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Prox1regulates the Subtype-Specific Development of Caudal Ganglionic
The Journal of Neuroscience, September 16, 2015 • 35(37):12869–12889 • 12869 Development/Plasticity/Repair Prox1 Regulates the Subtype-Specific Development of Caudal Ganglionic Eminence-Derived GABAergic Cortical Interneurons X Goichi Miyoshi,1 Allison Young,1 Timothy Petros,1 Theofanis Karayannis,1 Melissa McKenzie Chang,1 Alfonso Lavado,2 Tomohiko Iwano,3 Miho Nakajima,4 Hiroki Taniguchi,5 Z. Josh Huang,5 XNathaniel Heintz,4 Guillermo Oliver,2 Fumio Matsuzaki,3 Robert P. Machold,1 and Gord Fishell1 1Department of Neuroscience and Physiology, NYU Neuroscience Institute, Smilow Research Center, New York University School of Medicine, New York, New York 10016, 2Department of Genetics & Tumor Cell Biology, St. Jude Children’s Research Hospital, Memphis, Tennessee 38105, 3Laboratory for Cell Asymmetry, RIKEN Center for Developmental Biology, Kobe 650-0047, Japan, 4Laboratory of Molecular Biology, Howard Hughes Medical Institute, GENSAT Project, The Rockefeller University, New York, New York 10065, and 5Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724 Neurogliaform (RELNϩ) and bipolar (VIPϩ) GABAergic interneurons of the mammalian cerebral cortex provide critical inhibition locally within the superficial layers. While these subtypes are known to originate from the embryonic caudal ganglionic eminence (CGE), the specific genetic programs that direct their positioning, maturation, and integration into the cortical network have not been eluci- dated. Here, we report that in mice expression of the transcription factor Prox1 is selectively maintained in postmitotic CGE-derived cortical interneuron precursors and that loss of Prox1 impairs the integration of these cells into superficial layers. Moreover, Prox1 differentially regulates the postnatal maturation of each specific subtype originating from the CGE (RELN, Calb2/VIP, and VIP). -
Systematic Detection of Divergent Brain Proteins in Human Evolution and Their Roles in Cognition
bioRxiv preprint doi: https://doi.org/10.1101/658658; this version posted June 3, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. Systematic detection of divergent brain proteins in human evolution and their roles in cognition Guillaume Dumas1,*, Simon Malesys1 and Thomas Bourgeron1 Affiliations: 1 Human Genetics and Cognitive Functions, Institut Pasteur, UMR3571 CNRS, Université de Paris, Paris, (75015) France * Corresponding author: [email protected] 1 bioRxiv preprint doi: https://doi.org/10.1101/658658; this version posted June 3, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. Abstract The human brain differs from that of other primates, but the underlying genetic mechanisms remain unclear. Here we measured the evolutionary pressures acting on all human protein- coding genes (N=17,808) based on their divergence from early hominins such as Neanderthal, and non-human primates. We confirm that genes encoding brain-related proteins are among the most conserved of the human proteome. Conversely, several of the most divergent proteins in humans compared to other primates are associated with brain-associated diseases such as micro/macrocephaly, dyslexia, and autism. We identified specific eXpression profiles of a set of divergent genes in ciliated cells of the cerebellum, that might have contributed to the emergence of fine motor skills and social cognition in humans. -
T-Brain Regulates Archenteron Induction Signal 5207 Range of Amplification
Development 129, 5205-5216 (2002) 5205 Printed in Great Britain © The Company of Biologists Limited 2002 DEV5034 T-brain homologue (HpTb) is involved in the archenteron induction signals of micromere descendant cells in the sea urchin embryo Takuya Fuchikami1, Keiko Mitsunaga-Nakatsubo1, Shonan Amemiya2, Toshiya Hosomi1, Takashi Watanabe1, Daisuke Kurokawa1,*, Miho Kataoka1, Yoshito Harada3, Nori Satoh3, Shinichiro Kusunoki4, Kazuko Takata1, Taishin Shimotori1, Takashi Yamamoto1, Naoaki Sakamoto1, Hiraku Shimada1 and Koji Akasaka1,† 1Department of Mathematical and Life Sciences, Graduate School of Science, Hiroshima University, Higashi-Hiroshima 739-8526, Japan 2Department of Integrated Biosciences, Graduate School of Frontier Sciences, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113-0033, Japan 3Department of Zoology, Graduate School of Science, Kyoto University, Sakyo-ku, Kyoto 606-8502, Japan 4LSL, Nerima-ku, Tokyo 178-0061, Japan *Present address: Evolutionary Regeneration Biology Group, RIKEN Center for Developmental Biology, Kobe 650-0047, Japan †Author for correspondence (e-mail: [email protected]) Accepted 30 July 2002 SUMMARY Signals from micromere descendants play a crucial role in cells, the initial specification of primary mesenchyme cells, sea urchin development. In this study, we demonstrate that or the specification of endoderm. HpTb expression is these micromere descendants express HpTb, a T-brain controlled by nuclear localization of β-catenin, suggesting homolog of Hemicentrotus pulcherrimus. HpTb is expressed that -
Gene Expression Profiles of Estrogen Receptor–Positive and Estrogen Receptor–Negative Breast Cancers Are Detectable in Histologically Normal Breast Epithelium
Published OnlineFirst November 8, 2010; DOI: 10.1158/1078-0432.CCR-10-1369 Clinical Cancer Human Cancer Biology Research Gene Expression Profiles of Estrogen Receptor–Positive and Estrogen Receptor–Negative Breast Cancers Are Detectable in Histologically Normal Breast Epithelium Kelly Graham1, Xijin Ge4, Antonio de las Morenas2, Anusri Tripathi3, and Carol L. Rosenberg1,2,3 Abstract Purpose: Previously, we found that gene expression in histologically normal breast epithelium (NlEpi) from women at high breast cancer risk can resemble gene expression in NlEpi from cancer-containing breasts. Therefore, we hypothesized that gene expression characteristic of a cancer subtype might be seen in NlEpi of breasts containing that subtype. Experimental Design: We examined gene expression in 46 cases of microdissected NlEpi from untreated women undergoing breast cancer surgery. From 30 age-matched cases [15 estrogen receptor (ER)þ,15ERÀ] we used Affymetryix U133A arrays. From 16 independent cases (9 ERþ,7ERÀ), we validated selected genes using quantitative real-time PCR (qPCR). We then compared gene expression between NlEpi and invasive breast cancer using four publicly available data sets. Results: We identified 198 genes that are differentially expressed between NlEpi from breasts with ERþ (NlEpiERþ) compared with ERÀ cancers (NlEpiERÀ). These include genes characteristic of ERþ and ERÀ cancers (e.g., ESR1, GATA3, and CX3CL1, FABP7). qPCR validated the microarray results in both the 30 original cases and the 16 independent cases. Gene expression in NlEpiERþ and NlEpiERÀ resembled gene expression in ERþ and ERÀ cancers, respectively: 25% to 53% of the genes or probes examined in four external data sets overlapped between NlEpi and the corresponding cancer subtype. -
Accompanies CD8 T Cell Effector Function Global DNA Methylation
Global DNA Methylation Remodeling Accompanies CD8 T Cell Effector Function Christopher D. Scharer, Benjamin G. Barwick, Benjamin A. Youngblood, Rafi Ahmed and Jeremy M. Boss This information is current as of October 1, 2021. J Immunol 2013; 191:3419-3429; Prepublished online 16 August 2013; doi: 10.4049/jimmunol.1301395 http://www.jimmunol.org/content/191/6/3419 Downloaded from Supplementary http://www.jimmunol.org/content/suppl/2013/08/20/jimmunol.130139 Material 5.DC1 References This article cites 81 articles, 25 of which you can access for free at: http://www.jimmunol.org/content/191/6/3419.full#ref-list-1 http://www.jimmunol.org/ Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists by guest on October 1, 2021 • Fast Publication! 4 weeks from acceptance to publication *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2013 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Global DNA Methylation Remodeling Accompanies CD8 T Cell Effector Function Christopher D. Scharer,* Benjamin G. Barwick,* Benjamin A. Youngblood,*,† Rafi Ahmed,*,† and Jeremy M. -
UNIVERSITY of CALIFORNIA RIVERSIDE Investigations Into The
UNIVERSITY OF CALIFORNIA RIVERSIDE Investigations into the Role of TAF1-mediated Phosphorylation in Gene Regulation A Dissertation submitted in partial satisfaction of the requirements for the degree of Doctor of Philosophy in Cell, Molecular and Developmental Biology by Brian James Gadd December 2012 Dissertation Committee: Dr. Xuan Liu, Chairperson Dr. Frank Sauer Dr. Frances M. Sladek Copyright by Brian James Gadd 2012 The Dissertation of Brian James Gadd is approved Committee Chairperson University of California, Riverside Acknowledgments I am thankful to Dr. Liu for her patience and support over the last eight years. I am deeply indebted to my committee members, Dr. Frank Sauer and Dr. Frances Sladek for the insightful comments on my research and this dissertation. Thanks goes out to CMDB, especially Dr. Bachant, Dr. Springer and Kathy Redd for their support. Thanks to all the members of the Liu lab both past and present. A very special thanks to the members of the Sauer lab, including Silvia, Stephane, David, Matt, Stephen, Ninuo, Toby, Josh, Alice, Alex and Flora. You have made all the years here fly by and made them so enjoyable. From the Sladek lab I want to thank Eugene, John, Linh and Karthi. Special thanks go out to all the friends I’ve made over the years here. Chris, Amber, Stephane and David, thank you so much for feeding me, encouraging me and keeping me sane. Thanks to the brothers for all your encouragement and prayers. To any I haven’t mentioned by name, I promise I haven’t forgotten all you’ve done for me during my graduate years. -
Sporadic Autism Exomes Reveal a Highly Interconnected Protein Network of De Novo Mutations
LETTER doi:10.1038/nature10989 Sporadic autism exomes reveal a highly interconnected protein network of de novo mutations Brian J. O’Roak1,LauraVives1, Santhosh Girirajan1,EmreKarakoc1, Niklas Krumm1,BradleyP.Coe1,RoieLevy1,ArthurKo1,CholiLee1, Joshua D. Smith1, Emily H. Turner1, Ian B. Stanaway1, Benjamin Vernot1, Maika Malig1, Carl Baker1, Beau Reilly2,JoshuaM.Akey1, Elhanan Borenstein1,3,4,MarkJ.Rieder1, Deborah A. Nickerson1, Raphael Bernier2, Jay Shendure1 &EvanE.Eichler1,5 It is well established that autism spectrum disorders (ASD) have a per generation, in close agreement with our previous observations4, strong genetic component; however, for at least 70% of cases, the yet in general, higher than previous studies, indicating increased underlying genetic cause is unknown1. Under the hypothesis that sensitivity (Supplementary Table 2 and Supplementary Table 4)7. de novo mutations underlie a substantial fraction of the risk for We also observed complex classes of de novo mutation including: five developing ASD in families with no previous history of ASD or cases of multiple mutations in close proximity; two events consistent related phenotypes—so-called sporadic or simplex families2,3—we with paternal germline mosaicism (that is, where both siblings con- sequenced all coding regions of the genome (the exome) for tained a de novo event observed in neither parent); and nine events parent–child trios exhibiting sporadic ASD, including 189 new showing a weak minor allele profile consistent with somatic mosaicism trios and 20 that were previously reported4. Additionally, we also (Supplementary Table 3 and Supplementary Figs 2 and 3). sequenced the exomes of 50 unaffected siblings corresponding to Of the severe de novo events, 28% (33 of 120) are predicted to these new (n 5 31) and previously reported trios (n 5 19)4, for a truncate the protein. -
Supplementary Table 1: Genes Affected by Anoikis. A, Ratio of Signal
Supplementary Table 1: Genes affected by anoikis. a, ratio of signal intensity of nonanchored cells anchorage dependent cells (CasKoSrc) over anchored cells; b, induced by Src transformation of Cx43KO cells; c, decreased by Src transformation of Cx43Ko cells; *, induced by normalization of Src transformed cells by neighboring nontransformed cells. Gene Symbol Probe Set Fold Changea Gene Name increased Selenbp1 1450699_at 23.22 selenium binding protein 1 Dscr1l1 1450243_a_at 10.77 Down syndrome critical region gene 1-like 1 Dscr1l1 1421425_a_at 4.29 Down syndrome critical region gene 1-like 1 Ttyh1 1426617_a_at 6.70 tweety homolog 1 (Drosophila) 5730521E12Rik 1419065_at 6.16 RIKEN cDNA 5730521E12 gene c 6330406I15Rik 1452244_at 5.87 RIKEN cDNA 6330406I15 gene AF067063 1425160_at 5.73 clone L2 uniform group of 2-cell-stage gene family mRNA Morc 1419418_a_at 5.55 microrchidia c Gpr56 1421118_a_at 5.43 G protein-coupled receptor 56 Pax6 1452526_a_at 5.06 paired box gene 6 Tgfbi 1415871_at 3.73 transforming growth factor beta induced Adarb1 1434932_at 3.70 adenosine deaminase RNA-specific B1 Ddx3y 1452077_at 3.30 DEAD (Asp-Glu-Ala-Asp) box polypeptide 3 Y-linked b Ampd3 1422573_at 3.20 AMP deaminase 3 Gli2 1459211_at 3.07 GLI-Kruppel family member GLI2 Selenbp2 1417580_s_at 2.96 selenium binding protein 2 Adamts1 1450716_at 2.80 a disintegrin-like and metalloprotease with thrombospondin type 1 motif 1 Dusp15 1426189_at 2.70 dual specificity phosphatase-like 15 Dpep3 1429035_at 2.60 dipeptidase 3 Sepp1 1452141_a_at 2.57 selenoprotein P plasma -
Development and Validation of a Protein-Based Risk Score for Cardiovascular Outcomes Among Patients with Stable Coronary Heart Disease
Supplementary Online Content Ganz P, Heidecker B, Hveem K, et al. Development and validation of a protein-based risk score for cardiovascular outcomes among patients with stable coronary heart disease. JAMA. doi: 10.1001/jama.2016.5951 eTable 1. List of 1130 Proteins Measured by Somalogic’s Modified Aptamer-Based Proteomic Assay eTable 2. Coefficients for Weibull Recalibration Model Applied to 9-Protein Model eFigure 1. Median Protein Levels in Derivation and Validation Cohort eTable 3. Coefficients for the Recalibration Model Applied to Refit Framingham eFigure 2. Calibration Plots for the Refit Framingham Model eTable 4. List of 200 Proteins Associated With the Risk of MI, Stroke, Heart Failure, and Death eFigure 3. Hazard Ratios of Lasso Selected Proteins for Primary End Point of MI, Stroke, Heart Failure, and Death eFigure 4. 9-Protein Prognostic Model Hazard Ratios Adjusted for Framingham Variables eFigure 5. 9-Protein Risk Scores by Event Type This supplementary material has been provided by the authors to give readers additional information about their work. Downloaded From: https://jamanetwork.com/ on 10/02/2021 Supplemental Material Table of Contents 1 Study Design and Data Processing ......................................................................................................... 3 2 Table of 1130 Proteins Measured .......................................................................................................... 4 3 Variable Selection and Statistical Modeling ........................................................................................ -
Apoptotic Cells Inflammasome Activity During the Uptake of Macrophage
Downloaded from http://www.jimmunol.org/ by guest on September 29, 2021 is online at: average * The Journal of Immunology , 26 of which you can access for free at: 2012; 188:5682-5693; Prepublished online 20 from submission to initial decision 4 weeks from acceptance to publication April 2012; doi: 10.4049/jimmunol.1103760 http://www.jimmunol.org/content/188/11/5682 Complement Protein C1q Directs Macrophage Polarization and Limits Inflammasome Activity during the Uptake of Apoptotic Cells Marie E. Benoit, Elizabeth V. Clarke, Pedro Morgado, Deborah A. Fraser and Andrea J. Tenner J Immunol cites 56 articles Submit online. Every submission reviewed by practicing scientists ? is published twice each month by Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts http://jimmunol.org/subscription http://www.jimmunol.org/content/suppl/2012/04/20/jimmunol.110376 0.DC1 This article http://www.jimmunol.org/content/188/11/5682.full#ref-list-1 Information about subscribing to The JI No Triage! Fast Publication! Rapid Reviews! 30 days* Why • • • Material References Permissions Email Alerts Subscription Supplementary The Journal of Immunology The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2012 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. This information is current as of September 29, 2021. The Journal of Immunology Complement Protein C1q Directs Macrophage Polarization and Limits Inflammasome Activity during the Uptake of Apoptotic Cells Marie E. -
Effects of Chronic Stress on Prefrontal Cortex Transcriptome in Mice Displaying Different Genetic Backgrounds
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Springer - Publisher Connector J Mol Neurosci (2013) 50:33–57 DOI 10.1007/s12031-012-9850-1 Effects of Chronic Stress on Prefrontal Cortex Transcriptome in Mice Displaying Different Genetic Backgrounds Pawel Lisowski & Marek Wieczorek & Joanna Goscik & Grzegorz R. Juszczak & Adrian M. Stankiewicz & Lech Zwierzchowski & Artur H. Swiergiel Received: 14 May 2012 /Accepted: 25 June 2012 /Published online: 27 July 2012 # The Author(s) 2012. This article is published with open access at Springerlink.com Abstract There is increasing evidence that depression signaling pathway (Clic6, Drd1a,andPpp1r1b). LA derives from the impact of environmental pressure on transcriptome affected by CMS was associated with genetically susceptible individuals. We analyzed the genes involved in behavioral response to stimulus effects of chronic mild stress (CMS) on prefrontal cor- (Fcer1g, Rasd2, S100a8, S100a9, Crhr1, Grm5,and tex transcriptome of two strains of mice bred for high Prkcc), immune effector processes (Fcer1g, Mpo,and (HA)and low (LA) swim stress-induced analgesia that Igh-VJ558), diacylglycerol binding (Rasgrp1, Dgke, differ in basal transcriptomic profiles and depression- Dgkg,andPrkcc), and long-term depression (Crhr1, like behaviors. We found that CMS affected 96 and 92 Grm5,andPrkcc) and/or coding elements of dendrites genes in HA and LA mice, respectively. Among genes (Crmp1, Cntnap4,andPrkcc) and myelin proteins with the same expression pattern in both strains after (Gpm6a, Mal,andMog). The results indicate significant CMS, we observed robust upregulation of Ttr gene contribution of genetic background to differences in coding transthyretin involved in amyloidosis, seizures, stress response gene expression in the mouse prefrontal stroke-like episodes, or dementia. -
Ssecks/Gravin/AKAP12 Attenuates Expression of Proliferative And
BMC Cancer BioMed Central Research article Open Access SSeCKS/Gravin/AKAP12 attenuates expression of proliferative and angiogenic genes during suppression of v-Src-induced oncogenesis Yongzhong Liu1, Lingqiu Gao2 and Irwin H Gelman*2 Address: 1Mucosal Immunology Unit, National Institutes of Health, Bethesda, MD 20892, USA and 2Department of Cancer Genetics, Roswell Park Cancer Institute, Buffalo, NY 14263, USA Email: Yongzhong Liu - [email protected]; Lingqiu Gao - [email protected]; Irwin H Gelman* - [email protected] * Corresponding author Published: 25 April 2006 Received: 24 January 2006 Accepted: 25 April 2006 BMC Cancer2006, 6:105 doi:10.1186/1471-2407-6-105 This article is available from: http://www.biomedcentral.com/1471-2407/6/105 © 2006Liu 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: SSeCKS is a major protein kinase C substrate with kinase scaffolding and metastasis- suppressor activity whose expression is severely downregulated in Src- and Ras-transformed fibroblast and epithelial cells and in human prostate, breast, and gastric cancers. We previously used NIH3T3 cells with tetracycline-regulated SSeCKS expression plus a temperature-sensitive v-Src allele to show that SSeCKS re-expression inhibited parameters of v-Src-induced oncogenic growth without attenuating in vivo Src kinase activity. Methods: We use cDNA microarrays and semi-quantitative RT-PCR analysis to identify changes in gene expression correlating with i) SSeCKS expression in the absence of v-Src activity, ii) activation of v-Src activity alone, and iii) SSeCKS re-expression in the presence of active v-Src.