Minimal Peroxide Exposure of Neuronal Cells Induces Multifaceted Adaptive Responses
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Polyclonal Antibody to APIP (Full Length) - Purified
OriGene Technologies, Inc. OriGene Technologies GmbH 9620 Medical Center Drive, Ste 200 Schillerstr. 5 Rockville, MD 20850 32052 Herford UNITED STATES GERMANY Phone: +1-888-267-4436 Phone: +49-5221-34606-0 Fax: +1-301-340-8606 Fax: +49-5221-34606-11 [email protected] [email protected] AP08426PU-N Polyclonal Antibody to APIP (full length) - Purified Alternate names: APAF1-interacting protein, CGI-29 Quantity: 50 µg Concentration: 0.5 mg/ml Background: The mammalian homologues of the key cell death gene CED-4 in C. elegans has been identified recently from human and mouse and designated Apaf1 (for apoptosis protease activating factor 1). Apaf1 binds to cytochrome c (Apaf2) and caspase 9 (Apaf3), which leads to caspase 9 activation. Activated caspase 9 in turn cleaves and activates caspase 3 that is one of the key proteases, being responsible for the proteolytic cleavage of many key proteins in apoptosis. A new Apaf1 Interacting Protein (APIP) also known as CG129 and MMRP19, has been identified as a negative regulator of ischemic injury. APIP competes with Caspase 9 binding site of Apaf1. APIP is predicted to code for a 204 amino acid. An isoform of APIP, APIP2 encodes a 242 amino acid protein, which is an alternative splicing variant differing in its N terminus from APIP. APIP transcript is ubiquitously expressed in most adult tissue with high expression in skeletal muscle, heart, and kidney. Uniprot ID: Q96GX9 NCBI: NP_057041.2 GeneID: 51074 Host / Isotype: Rabbit / IgG Immunogen: Recombinant protein corresponding to a full-length His-tagged recombinant Human APIP protein Format: State: Liquid purified Ig fraction Purification: Protein G Chromatography Buffer System: PBS containing 0.2% Gelatin as stabilizer and 0.05% Sodium Azide as preservative Applications: Immunohistochemistry on Paraffin Sections: 10 µg/ml. -
Wo 2010/075007 A2
(12) INTERNATIONAL APPLICATION PUBLISHED UNDER THE PATENT COOPERATION TREATY (PCT) (19) World Intellectual Property Organization International Bureau (10) International Publication Number (43) International Publication Date 1 July 2010 (01.07.2010) WO 2010/075007 A2 (51) International Patent Classification: (81) Designated States (unless otherwise indicated, for every C12Q 1/68 (2006.01) G06F 19/00 (2006.01) kind of national protection available): AE, AG, AL, AM, C12N 15/12 (2006.01) AO, AT, AU, AZ, BA, BB, BG, BH, BR, BW, BY, BZ, CA, CH, CL, CN, CO, CR, CU, CZ, DE, DK, DM, DO, (21) International Application Number: DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, PCT/US2009/067757 HN, HR, HU, ID, IL, IN, IS, JP, KE, KG, KM, KN, KP, (22) International Filing Date: KR, KZ, LA, LC, LK, LR, LS, LT, LU, LY, MA, MD, 11 December 2009 ( 11.12.2009) ME, MG, MK, MN, MW, MX, MY, MZ, NA, NG, NI, NO, NZ, OM, PE, PG, PH, PL, PT, RO, RS, RU, SC, SD, (25) Filing Language: English SE, SG, SK, SL, SM, ST, SV, SY, TJ, TM, TN, TR, TT, (26) Publication Language: English TZ, UA, UG, US, UZ, VC, VN, ZA, ZM, ZW. (30) Priority Data: (84) Designated States (unless otherwise indicated, for every 12/3 16,877 16 December 2008 (16.12.2008) US kind of regional protection available): ARIPO (BW, GH, GM, KE, LS, MW, MZ, NA, SD, SL, SZ, TZ, UG, ZM, (71) Applicant (for all designated States except US): DODDS, ZW), Eurasian (AM, AZ, BY, KG, KZ, MD, RU, TJ, W., Jean [US/US]; 938 Stanford Street, Santa Monica, TM), European (AT, BE, BG, CH, CY, CZ, DE, DK, EE, CA 90403 (US). -
Androgen Receptor Binding Sites Identified by a GREF GATA Model
doi:10.1016/j.jmb.2005.09.009 J. Mol. Biol. (2005) 353, 763–771 COMMUNICATION Androgen Receptor Binding Sites Identified by a GREF_GATA Model Katsuaki Masuda1, Thomas Werner2, Shilpi Maheshwari1 Matthias Frisch2, Soyon Oh1, Gyorgy Petrovics1, Klaus May2 Vasantha Srikantan1, Shiv Srivastava1 and Albert Dobi1* 1Center for Prostate Disease Changes in transcriptional regulation can be permissive for tumor Research, Department of progression by allowing for selective growth advantage of tumor cells. Surgery, Uniformed Services Tumor suppressors can effectively inhibit this process. The PMEPA1 gene, a University, Rockville, MD potent inhibitor of prostate cancer cell growth is an androgen-regulated 20852, USA gene. We addressed the question of whether or not androgen receptor can directly bind to specific PMEPA1 promoter upstream sequences. To test this 2Genomatix Software GmbH hypothesis we extended in silico prediction of androgen receptor binding D-80339 Munich, Germany sites by a modeling approach and verified the actual binding by in vivo chromatin immunoprecipitation assay. Promoter upstream sequences of highly androgen-inducible genes were examined from microarray data of prostate cancer cells for transcription factor binding sites (TFBSs). Results were analyzed to formulate a model for the description of specific androgen receptor binding site context in these sequences. In silico analysis and subsequent experimental verification of the selected sequences suggested that a model that combined a GREF and a GATA TFBS was sufficient for predicting a class of functional androgen receptor binding sites. The GREF matrix family represents androgen receptor, glucocorticoid receptor and progesterone receptor binding sites and the GATA matrix family represents GATA binding protein 1–6 binding sites. -
Genomic Regions Associated with Muscularity in Beef Cattle Differ In
Doyle et al. Genet Sel Evol (2020) 52:2 https://doi.org/10.1186/s12711-020-0523-1 Genetics Selection Evolution RESEARCH ARTICLE Open Access Genomic regions associated with muscularity in beef cattle difer in fve contrasting cattle breeds Jennifer L. Doyle1,2, Donagh P. Berry1* , Roel F. Veerkamp3, Tara R. Carthy1, Ross D. Evans4, Siobhán W. Walsh2 and Deirdre C. Purfeld1 Abstract Background: Linear type traits, which refect the muscular characteristics of an animal, could provide insight into how, in some cases, morphologically very diferent animals can yield the same carcass weight. Such variability may contribute to diferences in the overall value of the carcass since primal cuts vary greatly in price; such variability may also hinder successful genome-based association studies. Therefore, the objective of our study was to identify genomic regions that are associated with fve muscularity linear type traits and to determine if these signifcant regions are common across fve diferent breeds. Analyses were carried out using linear mixed models on imputed whole-genome sequence data in each of the fve breeds, separately. Then, the results of the within-breed analyses were used to conduct an across-breed meta-analysis per trait. Results: We identifed many quantitative trait loci (QTL) that are located across the whole genome and associated with each trait in each breed. The only commonality among the breeds and traits was a large-efect pleiotropic QTL on BTA2 that contained the MSTN gene, which was associated with all traits in the Charolais and Limousin breeds. Other plausible candidate genes were identifed for muscularity traits including PDE1A, PPP1R1C and multiple col- lagen and HOXD genes. -
APIP (NM 015957) Human Tagged ORF Clone Product Data
OriGene Technologies, Inc. 9620 Medical Center Drive, Ste 200 Rockville, MD 20850, US Phone: +1-888-267-4436 [email protected] EU: [email protected] CN: [email protected] Product datasheet for RC203297 APIP (NM_015957) Human Tagged ORF Clone Product data: Product Type: Expression Plasmids Product Name: APIP (NM_015957) Human Tagged ORF Clone Tag: Myc-DDK Symbol: APIP Synonyms: APIP2; CGI-29; CGI29; hAPIP; MMRP19 Vector: pCMV6-Entry (PS100001) E. coli Selection: Kanamycin (25 ug/mL) Cell Selection: Neomycin ORF Nucleotide >RC203297 ORF sequence Sequence: Red=Cloning site Blue=ORF Green=Tags(s) TTTTGTAATACGACTCACTATAGGGCGGCCGGGAATTCGTCGACTGGATCCGGTACCGAGGAGATCTGCC GCCGCGATCGCC ATGTCTGGCTGTGATGCTCGGGAGGGAGACTGTTGTTCCCGGAGATGCGGCGCGCAGGACAAGGAGCGTC CAAGATACCTGATCCCAGAACTTTGCAAACAGTTTTACCATTTAGGCTGGGTCACTGGGACTGGAGGAGG AATTAGCTTGAAGCATGGCGATGAAATCTACATTGCTCCTTCAGGAGTGCAAAAGGAACGAATTCAGCCT GAAGACATGTTTGTTTGTGATATAAATGAAAAGGACATAAGTGGACCTTCGCCATCGAAGAAGCTAAAAA AAAGCCAGTGTACTCCTCTTTTCATGAATGCTTACACAATGAGAGGAGCAGGTGCAGTGATTCATACCCA CTCTAAAGCTGCTGTGATGGCCACACTTCTCTTTCCAGGACGGGAGTTTAAAATTACACATCAAGAGATG ATAAAAGGAATAAAGAAATGTACTTCCGGAGGGTATTATAGATATGATGATATGTTAGTGGTACCCATTA TTGAGAATACACCTGAGGAGAAAGACCTCAAAGATAGAATGGCTCATGCAGTGAATGAATACCCAGACTC CTGTGCAGTACTGGTCAGACGTCATGGAGTATATGTGTGGGGGGAAACATGGGAGAAGGCCAAAACCATG TGTGAGTGTTATGACTATTTATTTGATATTGCCGTATCAATGAAGAAAGTAGGACTTGATCCTTCACAGC TCCCAGTTGGAGAAAATGGAATTGTC ACGCGTACGCGGCCGCTCGAGCAGAAACTCATCTCAGAAGAGGATCTGGCAGCAAATGATATCCTGGATT ACAAGGATGACGACGATAAGGTTTAA This product is to be used for -
Genome-Wide Association Study of Multiplex Schizophrenia Pedigrees
Article Genome-Wide Association Study of Multiplex Schizophrenia Pedigrees Douglas F. Levinson, M.D. Anthony O’Neill, M.D. in the primary European-ancestry analyses). Association was tested for single SNPs and Jianxin Shi, Ph.D. George N. Papadimitriou, M.D. genetic pathways. Polygenic scores based Kai Wang, Ph.D. Dimitris Dikeos, M.D. on family study results were used to predict case-control status in the Schizophrenia Sang Oh, M.Sc. Wolfgang Maier, M.D. Psychiatric GWAS Consortium (PGC) data set, and consistency of direction of effect Brien Riley, Ph.D. Bernard Lerer, M.D. with the family study was determined for Ann E. Pulver, Ph.D. Dominique Campion, M.D., top SNPs in the PGC GWAS analysis. Within- family segregation was examined for Dieter B. Wildenauer, Ph.D. Ph.D. schizophrenia-associated rare CNVs. Claudine Laurent, M.D., Ph.D. David Cohen, M.D., Ph.D. Results: No genome-wide significant asso- Maurice Jay, M.D. ciations were observed for single SNPs or for Bryan J. Mowry, M.D., pathways. PGC case and control subjects F.R.A.N.Z.C.P. Ayman Fanous, M.D. had significantly different genome-wide Pablo V. Gejman, M.D. Peter Eichhammer, M.D. polygenic scores (computed by weighting their genotypes by log-odds ratios from the 2 Michael J. Owen, Ph.D., Jeremy M. Silverman, Ph.D. family study) (best p=10 17, explaining F.R.C.Psych. 0.4% of the variance). Family study and Nadine Norton, Ph.D. PGC analyses had consistent directions for Kenneth S. Kendler, M.D. -
Strand Breaks for P53 Exon 6 and 8 Among Different Time Course of Folate Depletion Or Repletion in the Rectosigmoid Mucosa
SUPPLEMENTAL FIGURE COLON p53 EXONIC STRAND BREAKS DURING FOLATE DEPLETION-REPLETION INTERVENTION Supplemental Figure Legend Strand breaks for p53 exon 6 and 8 among different time course of folate depletion or repletion in the rectosigmoid mucosa. The input of DNA was controlled by GAPDH. The data is shown as ΔCt after normalized to GAPDH. The higher ΔCt the more strand breaks. The P value is shown in the figure. SUPPLEMENT S1 Genes that were significantly UPREGULATED after folate intervention (by unadjusted paired t-test), list is sorted by P value Gene Symbol Nucleotide P VALUE Description OLFM4 NM_006418 0.0000 Homo sapiens differentially expressed in hematopoietic lineages (GW112) mRNA. FMR1NB NM_152578 0.0000 Homo sapiens hypothetical protein FLJ25736 (FLJ25736) mRNA. IFI6 NM_002038 0.0001 Homo sapiens interferon alpha-inducible protein (clone IFI-6-16) (G1P3) transcript variant 1 mRNA. Homo sapiens UDP-N-acetyl-alpha-D-galactosamine:polypeptide N-acetylgalactosaminyltransferase 15 GALNTL5 NM_145292 0.0001 (GALNT15) mRNA. STIM2 NM_020860 0.0001 Homo sapiens stromal interaction molecule 2 (STIM2) mRNA. ZNF645 NM_152577 0.0002 Homo sapiens hypothetical protein FLJ25735 (FLJ25735) mRNA. ATP12A NM_001676 0.0002 Homo sapiens ATPase H+/K+ transporting nongastric alpha polypeptide (ATP12A) mRNA. U1SNRNPBP NM_007020 0.0003 Homo sapiens U1-snRNP binding protein homolog (U1SNRNPBP) transcript variant 1 mRNA. RNF125 NM_017831 0.0004 Homo sapiens ring finger protein 125 (RNF125) mRNA. FMNL1 NM_005892 0.0004 Homo sapiens formin-like (FMNL) mRNA. ISG15 NM_005101 0.0005 Homo sapiens interferon alpha-inducible protein (clone IFI-15K) (G1P2) mRNA. SLC6A14 NM_007231 0.0005 Homo sapiens solute carrier family 6 (neurotransmitter transporter) member 14 (SLC6A14) mRNA. -
Molecular Cytogenetics Biomed Central
Molecular Cytogenetics BioMed Central Research Open Access MODY-like diabetes associated with an apparently balanced translocation: possible involvement of MPP7 gene and cell polarity in the pathogenesis of diabetes Elizabeth J Bhoj1, Stefano Romeo1,2, Marco G Baroni2, Guy Bartov3, Roger A Schultz3,5 and Andrew R Zinn*1,4 Address: 1McDermott Center for Human Growth and Development, The University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA, 2Department of Medical Sciences, Endocrinology, University of Cagliari, Cagliari, Italy, 3Department of Pathology, The University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA , 4Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA and 5Signature Genomic Laboratories, LLC, Spokane, WA, USA Email: Elizabeth J Bhoj - [email protected]; Stefano Romeo - [email protected]; Marco G Baroni - [email protected]; Guy Bartov - [email protected]; Roger A Schultz - [email protected]; Andrew R Zinn* - [email protected] * Corresponding author Published: 13 February 2009 Received: 26 September 2008 Accepted: 13 February 2009 Molecular Cytogenetics 2009, 2:5 doi:10.1186/1755-8166-2-5 This article is available from: http://www.molecularcytogenetics.org/content/2/1/5 © 2009 Bhoj et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Background: Characterization of disease-associated balanced translocations has led to the discovery of genes responsible for many disorders, including syndromes that include various forms of diabetes mellitus. -
Microrna Regulation and Human Protein Kinase Genes
MICRORNA REGULATION AND HUMAN PROTEIN KINASE GENES REQUIRED FOR INFLUENZA VIRUS REPLICATION by LAUREN ELIZABETH ANDERSEN (Under the Direction of Ralph A. Tripp) ABSTRACT Human protein kinases (HPKs) have profound effects on cellular responses. To better understand the role of HPKs and the signaling networks that influence influenza replication, a siRNA screen of 720 HPKs was performed. From the screen, 17 “hit” HPKs (NPR2, MAP3K1, DYRK3, EPHA6, TPK1, PDK2, EXOSC10, NEK8, PLK4, SGK3, NEK3, PANK4, ITPKB, CDC2L5, CALM2, PKN3, and HK2) were validated as important for A/WSN/33 influenza virus replication, and 6 HPKs (CDC2L5, HK2, NEK3, PANK4, PLK4 and SGK3) identified as important for A/New Caledonia/20/99 influenza virus replication. Meta-analysis of the hit HPK genes identified important for influenza virus replication showed a level of overlap, most notably with the p53/DNA damage pathway. In addition, microRNAs (miRNAs) predicted to target the validated HPK genes were determined based on miRNA seed site predictions from computational analysis and then validated using a panel of miRNA agonists and antagonists. The results identify miRNA regulation of hit HPK genes identified, specifically miR-148a by targeting CDC2L5 and miR-181b by targeting SGK3, and suggest these miRNAs also have a role in regulating influenza virus replication. Together these data advance our understanding of miRNA regulation of genes critical for virus replication and are important for development novel influenza intervention strategies. INDEX WORDS: Influenza virus, -
NLRP3 and ASC Differentially Affect the Lung Transcriptome During Pneumococcal Pneumonia
UvA-DARE (Digital Academic Repository) Cell-specific pattern recognition receptor signaling in antibacterial defense van Lieshout, M.H.P. Publication date 2015 Document Version Final published version Link to publication Citation for published version (APA): van Lieshout, M. H. P. (2015). Cell-specific pattern recognition receptor signaling in antibacterial defense. General rights It is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s), other than for strictly personal, individual use, unless the work is under an open content license (like Creative Commons). Disclaimer/Complaints regulations If you believe that digital publication of certain material infringes any of your rights or (privacy) interests, please let the Library know, stating your reasons. In case of a legitimate complaint, the Library will make the material inaccessible and/or remove it from the website. Please Ask the Library: https://uba.uva.nl/en/contact, or a letter to: Library of the University of Amsterdam, Secretariat, Singel 425, 1012 WP Amsterdam, The Netherlands. You will be contacted as soon as possible. UvA-DARE is a service provided by the library of the University of Amsterdam (https://dare.uva.nl) Download date:30 Sep 2021 Chapter 7 NLRP3 and ASC differentially affect the lung transcriptome during pneumococcal pneumonia American Journal of Respiratory Cell and Molecular Biology 2014 Apr;50(4):699-712 DOI: 10.1165/rcmb.2013-0015OC Miriam H.P. van Lieshout 1,2 Brendon P. Scicluna 1,2 Sandrine Florquin 3 Tom van der Poll 1,2,4 Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands: 1Center of Infection and Immunity Amsterdam 2Center of Experimental and Molecular Medicine 3Department of Pathology 4Division of Infectious Diseases Chapter 7 Abstract Streptococcus (S.) pneumoniae is the most frequently isolated causative pathogen of community-acquired pneumonia, a leading cause of mortality worldwide. -
Homologs of Genes Expressed in Caenorhabditis Elegans Gabaergic
Hammock et al. Neural Development 2010, 5:32 http://www.neuraldevelopment.com/content/5/1/32 RESEARCH ARTICLE Open Access Homologs of genes expressed in Caenorhabditis elegans GABAergic neurons are also found in the developing mouse forebrain Elizabeth AD Hammock1,2*, Kathie L Eagleson3, Susan Barlow4,6, Laurie R Earls4,7, David M Miller III2,4,5, Pat Levitt3* Abstract Background: In an effort to identify genes that specify the mammalian forebrain, we used a comparative approach to identify mouse homologs of transcription factors expressed in developing Caenorhabditis elegans GABAergic neurons. A cell-specific microarray profiling study revealed a set of transcription factors that are highly expressed in embryonic C. elegans GABAergic neurons. Results: Bioinformatic analyses identified mouse protein homologs of these selected transcripts and their expression pattern was mapped in the mouse embryonic forebrain by in situ hybridization. A review of human homologs indicates several of these genes are potential candidates in neurodevelopmental disorders. Conclusions: Our comparative approach has revealed several novel candidates that may serve as future targets for studies of mammalian forebrain development. Background As with other cell types, the diversity of GABAergic Proper forebrain patterning and cell-fate specification neurons has its basis in different developmental origins, lay the foundation for complex behaviors. These neuro- with timing and location of birth playing key roles in developmental events in large part depend on a series of cell fate [1,6-8]. gene expression refinements (reviewed in [1]) that com- Despite the phenotypic variety of GABAergic neurons, mit cells to express certain phenotypic features that all use GABA as a neurotransmitter. -
Defining Trends in Global Gene Expression in Arabian Horses with Cerebellar Abiotrophy
Cerebellum DOI 10.1007/s12311-016-0823-8 ORIGINAL PAPER Defining Trends in Global Gene Expression in Arabian Horses with Cerebellar Abiotrophy E. Y. Scott1 & M. C. T. Penedo2,3 & J. D. Murray1,3 & C. J. Finno3 # Springer Science+Business Media New York 2016 Abstract Equine cerebellar abiotrophy (CA) is a hereditary expression (DE) analysis were used (Tophat2/Cuffdiff2, neurodegenerative disease that affects the Purkinje neurons of Kallisto/EdgeR, and Kallisto/Sleuth) with 151 significant the cerebellum and causes ataxia in Arabian foals. Signs of DE genes identified by all three pipelines in CA-affected CA are typically first recognized either at birth to any time up horses. TOE1 (Log2(foldchange) = 0.92, p =0.66)and to 6 months of age. CA is inherited as an autosomal recessive MUTYH (Log2(foldchange) = 1.13, p = 0.66) were not dif- trait and is associated with a single nucleotide polymorphism ferentially expressed. Among the major pathways that were (SNP) on equine chromosome 2 (13074277G>A), located in differentially expressed, genes associated with calcium ho- the fourth exon of TOE1 and in proximity to MUTYH on the meostasis and specifically expressed in Purkinje neurons, antisense strand. We hypothesize that unraveling the func- CALB1 (Log2(foldchange) = −1.7, p < 0.01) and CA8 tional consequences of the CA SNP using RNA-seq will elu- (Log2(foldchange) = −0.97, p < 0.01), were significantly cidate the molecular pathways underlying the CA phenotype. down-regulated, confirming loss of Purkinje neurons. There RNA-seq (100 bp PE strand-specific) was performed in cer- was also a significant up-regulation of markers for microglial ebellar tissue from four CA-affected and five age-matched phagocytosis, TYROBP (Log2(foldchange) = 1.99, p <0.01) unaffected horses.