DOCSLIB.ORG

Supplementary Table 1A. Genes Significantly Altered in A4573 ESFT

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Supplementary Table 1A. Genes Significantly Altered in A4573 ESFT Supplementary Table 1A. Genes significantly altered in A4573 ESFT cells following BMI-1knockdown genesymbol genedescription siControl siBMI1 FC Direction P-value AASS aminoadipate-semialdehyde synthase | tetra-peptide repeat homeobox-like6.68 7.24 1.5 Up 0.007 ABCA2 ATP-binding cassette, sub-family A (ABC1), member 2 | neural5.44 proliferation,6.3 differentiation1.8 and Upcontrol, 1 0.006 ABHD4 abhydrolase domain containing 4 7.51 6.69 1.8 Down 0.002 ACACA acetyl-Coenzyme A carboxylase alpha | peroxiredoxin 5 | similar6.2 to High mobility7.26 group2.1 protein UpB1 (High mobility0.009 group protein 1) (HMG-1) (Amphoterin) (Heparin-binding protein p30) | Coenzyme A synthase ACAD9 acyl-Coenzyme A dehydrogenase family, member 9 9.25 8.59 1.6 Down 0.008 ACBD3 acyl-Coenzyme A binding domain containing 3 7.89 8.53 1.6 Up 0.008 ACCN2 amiloride-sensitive cation channel 2, neuronal 5.47 6.28 1.8 Up 0.005 ACIN1 apoptotic chromatin condensation inducer 1 7.15 7.79 1.6 Up 0.008 ACPL2 acid phosphatase-like 2 6.04 7.6 2.9 Up 0.000 ACSL4 acyl-CoA synthetase long-chain family member 4 6.72 5.8 1.9 Down 0.001 ACTA2 actin, alpha 2, smooth muscle, aorta 9.18 8.44 1.7 Down 0.003 ACYP1 acylphosphatase 1, erythrocyte (common) type 7.09 7.66 1.5 Up 0.009 ADA adenosine deaminase 6.34 7.1 1.7 Up 0.009 ADAL adenosine deaminase-like 7.88 6.89 2.0 Down 0.006 ADAMTS1 ADAM metallopeptidase with thrombospondin type 1 motif, 1 6.57 7.65 2.1 Up 0.000 ADARB1 adenosine deaminase, RNA-specific, B1 (RED1 homolog rat) 6.49 7.13 1.6 Up 0.008 ADCY9 adenylate cyclase 9 6.5 7.18 1.6 Up 0.002 ADCYAP1R1 adenylate cyclase activating polypeptide 1 (pituitary) receptor 5.71type I 6.38 1.6 Up 0.002 ADI1 acireductone dioxygenase 1 6.65 7.35 1.6 Up 0.009 ADRBK1 adrenergic, beta, receptor kinase 1 | ankyrin repeat domain 136.95 family, member7.59 D 1.6 Up 0.002 AES amino-terminal enhancer of split 7.72 8.45 1.7 Up 0.005 AGPAT3 1-acylglycerol-3-phosphate O-acyltransferase 3 9.42 8.76 1.6 Down 0.003 AGPAT5 1-acylglycerol-3-phosphate O-acyltransferase 5 (lysophosphatidic7.16 acid acyltransferase,8.23 2.1 epsilon) Up 0.005 AKAP2 A kinase (PRKA) anchor protein 2 | paralemmin 2 | PALM2-AKAP26.55 protein7.14 1.5 Up 0.005 AKAP8 A kinase (PRKA) anchor protein 8 6.08 7.13 2.1 Up 0.001 AKT1S1 AKT1 substrate 1 (proline-rich) 6.56 7.37 1.8 Up 0.001 ALDH1A3 aldehyde dehydrogenase 1 family, member A3 5.95 6.55 1.5 Up 0.006 ALDH9A1 aldehyde dehydrogenase 9 family, member A1 8.55 9.96 2.7 Up 0.000 AMDHD2 amidohydrolase domain containing 2 | cementum protein 1 7.39 6.66 1.7 Down 0.003 ANAPC1 anaphase promoting complex subunit 1 | 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase7.61 6.95 1.6 Down 2 0.007 ANGPTL2 angiopoietin-like 2 5.95 6.67 1.6 Up 0.007 ANKDD1A ankyrin repeat and death domain containing 1A 5.33 5.97 1.6 Up 0.005 ANKH ankylosis, progressive homolog (mouse) | CHK1 checkpoint homolog6.1 (S. pombe)6.63 1.4 Up 0.006 ANKRD29 ankyrin repeat domain 29 6.05 6.78 1.7 Up 0.002 ANKS1A ankyrin repeat and sterile alpha motif domain containing 1A 6.65 5.85 1.7 Down 0.006 AOF2 amine oxidase (flavin containing) domain 2 | similar to TFIIH basal8.9 transcription9.84 factor 1.9complex Upp44 subunit (Basic0.000 transcription factor 2 44 kDa subunit) (BTF2-p44) (General transcription factor IIH polypeptide 2) APAF1 apoptotic peptidase activating factor 1 8.76 6.92 3.6 Down 0.000 APBB3 amyloid beta (A4) precursor protein-binding, family B, member8.97 3 8.07 1.9 Down 0.002 APCDD1 adenomatosis polyposis coli down-regulated 1 9.22 9.87 1.6 Up 0.002 APEH N-acylaminoacyl-peptide hydrolase | macrophage stimulating, 6.77pseudogene7.46 9 1.6 Up 0.002 API5 apoptosis inhibitor 5 9.69 8.46 2.3 Down 0.000 APLP1 amyloid beta (A4) precursor-like protein 1 5.76 6.6 1.8 Up 0.010 APOBEC3D apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like7.17 3D (putative)6.64 1.4 Down 0.006 ARG2 arginase, type II | similar to High mobility group protein B1 (High5.9 mobility6.78 group protein1.8 1) (HMG-1)Up (Amphoterin)0.001 (Heparin-binding protein p30) | similar to protein kinase C, eta ARHGAP17 Rho GTPase activating protein 17 7.07 8.23 2.2 Up 0.003 ARHGAP19 Rho GTPase activating protein 19 8.94 7.94 2.0 Down 0.004 ARHGAP19 Rho GTPase activating protein 19 7.92 7.29 1.5 Down 0.003 ARID1B AT rich interactive domain 1B (SWI1-like) | similar to AT rich interactive5.67 domain6.22 1B (SWI1-like)1.5 Up isoform 1 0.008 ARL1 ADP-ribosylation factor-like 1 9.21 8.33 1.8 Down 0.008 ARL13B ADP-ribosylation factor-like 13B 7.36 8.3 1.9 Up 0.000 ARL5B ADP-ribosylation factor-like 5B | similar to Programmed cell death8.28 protein6.98 8, mitochondrial2.5 precursorDown (Apoptosis-inducing0.000 factor) ARL6IP1 ADP-ribosylation factor-like 6 interacting protein 1 11.42 10.76 1.6 Down 0.005 ARMCX1 armadillo repeat containing, X-linked 1 7.93 7.16 1.7 Down 0.007 ARNTL aryl hydrocarbon receptor nuclear translocator-like 6.15 5.56 1.5 Down 0.008 ASH1L ash1 (absent, small, or homeotic)-like (Drosophila) | KIAA17516.25 | TL132 pseudogene6.89 1.6 Up 0.005 ATE1 arginyltransferase 1 | KIAA1529 6.15 7.12 2.0 Up 0.001 ATF1 activating transcription factor 1 5.82 6.58 1.7 Up 0.001 ATF2 activating transcription factor 2 7.22 8.4 2.3 Up 0.001 ATG9A ATG9 autophagy related 9 homolog A (S. cerevisiae) | ATP-binding6.81 cassette,7.51 sub-family1.6 B (MDR/TAP),Up member0.004 6 ATP10D ATPase, Class V, type 10D 7.22 6.28 1.9 Down 0.006 ATP11C ATPase, Class VI, type 11C 7.34 8.9 2.9 Up 0.000 ATP13A3 ATPase type 13A3 7.94 8.75 1.8 Up 0.002 ATP1B1 ATPase, Na+/K+ transporting, beta 1 polypeptide 6.06 6.68 1.5 Up 0.004 ATP6V0D1 ATPase, H+ transporting, lysosomal 38kDa, V0 subunit d1 9.11 8.2 1.9 Down 0.008 ATP6V1A ATPase, H+ transporting, lysosomal 70kDa, V1 subunit A 9.92 9.22 1.6 Down 0.005 AYTL2 acyltransferase like 2 7.18 8.07 1.9 Up 0.001 AZIN1 antizyme inhibitor 1 10.53 9.28 2.4 Down 0.000 B3GAT1 beta-1,3-glucuronyltransferase 1 (glucuronosyltransferase P) 5.84 6.84 2.0 Up 0.000 B4GALNT3 beta-1,4-N-acetyl-galactosaminyl transferase 3 5.44 5.9 1.4 Up 0.008 B4GALT5 UDP-Gal:betaGlcNAc beta 1,4- galactosyltransferase, polypeptide7.49 5 8.35 1.8 Up 0.009 B4GALT6 UDP-Gal:betaGlcNAc beta 1,4- galactosyltransferase, polypeptide7.8 6 6.82 2.0 Down 0.002 BAALC brain and acute leukemia, cytoplasmic | hypothetical protein FLJ104895.89 7.07 2.3 Up 0.001 BAG4 BCL2-associated athanogene 4 8.15 9.01 1.8 Up 0.003 BAI2 brain-specific angiogenesis inhibitor 2 | collagen, type XVI, alpha5.79 1 6.45 1.6 Up 0.003 BARX1 BarH-like homeobox 1 6.4 7.07 1.6 Up 0.003 BASP1 brain abundant, membrane attached signal protein 1 | similar 8.26to Aurora kinase9.65 A-interacting2.6 proteinUp (AURKA-interacting0.000 protein) BCL2L13 BCL2-like 13 (apoptosis facilitator) | hypothetical protein ZD77D087.87 | CHK16.85 checkpoint 2.0homologDown (S. pombe) | 0.005ring finger protein 141 BCL9 B-cell CLL/lymphoma 9 7.05 7.64 1.5 Up 0.008 BCOR BCL6 co-repressor | hypothetical protein LOC730590 | hypothetical7.57 protein8.1 LOC7280681.4 Up 0.006 BET1 7.96 8.46 1.4 Up 0.010 BGN biglycan 6.6 7.66 2.1 Up 0.001 BHLHB5 basic helix-loop-helix domain containing, class B, 5 8.22 9.28 2.1 Up 0.001 BIRC2 baculoviral IAP repeat-containing 2 9.28 8.13 2.2 Down 0.010 BIRC3 baculoviral IAP repeat-containing 3 10.15 8.02 4.4 Down 0.000 BMI1 B lymphoma Mo-MLV insertion region (mouse) | COMM domain8.31 containing 36.2 4.3 Down 0.000 BMP7 bone morphogenetic protein 7 (osteogenic protein 1) 6.18 6.95 1.7 Up 0.001 BOC Boc homolog (mouse) 5.3 6.14 1.8 Up 0.002 BPGM 2,3-bisphosphoglycerate mutase 8.77 8.25 1.4 Down 0.008 BST2 bone marrow stromal cell antigen 2 7.14 6.2 1.9 Down 0.002 BTBD5 BTB (POZ) domain containing 5 8.26 6.76 2.8 Down 0.000 BTN3A1 butyrophilin, subfamily 3, member A1 8.28 7.18 2.1 Down 0.001 BVES blood vessel epicardial substance 6.92 6.14 1.7 Down 0.006 C10orf72 chromosome 10 open reading frame 72 5.82 6.55 1.7 Up 0.001 C11orf24 chromosome 11 open reading frame 24 6.99 7.86 1.8 Up 0.003 C11orf51 chromosome 11 open reading frame 51 7.49 8.3 1.8 Up 0.003 C11orf59 chromosome 11 open reading frame 59 7.46 8.44 2.0 Up 0.001 C11orf60 chromosome 11 open reading frame 60 8.57 7.8 1.7 Down 0.008 C12orf49 chromosome 12 open reading frame 49 6.61 7.39 1.7 Up 0.001 C14orf100 chromosome 14 open reading frame 100 9.32 7.89 2.7 Down 0.001 C14orf122 chromosome 14 open reading frame 122 7.06 8.22 2.2 Up 0.000 C14orf32 chromosome 14 open reading frame 32 9.12 9.7 1.5 Up 0.010 C15orf39 chromosome 15 open reading frame 39 | similar to COMM domain5.91 containing6.38 4 1.4 Up 0.010 C16orf58 chromosome 16 open reading frame 58 7.85 7.12 1.7 Down 0.004 C17orf68 chromosome 17 open reading frame 68 8.17 7.36 1.8 Down 0.002 C18orf25 chromosome 18 open reading frame 25 7.13 6.24 1.9 Down 0.001 C19orf24 chromosome 19 open reading frame 24 7.63 8.28 1.6 Up 0.008 C1orf124 chromosome 1 open reading frame 124 7.63 6.55 2.1 Down 0.003 C1orf128 chromosome 1 open reading frame 128 | SET domain containing7.51 5 | lysophospholipase8.4 1.9 II | lysophospholipaseUp 0.004 II pseudogene 1 | similar to Acyl-protein thioesterase 2 (Lysophospholipase II) (LPL-I) C1orf38 chromosome 1 open reading frame 38 5.26 5.84 1.5 Up 0.008 C1orf55 chromosome 1 open reading frame 55 8.76 8.01 1.7 Down 0.005 C1orf75 chromosome 1 open reading frame 75 6.93 7.6 1.6 Up 0.005 C1orf86 chromosome 1 open reading frame 86 6 6.67 1.6 Up 0.007 C1QL1 complement component 1, q subcomponent-like 1 6.26 7.17 1.9 Up 0.005 C20orf55 chromosome 20 open reading frame 55 6.69 7.31 1.5 Up 0.009 C20orf77 chromosome 20 open reading frame 77 7.54 6.99 1.5 Down 0.007 C21orf25
Load more

Recommended publications
  • A Genetic Screening Identifies a Component of the SWI/SNF Complex, Arid1b As a Senescence Regulator
    A genetic screening identifies a component of the SWI/SNF complex, Arid1b as a senescence regulator Sadaf Khan A thesis submitted to Imperial College London for the degree of Doctor in Philosophy MRC Clinical Sciences Centre Imperial College London, School of Medicine July 2013 Statement of originality All experiments included in this thesis were performed by myself unless otherwise stated. Copyright Declaration The copyright of this thesis rests with the author and is made available under a Creative Commons Attribution Non-Commercial No Derivatives license. Researchers are free to copy, distribute or transmit the thesis on the condition that they attribute it, that they do not use it for commercial purposes and that they do not alter, transform or build upon it. For any reuse or redistribution, researchers must make clear to others the license terms of this work. 2 Abstract Senescence is an important tumour suppressor mechanism, which prevents the proliferation of stressed or damaged cells. The use of RNA interference to identify genes with a role in senescence is an important tool in the discovery of novel cancer genes. In this work, a protocol was established for conducting bypass of senescence screenings, using shRNA libraries together with next-generation sequencing. Using this approach, the SWI/SNF subunit Arid1b was identified as a regulator of cellular lifespan in MEFs. SWI/SNF is a large multi-subunit complex that remodels chromatin. Mutations in SWI/SNF proteins are frequently associated with cancer, suggesting that SWI/SNF components are tumour suppressors. Here the role of ARID1B during senescence was investigated. Depletion of ARID1B extends the proliferative capacity of primary mouse and human fibroblasts.
    [Show full text]
  • Acetyl Group Coordinated Progression Through the Catalytic Cycle of an Arylalkylamine N-Acetyltransferase
    RESEARCH ARTICLE Acetyl group coordinated progression through the catalytic cycle of an arylalkylamine N-acetyltransferase Adam A. Aboalroub, Ashleigh B. Bachman, Ziming Zhang, Dimitra Keramisanou, David J. Merkler, Ioannis Gelis* Department of Chemistry, University of South Florida, Tampa, Florida, United States of America * [email protected] a1111111111 a1111111111 a1111111111 Abstract a1111111111 a1111111111 The transfer of an acetyl group from acetyl-CoA to an acceptor amine is a ubiquitous bio- chemical transformation catalyzed by Gcn5-related N-acetyltransferases (GNATs). Although it is established that the reaction proceeds through a sequential ordered mecha- nism, the role of the acetyl group in driving the ordered formation of binary and ternary com- OPEN ACCESS plexes remains elusive. Herein, we show that CoA and acetyl-CoA alter the conformation of the substrate binding site of an arylalkylamine N-acetyltransferase (AANAT) to facilitate Citation: Aboalroub AA, Bachman AB, Zhang Z, Keramisanou D, Merkler DJ, Gelis I (2017) Acetyl interaction with acceptor substrates. However, it is the presence of the acetyl group within group coordinated progression through the the catalytic funnel that triggers high affinity binding. Acetyl group occupancy is relayed catalytic cycle of an arylalkylamine N- through a conserved salt bridge between the P-loop and the acceptor binding site, and is acetyltransferase. PLoS ONE 12(5): e0177270. manifested as differential dynamics in the CoA and acetyl-CoA-bound states. The capacity https://doi.org/10.1371/journal.pone.0177270 of the acetyl group carried by an acceptor to promote its tight binding even in the absence of Editor: Viswanathan V. Krishnan, California State CoA, but also its mutually exclusive position to the acetyl group of acetyl-CoA underscore its University Fresno, UNITED STATES importance in coordinating the progression of the catalytic cycle.
    [Show full text]
  • Combination of Photodynamic Therapy with Fenretinide and C6
    Wayne State University Wayne State University Theses 1-1-2015 Combination Of Photodynamic Therapy With Fenretinide And C6-Pyridinium Ceramide Enhances Killing Of Scc17b Human Head And Neck Squamous Cell Carcinoma Cells Via The eD Novo Sphingolipid Biosynthesis And Mitochondrial Apoptosis Nithin Bhargava Boppana Wayne State University, Follow this and additional works at: https://digitalcommons.wayne.edu/oa_theses Part of the Medicinal Chemistry and Pharmaceutics Commons Recommended Citation Boppana, Nithin Bhargava, "Combination Of Photodynamic Therapy With Fenretinide And C6-Pyridinium Ceramide Enhances Killing Of Scc17b Human Head And Neck Squamous Cell Carcinoma Cells Via The eD Novo Sphingolipid Biosynthesis And Mitochondrial Apoptosis" (2015). Wayne State University Theses. 431. https://digitalcommons.wayne.edu/oa_theses/431 This Open Access Thesis is brought to you for free and open access by DigitalCommons@WayneState. It has been accepted for inclusion in Wayne State University Theses by an authorized administrator of DigitalCommons@WayneState. COMBINATION OF PHOTODYNAMIC THERAPY WITH FENRETINIDE AND C6-PYRIDINIUM CERAMIDE ENHANCES KILLING OF SCC17B HUMAN HEAD AND NECK SQUAMOUS CELL CARCINOMA CELLS VIA THE DE NOVO SPHINGOLIPID BIOSYNTHESIS AND MITOCHONDRIAL APOPTOSIS by NITHIN BHARGAVA BOPPANA THESIS Submitted to the Graduate School of Wayne State University, Detroit, Michigan in partial fulfillment of the requirements for the degree of MASTER OF SCIENCE 2015 MAJOR: PHARMACEUTICAL SCIENCES Approved By: ________________________________ Advisor Date © COPYRIGHT BY NITHIN BHARGAVA BOPPANA 2015 All Rights Reserved DEDICATION Dedicated to my mom Rekha Vasireddy for always believing in me and helping me in becoming the person who I am today. ii ACKNOWLEDGEMENTS I am grateful to my advisor, Dr. Duska Separovic for her invaluable mentorship throughout the project.
    [Show full text]
  • NDUFAF1 Antibody
    Efficient Professional Protein and Antibody Platforms NDUFAF1 Antibody Basic information: Catalog No.: UPA63763 Source: Rabbit Size: 50ul/100ul Clonality: monoclonal Concentration: 1mg/ml Isotype: Rabbit IgG Purification: Protein A purified. Useful Information: WB:1:1000 ICC:1:50-1:200 Applications: IHC:1:50-1:200 FC:1:50-1:100 Reactivity: Human Specificity: This antibody recognizes NDUFAF1 protein. Immunogen: Synthetic peptide within C terminal human NDUFAF1. This gene encodes a complex I assembly factor protein. Complex I (NADH-ubiquinone oxidoreductase) catalyzes the transfer of electrons from NADH to ubiquinone (coenzyme Q) in the first step of the mitochondrial respiratory chain, resulting in the translocation of protons across the inner mitochondrial membrane. The encoded protein is required for assembly of complex I, and mutations in this gene are a cause of mitochondrial complex I deficiency. Alternatively spliced transcript variants have been observed for Description: this gene, and a pseudogene of this gene is located on the long arm of chromosome 19. Part of the mitochondrial complex I assembly (MCIA) com- plex. The complex comprises at least TMEM126B, NDUFAF1, ECSIT, and ACAD9. Interacts with ECSIT. Interacts with ACAD9. At early stages of com- plex I assembly, it is found in intermediate subcomplexes that contain dif- ferent subunits including NDUFB6, NDUFA6, NDUFA9, NDUFS3, NDUFS7, ND1, ND2 and ND3 Uniprot: Q9Y375 Human BiowMW: 38 kDa Buffer: 1*TBS (pH7.4), 1%BSA, 50%Glycerol. Preservative: 0.05% Sodium Azide. Storage: Store at 4°C short term and -20°C long term. Avoid freeze-thaw cycles. Note: For research use only, not for use in diagnostic procedure.
    [Show full text]
  • Molecular Mechanism of ACAD9 in Mitochondrial Respiratory Complex 1 Assembly
    bioRxiv preprint doi: https://doi.org/10.1101/2021.01.07.425795; this version posted January 9, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Molecular mechanism of ACAD9 in mitochondrial respiratory complex 1 assembly Chuanwu Xia1, Baoying Lou1, Zhuji Fu1, Al-Walid Mohsen2, Jerry Vockley2, and Jung-Ja P. Kim1 1Department of Biochemistry, Medical College of Wisconsin, Milwaukee, Wisconsin, 53226, USA 2Department of Pediatrics, University of Pittsburgh School of Medicine, University of Pittsburgh, Children’s Hospital of Pittsburgh of UPMC, Pittsburgh, PA 15224, USA Abstract ACAD9 belongs to the acyl-CoA dehydrogenase family, which catalyzes the α-β dehydrogenation of fatty acyl-CoA thioesters. Thus, it is involved in fatty acid β-oxidation (FAO). However, it is now known that the primary function of ACAD9 is as an essential chaperone for mitochondrial respiratory complex 1 assembly. ACAD9 interacts with ECSIT and NDUFAF1, forming the mitochondrial complex 1 assembly (MCIA) complex. Although the role of MCIA in the complex 1 assembly pathway is well studied, little is known about the molecular mechanism of the interactions among these three assembly factors. Our current studies reveal that when ECSIT interacts with ACAD9, the flavoenzyme loses the FAD cofactor and consequently loses its FAO activity, demonstrating that the two roles of ACAD9 are not compatible. ACAD9 binds to the carboxy-terminal half (C-ECSIT), and NDUFAF1 binds to the amino-terminal half of ECSIT. Although the binary complex of ACAD9 with ECSIT or with C-ECSIT is unstable and aggregates easily, the ternary complex of ACAD9-ECSIT-NDUFAF1 (i.e., the MCIA complex) is soluble and extremely stable.
    [Show full text]
  • Molecular Biology and Biochemistry of The
    MOLECULAR BIOLOGY AND BIOCHEMISTRY OF THE REGULATION OF HRP/TYPE III SECRETION GENES IN THE CORN PATHOGEN PANTOEA STEWARTII SUBSP. STEWARTII DISSERTATION Presented in Partial Fulfillment of the Requirements for the Degree Doctor of Philosophy in the Graduate School of The Ohio State University By Massimo Merighi, B. S., M. S. ***** The Ohio State University 2003 Dissertation Committee: Professor David L. Coplin, Adviser Approved by Professor Brian Ahmer ______________________ Professor Dietz W. Bauer Adviser Professor Terrence L. Graham Plant Pathology Copyright by Massimo Merighi 2003 ii ABSTRACT Pantoea stewartii subsp. stewartii is a bacterial pathogen of corn. Its pathogenicity depends on the expression of a Hrp/type III protein secretion/translocation system. The regulatory region of the hrp gene cluster consists of three adjacent operons: hrpXY encodes a two- component regulatory system, consisting of the response regulator HrpY and sensor PAS-kinase HrpX; hrpS encodes an NtrC-like enhancer-binding protein; and hrpL encodes an ECF sigma factor. In this study, we used genetic and biochemical approaches to delineate the following regulatory cascade: 1) HrpY activates hrpS; 2) HrpS activates hrpL; and 3) HrpL activates secretion and effector genes with ‘Hrp-box’ promoters. This pathway responds to environmental signals and global regulators. Mutant analysis showed that HrpX is required for full virulence. Deletion of its individual PAS-sensory domains revealed that they are not redundant and each may have a different role in modulating kinase activity. HrpX probably senses an intracellular signal, possibly related to nitrogen metabolism. pH, osmolarity and nicotinic acid controlled expression of hrpS independently of HrpX/HrpY.
    [Show full text]
  • Supplemental Table S1
    Entrez Gene Symbol Gene Name Affymetrix EST Glomchip SAGE Stanford Literature HPA confirmed Gene ID Profiling profiling Profiling Profiling array profiling confirmed 1 2 A2M alpha-2-macroglobulin 0 0 0 1 0 2 10347 ABCA7 ATP-binding cassette, sub-family A (ABC1), member 7 1 0 0 0 0 3 10350 ABCA9 ATP-binding cassette, sub-family A (ABC1), member 9 1 0 0 0 0 4 10057 ABCC5 ATP-binding cassette, sub-family C (CFTR/MRP), member 5 1 0 0 0 0 5 10060 ABCC9 ATP-binding cassette, sub-family C (CFTR/MRP), member 9 1 0 0 0 0 6 79575 ABHD8 abhydrolase domain containing 8 1 0 0 0 0 7 51225 ABI3 ABI gene family, member 3 1 0 1 0 0 8 29 ABR active BCR-related gene 1 0 0 0 0 9 25841 ABTB2 ankyrin repeat and BTB (POZ) domain containing 2 1 0 1 0 0 10 30 ACAA1 acetyl-Coenzyme A acyltransferase 1 (peroxisomal 3-oxoacyl-Coenzyme A thiol 0 1 0 0 0 11 43 ACHE acetylcholinesterase (Yt blood group) 1 0 0 0 0 12 58 ACTA1 actin, alpha 1, skeletal muscle 0 1 0 0 0 13 60 ACTB actin, beta 01000 1 14 71 ACTG1 actin, gamma 1 0 1 0 0 0 15 81 ACTN4 actinin, alpha 4 0 0 1 1 1 10700177 16 10096 ACTR3 ARP3 actin-related protein 3 homolog (yeast) 0 1 0 0 0 17 94 ACVRL1 activin A receptor type II-like 1 1 0 1 0 0 18 8038 ADAM12 ADAM metallopeptidase domain 12 (meltrin alpha) 1 0 0 0 0 19 8751 ADAM15 ADAM metallopeptidase domain 15 (metargidin) 1 0 0 0 0 20 8728 ADAM19 ADAM metallopeptidase domain 19 (meltrin beta) 1 0 0 0 0 21 81792 ADAMTS12 ADAM metallopeptidase with thrombospondin type 1 motif, 12 1 0 0 0 0 22 9507 ADAMTS4 ADAM metallopeptidase with thrombospondin type 1
    [Show full text]
  • Enzymatic Encoding Methods for Efficient Synthesis Of
    (19) TZZ__T (11) EP 1 957 644 B1 (12) EUROPEAN PATENT SPECIFICATION (45) Date of publication and mention (51) Int Cl.: of the grant of the patent: C12N 15/10 (2006.01) C12Q 1/68 (2006.01) 01.12.2010 Bulletin 2010/48 C40B 40/06 (2006.01) C40B 50/06 (2006.01) (21) Application number: 06818144.5 (86) International application number: PCT/DK2006/000685 (22) Date of filing: 01.12.2006 (87) International publication number: WO 2007/062664 (07.06.2007 Gazette 2007/23) (54) ENZYMATIC ENCODING METHODS FOR EFFICIENT SYNTHESIS OF LARGE LIBRARIES ENZYMVERMITTELNDE KODIERUNGSMETHODEN FÜR EINE EFFIZIENTE SYNTHESE VON GROSSEN BIBLIOTHEKEN PROCEDES DE CODAGE ENZYMATIQUE DESTINES A LA SYNTHESE EFFICACE DE BIBLIOTHEQUES IMPORTANTES (84) Designated Contracting States: • GOLDBECH, Anne AT BE BG CH CY CZ DE DK EE ES FI FR GB GR DK-2200 Copenhagen N (DK) HU IE IS IT LI LT LU LV MC NL PL PT RO SE SI • DE LEON, Daen SK TR DK-2300 Copenhagen S (DK) Designated Extension States: • KALDOR, Ditte Kievsmose AL BA HR MK RS DK-2880 Bagsvaerd (DK) • SLØK, Frank Abilgaard (30) Priority: 01.12.2005 DK 200501704 DK-3450 Allerød (DK) 02.12.2005 US 741490 P • HUSEMOEN, Birgitte Nystrup DK-2500 Valby (DK) (43) Date of publication of application: • DOLBERG, Johannes 20.08.2008 Bulletin 2008/34 DK-1674 Copenhagen V (DK) • JENSEN, Kim Birkebæk (73) Proprietor: Nuevolution A/S DK-2610 Rødovre (DK) 2100 Copenhagen 0 (DK) • PETERSEN, Lene DK-2100 Copenhagen Ø (DK) (72) Inventors: • NØRREGAARD-MADSEN, Mads • FRANCH, Thomas DK-3460 Birkerød (DK) DK-3070 Snekkersten (DK) • GODSKESEN,
    [Show full text]
  • ARID1B Is a Specific Vulnerability in ARID1A-Mutant Cancers The
    ARID1B is a specific vulnerability in ARID1A-mutant cancers The Harvard community has made this article openly available. Please share how this access benefits you. Your story matters. Citation Helming, K. C., X. Wang, B. G. Wilson, F. Vazquez, J. R. Haswell, H. E. Manchester, Y. Kim, et al. 2014. “ARID1B is a specific vulnerability in ARID1A-mutant cancers.” Nature medicine 20 (3): 251-254. doi:10.1038/nm.3480. http://dx.doi.org/10.1038/nm.3480. Published Version doi:10.1038/nm.3480 Accessed February 16, 2015 10:04:32 PM EST Citable Link http://nrs.harvard.edu/urn-3:HUL.InstRepos:12987227 Terms of Use This article was downloaded from Harvard University's DASH repository, and is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of- use#LAA (Article begins on next page) NIH Public Access Author Manuscript Nat Med. Author manuscript; available in PMC 2014 September 01. NIH-PA Author ManuscriptPublished NIH-PA Author Manuscript in final edited NIH-PA Author Manuscript form as: Nat Med. 2014 March ; 20(3): 251–254. doi:10.1038/nm.3480. ARID1B is a specific vulnerability in ARID1A-mutant cancers Katherine C. Helming1,2,3,4,*, Xiaofeng Wang1,2,3,*, Boris G. Wilson1,2,3, Francisca Vazquez5, Jeffrey R. Haswell1,2,3, Haley E. Manchester1,2,3, Youngha Kim1,2,3, Gregory V. Kryukov5, Mahmoud Ghandi5, Andrew J. Aguirre5,6,7, Zainab Jagani8, Zhong Wang9, Levi A. Garraway6, William C. Hahn6,7, and Charles W.
    [Show full text]
  • A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus
    Page 1 of 781 Diabetes A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes Mellitus Robert N. Bone1,6,7, Olufunmilola Oyebamiji2, Sayali Talware2, Sharmila Selvaraj2, Preethi Krishnan3,6, Farooq Syed1,6,7, Huanmei Wu2, Carmella Evans-Molina 1,3,4,5,6,7,8* Departments of 1Pediatrics, 3Medicine, 4Anatomy, Cell Biology & Physiology, 5Biochemistry & Molecular Biology, the 6Center for Diabetes & Metabolic Diseases, and the 7Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; 2Department of BioHealth Informatics, Indiana University-Purdue University Indianapolis, Indianapolis, IN, 46202; 8Roudebush VA Medical Center, Indianapolis, IN 46202. *Corresponding Author(s): Carmella Evans-Molina, MD, PhD ([email protected]) Indiana University School of Medicine, 635 Barnhill Drive, MS 2031A, Indianapolis, IN 46202, Telephone: (317) 274-4145, Fax (317) 274-4107 Running Title: Golgi Stress Response in Diabetes Word Count: 4358 Number of Figures: 6 Keywords: Golgi apparatus stress, Islets, β cell, Type 1 diabetes, Type 2 diabetes 1 Diabetes Publish Ahead of Print, published online August 20, 2020 Diabetes Page 2 of 781 ABSTRACT The Golgi apparatus (GA) is an important site of insulin processing and granule maturation, but whether GA organelle dysfunction and GA stress are present in the diabetic β-cell has not been tested. We utilized an informatics-based approach to develop a transcriptional signature of β-cell GA stress using existing RNA sequencing and microarray datasets generated using human islets from donors with diabetes and islets where type 1(T1D) and type 2 diabetes (T2D) had been modeled ex vivo. To narrow our results to GA-specific genes, we applied a filter set of 1,030 genes accepted as GA associated.
    [Show full text]
  • Inborn Errors of Metabolism Test Requisition
    LABORATORY OF GENETICS AND GENOMICS Mailing Address: For local courier service and/or inquiries, please contact 513-636-4474 • Fax: 513-636-4373 3333 Burnet Avenue, Room R1042 www.cincinnatichildrens.org/moleculargenetics • Email: [email protected] Cincinnati, OH 45229 INBORN ERRORS OF METABOLISM TEST REQUISITION All Information Must Be Completed Before Sample Can Be Processed PATIENT INFORMATION ETHNIC/RACIAL BACKGROUND (Choose All) Patient Name: ___________________ , ___________________ , ________ European American (White) African-American (Black) Last First MI Native American or Alaskan Asian-American Address: ____________________________________________________ Pacific Islander Ashkenazi Jewish ancestry ____________________________________________________ Latino-Hispanic _____________________________________________ Home Phone: ________________________________________________ (specify country/region of origin) MR# __________________ Date of Birth ________ / ________ / _______ Other ____________________________________________________ (specify country/region of origin) Gender: Male Female BILLING INFORMATION (Choose ONE method of payment) o REFERRING INSTITUTION o COMMERCIAL INSURANCE* Insurance can only be billed if requested at the time of service. Institution: ____________________________________________________ Policy Holder Name: _____________________________________________ Address: _____________________________________________________ Gender: ________________ Date of Birth ________ / ________ / _______
    [Show full text]
  • 4-6 Weeks Old Female C57BL/6 Mice Obtained from Jackson Labs Were Used for Cell Isolation
    Methods Mice: 4-6 weeks old female C57BL/6 mice obtained from Jackson labs were used for cell isolation. Female Foxp3-IRES-GFP reporter mice (1), backcrossed to B6/C57 background for 10 generations, were used for the isolation of naïve CD4 and naïve CD8 cells for the RNAseq experiments. The mice were housed in pathogen-free animal facility in the La Jolla Institute for Allergy and Immunology and were used according to protocols approved by the Institutional Animal Care and use Committee. Preparation of cells: Subsets of thymocytes were isolated by cell sorting as previously described (2), after cell surface staining using CD4 (GK1.5), CD8 (53-6.7), CD3ε (145- 2C11), CD24 (M1/69) (all from Biolegend). DP cells: CD4+CD8 int/hi; CD4 SP cells: CD4CD3 hi, CD24 int/lo; CD8 SP cells: CD8 int/hi CD4 CD3 hi, CD24 int/lo (Fig S2). Peripheral subsets were isolated after pooling spleen and lymph nodes. T cells were enriched by negative isolation using Dynabeads (Dynabeads untouched mouse T cells, 11413D, Invitrogen). After surface staining for CD4 (GK1.5), CD8 (53-6.7), CD62L (MEL-14), CD25 (PC61) and CD44 (IM7), naïve CD4+CD62L hiCD25-CD44lo and naïve CD8+CD62L hiCD25-CD44lo were obtained by sorting (BD FACS Aria). Additionally, for the RNAseq experiments, CD4 and CD8 naïve cells were isolated by sorting T cells from the Foxp3- IRES-GFP mice: CD4+CD62LhiCD25–CD44lo GFP(FOXP3)– and CD8+CD62LhiCD25– CD44lo GFP(FOXP3)– (antibodies were from Biolegend). In some cases, naïve CD4 cells were cultured in vitro under Th1 or Th2 polarizing conditions (3, 4).
    [Show full text]