Transcriptome Analysis of Gravitational Effects on Mouse Skeletal Muscles Under Microgravity and Artificial 1 G Onboard Environm
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The Role of PU.1 and GATA-1 Transcription Factors During Normal and Leukemogenic Hematopoiesis
Leukemia (2010) 24, 1249–1257 & 2010 Macmillan Publishers Limited All rights reserved 0887-6924/10 www.nature.com/leu REVIEW The role of PU.1 and GATA-1 transcription factors during normal and leukemogenic hematopoiesis P Burda1, P Laslo2 and T Stopka1,3 1Department of Pathophysiology and Center of Experimental Hematology, First Faculty of Medicine, Charles University, Prague, Czech Republic; 2Section of Experimental Haematology, Leeds Institute of Molecular Medicine, University of Leads, St James’s University Hospital, Leeds, UK and 31st Department of Medicine-Hematology, General University Hospital, Prague, Czech Republic Hematopoiesis is coordinated by a complex regulatory network Additional domains include an N-terminal acidic domain and a of transcription factors and among them PU.1 (Spi1, Sfpi1) glutamine-rich domain, both involved in transcriptional activa- represents a key molecule. This review summarizes the tion, as well as a PEST domain involved in protein–protein indispensable requirement of PU.1 during hematopoietic cell fate decisions and how the function of PU.1 can be modulated interactions. PU.1 protein can be modified post-translationally by protein–protein interactions with additional factors. The by phosporylation at serines 41 (N-terminal acidic domain) and mutual negative regulation between PU.1 and GATA-1 is 142 and 148 (PEST domain), which results in augmented detailed within the context of normal and leukemogenic activity. hematopoiesis and the concept of ‘differentiation therapy’ to The PU.1 protein can physically interact with a variety of restore normal cellular differentiation of leukemic cells is regulatory factors including (i) general transcription factors discussed. Leukemia (2010) 24, 1249–1257; doi:10.1038/leu.2010.104; (TFIID, TBP), (ii) early hematopoietic transcription factors published online 3 June 2010 (GATA-2 and Runx-1), (iii) erythroid factor (GATA-1) and (iv) Keywords: PU.1; leukemia differentiation; GATA-1; chromatin; non-erythroid factors (C/EBPa, C/EBPb, IRF4/8 and c-Jun). -
5045.Full.Pdf
IFN Consensus Sequence Binding Protein (Icsbp) Is Critical for Eosinophil Development This information is current as Maja Milanovic, Grzegorz Terszowski, Daniela Struck, of September 28, 2021. Oliver Liesenfeld and Dirk Carstanjen J Immunol 2008; 181:5045-5053; ; doi: 10.4049/jimmunol.181.7.5045 http://www.jimmunol.org/content/181/7/5045 Downloaded from References This article cites 47 articles, 33 of which you can access for free at: http://www.jimmunol.org/content/181/7/5045.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 28, 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 © 2008 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology IFN Consensus Sequence Binding Protein (Icsbp) Is Critical for Eosinophil Development1 Maja Milanovic,2* Grzegorz Terszowski,2† Daniela Struck,2‡ Oliver Liesenfeld,‡ and Dirk Carstanjen3* IFN consensus sequence binding protein (Icsbp) (IFN response factor-8) is a hematopoietic transcription factor with dual functions in myelopoiesis and immunity. -
Expression of Wilms Tumor 1 Gene Distinguishes Vascular Malformations from Proliferative Endothelial Lesions
OBSERVATION Expression of Wilms Tumor 1 Gene Distinguishes Vascular Malformations From Proliferative Endothelial Lesions Leslie P. Lawley, MD; Francesca Cerimele, MD, PhD; Sharon W. Weiss, MD; Paula North, MD; Cynthia Cohen, MD; Harry P. W. Kozakewich, MD; John B. Mulliken, MD; Jack L. Arbiser, MD, PhD Background: Vascular malformations and hemangio- Observations: The biochemical differences between mas, which are endothelial lesions of childhood, may re- hemangiomas, which involute, and vascular malforma- sult in considerable morbidity because they can cause dis- tions, which do not involute, are not well understood. comfort and functional impairment and have a negative We found that the transcription factor encoded by the affect on the patient’s appearance. Although vascular mal- Wilms tumor 1 (WT1) gene is expressed in the endothe- formations may initially appear very similar to heman- lium of hemangiomas but not in vascular malforma- giomas, they have distinct clinical courses. Infantile hem- tions. angiomas progress through 3 stages: proliferative, involuting, and involuted. The proliferative phase is char- Conclusions: Defects in WT1 signaling may underlie the acterized by clinical growth. Once hemangiomas reach inability of malformation endothelial cells to undergo their maximum size, they begin to regress or involute. physiologic apoptosis and remodeling. The availability Histologically, this stage is characterized by endothelial of WT1 staining in hospital laboratories may allow the apoptosis. Finally, the involuted stage of the heman- clinician to distinguish hemangiomas from vascular mal- gioma occurs when the original lesion is replaced by a formations and thus to give appropriate therapy to the connective tissue remnant. In contrast to hemangio- patient. mas, vascular malformations do not involute but con- tinue to enlarge as the patient grows. -
L-Type Cav 1.2 Calcium Channel-Α-1C Regulates Response to Rituximab in Diffuse Large B-Cell Lymphoma
Published OnlineFirst March 1, 2019; DOI: 10.1158/1078-0432.CCR-18-2146 Translational Cancer Mechanisms and Therapy Clinical Cancer Research L-Type Cav 1.2 Calcium Channel-a-1C Regulates Response to Rituximab in Diffuse Large B-Cell Lymphoma Jiu-Yang Zhang1, Pei-Pei Zhang1,Wen-Ping Zhou1, Jia-Yu Yu2, Zhi-Hua Yao1, Jun-Feng Chu1, Shu-Na Yao1, Cheng Wang2, Waseem Lone2, Qing-Xin Xia3, Jie Ma3, Shu-Jun Yang1, Kang-Dong Liu4,5, Zi-Gang Dong4, Yong-Jun Guo3, Lynette M. Smith6, Timothy W. McKeithan7, Wing C. Chan7, Javeed Iqbal2, and Yan-Yan Liu1 Abstract Purpose: One third of patients with diffuse large B-cell an independent prognostic factor for RCHOP resistance after lymphoma (DLBCL) succumb to the disease partly due to adjusting for International Prognostic Index, cell-of-origin rituximab resistance. Rituximab-induced calcium flux is an classification, and MYC/BCL2 double expression. Loss of important inducer of apoptotic cell death, and we investigated CACNA1C expression reduced rituximab-induced apoptosis the potential role of calcium channels in rituximab resistance. and tumor shrinkage. We further demonstrated direct inter- Experimental Design: The distinctive expression of calcium action of CACNA1C with CD20 and its role in CD20 stabi- channel members was compared between patients sensitive lization. Functional modulators of L-type calcium channel and resistant to rituximab, cyclophosphamide, vincristine, showed expected alteration in rituximab-induced apoptosis doxorubicin, prednisone (RCHOP) regimen. The observation and tumor suppression. Furthermore, we demonstrated that was further validated through mechanistic in vitro and in vivo CACNA1C expression was directly regulated by miR-363 studies using cell lines and patient-derived xenograft mouse whose high expression is associated with worse prognosis in models. -
Letters to the Editor
LETTERS TO THE EDITOR The significant upregulation of Gata1 and EpoR mRNA Mice over-expressing human erythropoietin expression in hEPO over-expressing tg6 mice was con - indicate that erythropoietin enhances expression firmed by analyzing the spleen as a major source of of its receptor via up-regulated Gata1 and Tal1 hematopoiesis (Figure 2A and B). To further dissect the complexity of changes in the transcriptional network, the analysis of Myb mRNA expression served as marker for The development of medullary hematopoiesis is char - adult definitive erythroblasts, 10 showing significantly acterized by a specific expression profile of hematopoiet - ic transcription factors, including GATA transcription fac - tors. At mid-gestation, when hematopoiesis is newly A GATA 1 2 established in the bone marrow of human fetuses, initial - wt ly high GATA2 expression becomes subsequently down- regulated, while GATA1 expression increases in parallel. 1 1.5 Both transcription factors bind to overlapping sets of tg6 hematopoietic downstream target genes, often at distinct 1 sites, to regulate the balance between proliferation and differentiation. Chromatin occupancy by GATA1 and 0.5 GATA2 can change in the course of hematopoietic differ - entiation, leading to the so-called GATA switch. 2 Thus, a 0 n d7 d21 d49 i spatio-temporal regulation of GATA1 or GATA2 activities t c is required within lineage-specific differentiation. During a - erythroid differentiation GATA1 expression peaks at the b B GATA 2 3 o level of colony-forming units (CFU-E), where erythro - t 2 e poietin (Epo) exerts most specifically its effects, but v i t blocks terminal maturation if constitutively over- a 1.5 l 4 e expressed. -
Enhancer of WT1 Gene Is Essential for Its Transcription in Acute Leukemia and Solid Tumor Cell Lines
Leukemia (2009) 23, 1270–1277 & 2009 Macmillan Publishers Limited All rights reserved 0887-6924/09 $32.00 www.nature.com/leu ORIGINAL ARTICLE GATA-1 and GATA-2 binding to 30 enhancer of WT1 gene is essential for its transcription in acute leukemia and solid tumor cell lines A Furuhata1, M Murakami1, H Ito1, S Gao1, K Yoshida1, S Sobue2, R Kikuchi3, T Iwasaki3, A Takagi1, T Kojima1, M Suzuki4, A Abe5, T Naoe5 and T Murate1 1Department of Medical Technology, Nagoya University Graduate School of Health Sciences, Nagoya, Japan; 2Department of Pathology, College of Life and Health Sciences, Chubu University, Kasugai, Japan; 3Department of Laboratory Medicine, Nagoya University School of Medicine, Nagoya, Japan; 4Division of Molecular Carcinogenesis, Nagoya University Graduate School of Medicine, Nagoya, Japan and 5Department of Hematology and Oncology, Nagoya University Graduate School of Medicine, Nagoya, Japan Although oncogenic functions and the clinical significance of WT1 have been well documented, its gene-expression mecha- Wilms tumor 1 (WT1) have been extensively studied in acute nism remains undetermined. leukemia, the regulatory mechanism of its transcription still 13 remains to be determined. We found a significant correlation In the promoter analysis of WT1 gene, Cohen et al. reported among the amounts of WT1, GATA-1 and GATA-2 mRNAs from the importance of Sp1 for mRNA expression, although the leukemia and solid tumor cell lines. Overexpression and small promoter region may not determine the tissue-specific manner interfering RNA (siRNA) transfection experiments of GATA-1 of WT1 expression.13,14 Regarding this point, the 30 enhancer and GATA-2 showed that these GATA transcription factors located 450 kb downstream of the promoter was identified as could induce WT1 expression. -
Supplementary Table 2
Supplementary Table 2. Differentially Expressed Genes following Sham treatment relative to Untreated Controls Fold Change Accession Name Symbol 3 h 12 h NM_013121 CD28 antigen Cd28 12.82 BG665360 FMS-like tyrosine kinase 1 Flt1 9.63 NM_012701 Adrenergic receptor, beta 1 Adrb1 8.24 0.46 U20796 Nuclear receptor subfamily 1, group D, member 2 Nr1d2 7.22 NM_017116 Calpain 2 Capn2 6.41 BE097282 Guanine nucleotide binding protein, alpha 12 Gna12 6.21 NM_053328 Basic helix-loop-helix domain containing, class B2 Bhlhb2 5.79 NM_053831 Guanylate cyclase 2f Gucy2f 5.71 AW251703 Tumor necrosis factor receptor superfamily, member 12a Tnfrsf12a 5.57 NM_021691 Twist homolog 2 (Drosophila) Twist2 5.42 NM_133550 Fc receptor, IgE, low affinity II, alpha polypeptide Fcer2a 4.93 NM_031120 Signal sequence receptor, gamma Ssr3 4.84 NM_053544 Secreted frizzled-related protein 4 Sfrp4 4.73 NM_053910 Pleckstrin homology, Sec7 and coiled/coil domains 1 Pscd1 4.69 BE113233 Suppressor of cytokine signaling 2 Socs2 4.68 NM_053949 Potassium voltage-gated channel, subfamily H (eag- Kcnh2 4.60 related), member 2 NM_017305 Glutamate cysteine ligase, modifier subunit Gclm 4.59 NM_017309 Protein phospatase 3, regulatory subunit B, alpha Ppp3r1 4.54 isoform,type 1 NM_012765 5-hydroxytryptamine (serotonin) receptor 2C Htr2c 4.46 NM_017218 V-erb-b2 erythroblastic leukemia viral oncogene homolog Erbb3 4.42 3 (avian) AW918369 Zinc finger protein 191 Zfp191 4.38 NM_031034 Guanine nucleotide binding protein, alpha 12 Gna12 4.38 NM_017020 Interleukin 6 receptor Il6r 4.37 AJ002942 -
Pflugers Final
CORE Metadata, citation and similar papers at core.ac.uk Provided by Serveur académique lausannois A comprehensive analysis of gene expression profiles in distal parts of the mouse renal tubule. Sylvain Pradervand2, Annie Mercier Zuber1, Gabriel Centeno1, Olivier Bonny1,3,4 and Dmitri Firsov1,4 1 - Department of Pharmacology and Toxicology, University of Lausanne, 1005 Lausanne, Switzerland 2 - DNA Array Facility, University of Lausanne, 1015 Lausanne, Switzerland 3 - Service of Nephrology, Lausanne University Hospital, 1005 Lausanne, Switzerland 4 – these two authors have equally contributed to the study to whom correspondence should be addressed: Dmitri FIRSOV Department of Pharmacology and Toxicology, University of Lausanne, 27 rue du Bugnon, 1005 Lausanne, Switzerland Phone: ++ 41-216925406 Fax: ++ 41-216925355 e-mail: [email protected] and Olivier BONNY Department of Pharmacology and Toxicology, University of Lausanne, 27 rue du Bugnon, 1005 Lausanne, Switzerland Phone: ++ 41-216925417 Fax: ++ 41-216925355 e-mail: [email protected] 1 Abstract The distal parts of the renal tubule play a critical role in maintaining homeostasis of extracellular fluids. In this review, we present an in-depth analysis of microarray-based gene expression profiles available for microdissected mouse distal nephron segments, i.e., the distal convoluted tubule (DCT) and the connecting tubule (CNT), and for the cortical portion of the collecting duct (CCD) (Zuber et al., 2009). Classification of expressed transcripts in 14 major functional gene categories demonstrated that all principal proteins involved in maintaining of salt and water balance are represented by highly abundant transcripts. However, a significant number of transcripts belonging, for instance, to categories of G protein-coupled receptors (GPCR) or serine-threonine kinases exhibit high expression levels but remain unassigned to a specific renal function. -
Differentially Methylated Genes
10/30/2013 Disclosures Key Rheumatoid Arthritis-Associated Pathogenic Pathways Revealed by Integrative Analysis of RA Omics Datasets Consultant: IGNYTA Funding: Rheumatology Research Foundation By John W. Whitaker, Wei Wang and Gary S. Firestein DNA methylation and gene regulation The RA methylation signature in FLS DNA methylation – DNMT1 (maintaining methylation) OA – DNMT3a, 3b (de novo methylation) RA % of CpG methylation: 0% 100% Nakano et al. 2013 ARD AA06 AANAT AARS ABCA6 ABCC12 ABCG1 ABHD8 ABL2 ABR ABRA ACACA ACAN ACAP3 ACCSL ACN9 ACOT7 ACOX2 ACP5 ACP6 ACPP ACSL1 ACSL3 ACSM5 ACVRL1 ADAM10 ADAM32 ADAM33 ADAMTS12 ADAMTS15 ADAMTS19 ADAMTS4 ADAT3 ADCK4 ADCK5 ADCY2 ADCY3 ADCY6 ADORA1 ADPGK ADPRHL1 ADTRP AFAP1 AFAP1L2 AFF3 AFG3L1P AGAP11 AGER AGTR1 AGXT AIF1L AIM2 AIRE AJUBA AK4 AKAP12 AKAP2 AKR1C2 AKR1E2 AKT2 ALAS1 ALDH1L1-AS1 ALDH3A1 ALDH3B1 ALDH8A1 ALDOB ALDOC ALOX12 ALPK3 ALS2CL ALX4 AMBRA1 AMPD2 AMPD3 ANGPT1 ANGPT2 ANGPTL5 ANGPTL6 ANK1 ANKMY2 ANKRD29 ANKRD37 ANKRD53 ANO3 ANO6 ANO7 ANP32C ANXA6 ANXA8L2 AP1G1 AP2A2 AP2M1 AP5B1 APBA2 APC APCDD1 APOBEC3B APOBEC3G APOC1 APOH APOL6 APOLD1 APOM AQP1 AQP10 AQP6 AQP9 ARAP1 ARHGAP24 ARHGAP42 ARHGEF19 ARHGEF25 ARHGEF3 ARHGEF37 ARHGEF7 ARL4C ARL6IP 5 ARL8B ARMC3 ARNTL2 ARPP21 ARRB1 ARSI ASAH2B ASB10 ASB2 ASCL2 ASIC4 ASPH ATF3 ATF7 ATL1 ATL3 ATP10A ATP1A1 ATP1A4 ATP2C1 ATP5A1 ATP5EP2 ATP5L2 ATP6V0CP3 ATP6V1C1 ATP6V1E2 ATXN7L1 ATXN7L2 AVPI1 AXIN2 B3GNT7 B3GNT8 B3GNTL1 BACH1 BAG3 Differential methylated genes in RA FLS BAIAP2L2 BANP BATF BATF2 BBS2 BCAS4 BCAT1 BCL7C BDKRB2 BEGAIN BEST1 BEST3 -
GATA1 Gene GATA Binding Protein 1
GATA1 gene GATA binding protein 1 Normal Function The GATA1 gene provides instructions for making a protein that attaches (binds) to specific regions of DNA and helps control the activity of many other genes. On the basis of this action, the GATA1 protein is known as a transcription factor. The GATA1 protein is involved in the specialization (differentiation) of immature blood cells. To function properly, these immature cells must differentiate into specific types of mature blood cells. By binding to DNA and interacting with other proteins, the GATA1 protein regulates the growth and division (proliferation) of immature red blood cells and platelet-precursor cells (megakaryocytes) to facilitate their differentiation. Red blood cells help carry oxygen to various tissues throughout the body and platelets aid in blood clotting. The GATA1 protein is also important for the maturation of several types of white blood cells that help fight infection, including eosinophils, mast cells, and dendritic cells. Two versions of the GATA1 protein are produced from the GATA1 gene: a regular length protein and a shorter version called GATA1s. The GATA1s protein lacks a specific region called the transactivation domain. Although the specific function of this region is unclear, researchers believe that it interacts with other proteins to modify GATA1 protein function. Health Conditions Related to Genetic Changes Dyserythropoietic anemia and thrombocytopenia At least eight different mutations in the GATA1 gene have been found to cause dyserythropoietic anemia and thrombocytopenia. Most of these mutations change a single protein building block (amino acid) in the GATA1 protein. GATA1 gene mutations disrupt the protein's ability to bind with DNA or interact with other proteins. -
Germline Mutations in Etv6 Result in Autosomal Dominant
GERMLINE MUTATIONS IN ETV6 RESULT IN AUTOSOMAL DOMINANT THROMBOCYTOPENIA By LEILA J. NOETZLI B.S., University of California San Diego, 2007 A thesis submitted to the Faculty of the Graduate School of the University of Colorado in partial fulfillment of the requirements for the degree of Doctor of Philosophy Human Medical Genetics and Genomics Program 2017 This thesis for the Doctor of Philosophy degree by Leila J. Noetzli has been approved for the Human Medical Genetics and Genomics Program by Robert Sclafani, Chair Jorge Di Paola, Advisor Jay Hesselberth Richard Spritz Rytis Prekeris Date: May 19, 2017 ii Noetzli, Leila J. (Ph.D., Human Medical Genetics and Genomics) Germline mutations in ETV6 result in autosomal dominant thrombocytopenia Thesis directed by Associate Professor Jorge Di Paola ABSTRACT Whole exome sequencing on a family with autosomal dominant thrombocytopenia and two occurrences of acute lymphoblastic leukemia (ALL) of unknown cause identified a heterozygous single nucleotide change in the gene ETV6, encoding a p.Pro214Leu amino acid substitution. We screened families with the same phenotype and found mutations in ETV6 in two additional families: one with the identical p.Pro214Leu mutation and one with a p.Arg418Gly substitution. ETV6 is a transcriptional repressor that functions through self-oligomerization and is essential for hematopoietic stem cell proliferation and platelet production in mice. Our report was among the first to describe pathogenic germline mutations in ETV6. Functional characterization of the corresponding ETV6 protein mutations showed aberrant cytoplasmic localization, impaired transcriptional repression, and delayed megakaryocyte maturation. Furthermore, we found that mutant ETV6 protein oligomerizes with WT ETV6 and sequesters it from the nucleus suggesting a dominant negative mechanism. -
Global Analysis of Estrogen Receptor Beta Binding to Breast Cancer Cell Genome Reveals an Extensive Interplay with Estrogen Rece
Grober et al. BMC Genomics 2011, 12:36 http://www.biomedcentral.com/1471-2164/12/36 RESEARCHARTICLE Open Access Global analysis of estrogen receptor beta binding to breast cancer cell genome reveals an extensive interplay with estrogen receptor alpha for target gene regulation Oli MV Grober1†, Margherita Mutarelli1†, Giorgio Giurato1, Maria Ravo1,2, Luigi Cicatiello1, Maria Rosaria De Filippo1, Lorenzo Ferraro1, Giovanni Nassa1,2, Maria Francesca Papa1, Ornella Paris1, Roberta Tarallo1,2, Shujun Luo3, Gary P Schroth3, Vladimir Benes4, Alessandro Weisz1,2* Abstract Background: Estrogen receptors alpha (ERa) and beta (ERb) are transcription factors (TFs) that mediate estrogen signaling and define the hormone-responsive phenotype of breast cancer (BC). The two receptors can be found co-expressed and play specific, often opposite, roles, with ERb being able to modulate the effects of ERa on gene transcription and cell proliferation. ERb is frequently lost in BC, where its presence generally correlates with a better prognosis of the disease. The identification of the genomic targets of ERb in hormone-responsive BC cells is thus a critical step to elucidate the roles of this receptor in estrogen signaling and tumor cell biology. Results: Expression of full-length ERb in hormone-responsive, ERa-positive MCF-7 cells resulted in a marked reduction in cell proliferation in response to estrogen and marked effects on the cell transcriptome. By ChIP-Seq we identified 9702 ERb and 6024 ERa binding sites in estrogen-stimulated cells, comprising sites occupied by either ERb,ERa or both ER subtypes. A search for TF binding matrices revealed that the majority of the binding sites identified comprise one or more Estrogen Response Element and the remaining show binding matrixes for other TFs known to mediate ER interaction with chromatin by tethering, including AP2, E2F and SP1.