High-Resolution Hi-C Maps Highlight Multiscale 3D Epigenome
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Ovarian Gene Expression in the Absence of FIGLA, an Oocyte
BMC Developmental Biology BioMed Central Research article Open Access Ovarian gene expression in the absence of FIGLA, an oocyte-specific transcription factor Saurabh Joshi*1, Holly Davies1, Lauren Porter Sims2, Shawn E Levy2 and Jurrien Dean1 Address: 1Laboratory of Cellular and Developmental Biology, NIDDK, National Institutes of Health, Bethesda, MD 20892, USA and 2Department of Biomedical Informatics, Vanderbilt University Medical Center, Nashville, TN 37232, USA Email: Saurabh Joshi* - [email protected]; Holly Davies - [email protected]; Lauren Porter Sims - [email protected]; Shawn E Levy - [email protected]; Jurrien Dean - [email protected] * Corresponding author Published: 13 June 2007 Received: 11 December 2006 Accepted: 13 June 2007 BMC Developmental Biology 2007, 7:67 doi:10.1186/1471-213X-7-67 This article is available from: http://www.biomedcentral.com/1471-213X/7/67 © 2007 Joshi 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: Ovarian folliculogenesis in mammals is a complex process involving interactions between germ and somatic cells. Carefully orchestrated expression of transcription factors, cell adhesion molecules and growth factors are required for success. We have identified a germ-cell specific, basic helix-loop-helix transcription factor, FIGLA (Factor In the GermLine, Alpha) and demonstrated its involvement in two independent developmental processes: formation of the primordial follicle and coordinate expression of zona pellucida genes. Results: Taking advantage of Figla null mouse lines, we have used a combined approach of microarray and Serial Analysis of Gene Expression (SAGE) to identify potential downstream target genes. -
Table S1 the Four Gene Sets Derived from Gene Expression Profiles of Escs and Differentiated Cells
Table S1 The four gene sets derived from gene expression profiles of ESCs and differentiated cells Uniform High Uniform Low ES Up ES Down EntrezID GeneSymbol EntrezID GeneSymbol EntrezID GeneSymbol EntrezID GeneSymbol 269261 Rpl12 11354 Abpa 68239 Krt42 15132 Hbb-bh1 67891 Rpl4 11537 Cfd 26380 Esrrb 15126 Hba-x 55949 Eef1b2 11698 Ambn 73703 Dppa2 15111 Hand2 18148 Npm1 11730 Ang3 67374 Jam2 65255 Asb4 67427 Rps20 11731 Ang2 22702 Zfp42 17292 Mesp1 15481 Hspa8 11807 Apoa2 58865 Tdh 19737 Rgs5 100041686 LOC100041686 11814 Apoc3 26388 Ifi202b 225518 Prdm6 11983 Atpif1 11945 Atp4b 11614 Nr0b1 20378 Frzb 19241 Tmsb4x 12007 Azgp1 76815 Calcoco2 12767 Cxcr4 20116 Rps8 12044 Bcl2a1a 219132 D14Ertd668e 103889 Hoxb2 20103 Rps5 12047 Bcl2a1d 381411 Gm1967 17701 Msx1 14694 Gnb2l1 12049 Bcl2l10 20899 Stra8 23796 Aplnr 19941 Rpl26 12096 Bglap1 78625 1700061G19Rik 12627 Cfc1 12070 Ngfrap1 12097 Bglap2 21816 Tgm1 12622 Cer1 19989 Rpl7 12267 C3ar1 67405 Nts 21385 Tbx2 19896 Rpl10a 12279 C9 435337 EG435337 56720 Tdo2 20044 Rps14 12391 Cav3 545913 Zscan4d 16869 Lhx1 19175 Psmb6 12409 Cbr2 244448 Triml1 22253 Unc5c 22627 Ywhae 12477 Ctla4 69134 2200001I15Rik 14174 Fgf3 19951 Rpl32 12523 Cd84 66065 Hsd17b14 16542 Kdr 66152 1110020P15Rik 12524 Cd86 81879 Tcfcp2l1 15122 Hba-a1 66489 Rpl35 12640 Cga 17907 Mylpf 15414 Hoxb6 15519 Hsp90aa1 12642 Ch25h 26424 Nr5a2 210530 Leprel1 66483 Rpl36al 12655 Chi3l3 83560 Tex14 12338 Capn6 27370 Rps26 12796 Camp 17450 Morc1 20671 Sox17 66576 Uqcrh 12869 Cox8b 79455 Pdcl2 20613 Snai1 22154 Tubb5 12959 Cryba4 231821 Centa1 17897 -
Redefining the Specificity of Phosphoinositide-Binding by Human
bioRxiv preprint doi: https://doi.org/10.1101/2020.06.20.163253; this version posted June 21, 2020. 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-NC 4.0 International license. Redefining the specificity of phosphoinositide-binding by human PH domain-containing proteins Nilmani Singh1†, Adriana Reyes-Ordoñez1†, Michael A. Compagnone1, Jesus F. Moreno Castillo1, Benjamin J. Leslie2, Taekjip Ha2,3,4,5, Jie Chen1* 1Department of Cell & Developmental Biology, University of Illinois at Urbana-Champaign, Urbana, IL 61801; 2Department of Biophysics and Biophysical Chemistry, Johns Hopkins University School of Medicine, Baltimore, MD 21205; 3Department of Biophysics, Johns Hopkins University, Baltimore, MD 21218; 4Department of Biomedical Engineering, Johns Hopkins University, Baltimore, MD 21205; 5Howard Hughes Medical Institute, Baltimore, MD 21205, USA †These authors contributed equally to this work. *Correspondence: [email protected]. bioRxiv preprint doi: https://doi.org/10.1101/2020.06.20.163253; this version posted June 21, 2020. 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-NC 4.0 International license. ABSTRACT Pleckstrin homology (PH) domains are presumed to bind phosphoinositides (PIPs), but specific interaction with and regulation by PIPs for most PH domain-containing proteins are unclear. Here we employed a single-molecule pulldown assay to study interactions of lipid vesicles with full-length proteins in mammalian whole cell lysates. -
Aneuploidy: Using Genetic Instability to Preserve a Haploid Genome?
Health Science Campus FINAL APPROVAL OF DISSERTATION Doctor of Philosophy in Biomedical Science (Cancer Biology) Aneuploidy: Using genetic instability to preserve a haploid genome? Submitted by: Ramona Ramdath In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biomedical Science Examination Committee Signature/Date Major Advisor: David Allison, M.D., Ph.D. Academic James Trempe, Ph.D. Advisory Committee: David Giovanucci, Ph.D. Randall Ruch, Ph.D. Ronald Mellgren, Ph.D. Senior Associate Dean College of Graduate Studies Michael S. Bisesi, Ph.D. Date of Defense: April 10, 2009 Aneuploidy: Using genetic instability to preserve a haploid genome? Ramona Ramdath University of Toledo, Health Science Campus 2009 Dedication I dedicate this dissertation to my grandfather who died of lung cancer two years ago, but who always instilled in us the value and importance of education. And to my mom and sister, both of whom have been pillars of support and stimulating conversations. To my sister, Rehanna, especially- I hope this inspires you to achieve all that you want to in life, academically and otherwise. ii Acknowledgements As we go through these academic journeys, there are so many along the way that make an impact not only on our work, but on our lives as well, and I would like to say a heartfelt thank you to all of those people: My Committee members- Dr. James Trempe, Dr. David Giovanucchi, Dr. Ronald Mellgren and Dr. Randall Ruch for their guidance, suggestions, support and confidence in me. My major advisor- Dr. David Allison, for his constructive criticism and positive reinforcement. -
Supplementary Materials
Supplementary materials Supplementary Table S1: MGNC compound library Ingredien Molecule Caco- Mol ID MW AlogP OB (%) BBB DL FASA- HL t Name Name 2 shengdi MOL012254 campesterol 400.8 7.63 37.58 1.34 0.98 0.7 0.21 20.2 shengdi MOL000519 coniferin 314.4 3.16 31.11 0.42 -0.2 0.3 0.27 74.6 beta- shengdi MOL000359 414.8 8.08 36.91 1.32 0.99 0.8 0.23 20.2 sitosterol pachymic shengdi MOL000289 528.9 6.54 33.63 0.1 -0.6 0.8 0 9.27 acid Poricoic acid shengdi MOL000291 484.7 5.64 30.52 -0.08 -0.9 0.8 0 8.67 B Chrysanthem shengdi MOL004492 585 8.24 38.72 0.51 -1 0.6 0.3 17.5 axanthin 20- shengdi MOL011455 Hexadecano 418.6 1.91 32.7 -0.24 -0.4 0.7 0.29 104 ylingenol huanglian MOL001454 berberine 336.4 3.45 36.86 1.24 0.57 0.8 0.19 6.57 huanglian MOL013352 Obacunone 454.6 2.68 43.29 0.01 -0.4 0.8 0.31 -13 huanglian MOL002894 berberrubine 322.4 3.2 35.74 1.07 0.17 0.7 0.24 6.46 huanglian MOL002897 epiberberine 336.4 3.45 43.09 1.17 0.4 0.8 0.19 6.1 huanglian MOL002903 (R)-Canadine 339.4 3.4 55.37 1.04 0.57 0.8 0.2 6.41 huanglian MOL002904 Berlambine 351.4 2.49 36.68 0.97 0.17 0.8 0.28 7.33 Corchorosid huanglian MOL002907 404.6 1.34 105 -0.91 -1.3 0.8 0.29 6.68 e A_qt Magnogrand huanglian MOL000622 266.4 1.18 63.71 0.02 -0.2 0.2 0.3 3.17 iolide huanglian MOL000762 Palmidin A 510.5 4.52 35.36 -0.38 -1.5 0.7 0.39 33.2 huanglian MOL000785 palmatine 352.4 3.65 64.6 1.33 0.37 0.7 0.13 2.25 huanglian MOL000098 quercetin 302.3 1.5 46.43 0.05 -0.8 0.3 0.38 14.4 huanglian MOL001458 coptisine 320.3 3.25 30.67 1.21 0.32 0.9 0.26 9.33 huanglian MOL002668 Worenine -
ARHGAP25 (A-12): Sc-137297
SAN TA C RUZ BI OTEC HNOL OG Y, INC . ARHGAP25 (A-12): sc-137297 BACKGROUND SOURCE GTPase-activating proteins (GAPs) accelerate the intrinsic rate of GTP ARHGAP25 (A-12) is an affinity purified goat polyclonal antibody raised hydrolysis of Ras-related proteins, resulting in downregulation of their active against a peptide mapping within an internal region of ARHGAP25 of human form. ARHGAP25 (Rho GTPase activating protein 25), also known as Rho-type origin. GTPase-activating protein 25, is a 645 amino acid protein that contains one Pleckstrin homology (PH) domain and one Rho-GAP domain. Encoded by a PRODUCT gene that maps to human chromosome 2p14, ARHGAP25 exists as four alter - Each vial contains 200 µg IgG in 1.0 ml of PBS with < 0.1% sodium azide natively spliced isoforms and shares significant homology with ARHGAP22 and 0.1% gelatin. and ARHGAP24 by exhibiting a common domain structure (PH-RhoGAP-CC); however, tissue expression of ARHGAP25 is myeloid-specific. ARHGAP25 is Blocking peptide available for competition studies, sc-137297 P, (100 µg a candidate epigenetic biomarker for non-invasive prenatal diagnosis of Down peptide in 0.5 ml PBS containing < 0.1% sodium azide and 0.2% BSA). syndrome, as well as a candidate gene in a chromosome 2p susceptibility locus linked to salt-sensitive hypertension and drug response. APPLICATIONS ARHGAP25 (A-12) is recommended for detection of ARHGAP25 isoforms 1 REFERENCES and 2 of mouse, rat and human origin by Western Blotting (starting dilution 1. Katoh, M., et al. 2004. Identification and characterization of ARHGAP24 1:100, dilution range 1:50-1:500), immunofluorescence (starting dilution 1:25, and ARHGAP25 genes in silico. -
TCF3 Antibody Product Type: Primary Antibodies Description: Rabbit Polyclonal to TCF3 Immunogen:3 Synthetic Peptides (Human) Conjugated to KLH
PRODUCT INFORMATION Product name: TCF3 antibody Product type: Primary antibodies Description: Rabbit polyclonal to TCF3 Immunogen:3 synthetic peptides (human) conjugated to KLH. Reacts with: Hu, Ms Tested applications: ELISA and WB. GENE INFORMATION Gene Symbol: TCF3 Gene Name: transcription factor 3 (E2A immunoglobulin enhancer binding factors E12/E47) Ensembl ID: ENSG00000071564 Entrez GeneID:6929 GenBank Accession number: M65214.1 Omim ID:147141 SwissProt:P15923 Molecular weight of TCF3: 67.6kDa (Isoform E12) and 67.265kDa (Isoform E47) Function: Heterodimers between TCF3 and tissuespecific basic helixloophelix (bHLH) proteins play major roles in determining tissuespecific cell fate during embryogenesis, like muscle or early Bcell differentiation. Dimers bind DNA on Ebox motifs: 5'CANNTG3'. Binds to the kappaE2 site in the kappa immunoglobulin gene enhancer. Subunit structure: Efficient DNA binding requires dimerization with another bHLH protein. Forms a heterodimer with ASH1 and TWIST2. Isoform E12 interacts with GRIPE and FIGLA By similarity. Interacts with PTF1A and TGFB1I1. Component of a nuclear TAL1 complex composed at least of CBFA2T3, LDB1, TAL1 and TCF3 By similarity. Interacts with UBE2I. Subcellular localization: Nucleus Involvement in disease:Chromosomal aberrations involving TCF3 are cause of forms of preBcell acute lymphoblastic leukemia (BALL). Translocation t(1;19)(q23;p13.3) with PBX1; Translocation t(17;19)(q22;p13.3) with HLF. Inversion inv(19)(p13;q13) with TFPT. APPLICATION NOTE Recommended dilution: • ELISA: Antibody specificity was verified by direct ELISA against the 3 immunogen peptides. A titer of 1/15000 has been determined. Appropriate specificity controls were run. -
Malaria Polyclonal B Cell Activator Activation of the Memory
Increased B Cell Survival and Preferential Activation of the Memory Compartment by a Malaria Polyclonal B Cell Activator This information is current as Daria Donati, Bobo Mok, Arnaud Chêne, Hong Xu, Mathula of October 2, 2021. Thangarajh, Rickard Glas, Qijun Chen, Mats Wahlgren and Maria Teresa Bejarano J Immunol 2006; 177:3035-3044; ; doi: 10.4049/jimmunol.177.5.3035 http://www.jimmunol.org/content/177/5/3035 Downloaded from References This article cites 35 articles, 15 of which you can access for free at: http://www.jimmunol.org/content/177/5/3035.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 • Fast Publication! 4 weeks from acceptance to publication by guest on October 2, 2021 *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 © 2006 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Increased B Cell Survival and Preferential Activation of the Memory Compartment by a Malaria Polyclonal B Cell Activator1 Daria Donati,2† Bobo Mok,* Arnaud Cheˆne,*† Hong Xu,† Mathula Thangarajh,‡ Rickard Glas,† Qijun Chen,§ Mats Wahlgren,* and Maria Teresa Bejarano*† Chronic malaria infection is characterized by polyclonal B cell activation, hyperglobulinemia, and elevated titers of autoantibod- ies. -
Genomic and Functional Profiling of Duplicated Chromosome
Human Molecular Genetics, 2006, Vol. 15, No. 6 853–869 doi:10.1093/hmg/ddl004 Advance Access published on January 30, 2006 Genomic and functional profiling of duplicated chromosome 15 cell lines reveal regulatory alterations in UBE3A-associated ubiquitin–proteasome pathway processes Colin A. Baron1, Clifford G. Tepper2, Stephenie Y. Liu1, Ryan R. Davis1, Nicholas J. Wang3, N. Carolyn Schanen4 and Jeffrey P. Gregg1,* 1Department of Pathology and 2Department of Biochemistry and Molecular Medicine, University of California, Davis School of Medicine, Sacramento, CA 95817, USA, 3Department of Human Genetics, University of 4 California–Los Angeles, Los Angeles, CA, USA and Center for Pediatric Research, Nemours Biomedical Research, Downloaded from Alfred I. duPont Hospital for Children, Wilmington, DE, USA Received November 21, 2005; Revised and Accepted January 25, 2006 Autism is a complex neurodevelopmental disorder having both genetic and epigenetic etiological elements. hmg.oxfordjournals.org Isodicentric chromosome 15 (Idic15), characterized by duplications of the multi-disorder critical region of 15q11–q14, is a relatively common cytogenetic event. When the duplication involves maternally derived con- tent, this abnormality is strongly correlated with autism disorder. However, the mechanistic links between Idic15 and autism are ill-defined. To gain insight into the potential role of these duplications, we performed a comprehensive, genomics-based characterization of an in vitro model system consisting of lymphoblast cell lines derived from individuals with both autism and Idic15. Array-based comparative genomic hybridiz- ation using commercial single nucleotide polymorphism arrays was conducted and found to be capable of by guest on December 17, 2010 sub-classifying Idic15 samples by virtue of the lengths of the duplicated chromosomal region. -
Phosphoinositide 3-Kinase Enables Phagocytosis of Large Particles by Terminating Actin Assembly Through Rac/Cdc42 Gtpase-Activating Proteins
ARTICLE Received 13 Apr 2015 | Accepted 11 Sep 2015 | Published 14 Oct 2015 DOI: 10.1038/ncomms9623 OPEN Phosphoinositide 3-kinase enables phagocytosis of large particles by terminating actin assembly through Rac/Cdc42 GTPase-activating proteins Daniel Schlam1,2, Richard D. Bagshaw3, Spencer A. Freeman1, Richard F. Collins1, Tony Pawson3, Gregory D. Fairn2,4 & Sergio Grinstein1,2,4 Phagocytosis is responsible for the elimination of particles of widely disparate sizes, from large fungi or effete cells to small bacteria. Though superficially similar, the molecular mechanisms involved differ: engulfment of large targets requires phosphoinositide 3-kinase (PI3K), while that of small ones does not. Here, we report that inactivation of Rac and Cdc42 at phagocytic cups is essential to complete internalization of large particles. Through a screen of 62 RhoGAP-family members, we demonstrate that ARHGAP12, ARHGAP25 and SH3BP1 are responsible for GTPase inactivation. Silencing these RhoGAPs impairs phagocytosis of large targets. The GAPs are recruited to large—but not small—phagocytic cups by products of PI3K, where they synergistically inactivate Rac and Cdc42. Remarkably, the prominent accumulation of phosphatidylinositol 3,4,5-trisphosphate characteristic of large-phagosome formation is less evident during phagocytosis of small targets, accounting for the contrasting RhoGAP distribution and the differential requirement for PI3K during phagocytosis of dissimilarly sized particles. 1 Division of Cell Biology, The Hospital for Sick Children, 555 University Avenue, Toronto, Ontario, Canada M5G1X8. 2 Institute of Medical Science, University of Toronto, Faculty of Medicine, 1 King’s College Circle, Toronto, Ontario, Canada M5S1A8. 3 Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, 600 University Avenue, Toronto, Ontario, Canada M5G1X5. -
Dynamic Transcriptional and Chromatin Accessibility Landscape of Medaka Embryogenesis
Downloaded from genome.cshlp.org on October 8, 2021 - Published by Cold Spring Harbor Laboratory Press Dynamic Transcriptional and Chromatin Accessibility Landscape of Medaka Embryogenesis Yingshu Li1,2,3,+, Yongjie Liu1,2,3,+, Hang Yang1,2,3, Ting Zhang1,2, Kiyoshi Naruse4,*, Qiang Tu1,2,3,* 1 State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Innovation Academy for Seed Design, Chinese Academy of Sciences, Beijing 100101, China 2 Key Laboratory of Genetic Network Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China 3 University of Chinese Academy of Sciences, Beijing 100049, China 4 Laboratory of Bioresources, National Institute for Basic Biology, Okazaki 444-8585, Aichi, Japan + These authors are joint first authors and contributed equally to this work. * Corresponding authors: [email protected], [email protected] Abstract Medaka (Oryzias latipes) has become an important vertebrate model widely used in genetics, developmental biology, environmental sciences, and many other fields. A high-quality genome sequence and a variety of genetic tools are available for this model organism. However, existing genome annotation is still rudimentary, as it was mainly based on computational prediction and short-read RNA-seq data. Here we report a dynamic transcriptome landscape of medaka embryogenesis profiled by long-read RNA-seq, short-read RNA-seq, and ATAC-seq. Integrating these datasets, we constructed a much-improved gene model set including about 17,000 novel isoforms, identified 1600 transcription factors, 1100 long non-coding RNAs, and 150,000 potential cis-regulatory elements as well. Time-series datasets provided another dimension of information. -
Mouse Arhgap25 Knockout Project (CRISPR/Cas9)
https://www.alphaknockout.com Mouse Arhgap25 Knockout Project (CRISPR/Cas9) Objective: To create a Arhgap25 knockout Mouse model (C57BL/6J) by CRISPR/Cas-mediated genome engineering. Strategy summary: The Arhgap25 gene (NCBI Reference Sequence: NM_001037727 ; Ensembl: ENSMUSG00000030047 ) is located on Mouse chromosome 6. 11 exons are identified, with the ATG start codon in exon 1 and the TGA stop codon in exon 11 (Transcript: ENSMUST00000113637). Exon 3~4 will be selected as target site. Cas9 and gRNA will be co-injected into fertilized eggs for KO Mouse production. The pups will be genotyped by PCR followed by sequencing analysis. Note: Mice homozygous for a knock-out allele exhibit altered leukocyte transendothelial migration. Exon 3 starts from about 13.48% of the coding region. Exon 3~4 covers 10.55% of the coding region. The size of effective KO region: ~4074 bp. The KO region does not have any other known gene. Page 1 of 8 https://www.alphaknockout.com Overview of the Targeting Strategy Wildtype allele 5' gRNA region gRNA region 3' 1 3 4 11 Legends Exon of mouse Arhgap25 Knockout region Page 2 of 8 https://www.alphaknockout.com Overview of the Dot Plot (up) Window size: 15 bp Forward Reverse Complement Sequence 12 Note: The 2000 bp section upstream of Exon 3 is aligned with itself to determine if there are tandem repeats. No significant tandem repeat is found in the dot plot matrix. So this region is suitable for PCR screening or sequencing analysis. Overview of the Dot Plot (down) Window size: 15 bp Forward Reverse Complement Sequence 12 Note: The 2000 bp section downstream of Exon 4 is aligned with itself to determine if there are tandem repeats.