Supplementary Table 1. a List of All 142 Genes Important in the P53 Stress Response and Included Into the Genomic Scan for Natural Selection

Total Page:16

File Type:pdf, Size:1020Kb

Supplementary Table 1. a List of All 142 Genes Important in the P53 Stress Response and Included Into the Genomic Scan for Natural Selection Supplementary table 1. A list of all 142 genes important in the p53 stress response and included into the genomic scan for natural selection. Gene Symbol Description AKT1 v-akt murine thymoma viral oncogene homolog 1 AKT2 v-akt murine thymoma viral oncogene homolog 2 APAF1 apoptotic peptidase activating factor 1 APC adenomatous polyposis coli APEX1 APEX nuclease (multifunctional DNA repair enzyme) 1 ATM ataxia telangiectasia mutated ATR ataxia telangiectasia and Rad3 related AURKA aurora kinase A BAI1 brain-specific angiogenesis inhibitor 1 BAX BCL2-associated X protein BBC3 BCL2 binding component 3 CCNG1 cyclin G1 CD82 CD82 molecule CDK2 cyclin-dependent kinase 2 CDK8 cyclin-dependent kinase 8 CDKN1A cyclin-dependent kinase inhibitor 1A (p21, Cip1) CDKN1B cyclin-dependent kinase inhibitor 1B (p27, Kip1) CDKN2A cyclin-dependent kinase inhibitor 2A (melanoma, p16, inhibits CDK4) CHEK2 CHK2 checkpoint homolog (S. pombe) CORO1B coronin, actin binding protein, 1B CREB1 cAMP responsive element binding protein 1 CREBBP CREB binding protein (Rubinstein-Taybi syndrome) CSE1L CSE1 chromosome segregation 1-like (yeast) CSNK2A1 casein kinase 2, alpha 1 polypeptide CTNNB1 catenin (cadherin-associated protein), beta 1, 88kDa CUL7 cullin 7 DUSP1 dual specificity phosphatase 1 DUSP16 dual specificity phosphatase 16 DYRK2 dual-specificity tyrosine-(Y)-phosphorylation regulated kinase 2 E2F1 E2F transcription factor 1 E4F1 E4F transcription factor 1 EEF1A1 eukaryotic translation elongation factor 1 alpha 1 EIF4EBP1 eukaryotic translation initiation factor 4E binding protein 1 ESR1 estrogen receptor 1 ESR2 estrogen receptor 2 (ER beta) FAS Fas (TNF receptor superfamily, member 6) FCGR1A Fc fragment of IgG, high affinity Ia, receptor (CD64) FHL2 four and a half LIM domains 2 FLT1 fms-related tyrosine kinase 1 (vasc. endoth. growth factor/vasc. permeability factor rec.) FNIP1 folliculin interacting protein 1 FOS v-fos FBJ murine osteosarcoma viral oncogene homolog FOXO1A forkhead box O1 FRAP1 FK506 binding protein 12-rapamycin associated protein 1 GADD45A growth arrest and DNA-damage-inducible, alpha GTF2H2 general transcription factor IIH, polypeptide 2, 44kDa GTSE1 G-2 and S-phase expressed 1 HIPK2 homeodomain interacting protein kinase 2 IGF1 insulin-like growth factor 1 (somatomedin C) IGFBP3 insulin-like growth factor binding protein 3 JMY junction-mediating and regulatory protein KDR kinase insert domain receptor (a type III receptor tyrosine kinase) LRDD leucine-rich repeats and death domain containing MAP2K4 mitogen-activated protein kinase kinase 4 MAP3K5 mitogen-activated protein kinase kinase kinase 5 MAP4 microtubule-associated protein 4 MAPK1 mitogen-activated protein kinase 1 MAPK8 mitogen-activated protein kinase 8 MAPK9 mitogen-activated protein kinase 9 MAPT microtubule-associated protein tau MDM2 Mdm2 p53 binding protein homolog (mouse) MDM4 Mdm4 p53 binding protein homolog (mouse) MMP2 matrix metallopeptidase 2 (gelatinase A, 72kDa gelatinase, 72kDa type IV collagenase) MTA2 metastasis associated 1 family, member 2 MYST1 MYST histone acetyltransferase 1 NFKB1 nuclear factor of kappa light polypeptide gene enhancer in B-cells 1 NUMB numb homolog (Drosophila) p53AIP1 p53-regulated apoptosis-inducing protein 1 PARC p53-associated parkin-like cytoplasmic protein PARP1 poly (ADP-ribose) polymerase 1 PCAF K(lysine) acetyltransferase 2B PDK1 pyruvate dehydrogenase kinase, isozyme 1 PIAS1 protein inhibitor of activated STAT, 1 PIAS4 protein inhibitor of activated STAT, 4 PIK3CA phosphoinositide-3-kinase, catalytic, alpha polypeptide PIK3R1 phosphoinositide-3-kinase, regulatory subunit 1 (alpha) PIK3R2 phosphoinositide-3-kinase, regulatory subunit 2 (beta) PIN1 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 PMAIP1 phorbol-12-myristate-13-acetate-induced protein 1 POU4F1 POU class 4 homeobox 1 POU4F2 POU class 4 homeobox 2 PPM1D protein phosphatase 1D magnesium-dependent, delta isoform PPP1R13B protein phosphatase 1, regulatory (inhibitor) subunit 13B PPP1R13L protein phosphatase 1, regulatory (inhibitor) subunit 13 like PPP2CA protein phosphatase 2 (formerly 2A), catalytic subunit, alpha isoform PPP2CB protein phosphatase 2 (formerly 2A), catalytic subunit, beta isoform PPP2R1A protein phosphatase 2 (formerly 2A), regulatory subunit A , alpha isoform PPP2R1B protein phosphatase 2 (formerly 2A), regulatory subunit A, beta isoform PPP2R2A protein phosphatase 2 (formerly 2A), regulatory subunit B, alpha isoform PPP2R2B protein phosphatase 2 (formerly 2A), regulatory subunit B, beta isoform PPP2R2C protein phosphatase 2 (formerly 2A), regulatory subunit B, gamma isoform PPP2R3A protein phosphatase 2 (formerly 2A), regulatory subunit B'', alpha PPP2R3B protein phosphatase 2 (formerly 2A), regulatory subunit B'', beta PPP2R4 protein phosphatase 2A activator, regulatory subunit 4 PPP2R5A protein phosphatase 2, regulatory subunit B', alpha isoform PPP2R5B protein phosphatase 2, regulatory subunit B', beta isoform PPP2R5C protein phosphatase 2, regulatory subunit B', gamma isoform PPP2R5D protein phosphatase 2, regulatory subunit B', delta isoform PPP2R5E protein phosphatase 2, regulatory subunit B', epsilon isoform PRKAA1 protein kinase, AMP-activated, alpha 1 catalytic subunit PRKAB1 protein kinase, AMP-activated, beta 1 non-catalytic subunit PRKAB2 protein kinase, AMP-activated, beta 2 non-catalytic subunit PRKAG2 protein kinase, AMP-activated, gamma 2 non-catalytic subunit PSRC1 proline/serine-rich coiled-coil 1 PTEN phosphatase and tensin homolog RAB13 RAB13, member RAS oncogene family RB1 retinoblastoma 1 RBBP4 retinoblastoma binding protein 4 RCHY1 ring finger and CHY zinc finger domain containing 1 RFWD2 ring finger and WD repeat domain 2 RHEB Ras homolog enriched in brain RPRM reprimo, TP53 dependent G2 arrest mediator candidate RPS6KB1 ribosomal protein S6 kinase, 70kDa, polypeptide 1 RRM2 ribonucleotide reductase M2 polypeptide SERPINB2 serpin peptidase inhibitor, clade B (ovalbumin), member 2 SERPINB5 serpin peptidase inhibitor, clade B (ovalbumin), member 5 SFN stratifin SIAH1 seven in absentia homolog 1 (Drosophila) SKP2 S-phase kinase-associated protein 2 (p45) STEAP3 STEAP family member 3 STK11 serine/threonine kinase 11 STMN1 stathmin 1/oncoprotein 18 STRAP serine/threonine kinase receptor associated protein SUMO1 SMT3 suppressor of mif two 3 homolog 1 (S. cerevisiae) TDG thymine-DNA glycosylase THBS1 thrombospondin 1 TNFRSF10B tumor necrosis factor receptor superfamily, member 10b TP53 tumor protein p53 TP53BP1 tumor protein p53 binding protein 1 TP53BP2 tumor protein p53 binding protein, 2 TP63/TP73L tumor protein p63 TP73 tumor protein p73 TSC1 tuberous sclerosis 1 TSC2 tuberous sclerosis 2 USP7 ubiquitin specific peptidase 7 (herpes virus-associated) VEGFA vascular endothelial growth factor A WNT1 wingless-type MMTV integration site family, member 1 WWP1 WW domain containing E3 ubiquitin protein ligase 1 XPA xeroderma pigmentosum, complementation group A XPC xeroderma pigmentosum, complementation group C XPO1 exportin 1 (CRM1 homolog, yeast) YWHAQ tyrosine 3-monooxygenase/tryptophan 5-monooxyg. activation protein, theta polypeptide ZNF385A zinc finger protein 385A.
Recommended publications
  • Deregulated Gene Expression Pathways in Myelodysplastic Syndrome Hematopoietic Stem Cells
    Leukemia (2010) 24, 756–764 & 2010 Macmillan Publishers Limited All rights reserved 0887-6924/10 $32.00 www.nature.com/leu ORIGINAL ARTICLE Deregulated gene expression pathways in myelodysplastic syndrome hematopoietic stem cells A Pellagatti1, M Cazzola2, A Giagounidis3, J Perry1, L Malcovati2, MG Della Porta2,MJa¨dersten4, S Killick5, A Verma6, CJ Norbury7, E Hellstro¨m-Lindberg4, JS Wainscoat1 and J Boultwood1 1LRF Molecular Haematology Unit, NDCLS, John Radcliffe Hospital, Oxford, UK; 2Department of Hematology Oncology, University of Pavia Medical School, Fondazione IRCCS Policlinico San Matteo, Pavia, Italy; 3Medizinische Klinik II, St Johannes Hospital, Duisburg, Germany; 4Division of Hematology, Department of Medicine, Karolinska Institutet, Stockholm, Sweden; 5Department of Haematology, Royal Bournemouth Hospital, Bournemouth, UK; 6Albert Einstein College of Medicine, Bronx, NY, USA and 7Sir William Dunn School of Pathology, University of Oxford, Oxford, UK To gain insight into the molecular pathogenesis of the the World Health Organization.6,7 Patients with refractory myelodysplastic syndromes (MDS), we performed global gene anemia (RA) with or without ringed sideroblasts, according to expression profiling and pathway analysis on the hemato- poietic stem cells (HSC) of 183 MDS patients as compared with the the French–American–British classification, were subdivided HSC of 17 healthy controls. The most significantly deregulated based on the presence or absence of multilineage dysplasia. In pathways in MDS include interferon signaling, thrombopoietin addition, patients with RA with excess blasts (RAEB) were signaling and the Wnt pathways. Among the most signifi- subdivided into two categories, RAEB1 and RAEB2, based on the cantly deregulated gene pathways in early MDS are immuno- percentage of bone marrow blasts.
    [Show full text]
  • Human CD64 / FCGR1A Protein (His Tag), Biotinylated
    Human CD64 / FCGR1A Protein (His Tag), Biotinylated Catalog Number: 10256-H08S-B General Information SDS-PAGE: Gene Name Synonym: CD64; Fc gamma RI Protein Construction: A DNA sequence encoding the human FCGR1A (NP_000557.1) (Met1- Pro288) was expressed with a polyhistidine tag at the C-terminus. The purified protein was biotinylated in vitro. Source: Human Expression Host: CHO Stable Cells QC Testing Purity: > 95 % as determined by SDS-PAGE. Bio Activity: Protein Description Measured by its binding ability in a functional ELISA.Immobilized High affinity immunoglobulin gamma Fc receptor I, also known as FCGR1 biotinylated Human CD64 Protein (Cat:10256-H08S-B)at 10 μg/mL can and CD64, is an integral membraneglycoprotein and a member of the bind human IgG1,The EC50 of human IgG1 is 6-14 ng/mL. immunoglobulin superfamily. CD64 is a high affinity receptor for the Fc region of IgG gamma and functions in both innate and adaptive immune Endotoxin: responses. Receptors that recognize the Fc portion of IgG function in the regulation of immune response and are divided into three classes < 1.0 EU per μg protein as determined by the LAL method. designated CD64, CD32, and CD16. CD64 is structurally composed of asignal peptidethat allows its transport to the surface of a cell, Stability: threeextracellularimmunoglobulin domainsof the C2-type that it uses to Samples are stable for up to twelve months from date of receipt at -70 ℃ bind antibody, a hydrophobictransmembrane domain, and a short cytoplasmic tail. CD64 isconstitutivelyfound on only macrophages and Predicted N terminal: Gln 16 monocytes, but treatment of polymorphonuclear leukocyteswith cytokines likeIFNγandG-CSFcan induce CD64 expression on these cells.
    [Show full text]
  • Analysis of Trans Esnps Infers Regulatory Network Architecture
    Analysis of trans eSNPs infers regulatory network architecture Anat Kreimer Submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Graduate School of Arts and Sciences COLUMBIA UNIVERSITY 2014 © 2014 Anat Kreimer All rights reserved ABSTRACT Analysis of trans eSNPs infers regulatory network architecture Anat Kreimer eSNPs are genetic variants associated with transcript expression levels. The characteristics of such variants highlight their importance and present a unique opportunity for studying gene regulation. eSNPs affect most genes and their cell type specificity can shed light on different processes that are activated in each cell. They can identify functional variants by connecting SNPs that are implicated in disease to a molecular mechanism. Examining eSNPs that are associated with distal genes can provide insights regarding the inference of regulatory networks but also presents challenges due to the high statistical burden of multiple testing. Such association studies allow: simultaneous investigation of many gene expression phenotypes without assuming any prior knowledge and identification of unknown regulators of gene expression while uncovering directionality. This thesis will focus on such distal eSNPs to map regulatory interactions between different loci and expose the architecture of the regulatory network defined by such interactions. We develop novel computational approaches and apply them to genetics-genomics data in human. We go beyond pairwise interactions to define network motifs, including regulatory modules and bi-fan structures, showing them to be prevalent in real data and exposing distinct attributes of such arrangements. We project eSNP associations onto a protein-protein interaction network to expose topological properties of eSNPs and their targets and highlight different modes of distal regulation.
    [Show full text]
  • Disruption of the Neuronal PAS3 Gene in a Family Affected with Schizophrenia D Kamnasaran, W J Muir, M a Ferguson-Smith,Dwcox
    325 ORIGINAL ARTICLE J Med Genet: first published as 10.1136/jmg.40.5.325 on 1 May 2003. Downloaded from Disruption of the neuronal PAS3 gene in a family affected with schizophrenia D Kamnasaran, W J Muir, M A Ferguson-Smith,DWCox ............................................................................................................................. J Med Genet 2003;40:325–332 Schizophrenia and its subtypes are part of a complex brain disorder with multiple postulated aetiolo- gies. There is evidence that this common disease is genetically heterogeneous, with many loci involved. See end of article for In this report, we describe a mother and daughter affected with schizophrenia, who are carriers of a authors’ affiliations t(9;14)(q34;q13) chromosome. By mapping on flow sorted aberrant chromosomes isolated from lym- ....................... phoblast cell lines, both subjects were found to have a translocation breakpoint junction between the Correspondence to: markers D14S730 and D14S70, a 683 kb interval on chromosome 14q13. This interval was found to Dr D W Cox, 8-39 Medical contain the neuronal PAS3 gene (NPAS3), by annotating the genomic sequence for ESTs and perform- Sciences Building, ing RACE and cDNA library screenings. The NPAS3 gene was characterised with respect to the University of Alberta, genomic structure, human expression profile, and protein cellular localisation to gain insight into gene Edmonton, Alberta T6G function. The translocation breakpoint junction lies within the third intron of NPAS3, resulting in the dis- 2H7, Canada; [email protected] ruption of the coding potential. The fact that the bHLH and PAS domains are disrupted from the remain- ing parts of the encoded protein suggests that the DNA binding and dimerisation functions of this Revised version received protein are destroyed.
    [Show full text]
  • PPP2R3C Gene Variants Cause Syndromic 46,XY Gonadal
    5 180 T Guran and others PPP2R3C in testis developmentQ1 180:5 291–309 Clinical Study and spermatogenesis PPP2R3C gene variants cause syndromic 46,XY gonadal dysgenesis and impaired spermatogenesis in humans Tulay Guran1, Gozde Yesil2, Serap Turan1, Zeynep Atay3, Emine Bozkurtlar4, AghaRza Aghayev5, Sinem Gul6, Ilker Tinay7, Basak Aru8, Sema Arslan9, M Kutay Koroglu10, Feriha Ercan10, Gulderen Y Demirel8, Funda S Eren4, Betul Karademir9 and Abdullah Bereket1 1Department of Paediatric Endocrinology and Diabetes, Marmara University, 2Department of Genetics, Bezm-i Alem University, 3Department of Paediatric Endocrinology and Diabetes, Medipol University, 4Department of Pathology, Marmara University, School of Medicine, Istanbul, Turkey, 5Department of Medical Genetics, Istanbul Faculty of Medicine, Istanbul University, Istanbul, Turkey, 6Department of Molecular Biology and Genetics, Gebze Technical University, Kocaeli, Turkey, 7Department of Urology, Marmara University, School of Medicine, Istanbul, Turkey, 8Department of Immunology, Yeditepe Correspondence University, Faculty of Medicine, Istanbul, Turkey, 9Department of Biochemistry, Genetic and Metabolic Diseases should be addressed Research and Investigation Center, and 10Department of Histology and Embryology, Marmara University, School of to T Guran Medicine, Istanbul, Turkey Email [email protected] Abstract Context: Most of the knowledge on the factors involved in human sexual development stems from studies of rare cases with disorders of sex development. Here, we have described a novel 46, XY complete gonadal dysgenesis syndrome caused by homozygous variants in PPP2R3C gene. This gene encodes B″gamma regulatory subunit of the protein phosphatase 2A (PP2A), which is a serine/threonine phosphatase involved in the phospho-regulation processes of most mammalian cell types. PPP2R3C gene is most abundantly expressed in testis in humans, while its function was hitherto unknown.
    [Show full text]
  • Chromosomal Aberrations in Head and Neck Squamous Cell Carcinomas in Norwegian and Sudanese Populations by Array Comparative Genomic Hybridization
    825-843 12/9/08 15:31 Page 825 ONCOLOGY REPORTS 20: 825-843, 2008 825 Chromosomal aberrations in head and neck squamous cell carcinomas in Norwegian and Sudanese populations by array comparative genomic hybridization ERIC ROMAN1,2, LEONARDO A. MEZA-ZEPEDA3, STINE H. KRESSE3, OLA MYKLEBOST3,4, ENDRE N. VASSTRAND2 and SALAH O. IBRAHIM1,2 1Department of Biomedicine, Faculty of Medicine and Dentistry, University of Bergen, Jonas Lies vei 91; 2Department of Oral Sciences - Periodontology, Faculty of Medicine and Dentistry, University of Bergen, Årstadveien 17, 5009 Bergen; 3Department of Tumor Biology, Institute for Cancer Research, Rikshospitalet-Radiumhospitalet Medical Center, Montebello, 0310 Oslo; 4Department of Molecular Biosciences, University of Oslo, Blindernveien 31, 0371 Oslo, Norway Received January 30, 2008; Accepted April 29, 2008 DOI: 10.3892/or_00000080 Abstract. We used microarray-based comparative genomic logical parameters showed little correlation, suggesting an hybridization to explore genome-wide profiles of chromosomal occurrence of gains/losses regardless of ethnic differences and aberrations in 26 samples of head and neck cancers compared clinicopathological status between the patients from the two to their pair-wise normal controls. The samples were obtained countries. Our findings indicate the existence of common from Sudanese (n=11) and Norwegian (n=15) patients. The gene-specific amplifications/deletions in these tumors, findings were correlated with clinicopathological variables. regardless of the source of the samples or attributed We identified the amplification of 41 common chromosomal carcinogenic risk factors. regions (harboring 149 candidate genes) and the deletion of 22 (28 candidate genes). Predominant chromosomal alterations Introduction that were observed included high-level amplification at 1q21 (harboring the S100A gene family) and 11q22 (including Head and neck squamous cell carcinoma (HNSCC), including several MMP family members).
    [Show full text]
  • Genome-Wide Approach to Identify Risk Factors for Therapy-Related Myeloid Leukemia
    Leukemia (2006) 20, 239–246 & 2006 Nature Publishing Group All rights reserved 0887-6924/06 $30.00 www.nature.com/leu ORIGINAL ARTICLE Genome-wide approach to identify risk factors for therapy-related myeloid leukemia A Bogni1, C Cheng2, W Liu2, W Yang1, J Pfeffer1, S Mukatira3, D French1, JR Downing4, C-H Pui4,5,6 and MV Relling1,6 1Department of Pharmaceutical Sciences, The University of Tennessee, Memphis, TN, USA; 2Department of Biostatistics, The University of Tennessee, Memphis, TN, USA; 3Hartwell Center, The University of Tennessee, Memphis, TN, USA; 4Department of Pathology, The University of Tennessee, Memphis, TN, USA; 5Department of Hematology/Oncology St Jude Children’s Research Hospital, The University of Tennessee, Memphis, TN, USA; and 6Colleges of Medicine and Pharmacy, The University of Tennessee, Memphis, TN, USA Using a target gene approach, only a few host genetic risk therapy increases, the importance of identifying host factors for factors for treatment-related myeloid leukemia (t-ML) have been secondary neoplasms increases. defined. Gene expression microarrays allow for a more 4 genome-wide approach to assess possible genetic risk factors Because DNA microarrays interrogate multiple ( 10 000) for t-ML. We assessed gene expression profiles (n ¼ 12 625 genes in one experiment, they allow for a ‘genome-wide’ probe sets) in diagnostic acute lymphoblastic leukemic cells assessment of genes that may predispose to leukemogenesis. from 228 children treated on protocols that included leukemo- DNA microarray analysis of gene expression has been used to genic agents such as etoposide, 13 of whom developed t-ML. identify distinct expression profiles that are characteristic of Expression of 68 probes, corresponding to 63 genes, was different leukemia subtypes.13,14 Studies using this method have significantly related to risk of t-ML.
    [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]
  • FCGR1A Recombinant Protein
    FCGR1A Recombinant Protein CATALOG NUMBER: 96-305 The purity of rh CD64 / FCGR1A was determined by DTT-reduced (+) SDS- PAGE and staining overnight with Coomassie Blue. Specifications SPECIES: Human SOURCE SPECIES: HEK293 cells SEQUENCE: Gln 16 - Pro 288 FUSION TAG: His Tag TESTED APPLICATIONS: WB APPLICATIONS: This recombinant protein can be used for WB. For research use only. BIOLOGICAL ACTIVITY: Measured by its ability to bind human IgG1 in the SPR assay (Biacore 2000) with the KD < 5 nM. Measured by its binding ability in a functional ELISA. Immobilized Human IgG4 at 10ug/mL (100 µl/well),can bind Human Fc gamma RI, His Tag (Cat# FCA-H52H2) with a linear of 0.1-2 ng/mL. Properties PURITY: >90% as determined by SDS-PAGE. PREDICTED MOLECULAR 32.5 kDa WEIGHT: PHYSICAL STATE: Lyopholized BUFFER: PBS, pH7.4 STORAGE CONDITIONS: Lyophilized Protein should be stored at -20˚C or lower for long term storage. Upon reconstitution, working aliquots should be stored at -20˚C or -70˚C. Avoid repeated freeze-thaw cycles. Additional Info ALTERNATE NAMES: FCGR1A, FCG1, FCGR1, IGFR1, CD64, CD64A, FCRI ACCESSION NO.: AAH32634 Background Receptors that recognize the Fc portion of IgG are divided into three groups designated Fc gamma RI, RII, and RIII, also known respectively as CD64, CD32, and CD16. Fc gamma RI binds IgG with high affinity and functions during early immune responses. Fc gamma RII and RIII are low affinity receptors that recognize IgG as aggregates surrounding multivalent antigens during late immune responses. High affinity immunoglobulin gamma Fc receptor I is also known as FCGR1A, FCG1, FCGR1, CD64 and IGFR1, is a type of integral membrane glycoprotein that binds monomeric IgG-type antibodies with high affinity, which belongs to the immunoglobulin superfamily or FCGR1 family.
    [Show full text]
  • The Cardiomyocyte Cell Cycle," Novartis Found Symposium 274 (2006): 196-276
    DePauw University Scholarly and Creative Work from DePauw University Biology Faculty publications Biology 2006 The ac rdiomyocyte cell cycle Pascal J. Lafontant DePauw University, [email protected] Follow this and additional works at: http://scholarship.depauw.edu/bio_facpubs Part of the Biology Commons Recommended Citation Lafontant, Pascal J. E. and Loren J. Field. "The cardiomyocyte cell cycle," Novartis Found Symposium 274 (2006): 196-276. This Article is brought to you for free and open access by the Biology at Scholarly and Creative Work from DePauw University. It has been accepted for inclusion in Biology Faculty publications by an authorized administrator of Scholarly and Creative Work from DePauw University. For more information, please contact [email protected]. NIH Public Access Author Manuscript Novartis Found Symp. Author manuscript; available in PMC 2009 January 20. NIH-PA Author ManuscriptPublished NIH-PA Author Manuscript in final edited NIH-PA Author Manuscript form as: Novartis Found Symp. 2006 ; 274: 196±276. The cardiomyocyte cell cycle Pascal J. E. Lafontant and Loren J. Field From the Wells Center for Pediatric Research and Krannert Institute of Cardiology, Indiana University School of Medicine, Indianapolis, IN 46202-5225. Abstract Many forms of cardiac disease are characterized by cardiomyocyte death due to necrosis, apoptosis and/or oncosis. Recently, the notion of promoting cardiac regeneration as a means to replace damaged heart tissue has engendered considerable interest. One approach to accomplish heart muscle regeneration entails promoting cardiomyocyte cell cycle activity in the surviving myocardium. Genetically modified mice have provided useful model systems to test the efficacy of specific pathways to promote cardiomyocyte proliferation in normal and diseased hearts.
    [Show full text]
  • Expression Profiling of KLF4
    Expression Profiling of KLF4 AJCR0000006 Supplemental Data Figure S1. Snapshot of enriched gene sets identified by GSEA in Klf4-null MEFs. Figure S2. Snapshot of enriched gene sets identified by GSEA in wild type MEFs. 98 Am J Cancer Res 2011;1(1):85-97 Table S1: Functional Annotation Clustering of Genes Up-Regulated in Klf4 -Null MEFs ILLUMINA_ID Gene Symbol Gene Name (Description) P -value Fold-Change Cell Cycle 8.00E-03 ILMN_1217331 Mcm6 MINICHROMOSOME MAINTENANCE DEFICIENT 6 40.36 ILMN_2723931 E2f6 E2F TRANSCRIPTION FACTOR 6 26.8 ILMN_2724570 Mapk12 MITOGEN-ACTIVATED PROTEIN KINASE 12 22.19 ILMN_1218470 Cdk2 CYCLIN-DEPENDENT KINASE 2 9.32 ILMN_1234909 Tipin TIMELESS INTERACTING PROTEIN 5.3 ILMN_1212692 Mapk13 SAPK/ERK/KINASE 4 4.96 ILMN_2666690 Cul7 CULLIN 7 2.23 ILMN_2681776 Mapk6 MITOGEN ACTIVATED PROTEIN KINASE 4 2.11 ILMN_2652909 Ddit3 DNA-DAMAGE INDUCIBLE TRANSCRIPT 3 2.07 ILMN_2742152 Gadd45a GROWTH ARREST AND DNA-DAMAGE-INDUCIBLE 45 ALPHA 1.92 ILMN_1212787 Pttg1 PITUITARY TUMOR-TRANSFORMING 1 1.8 ILMN_1216721 Cdk5 CYCLIN-DEPENDENT KINASE 5 1.78 ILMN_1227009 Gas2l1 GROWTH ARREST-SPECIFIC 2 LIKE 1 1.74 ILMN_2663009 Rassf5 RAS ASSOCIATION (RALGDS/AF-6) DOMAIN FAMILY 5 1.64 ILMN_1220454 Anapc13 ANAPHASE PROMOTING COMPLEX SUBUNIT 13 1.61 ILMN_1216213 Incenp INNER CENTROMERE PROTEIN 1.56 ILMN_1256301 Rcc2 REGULATOR OF CHROMOSOME CONDENSATION 2 1.53 Extracellular Matrix 5.80E-06 ILMN_2735184 Col18a1 PROCOLLAGEN, TYPE XVIII, ALPHA 1 51.5 ILMN_1223997 Crtap CARTILAGE ASSOCIATED PROTEIN 32.74 ILMN_2753809 Mmp3 MATRIX METALLOPEPTIDASE
    [Show full text]
  • Genome-Wide DNA Methylation Analysis of KRAS Mutant Cell Lines Ben Yi Tew1,5, Joel K
    www.nature.com/scientificreports OPEN Genome-wide DNA methylation analysis of KRAS mutant cell lines Ben Yi Tew1,5, Joel K. Durand2,5, Kirsten L. Bryant2, Tikvah K. Hayes2, Sen Peng3, Nhan L. Tran4, Gerald C. Gooden1, David N. Buckley1, Channing J. Der2, Albert S. Baldwin2 ✉ & Bodour Salhia1 ✉ Oncogenic RAS mutations are associated with DNA methylation changes that alter gene expression to drive cancer. Recent studies suggest that DNA methylation changes may be stochastic in nature, while other groups propose distinct signaling pathways responsible for aberrant methylation. Better understanding of DNA methylation events associated with oncogenic KRAS expression could enhance therapeutic approaches. Here we analyzed the basal CpG methylation of 11 KRAS-mutant and dependent pancreatic cancer cell lines and observed strikingly similar methylation patterns. KRAS knockdown resulted in unique methylation changes with limited overlap between each cell line. In KRAS-mutant Pa16C pancreatic cancer cells, while KRAS knockdown resulted in over 8,000 diferentially methylated (DM) CpGs, treatment with the ERK1/2-selective inhibitor SCH772984 showed less than 40 DM CpGs, suggesting that ERK is not a broadly active driver of KRAS-associated DNA methylation. KRAS G12V overexpression in an isogenic lung model reveals >50,600 DM CpGs compared to non-transformed controls. In lung and pancreatic cells, gene ontology analyses of DM promoters show an enrichment for genes involved in diferentiation and development. Taken all together, KRAS-mediated DNA methylation are stochastic and independent of canonical downstream efector signaling. These epigenetically altered genes associated with KRAS expression could represent potential therapeutic targets in KRAS-driven cancer. Activating KRAS mutations can be found in nearly 25 percent of all cancers1.
    [Show full text]