorectal Diseases, Zhongnan Hospital, Wuhan University, Wuhan, Hubei 430072, China #Equal contribution to the study. Contact information *Correspondence should be addressed to Dr. Min Wu, Email: [email protected], Tel: 86-27-68756620, or Dr. -
The Basic Region and Leucine Zipper Transcription Factor Mafk Is a New Nerve Growth Factor-Responsive Immediate Early Gene That Regulates Neurite Outgrowth
The Journal of Neuroscience, October 15, 2002, 22(20):8971–8980 The Basic Region and Leucine Zipper Transcription Factor MafK Is a New Nerve Growth Factor-Responsive Immediate Early Gene That Regulates Neurite Outgrowth Be´ ata To¨ro¨ csik, James M. Angelastro, and Lloyd A. Greene Department of Pathology and Center for Neurobiology and Behavior, Columbia University College of Physicians and Surgeons, New York, New York 10032 We used serial analysis of gene expression to identify new mediated by an atypical isoform of PKC but not by mitogen- NGF-responsive immediate early genes (IEGs) with potential activated kinase kinase, phospholipase C␥, or phosphoinositide roles in neuronal differentiation. Among those identified was 3Ј-kinase. Interference with MafK expression or activity by small MafK, a small Maf family basic region and leucine zipper tran- interfering RNA and dominant negative strategies, respectively, scriptional repressor and coactivator expressed in immature suppresses NGF-promoted outgrowth and maintenance of neu- neurons. NGF treatment elevates the levels of both MafK tran- rites by PC12 cells and neurite outgrowth by immature telence- scripts and protein. In contrast, there is no effect on expression phalic neurons. Our findings support a role for MafK as a novel of the closely related MafG. Unlike many other NGF-responsive regulator of neuronal differentiation. IEGs, MafK regulation shows selectivity and is unresponsive to epidermal growth factor, depolarization, or cAMP derivatives. Key words: MafK; NGF; immediate early -
Human Small Maf Proteins Form Heterodimers with CNC Family Transcription Factors and Recognize the NF-E2 Motif
Oncogene (1997) 14, 1901 ± 1910 1997 Stockton Press All rights reserved 0950 ± 9232/97 $12.00 Human small Maf proteins form heterodimers with CNC family transcription factors and recognize the NF-E2 motif Tsutomu Toki1, Jugou Itoh2, Jun'ichi Kitazawa1, Koji Arai1, Koki Hatakeyama3, Jun-itsu Akasaka4, Kazuhiko Igarashi5, Nobuo Nomura6, Masaru Yokoyama1, Masayuki Yamamoto5 and Etsuro Ito1 1Department of Pediatrics, 2Medicine, School of Medicine; 3Department of Biology, Faculty of Sciences, Hirosaki University, Hirosaki 036; 4Department of Biochemistry, Tohoku University School of Medicine, Sendai 980-77; 5Center for TARA and Institute of Basic Medical Sciences, University of Tsukuba, Tsukuba 305; 6Kazusa DNA Institute, Kisarazu 292, Japan The transcription factor NF-E2, a heterodimeric protein Talbot et al., 1990; Talbot and Grosveld, 1991; complex composed of p45 and small Maf family Kotkow and Orkin, 1995). Recent analyses demon- proteins, is considered crucial for the regulation of strated that NF-E2 is composed of two subunits erythroid gene expression and platelet formation. To (Andrews et al., 1993a,b; Igarashi et al., 1994). The facilitate the characterization of NF-E2 functions in large p45 subunit belongs to a family of basic leucine- human cells, we isolated cDNAs encoding two members zipper (bZip) proteins that is closely related to the of the small Maf family, MafK and MafG. The human Drosophila Cap`n'colar (the CNC family) factor mafK and mafG genes encode proteins of 156 and 162 (Mohler et al., 1991). It cannot bind to the NF-E2 amino acid residues, respectively, whose deduced amino sequence as a homodimer, but does do after forming acid sequences show approximately 95% identity to their heterodimers with chicken small Maf family proteins, respective chicken counterparts. -
860.Full.Pdf
Repression of IL-2 Promoter Activity by the Novel Basic Leucine Zipper p21 SNFT Protein This information is current as Milena Iacobelli, William Wachsman and Kathleen L. of September 29, 2021. McGuire J Immunol 2000; 165:860-868; ; doi: 10.4049/jimmunol.165.2.860 http://www.jimmunol.org/content/165/2/860 Downloaded from References This article cites 49 articles, 31 of which you can access for free at: http://www.jimmunol.org/content/165/2/860.full#ref-list-1 http://www.jimmunol.org/ Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication by guest on September 29, 2021 *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2000 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Repression of IL-2 Promoter Activity by the Novel Basic Leucine Zipper p21SNFT Protein1,2 Milena Iacobelli,* William Wachsman,† and Kathleen L. McGuire3* IL-2 is the major autocrine and paracrine growth factor produced by T cells upon T cell stimulation. The inducible expression of IL-2 is highly regulated by multiple transcription factors, particularly AP-1, which coordinately activate the promoter. -
Jdp2 Downregulates Trp53 Transcription to Promote Leukaemogenesis in the Context of Trp53 Heterozygosity
Oncogene (2013) 32, 397 --402 & 2013 Macmillan Publishers Limited All rights reserved 0950-9232/13 www.nature.com/onc SHORT COMMUNICATION Jdp2 downregulates Trp53 transcription to promote leukaemogenesis in the context of Trp53 heterozygosity L van der Weyden1, AG Rust1,4, RE McIntyre1,4, CD Robles-Espinoza1, M del Castillo Velasco-Herrera1, R Strogantsev2, AC Ferguson-Smith2, S McCarthy1, TM Keane1, MJ Arends3 and DJ Adams1 We performed a genetic screen in mice to identify candidate genes that are associated with leukaemogenesis in the context of Trp53 heterozygosity. To do this we generated Trp53 heterozygous mice carrying the T2/Onc transposon and SB11 transposase alleles to allow transposon-mediated insertional mutagenesis to occur. From the resulting leukaemias/lymphomas that developed in these mice, we identified nine loci that are potentially associated with tumour formation in the context of Trp53 heterozygosity, including AB041803 and the Jun dimerization protein 2 (Jdp2). We show that Jdp2 transcriptionally regulates the Trp53 promoter, via an atypical AP-1 site, and that Jdp2 expression negatively regulates Trp53 expression levels. This study is the first to identify a genetic mechanism for tumour formation in the context of Trp53 heterozygosity. Oncogene (2013) 32, 397--402; doi:10.1038/onc.2012.56; published online 27 February 2012 Keywords: p53; Jdp2; transposon; heterozygosity; lymphoma; mice INTRODUCTION targeted by transposon insertion events leading to upregulated Genetic alterations of TP53 are frequent events in tumourigenesis Jdp2 expression and a decrease in Trp53 expression levels. Further and promote genomic instability, impair apoptosis, and contribute we illustrate that Jdp2 regulates the Trp53 promoter via an atypical to aberrant self-renewal.1--4 The spectrum of mutations that occur AP-1 binding site. -
Heterogeneous Nuclear Ribonucleoprotein C1 C2, Mecp1
Heterogeneous nuclear ribonucleoprotein C1͞C2, MeCP1, and SWI͞SNF form a chromatin remodeling complex at the -globin locus control region Milind C. Mahajan*, Geeta J. Narlikar†, Gokul Boyapaty*, Robert E. Kingston‡, and Sherman M. Weissman*§ *Department of Genetics, The Anlyan Center, Yale University School of Medicine, New Haven, CT 06511; †Department of Biochemistry and Biophysics, University of California, San Francisco, CA 94143; and ‡Department of Molecular Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114 Contributed by Sherman M. Weissman, August 31, 2005 Locus control regions (LCRs) are regulatory DNA sequences that are promoter (20–23). These studies suggest the possible association situated many kilobases away from their cognate promoters. LCRs of the LCR with specific chromatin remodeling activities, al- protect transgenes from position effect variegation and hetero- though such a LCR-specific chromatin remodeling activity has chromatinization and also promote copy-number dependence of not been isolated. In the present work, we describe the biochem- the levels of transgene expression. In this work, we describe the ical purification and properties of a previously undescribed biochemical purification of a previously undescribed LCR-associ- chromatin-remodeling complex that binds to the human -globin ated remodeling complex (LARC) that consists of heterogeneous LCR HS2 in a sequence-specific manner. nuclear ribonucleoprotein C1͞C2, nucleosome remodeling SWI͞ SNF, and nucleosome remodeling and deacetylating (NuRD)͞ Materials and Methods MeCP1 as a single homogeneous complex. LARC binds to the Cell Culture and Preparation of Nuclear Extracts. Growth of the K562 hypersensitive 2 (HS2)-Maf recognition element (MARE) DNA in a cells and preparation of the nuclear extract is described in ref. -
The Chemical Defensome of Five Model Teleost Fish
www.nature.com/scientificreports OPEN The chemical defensome of fve model teleost fsh Marta Eide1,5, Xiaokang Zhang2,3,5, Odd André Karlsen1, Jared V. Goldstone4, John Stegeman4, Inge Jonassen2 & Anders Goksøyr1* How an organism copes with chemicals is largely determined by the genes and proteins that collectively function to defend against, detoxify and eliminate chemical stressors. This integrative network includes receptors and transcription factors, biotransformation enzymes, transporters, antioxidants, and metal- and heat-responsive genes, and is collectively known as the chemical defensome. Teleost fsh is the largest group of vertebrate species and can provide valuable insights into the evolution and functional diversity of defensome genes. We have previously shown that the xenosensing pregnane x receptor (pxr, nr1i2) is lost in many teleost species, including Atlantic cod (Gadus morhua) and three-spined stickleback (Gasterosteus aculeatus), but it is not known if compensatory mechanisms or signaling pathways have evolved in its absence. In this study, we compared the genes comprising the chemical defensome of fve fsh species that span the teleosteii evolutionary branch often used as model species in toxicological studies and environmental monitoring programs: zebrafsh (Danio rerio), medaka (Oryzias latipes), Atlantic killifsh (Fundulus heteroclitus), Atlantic cod, and three-spined stickleback. Genome mining revealed evolved diferences in the number and composition of defensome genes that can have implication for how these species sense and respond to environmental pollutants, but we did not observe any candidates of compensatory mechanisms or pathways in cod and stickleback in the absence of pxr. The results indicate that knowledge regarding the diversity and function of the defensome will be important for toxicological testing and risk assessment studies. -
NF-E2p18/Mafk Is Required in DMSO-Induced Differentiation Of
Leukemia (1997) 11, 273–280 1997 Stockton Press All rights reserved 0887-6924/97 $12.00 NF-E2p18/mafK is required in DMSO-induced differentiation of Friend erythroleukemia cells by enhancing NF-E2 activity C Francastel, V Poindessous-Jazat, Y Augery-Bourget and J Robert-Le´ze´ne`s INSERM U268, Hoˆpital Paul Brousse, 94800 Villejuif, France When Friend murine erythroleukemia (F-MEL) cells are induced (LCR).6 The b-globin complex LCR (b-LCR) include four to differentiate by dimethylsulfoxide (DMSO), erythroid-specific erythroid-specific DNasel hypersensitive sites (designated HS- genes are transcriptionally activated. The erythroid transcrip- 1 to HS-4) and acts as a powerful enhancer of transcription tion factor NF-E2 is essential for enhancer activity of the globin 7,8 locus control regions. NF-E2 functions as a heterocomplex of globin promoters. While all four HS have LCR activity in consisting of a 45-kDa subunit (NF-E2p45) and a 18-kDa sub- transgenic mice, only one region (HS-2) is crucial for unit (NF-E2p18). The larger subunit NF-E2p45 is tissue-restric- enhancer activity when assayed in transient transfection ted and is believed to play a role in globin gene expression in systems.9–11 Within HS-2, the enhancer activity for globin F-MEL cells. The expression of the smaller subunit NF-E2p18, expression requires a tandem repeat of AP-1-like which is a Maf family member (MafK), is cell type- and develop- 12,13 mental stage-specific. We have investigated the possible role elements. This tandem motif was shown to bind two tran- of NF-E2p18 in Friend erythroid differentiation by stably trans- scription factors: the ubiquitous AP-1 protein and the lineage fecting either sense and antisense p18 constructs into differen- limited NF-E2 protein.14,15 The NF-E2 complex is a hetero- tiation-sensitive 745A and partially defective-differentiation dimer of two b-Zip proteins of 45 and 18 kDa.16,17 While NF- TFP10 cell lines. -
Supplementary Table 1
Supplementary Table 1. 492 genes are unique to 0 h post-heat timepoint. The name, p-value, fold change, location and family of each gene are indicated. Genes were filtered for an absolute value log2 ration 1.5 and a significance value of p ≤ 0.05. Symbol p-value Log Gene Name Location Family Ratio ABCA13 1.87E-02 3.292 ATP-binding cassette, sub-family unknown transporter A (ABC1), member 13 ABCB1 1.93E-02 −1.819 ATP-binding cassette, sub-family Plasma transporter B (MDR/TAP), member 1 Membrane ABCC3 2.83E-02 2.016 ATP-binding cassette, sub-family Plasma transporter C (CFTR/MRP), member 3 Membrane ABHD6 7.79E-03 −2.717 abhydrolase domain containing 6 Cytoplasm enzyme ACAT1 4.10E-02 3.009 acetyl-CoA acetyltransferase 1 Cytoplasm enzyme ACBD4 2.66E-03 1.722 acyl-CoA binding domain unknown other containing 4 ACSL5 1.86E-02 −2.876 acyl-CoA synthetase long-chain Cytoplasm enzyme family member 5 ADAM23 3.33E-02 −3.008 ADAM metallopeptidase domain Plasma peptidase 23 Membrane ADAM29 5.58E-03 3.463 ADAM metallopeptidase domain Plasma peptidase 29 Membrane ADAMTS17 2.67E-04 3.051 ADAM metallopeptidase with Extracellular other thrombospondin type 1 motif, 17 Space ADCYAP1R1 1.20E-02 1.848 adenylate cyclase activating Plasma G-protein polypeptide 1 (pituitary) receptor Membrane coupled type I receptor ADH6 (includes 4.02E-02 −1.845 alcohol dehydrogenase 6 (class Cytoplasm enzyme EG:130) V) AHSA2 1.54E-04 −1.6 AHA1, activator of heat shock unknown other 90kDa protein ATPase homolog 2 (yeast) AK5 3.32E-02 1.658 adenylate kinase 5 Cytoplasm kinase AK7 -
Using PU.1 and Jun Dimerization Protein 2 Transcription Factor Expression in Myelodysplastic Syndromes to Predict Treatment Response and Leukaemia Transformation
Annals of Hematology (2019) 98:1529–1531 https://doi.org/10.1007/s00277-019-03627-9 LETTER TO THE EDITOR Using PU.1 and Jun dimerization protein 2 transcription factor expression in myelodysplastic syndromes to predict treatment response and leukaemia transformation Kristian Boasman1 & Matthew James Simmonds1 & Ciaren Graham2 & Yogen Saunthararajah3 & Ciro Roberto Rinaldi1 Received: 2 January 2019 /Accepted: 28 January 2019 /Published online: 5 February 2019 # Springer-Verlag GmbH Germany, part of Springer Nature 2019 Dear Editor, Dimerization Protein 2 (JDP2), a downstream target of Myelodysplastic syndromes (MDS) are malignant disor- PU.1 which represses acetylation of core histones in vitro ders of myeloid progenitors, characterised by bone marrow and in vivo, was significantly suppressed [5]. JDP2 medi- failure, peripheral cytopenias and progression to acute my- ates broader effects on regulation of lineage-differentiation eloid leukaemia (AML) [1]. Currently, the DNA methyl- programs [6, 7] and has also been found downregulated in transferase 1 (DNMT1) depleting drugs 5-azacytidine and AML patients [6] but its role in MDS has not been ex- decitabine are the only drugs approved in the USA to treat plored. In this study, we measured the gene expression of all subtypes of MDS. Unfortunately, only 40–50% of pa- PU.1 and JDP2 in total bone marrow and selected CD34+ tients achieve some response with these drugs, and these cells from 12 newly diagnosed MDS patients stratified ac- are not typically durable beyond some months or years. cording to IPSS-R score (6-low, 3-intermediate, 3-high Whilst it is known, these drugs repressive epigenetic mod- risk), 2 AML patient and 10 normal controls.