Sex-Specific Transcriptome Differences in Human Adipose
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Metallothionein Monoclonal Antibody, Clone N11-G
Metallothionein monoclonal antibody, clone N11-G Catalog # : MAB9787 規格 : [ 50 uL ] List All Specification Application Image Product Rabbit monoclonal antibody raised against synthetic peptide of MT1A, Western Blot (Recombinant protein) Description: MT1B, MT1E, MT1F, MT1G, MT1H, MT1IP, MT1L, MT1M, MT2A. Immunogen: A synthetic peptide corresponding to N-terminus of human MT1A, MT1B, MT1E, MT1F, MT1G, MT1H, MT1IP, MT1L, MT1M, MT2A. Host: Rabbit enlarge Reactivity: Human, Mouse Immunoprecipitation Form: Liquid Enzyme-linked Immunoabsorbent Assay Recommend Western Blot (1:1000) Usage: ELISA (1:5000-1:10000) The optimal working dilution should be determined by the end user. Storage Buffer: In 20 mM Tris-HCl, pH 8.0 (10 mg/mL BSA, 0.05% sodium azide) Storage Store at -20°C. Instruction: Note: This product contains sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only. Datasheet: Download Applications Western Blot (Recombinant protein) Western blot analysis of recombinant Metallothionein protein with Metallothionein monoclonal antibody, clone N11-G (Cat # MAB9787). Lane 1: 1 ug. Lane 2: 3 ug. Lane 3: 5 ug. Immunoprecipitation Enzyme-linked Immunoabsorbent Assay ASSP5 MT1A MT1B MT1E MT1F MT1G MT1H MT1M MT1L MT1IP Page 1 of 5 2021/6/2 Gene Information Entrez GeneID: 4489 Protein P04731 (Gene ID : 4489);P07438 (Gene ID : 4490);P04732 (Gene ID : Accession#: 4493);P04733 (Gene ID : 4494);P13640 (Gene ID : 4495);P80294 (Gene ID : 4496);P80295 (Gene ID : 4496);Q8N339 (Gene ID : 4499);Q86YX0 (Gene ID : 4490);Q86YX5 -
Evaluation of Chromatin Accessibility in Prefrontal Cortex of Individuals with Schizophrenia
ARTICLE DOI: 10.1038/s41467-018-05379-y OPEN Evaluation of chromatin accessibility in prefrontal cortex of individuals with schizophrenia Julien Bryois 1, Melanie E. Garrett2, Lingyun Song3, Alexias Safi3, Paola Giusti-Rodriguez 4, Graham D. Johnson 3, Annie W. Shieh13, Alfonso Buil5, John F. Fullard6, Panos Roussos 6,7,8, Pamela Sklar6, Schahram Akbarian 6, Vahram Haroutunian 6,9, Craig A. Stockmeier 10, Gregory A. Wray3,11, Kevin P. White12, Chunyu Liu13, Timothy E. Reddy 3,14, Allison Ashley-Koch2,15, Patrick F. Sullivan 1,4,16 & Gregory E. Crawford 3,17 1234567890():,; Schizophrenia genome-wide association studies have identified >150 regions of the genome associated with disease risk, yet there is little evidence that coding mutations contribute to this disorder. To explore the mechanism of non-coding regulatory elements in schizophrenia, we performed ATAC-seq on adult prefrontal cortex brain samples from 135 individuals with schizophrenia and 137 controls, and identified 118,152 ATAC-seq peaks. These accessible chromatin regions in the brain are highly enriched for schizophrenia SNP heritability. Accessible chromatin regions that overlap evolutionarily conserved regions exhibit an even higher heritability enrichment, indicating that sequence conservation can further refine functional risk variants. We identify few differences in chromatin accessibility between cases and controls, in contrast to thousands of age-related differential accessible chromatin regions. Altogether, we characterize chromatin accessibility in the human prefrontal cortex, the effect of schizophrenia and age on chromatin accessibility, and provide evidence that our dataset will allow for fine mapping of risk variants. 1 Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, SE-17177 Stockholm, Sweden. -
Supplemental Tables4.Pdf
Yano_Supplemental_Table_S4 Gene ontology – Biological process 1 of 9 Fold List Pop Pop GO Term Count % PValue Bonferroni Benjamini FDR Genes Total Hits Total Enrichment DLC1, CADM1, NELL2, CLSTN1, PCDHGA8, CTNNB1, NRCAM, APP, CNTNAP2, FERT2, RAPGEF1, PTPRM, MPDZ, SDK1, PCDH9, PTPRS, VEZT, NRXN1, MYH9, GO:0007155~cell CTNNA2, NCAM1, NCAM2, DDR1, LSAMP, CNTN1, 50 5.61 2.14E-08 510 311 7436 2.34 4.50E-05 4.50E-05 3.70E-05 adhesion ROR2, VCAN, DST, LIMS1, TNC, ASTN1, CTNND2, CTNND1, CDH2, NEO1, CDH4, CD24A, FAT3, PVRL3, TRO, TTYH1, MLLT4, LPP, NLGN1, PCDH19, LAMA1, ITGA9, CDH13, CDON, PSPC1 DLC1, CADM1, NELL2, CLSTN1, PCDHGA8, CTNNB1, NRCAM, APP, CNTNAP2, FERT2, RAPGEF1, PTPRM, MPDZ, SDK1, PCDH9, PTPRS, VEZT, NRXN1, MYH9, GO:0022610~biological CTNNA2, NCAM1, NCAM2, DDR1, LSAMP, CNTN1, 50 5.61 2.14E-08 510 311 7436 2.34 4.50E-05 4.50E-05 3.70E-05 adhesion ROR2, VCAN, DST, LIMS1, TNC, ASTN1, CTNND2, CTNND1, CDH2, NEO1, CDH4, CD24A, FAT3, PVRL3, TRO, TTYH1, MLLT4, LPP, NLGN1, PCDH19, LAMA1, ITGA9, CDH13, CDON, PSPC1 DCC, ENAH, PLXNA2, CAPZA2, ATP5B, ASTN1, PAX6, ZEB2, CDH2, CDH4, GLI3, CD24A, EPHB1, NRCAM, GO:0006928~cell CTTNBP2, EDNRB, APP, PTK2, ETV1, CLASP2, STRBP, 36 4.04 3.46E-07 510 205 7436 2.56 7.28E-04 3.64E-04 5.98E-04 motion NRG1, DCLK1, PLAT, SGPL1, TGFBR1, EVL, MYH9, YWHAE, NCKAP1, CTNNA2, SEMA6A, EPHA4, NDEL1, FYN, LRP6 PLXNA2, ADCY5, PAX6, GLI3, CTNNB1, LPHN2, EDNRB, LPHN3, APP, CSNK2A1, GPR45, NRG1, RAPGEF1, WWOX, SGPL1, TLE4, SPEN, NCAM1, DDR1, GRB10, GRM3, GNAQ, HIPK1, GNB1, HIPK2, PYGO1, GO:0007166~cell RNF138, ROR2, CNTN1, -
The Ribosomal Protein Rpl22 Controls Ribosome Composition by Directly Repressing Expression of Its Own Paralog, Rpl22l1
The Ribosomal Protein Rpl22 Controls Ribosome Composition by Directly Repressing Expression of Its Own Paralog, Rpl22l1 Monique N. O’Leary1,2, Katherine H. Schreiber1,2, Yong Zhang3, Anne-Ce´cile E. Duc3, Shuyun Rao3,J. Scott Hale4¤, Emmeline C. Academia2, Shreya R. Shah1, John F. Morton5, Carly A. Holstein6, Dan B. Martin6, Matt Kaeberlein7, Warren C. Ladiges5, Pamela J. Fink4, Vivian L. MacKay1, David L. Wiest3, Brian K. Kennedy1,2* 1 Department of Biochemistry, University of Washington, Seattle, Washington, United States of America, 2 Buck Institute for Research on Aging, Novato, California, United States of America, 3 Blood Cell Development and Cancer Keystone, Immune Cell Development and Host Defense Program, Fox Chase Cancer Center, Philadelphia, Pennsylvania, United States of America, 4 Department of Immunology, University of Washington, Seattle, Washington, United States of America, 5 Department of Comparative Medicine, University of Washington, Seattle, Washington, United States of America, 6 Institute for Systems Biology, Seattle, Washington, United States of America, 7 Department of Pathology, University of Washington, Seattle, Washington, United States of America Abstract Most yeast ribosomal protein genes are duplicated and their characterization has led to hypotheses regarding the existence of specialized ribosomes with different subunit composition or specifically-tailored functions. In yeast, ribosomal protein genes are generally duplicated and evidence has emerged that paralogs might have specific roles. Unlike yeast, most mammalian ribosomal proteins are thought to be encoded by a single gene copy, raising the possibility that heterogenous populations of ribosomes are unique to yeast. Here, we examine the roles of the mammalian Rpl22, finding that Rpl222/2 mice have only subtle phenotypes with no significant translation defects. -
Supplementary Table 1.Xlsx
SUPPLEMENTARY APPENDIX Chromothripsis is linked to TP53 alteration, cell cycle impairment, and dismal outcome in acute myeloid leukemia with complex karyotype Frank G. Rücker, 1 Anna Dolnik, 1 Tamara J. Blätte, 1 Veronica Teleanu, 1 Aurélie Ernst, 2 Felicitas Thol, 3 Michael Heuser, 3 Arnold Ganser, 3 Hartmut Döhner, 1 Konstanze Döhner *1 and Lars Bullinger *1,4 1Department of Internal Medicine III, University Hospital of Ulm, Albert-Einstein-Allee 23; 2Division of Molecular Genetics, German Cancer Consor - tium (DKTK), German Cancer Research Center (DKFZ), Heidelberg; 3Department of Hematology, Hemostasis, Oncology, and Stem Cell Transplanta - tion, Hannover Medical School and 4Department of Hematology, Oncology and Tumor Immunology, Charité-University Medicine Berlin, Campus Virchow Klinikum, Berlin, Germany *KD and LB contributed equally to this work. Correspondence: [email protected] doi:10.3324/haematol.2017.180497 Supplementary Table 1 Top 200 differentially expressed genes in chromothripsis‐positive (n=13) vs –negative (n=14) CK‐AML (p‐value <.05) Symbol ID LogFC p value PSMB10 5699 ‐1,652 4,81E‐05 ADAMTS6 11174 ‐1,736 1,50E‐04 SLC7A6 9057 ‐1,317 6,80E‐04 VANGL1 81839 2,403 6,94E‐04 ZNF197 10168 1,409 7,30E‐04 TAS2R62P 338399 ‐1,404 9,22E‐04 PLA2G15 23659 ‐1,455 0,001 CBFB 865 ‐1,453 0,001 CNOT8 9337 ‐1,449 0,001 ACD 65057 ‐1,329 0,001 CKLF 51192 ‐1,657 0,002 CMTM3 123920 ‐1,48 0,002 FAM192A 80011 ‐1,408 0,002 SSH3 54961 ‐1,279 0,002 ZNF415 55786 1,425 0,002 BEX2 84707 1,57 0,002 GCNT2 2651 1,732 0,002 PIM1 5292 1,935 -
Assessment of Hematopoietic Failure Due to Rpl11 Deficiency in a Zebrafish Model of Diamond-Blackfan Anemia by Deep Sequencing
Zhang et al. BMC Genomics 2013, 14:896 http://www.biomedcentral.com/1471-2164/14/896 RESEARCH ARTICLE Open Access Assessment of hematopoietic failure due to Rpl11 deficiency in a zebrafish model of Diamond- Blackfan anemia by deep sequencing Zhaojun Zhang1†, Haibo Jia2†, Qian Zhang1, Yang Wan3, Yang Zhou2, Qiong Jia2, Wanguang Zhang4, Weiping Yuan3, Tao Cheng3, Xiaofan Zhu3* and Xiangdong Fang1* Abstract Background: Diamond–Blackfan anemia is a rare congenital red blood cell dysplasia that develops soon after birth. RPL11 mutations account for approximately 4.8% of human DBA cases with defective hematopoietic phenotypes. However, the mechanisms by which RPL11 regulates hematopoiesis in DBA remain elusive. In this study, we analyzed the transcriptome using deep sequencing data from an Rpl11-deficient zebrafish model to identify Rpl11-mediated hematopoietic failure and investigate the underlying mechanisms. Results: We characterized hematological defects in Rpl11-deficient zebrafish embryos by identifying affected hematological genes, hematopoiesis-associated pathways, and regulatory networks. We found that hemoglobin biosynthetic and hematological defects in Rpl11-deficient zebrafish were related to dysregulation of iron metabolism-related genes, including tfa, tfr1b, alas2 and slc25a37, which are involved in heme and hemoglobin biosynthesis. In addition, we found reduced expression of the hematopoietic stem cells (HSC) marker cmyb and HSC transcription factors tal1 and hoxb4a in Rpl11-deficient zebrafish embryos, indicating that the hematopoietic defects may be related to impaired HSC formation, differentiation, and proliferation. However, Rpl11 deficiency did not affect the development of other blood cell lineages such as granulocytes and myelocytes. Conclusion: We identified hematopoietic failure of Rpl11-deficient zebrafish embryos using transcriptome deep sequencing and elucidated potential underlying mechanisms. -
UC Riverside UCR Honors Capstones 2019-2020
UC Riverside UCR Honors Capstones 2019-2020 Title Development of a Method for Heterologous Expression of Moss Methyltransferases in Pichia Pastoris Yeast Permalink https://escholarship.org/uc/item/4f71h39k Author Fogel, Dustin Publication Date 2021-01-08 Data Availability The data associated with this publication are within the manuscript. eScholarship.org Powered by the California Digital Library University of California By A capstone project submitted for Graduation with University Honors University Honors University of California, Riverside APPROVED _______________________________________________ Dr. Department of _______________________________________________ Dr. Richard Cardullo, Howard H Hays Jr. Chair, University Honors Abstract Acknowledgements: I would like to thanks to Anjin Huang for her extensive work on designing and leading a significant part of the transformation of new Pichia cultures. I would also like to thank Dr. Eugene A. Nothnagel, my faculty mentor, for his unending dedication, guidance, and support throughout both this capstone project and my time as an undergraduate student at UCR. Additionally, I would like to thank Dr. Martha L. Orozco-Cárdenas for aiding in this project by donating both lab space and time to developing this project. Finally, I would like to thank other student collaborators, Carlos Aguilar, James Yen, Maivy Ngoc Le, and others in assisting with conducting many of the experiments that culminated in this capstone project. 1 Table of Contents Abstract_____________________________________________________________________ -
Hedgehog Signaling, Epithelial-To-Mesenchymal Transition and Mirna (Review)
271-275 1/8/08 15:18 Page 271 INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE 22: 271-275, 2008 271 Hedgehog signaling, epithelial-to-mesenchymal transition and miRNA (Review) YURIKO KATOH1 and MASARU KATOH2 1M&M Medical Bioinformatics, Hongo 113-0033; 2Genetics and Cell Biology Section, National Cancer Center, Tokyo 104-0045, Japan Received May 19, 2008; Accepted June 26, 2008 DOI: 10.3892/ijmm_00000019 Abstract. SHH, IHH, and DHH are lipid-modified secreted strictly controlled before clinical application of synthetic proteins binding to Patched receptors, and CDON, BOC or miRNA. Peptide mimetic and RNA aptamer could also be GAS1 co-receptors. In the absence of Hedgehog signaling, utilized as Hedgehog signaling inhibitors or EMT suppressors. GLI1 is transcriptionally repressed, GLI2 is phosphorylated by GSK3 and CK1 for the FBXW11 (ßTRCP2)-mediated degradation, and GLI3 is processed to a cleaved repressor. In Contents the presence of Hedgehog signaling, Smoothened is relieved from Patched-mediated suppression due to the Hedgehog- 1. Introduction dependent internalization of Patched, which leads to 2. Hedgehog signaling pathway MAP3K10 (MST) activation and SUFU inactivation for the 3. Epithelial-to-mesenchymal transition (EMT) stabilization and nuclear accumulation of GLI family 4. Hedgehog and EMT members. GLI activators then upregulate CCND1, CCND2 5. MicroRNA (miRNA) for cell cycle acceleration, FOXA2, FOXC2, FOXE1, 6. Perspectives FOXF1, FOXL1, FOXP3, POU3F1, RUNX2, SOX13, TBX2 for cell fate determination, JAG2, INHBC, and INHBE for 1. Introduction stem cell signaling regulation. Hedgehog signals also up- regulate SFRP1 in mesenchymal cells for WNT signaling Hedgehog family members are key regulators of embryo- regulation. Epithelial-to-mesenchymal transition (EMT) during genesis, adult tissue homeostasis, and carcinogenesis (1-5). -
Mutations in CDON, Encoding a Hedgehog Receptor, Result in Holoprosencephaly and Defective Interactions with Other Hedgehog Receptors
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector ARTICLE Mutations in CDON, Encoding a Hedgehog Receptor, Result in Holoprosencephaly and Defective Interactions with Other Hedgehog Receptors Gyu-Un Bae,1,2,4,6 Sabina Domene´,3,4,7 Erich Roessler,3 Karen Schachter,1,8 Jong-Sun Kang,2,5,* Maximilian Muenke,3,5,* and Robert S. Krauss1,5 Holoprosencephaly (HPE), a common human congenital anomaly defined by a failure to delineate the midline of the forebrain and/or midface, is associated with diminished Sonic hedgehog (SHH)-pathway activity in development of these structures. SHH signaling is regulated by a network of ligand-binding factors, including the primary receptor PTCH1 and the putative coreceptors, CDON (also called CDO), BOC, and GAS1. Although binding of SHH to these receptors promotes pathway activity, it is not known whether interactions between these receptors are important. We report here identification of missense CDON mutations in human HPE. These mutations diminish CDON’s ability to support SHH-dependent gene expression in cell-based signaling assays. The mutations occur outside the SHH-binding domain of CDON, and the encoded variant CDON proteins do not display defects in binding to SHH. In contrast, wild-type CDON associates with PTCH1 and GAS1, but the variants do so inefficiently, in a manner that parallels their activity in cell-based assays. Our findings argue that CDON must associate with both ligand and other hedgehog-receptor components, particularly PTCH1, for signaling to occur and that disruption of the latter interactions is a mechanism of HPE. -
Role and Regulation of the P53-Homolog P73 in the Transformation of Normal Human Fibroblasts
Role and regulation of the p53-homolog p73 in the transformation of normal human fibroblasts Dissertation zur Erlangung des naturwissenschaftlichen Doktorgrades der Bayerischen Julius-Maximilians-Universität Würzburg vorgelegt von Lars Hofmann aus Aschaffenburg Würzburg 2007 Eingereicht am Mitglieder der Promotionskommission: Vorsitzender: Prof. Dr. Dr. Martin J. Müller Gutachter: Prof. Dr. Michael P. Schön Gutachter : Prof. Dr. Georg Krohne Tag des Promotionskolloquiums: Doktorurkunde ausgehändigt am Erklärung Hiermit erkläre ich, dass ich die vorliegende Arbeit selbständig angefertigt und keine anderen als die angegebenen Hilfsmittel und Quellen verwendet habe. Diese Arbeit wurde weder in gleicher noch in ähnlicher Form in einem anderen Prüfungsverfahren vorgelegt. Ich habe früher, außer den mit dem Zulassungsgesuch urkundlichen Graden, keine weiteren akademischen Grade erworben und zu erwerben gesucht. Würzburg, Lars Hofmann Content SUMMARY ................................................................................................................ IV ZUSAMMENFASSUNG ............................................................................................. V 1. INTRODUCTION ................................................................................................. 1 1.1. Molecular basics of cancer .......................................................................................... 1 1.2. Early research on tumorigenesis ................................................................................. 3 1.3. Developing -
Genome-Wide Association Study of Nicotine Dependence in American Populations: Identification of Novel Risk Loci in Both African-Americans and European-Americans
Biological Archival Report Psychiatry Genome-Wide Association Study of Nicotine Dependence in American Populations: Identification of Novel Risk Loci in Both African-Americans and European-Americans Joel Gelernter, Henry R. Kranzler, Richard Sherva, Laura Almasy, Aryeh I. Herman, Ryan Koesterer, Hongyu Zhao, and Lindsay A. Farrer ABSTRACT BACKGROUND: We report a genome-wide association study (GWAS) of nicotine dependence defined on the basis of scores on the Fagerström Test for Nicotine Dependence in European-American (EA) and African-American (AA) populations. METHODS: Our sample, from the one used in our previous GWAS, included only subjects who had smoked .100 cigarettes lifetime (2114 EA and 2602 AA subjects) and an additional 927 AA and 2003 EA subjects from the Study of Addiction: Genetics and Environment project [via the database of Genotypes and Phenotypes (dbGAP)]. GWAS analysis considered Fagerström Test for Nicotine Dependence score as an ordinal trait, separately in each population and sample and by combining the results in meta-analysis. We also conducted analyses that were adjusted for other substance use disorder criteria in a single nucleotide polymorphism (SNP) subset. RESULTS: In EAs, one chromosome 7 intergenic region was genome-wide significant (GWS): rs13225753, p 5 3.48 3 1028 (adjusted). In AAs, GWS associations were observed at numerous SNPs mapped to a region on chromosome 14 of .305,000 base pairs (minimal p 5 4.74 3 10210). Two chromosome 8 regions were associated: p 5 4.45 3 1028 at DLC1 SNP rs289519 (unadjusted) and p 5 1.10 3 1029 at rs6996964 (adjusted for other substances), located between CSGALNACT1 and INTS10. -
WO 2012/174282 A2 20 December 2012 (20.12.2012) P O P C T
(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 WO 2012/174282 A2 20 December 2012 (20.12.2012) P O P C T (51) International Patent Classification: David [US/US]; 13539 N . 95th Way, Scottsdale, AZ C12Q 1/68 (2006.01) 85260 (US). (21) International Application Number: (74) Agent: AKHAVAN, Ramin; Caris Science, Inc., 6655 N . PCT/US20 12/0425 19 Macarthur Blvd., Irving, TX 75039 (US). (22) International Filing Date: (81) Designated States (unless otherwise indicated, for every 14 June 2012 (14.06.2012) kind of national protection available): AE, AG, AL, AM, AO, AT, AU, AZ, BA, BB, BG, BH, BR, BW, BY, BZ, English (25) Filing Language: CA, CH, CL, CN, CO, CR, CU, CZ, DE, DK, DM, DO, Publication Language: English DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, HN, HR, HU, ID, IL, IN, IS, JP, KE, KG, KM, KN, KP, KR, (30) Priority Data: KZ, LA, LC, LK, LR, LS, LT, LU, LY, MA, MD, ME, 61/497,895 16 June 201 1 (16.06.201 1) US MG, MK, MN, MW, MX, MY, MZ, NA, NG, NI, NO, NZ, 61/499,138 20 June 201 1 (20.06.201 1) US OM, PE, PG, PH, PL, PT, QA, RO, RS, RU, RW, SC, SD, 61/501,680 27 June 201 1 (27.06.201 1) u s SE, SG, SK, SL, SM, ST, SV, SY, TH, TJ, TM, TN, TR, 61/506,019 8 July 201 1(08.07.201 1) u s TT, TZ, UA, UG, US, UZ, VC, VN, ZA, ZM, ZW.