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Activated Peripheral-Blood-Derived Mononuclear Cells
Transcription factor expression in lipopolysaccharide- activated peripheral-blood-derived mononuclear cells Jared C. Roach*†, Kelly D. Smith*‡, Katie L. Strobe*, Stephanie M. Nissen*, Christian D. Haudenschild§, Daixing Zhou§, Thomas J. Vasicek¶, G. A. Heldʈ, Gustavo A. Stolovitzkyʈ, Leroy E. Hood*†, and Alan Aderem* *Institute for Systems Biology, 1441 North 34th Street, Seattle, WA 98103; ‡Department of Pathology, University of Washington, Seattle, WA 98195; §Illumina, 25861 Industrial Boulevard, Hayward, CA 94545; ¶Medtronic, 710 Medtronic Parkway, Minneapolis, MN 55432; and ʈIBM Computational Biology Center, P.O. Box 218, Yorktown Heights, NY 10598 Contributed by Leroy E. Hood, August 21, 2007 (sent for review January 7, 2007) Transcription factors play a key role in integrating and modulating system. In this model system, we activated peripheral-blood-derived biological information. In this study, we comprehensively measured mononuclear cells, which can be loosely termed ‘‘macrophages,’’ the changing abundances of mRNAs over a time course of activation with lipopolysaccharide (LPS). We focused on the precise mea- of human peripheral-blood-derived mononuclear cells (‘‘macro- surement of mRNA concentrations. There is currently no high- phages’’) with lipopolysaccharide. Global and dynamic analysis of throughput technology that can precisely and sensitively measure all transcription factors in response to a physiological stimulus has yet to mRNAs in a system, although such technologies are likely to be be achieved in a human system, and our efforts significantly available in the near future. To demonstrate the potential utility of advanced this goal. We used multiple global high-throughput tech- such technologies, and to motivate their development and encour- nologies for measuring mRNA levels, including massively parallel age their use, we produced data from a combination of two distinct signature sequencing and GeneChip microarrays. -
Molecular Profile of Tumor-Specific CD8+ T Cell Hypofunction in a Transplantable Murine Cancer Model
Downloaded from http://www.jimmunol.org/ by guest on September 25, 2021 T + is online at: average * The Journal of Immunology , 34 of which you can access for free at: 2016; 197:1477-1488; Prepublished online 1 July from submission to initial decision 4 weeks from acceptance to publication 2016; doi: 10.4049/jimmunol.1600589 http://www.jimmunol.org/content/197/4/1477 Molecular Profile of Tumor-Specific CD8 Cell Hypofunction in a Transplantable Murine Cancer Model Katherine A. Waugh, Sonia M. Leach, Brandon L. Moore, Tullia C. Bruno, Jonathan D. Buhrman and Jill E. Slansky J Immunol cites 95 articles Submit online. Every submission reviewed by practicing scientists ? is published twice each month by Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts http://jimmunol.org/subscription Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html http://www.jimmunol.org/content/suppl/2016/07/01/jimmunol.160058 9.DCSupplemental This article http://www.jimmunol.org/content/197/4/1477.full#ref-list-1 Information about subscribing to The JI No Triage! Fast Publication! Rapid Reviews! 30 days* Why • • • Material References Permissions Email Alerts Subscription Supplementary The Journal of Immunology The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2016 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. This information is current as of September 25, 2021. The Journal of Immunology Molecular Profile of Tumor-Specific CD8+ T Cell Hypofunction in a Transplantable Murine Cancer Model Katherine A. -
A Genome-Wide Analysis of the ERF Gene Family in Sorghum
A genome-wide analysis of the ERF gene family in sorghum H.W. Yan, L. Hong, Y.Q. Zhou, H.Y. Jiang, S.W. Zhu, J. Fan and B.J. Cheng Key Laboratory of Crop Biology of Anhui Province, Anhui Agricultural University, Hefei, China Corresponding author: B.J. Cheng E-mail: [email protected] Genet. Mol. Res. 12 (2): 2038-2055 (2013) Received November 9, 2012 Accepted March 8, 2013 Published May 13, 2013 DOI http://dx.doi.org/10.4238/2013.May.13.1 ABSTRACT. The ethylene response factor (ERF) family are members of the APETALA2 (AP2)/ERF transcription factor superfamily; they are known to play an important role in plant adaptation to biotic and abiotic stress. ERF genes have been studied in Arabidopsis, rice, grape, and maize; however, there are few reports of ERF genes in sorghum. We identified 105 sorghum ERF (SbERF) genes, which were categorized into 12 groups (A-1 to A-6 and B-1 to B-6) based on their sequence similarity, and this new method of classification for ERF genes was then further characterized. A comprehensive bioinformatic analysis of SbERF genes was performed using a sorghum genomic database, to analyze the phylogeny of SbERF genes, identify other conserved motifs apart from the AP2/ERF domain, map SbERF genes to the 10 sorghum chromosomes, and determine the tissue-specific expression patterns of SbERF genes. Gene clustering indicates that SbERF genes were generated by tandem duplications. Comparison of SbERF genes with maize ERF homologs suggests lateral gene transfer between monocot species. These results can contribute to our understanting of Genetics and Molecular Research 12 (2): 2038-2055 (2013) ©FUNPEC-RP www.funpecrp.com.br Analysis of the ERF gene family in sorghum 2039 the evolution of the ERF gene family. -
Supplemental Materials ZNF281 Enhances Cardiac Reprogramming
Supplemental Materials ZNF281 enhances cardiac reprogramming by modulating cardiac and inflammatory gene expression Huanyu Zhou, Maria Gabriela Morales, Hisayuki Hashimoto, Matthew E. Dickson, Kunhua Song, Wenduo Ye, Min S. Kim, Hanspeter Niederstrasser, Zhaoning Wang, Beibei Chen, Bruce A. Posner, Rhonda Bassel-Duby and Eric N. Olson Supplemental Table 1; related to Figure 1. Supplemental Table 2; related to Figure 1. Supplemental Table 3; related to the “quantitative mRNA measurement” in Materials and Methods section. Supplemental Table 4; related to the “ChIP-seq, gene ontology and pathway analysis” and “RNA-seq” and gene ontology analysis” in Materials and Methods section. Supplemental Figure S1; related to Figure 1. Supplemental Figure S2; related to Figure 2. Supplemental Figure S3; related to Figure 3. Supplemental Figure S4; related to Figure 4. Supplemental Figure S5; related to Figure 6. Supplemental Table S1. Genes included in human retroviral ORF cDNA library. Gene Gene Gene Gene Gene Gene Gene Gene Symbol Symbol Symbol Symbol Symbol Symbol Symbol Symbol AATF BMP8A CEBPE CTNNB1 ESR2 GDF3 HOXA5 IL17D ADIPOQ BRPF1 CEBPG CUX1 ESRRA GDF6 HOXA6 IL17F ADNP BRPF3 CERS1 CX3CL1 ETS1 GIN1 HOXA7 IL18 AEBP1 BUD31 CERS2 CXCL10 ETS2 GLIS3 HOXB1 IL19 AFF4 C17ORF77 CERS4 CXCL11 ETV3 GMEB1 HOXB13 IL1A AHR C1QTNF4 CFL2 CXCL12 ETV7 GPBP1 HOXB5 IL1B AIMP1 C21ORF66 CHIA CXCL13 FAM3B GPER HOXB6 IL1F3 ALS2CR8 CBFA2T2 CIR1 CXCL14 FAM3D GPI HOXB7 IL1F5 ALX1 CBFA2T3 CITED1 CXCL16 FASLG GREM1 HOXB9 IL1F6 ARGFX CBFB CITED2 CXCL3 FBLN1 GREM2 HOXC4 IL1F7 -
Gene Expression Analysis of Angioimmunoblastic Lymphoma Indicates Derivation from T Follicular Helper Cells and Vascular Endothelial Growth Factor Deregulation
Research Article Gene Expression Analysis of Angioimmunoblastic Lymphoma Indicates Derivation from T Follicular Helper Cells and Vascular Endothelial Growth Factor Deregulation Pier Paolo Piccaluga,1,2 Claudio Agostinelli,1 Andrea Califano,3 Antonino Carbone,4 Luca Fantoni,6 Sergio Ferrari,5 Anna Gazzola,1 Annunziata Gloghini,6 Simona Righi,1 Maura Rossi,1 Enrico Tagliafico,5 Pier Luigi Zinzani,1 Simonetta Zupo,7 Michele Baccarani,1 and Stefano A. Pileri1 1Institute of Hematology and Medical Oncology ‘‘L. and A. Sera`gnoli,’’ S. Orsola-Malpighi Hospital, University of Bologna, Bologna, Italy; 2Institute for Cancer Genetics and 3Center for Computational Biology and Biochemistry, Columbia University, New York, New York; 4Department of Pathology, Istituto Nazionale Tumori, Milan, Italy; 5Department of Biomedical Sciences, University of Modena and Reggio Emilia, Modena, Italy; 6Division of Experimental Oncology, Centro di Riferimento Oncologico, Aviano, Italy; and 7S.S.D. Diagnostica Malattie Linfoproliferative, Istituto Nazionale per la Ricerca sul Cancro, Genova, Italy Abstract Introduction Angioimmunoblastic lymphoma (AILT) is the second most Peripheral T-cell lymphomas (PTCL) represent 10% to 15% of common subtype of peripheral T-cell lymphoma (PTCL) and all lymphoid neoplasms (1). They are a heterogeneous group of is characterized by dismal prognosis. Thus far, only a fewstu- tumors that in the Revised European-American Lymphoma dies have dealt with its molecular pathogenesis. We performed (REAL)/WHO classification are subdivided into -
The UVB-Induced Gene Expression Profile of Human Epidermis in Vivo Is Different from That of Cultured Keratinocytes
Oncogene (2006) 25, 2601–2614 & 2006 Nature Publishing Group All rights reserved 0950-9232/06 $30.00 www.nature.com/onc ORIGINAL ARTICLE The UVB-induced gene expression profile of human epidermis in vivo is different from that of cultured keratinocytes CD Enk1, J Jacob-Hirsch2, H Gal3, I Verbovetski4, N Amariglio2, D Mevorach4, A Ingber1, D Givol3, G Rechavi2 and M Hochberg1 1Department of Dermatology, The Hadassah-Hebrew University Medical Center, Jerusalem, Israel; 2Department of Pediatric Hemato-Oncology and Functional Genomics, Safra Children’s Hospital, Sheba Medical Center and Sackler School of Medicine, Tel-Aviv University,Tel Aviv, Israel; 3Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel and 4The Laboratory for Cellular and Molecular Immunology, Department of Medicine, The Hadassah-Hebrew University Medical Center, Jerusalem, Israel In order to obtain a comprehensive picture of the radiation. UVB, with a wavelength range between 290 molecular events regulating cutaneous photodamage of and 320 nm, represents one of the most important intact human epidermis, suction blister roofs obtained environmental hazards affectinghuman skin (Hahn after a single dose of in vivo ultraviolet (UV)B exposure and Weinberg, 2002). To protect itself against the were used for microarray profiling. We found a changed DNA-damaging effects of sunlight, the skin disposes expression of 619 genes. Half of the UVB-regulated genes over highly complicated cellular programs, including had returned to pre-exposure baseline levels at 72 h, cell-cycle arrest, DNA repair and apoptosis (Brash et al., underscoring the transient character of the molecular 1996). Failure in selected elements of these defensive cutaneous UVB response. -
The Eif2 Phosphatase: Characterization and Modulation
The eIF2 phosphatase: characterization and modulation Ana Crespillo Casado Darwin College July 2018 Ana Crespillo Casado The eIF2 phosphatase: characterization and modulation Abstract Cellular needs are fulfilled by the combined activity of functional proteins. Consequently, cells are equipped with a complex proteostatic network that controls protein production in response to cellular requisites. Thereby, protein synthesis is induced or attenuated depending on the particular cellular conditions. One of the mechanisms to control protein synthesis is the phosphorylation of eIF2, which triggers the so-called Integrated Stress Response (ISR). Kinases that sense stresses induce the phosphorylation of eIF2, which, on the one hand, attenuates global rates of protein synthesis and, on the other hand, activates the expression of specific proteins that help to alleviate the stress. One of the proteins preferentially expressed during the ISR is PPP1R15A, a regulatory subunit of Protein Phosphatase 1 (PP1). The PP1/PPP1R15A holophosphatase dephosphorylates eIF2 and terminates the ISR once the stresses are resolved. Hence, eIF2 kinases and phosphatases work together to control levels of phosphorylated eIF2. Maintaining the right balance between the activity of these kinases and phosphatases is important, as is seen by the correlation between their perturbance and the appearance of certain cellular malfunctions or diseases. However, affecting this balance has been also suggested to have beneficial effects. For example, genetic interference with the PPP1R15A regulatory subunit is proposed to confer protection to mice and cells under ER-stress conditions. This observation led to the search for compounds with the ability to modulate the ISR, in particular, by acting on the eIF2 phosphatases. -
University of Birmingham Obeticholic Acid for the Treatment of Primary Biliary Cirrhosis
University of Birmingham Obeticholic acid for the treatment of primary biliary cirrhosis Trivedi, Palak J; Hirschfield, Gideon M; Gershwin, M Eric DOI: 10.1586/17512433.2015.1092381 License: None: All rights reserved Document Version Peer reviewed version Citation for published version (Harvard): Trivedi, PJ, Hirschfield, GM & Gershwin, ME 2016, 'Obeticholic acid for the treatment of primary biliary cirrhosis', Expert Review of Clinical Pharmacology, vol. 9, no. 1, pp. 13-26. https://doi.org/10.1586/17512433.2015.1092381 Link to publication on Research at Birmingham portal Publisher Rights Statement: Eligibility for repository: Checked on 29/2/2016 General rights Unless a licence is specified above, all rights (including copyright and moral rights) in this document are retained by the authors and/or the copyright holders. The express permission of the copyright holder must be obtained for any use of this material other than for purposes permitted by law. •Users may freely distribute the URL that is used to identify this publication. •Users may download and/or print one copy of the publication from the University of Birmingham research portal for the purpose of private study or non-commercial research. •User may use extracts from the document in line with the concept of ‘fair dealing’ under the Copyright, Designs and Patents Act 1988 (?) •Users may not further distribute the material nor use it for the purposes of commercial gain. Where a licence is displayed above, please note the terms and conditions of the licence govern your use of this document. When citing, please reference the published version. Take down policy While the University of Birmingham exercises care and attention in making items available there are rare occasions when an item has been uploaded in error or has been deemed to be commercially or otherwise sensitive. -
Combinatorial Bzip Dimers Display Complex DNA-Binding Specificity Landscapes
Combinatorial bZIP dimers display complex DNA-binding specificity landscapes The MIT Faculty has made this article openly available. Please share how this access benefits you. Your story matters. Citation Rodriguez-Martinez, Jose A et al. “Combinatorial bZIP Dimers Display Complex DNA-Binding Specificity Landscapes.” eLife 6 (2017): n. pag. As Published http://dx.doi.org/10.7554/eLife.19272 Publisher eLife Sciences Publications, Ltd. Version Final published version Citable link http://hdl.handle.net/1721.1/110147 Terms of Use Creative Commons Attribution 4.0 International License Detailed Terms http://creativecommons.org/licenses/by-nc/4.0/ RESEARCH ARTICLE Combinatorial bZIP dimers display complex DNA-binding specificity landscapes Jose´ A Rodrı´guez-Martı´nez1†, Aaron W Reinke2†, Devesh Bhimsaria1,3†, Amy E Keating2,4, Aseem Z Ansari1,5* 1Department of Biochemistry, University of Wisconsin-Madison, Madison, United States; 2Department of Biology, Massachusetts Institute of Technology, Cambridge, United States; 3Department of Electrical and Computer Engineering, University of Wisconsin-Madison, Madison, Unites States; 4Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, United States; 5The Genome Center of Wisconsin, University of Wisconsin-Madison, Madison, United States Abstract How transcription factor dimerization impacts DNA-binding specificity is poorly understood. Guided by protein dimerization properties, we examined DNA binding specificities of 270 human bZIP pairs. DNA interactomes of 80 heterodimers and 22 homodimers revealed that 72% of heterodimer motifs correspond to conjoined half-sites preferred by partnering monomers. Remarkably, the remaining motifs are composed of variably-spaced half-sites (12%) or ‘emergent’ sites (16%) that cannot be readily inferred from half-site preferences of partnering monomers. -
1714 Gene Comprehensive Cancer Panel Enriched for Clinically Actionable Genes with Additional Biologically Relevant Genes 400-500X Average Coverage on Tumor
xO GENE PANEL 1714 gene comprehensive cancer panel enriched for clinically actionable genes with additional biologically relevant genes 400-500x average coverage on tumor Genes A-C Genes D-F Genes G-I Genes J-L AATK ATAD2B BTG1 CDH7 CREM DACH1 EPHA1 FES G6PC3 HGF IL18RAP JADE1 LMO1 ABCA1 ATF1 BTG2 CDK1 CRHR1 DACH2 EPHA2 FEV G6PD HIF1A IL1R1 JAK1 LMO2 ABCB1 ATM BTG3 CDK10 CRK DAXX EPHA3 FGF1 GAB1 HIF1AN IL1R2 JAK2 LMO7 ABCB11 ATR BTK CDK11A CRKL DBH EPHA4 FGF10 GAB2 HIST1H1E IL1RAP JAK3 LMTK2 ABCB4 ATRX BTRC CDK11B CRLF2 DCC EPHA5 FGF11 GABPA HIST1H3B IL20RA JARID2 LMTK3 ABCC1 AURKA BUB1 CDK12 CRTC1 DCUN1D1 EPHA6 FGF12 GALNT12 HIST1H4E IL20RB JAZF1 LPHN2 ABCC2 AURKB BUB1B CDK13 CRTC2 DCUN1D2 EPHA7 FGF13 GATA1 HLA-A IL21R JMJD1C LPHN3 ABCG1 AURKC BUB3 CDK14 CRTC3 DDB2 EPHA8 FGF14 GATA2 HLA-B IL22RA1 JMJD4 LPP ABCG2 AXIN1 C11orf30 CDK15 CSF1 DDIT3 EPHB1 FGF16 GATA3 HLF IL22RA2 JMJD6 LRP1B ABI1 AXIN2 CACNA1C CDK16 CSF1R DDR1 EPHB2 FGF17 GATA5 HLTF IL23R JMJD7 LRP5 ABL1 AXL CACNA1S CDK17 CSF2RA DDR2 EPHB3 FGF18 GATA6 HMGA1 IL2RA JMJD8 LRP6 ABL2 B2M CACNB2 CDK18 CSF2RB DDX3X EPHB4 FGF19 GDNF HMGA2 IL2RB JUN LRRK2 ACE BABAM1 CADM2 CDK19 CSF3R DDX5 EPHB6 FGF2 GFI1 HMGCR IL2RG JUNB LSM1 ACSL6 BACH1 CALR CDK2 CSK DDX6 EPOR FGF20 GFI1B HNF1A IL3 JUND LTK ACTA2 BACH2 CAMTA1 CDK20 CSNK1D DEK ERBB2 FGF21 GFRA4 HNF1B IL3RA JUP LYL1 ACTC1 BAG4 CAPRIN2 CDK3 CSNK1E DHFR ERBB3 FGF22 GGCX HNRNPA3 IL4R KAT2A LYN ACVR1 BAI3 CARD10 CDK4 CTCF DHH ERBB4 FGF23 GHR HOXA10 IL5RA KAT2B LZTR1 ACVR1B BAP1 CARD11 CDK5 CTCFL DIAPH1 ERCC1 FGF3 GID4 HOXA11 IL6R KAT5 ACVR2A -
The Cis-Trans Binding Strength Defined by Motif Frequencies Facilitates Statistical Inference of Transcriptional Regulation
Feng et al. BMC Bioinformatics 2019, 20(Suppl 7):201 https://doi.org/10.1186/s12859-019-2732-6 RESEARCH Open Access The cis-trans binding strength defined by motif frequencies facilitates statistical inference of transcriptional regulation Yance Feng1,2†, Sheng Zhang1,2†, Liang Li1,2 and Lei M. Li1,2,3* From The 12th International Conference on Computational Systems Biology (ISB 2018) Guiyang, China. 18-21 August 2018 Abstract Background: A key problem in systems biology is the determination of the regulatory mechanism corresponding to a phenotype. An empirical approach in this regard is to compare the expression profiles of cells under two conditions or tissues from two phenotypes and to unravel the underlying transcriptional regulation. We have proposed the method BASE to statistically infer the effective regulatory factors that are responsible for the gene expression differentiation with the help from the binding data between factors and genes. Usually the protein-DNA binding data are obtained by ChIP-seq experiments, which could be costly and are condition-specific. Results: Here we report a definition of binding strength based on a probability model. Using this condition-free definition, the BASE method needs only the frequencies of cis-motifs in regulatory regions, thereby the inferences can be carried out in silico. The directional regulation can be inferred by considering down- and up-regulation separately.Weshowedtheeffectivenessoftheapproachbyonecasestudy.Inthestudyoftheeffectsof polyunsaturated fatty acids (PUFA), namely, docosahexaenoic (DHA) and eicosapentaenoic (EPA) diets on mouse small intestine cells, the inferences of regulations are consistent with those reported in the literature, including PPARα and NFκB, respectively corresponding to enhanced adipogenesis and reduced inflammation. -
PPP1R15A-Mediated Dephosphorylation of Eif2a
RESEARCH ARTICLE PPP1R15A-mediated dephosphorylation of eIF2a is unaffected by Sephin1 or Guanabenz Ana Crespillo-Casado1*, Joseph E Chambers1, Peter M Fischer2,3, Stefan J Marciniak1, David Ron1* 1Cambridge Institute for Medical Research, University of Cambridge, Cambridge, United Kingdom; 2Division of Biomolecular Science and Medicinal Chemistry, School of Pharmacy, University of Nottingham, Nottingham, United Kingdom; 3Centre for Biomolecular Sciences, University of Nottingham, Nottingham, United Kingdom Abstract Dephosphorylation of translation initiation factor 2 (eIF2a) terminates signalling in the mammalian integrated stress response (ISR) and has emerged as a promising target for modifying the course of protein misfolding diseases. The [(o-chlorobenzylidene)amino]guanidines (Guanabenz and Sephin1) have been proposed to exert protective effects against misfolding by interfering with eIF2a-P dephosphorylation through selective disruption of a PP1-PPP1R15A holophosphatase complex. Surprisingly, they proved inert in vitro affecting neither stability of the PP1-PPP1R15A complex nor substrate-specific dephosphorylation. Furthermore, eIF2a-P dephosphorylation, assessed by a kinase shut-off experiment, progressed normally in Sephin1-treated cells. Consistent with its role in defending proteostasis, Sephin1 attenuated the IRE1 branch of the endoplasmic reticulum unfolded protein response. However, repression was noted in both wildtype and Ppp1r15a deleted cells and in cells rendered ISR-deficient by CRISPR editing of the Eif2s1 locus to encode a non-phosphorylatable eIF2a (eIF2aS51A). These findings challenge the view that [(o- chlorobenzylidene)amino]guanidines restore proteostasis by interfering with eIF2a-P *For correspondence: ac880@ dephosphorylation. cam.ac.uk (AC-C); dr360@ DOI: 10.7554/eLife.26109.001 medschl.cam.ac.uk (DR) Competing interest: See page 26 Introduction Funding: See page 26 Protein folding homeostasis (proteostasis) is achieved by balancing the rate of production, folding Received: 16 February 2017 and protein degradation.