Mouse Fchsd2 Knockout Project (CRISPR/Cas9)
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Newly Identified Gon4l/Udu-Interacting Proteins
www.nature.com/scientificreports OPEN Newly identifed Gon4l/ Udu‑interacting proteins implicate novel functions Su‑Mei Tsai1, Kuo‑Chang Chu1 & Yun‑Jin Jiang1,2,3,4,5* Mutations of the Gon4l/udu gene in diferent organisms give rise to diverse phenotypes. Although the efects of Gon4l/Udu in transcriptional regulation have been demonstrated, they cannot solely explain the observed characteristics among species. To further understand the function of Gon4l/Udu, we used yeast two‑hybrid (Y2H) screening to identify interacting proteins in zebrafsh and mouse systems, confrmed the interactions by co‑immunoprecipitation assay, and found four novel Gon4l‑interacting proteins: BRCA1 associated protein‑1 (Bap1), DNA methyltransferase 1 (Dnmt1), Tho complex 1 (Thoc1, also known as Tho1 or HPR1), and Cryptochrome circadian regulator 3a (Cry3a). Furthermore, all known Gon4l/Udu‑interacting proteins—as found in this study, in previous reports, and in online resources—were investigated by Phenotype Enrichment Analysis. The most enriched phenotypes identifed include increased embryonic tissue cell apoptosis, embryonic lethality, increased T cell derived lymphoma incidence, decreased cell proliferation, chromosome instability, and abnormal dopamine level, characteristics that largely resemble those observed in reported Gon4l/udu mutant animals. Similar to the expression pattern of udu, those of bap1, dnmt1, thoc1, and cry3a are also found in the brain region and other tissues. Thus, these fndings indicate novel mechanisms of Gon4l/ Udu in regulating CpG methylation, histone expression/modifcation, DNA repair/genomic stability, and RNA binding/processing/export. Gon4l is a nuclear protein conserved among species. Animal models from invertebrates to vertebrates have shown that the protein Gon4-like (Gon4l) is essential for regulating cell proliferation and diferentiation. -
856 1. ABSTRACT Analysis for Carom Complex, Signaling and Function By
[Frontiers in Bioscience, Landmark, 21, 856-872, January 1, 2016] Analysis for Carom complex, signaling and function by database mining Suxuan Liu1,2, Xinyu Xiong2, Sam Varghese Thomas2, Yanjie Xu2,6, Xiaoshu Cheng6, Xianxian Zhao1, Xiaofeng Yang2,3,4,5, Hong Wang2,3,4,5 1Department of Cardiology, Changhai Hospital, Second Military Medical University, Shanghai, 200433, China, 2Center for Metabolic Disease Research,Temple University School of Medicine, Philadelphia, PA, 19140, 3Cardiovascular Research, Temple University School of Medicine, Philadelphia, PA, 19140, 4Thrombosis Research, Temple University School of Medicine, Philadelphia, PA, 19140, 5Department of Pharmacology, Temple University School of Medicine, Philadelphia, PA, 19140, 6Department of Cardiology, Second Hospital of Nanchang University, Institute of Cardiovascular Disease in Nanchang University, Nan Chang, Jiang Xi, 330006, China TABLE OF CONTENTS 1. Abstract 2. Introduciton 3. Materials and methods 3.1. Identification of Carom partners (NCBI Gene database) 3.2. Tissue mRNA distribution profiles of Carom and partners (EST database) 3.3. Identification for conditions altering Carom expression (GEO database) 3.4. Pathway analysis of Carom and partners (Ingenuity pathway analysis) 3.5. Predicted function of Carom complex signaling (PubMed) 4. Results 4.1. Identification of 26 Carom partners 4.2. Carom and 26 partners are differentially expressed in human and mouse tissues 4.3. Inflammatory and reprogramming conditions altered Carom expression 4.4. Paired Carom partners in inflammatory and reprogramming conditions 4.5. Carom complex pathway analysis 5. Discussion 5.1. Carom and partner proteins are differentially expressed in tissues 5.2. Expression of Carom complex is altered in inflammatory and reprogramming conditions 5.3. -
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bioRxiv preprint doi: https://doi.org/10.1101/017566; this version posted November 19, 2015. 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-ND 4.0 International license. 1 1 Testing for ancient selection using cross-population allele 2 frequency differentiation 1;∗ 3 Fernando Racimo 4 1 Department of Integrative Biology, University of California, Berkeley, CA, USA 5 ∗ E-mail: [email protected] 6 1 Abstract 7 A powerful way to detect selection in a population is by modeling local allele frequency changes in a 8 particular region of the genome under scenarios of selection and neutrality, and finding which model is 9 most compatible with the data. Chen et al. [2010] developed a composite likelihood method called XP- 10 CLR that uses an outgroup population to detect departures from neutrality which could be compatible 11 with hard or soft sweeps, at linked sites near a beneficial allele. However, this method is most sensitive 12 to recent selection and may miss selective events that happened a long time ago. To overcome this, 13 we developed an extension of XP-CLR that jointly models the behavior of a selected allele in a three- 14 population tree. Our method - called 3P-CLR - outperforms XP-CLR when testing for selection that 15 occurred before two populations split from each other, and can distinguish between those events and 16 events that occurred specifically in each of the populations after the split. -
Development of Novel Analysis and Data Integration Systems to Understand Human Gene Regulation
Development of novel analysis and data integration systems to understand human gene regulation Dissertation zur Erlangung des Doktorgrades Dr. rer. nat. der Fakult¨atf¨urMathematik und Informatik der Georg-August-Universit¨atG¨ottingen im PhD Programme in Computer Science (PCS) der Georg-August University School of Science (GAUSS) vorgelegt von Raza-Ur Rahman aus Pakistan G¨ottingen,April 2018 Prof. Dr. Stefan Bonn, Zentrum f¨urMolekulare Neurobiologie (ZMNH), Betreuungsausschuss: Institut f¨urMedizinische Systembiologie, Hamburg Prof. Dr. Tim Beißbarth, Institut f¨urMedizinische Statistik, Universit¨atsmedizin, Georg-August Universit¨at,G¨ottingen Prof. Dr. Burkhard Morgenstern, Institut f¨urMikrobiologie und Genetik Abtl. Bioinformatik, Georg-August Universit¨at,G¨ottingen Pr¨ufungskommission: Prof. Dr. Stefan Bonn, Zentrum f¨urMolekulare Neurobiologie (ZMNH), Referent: Institut f¨urMedizinische Systembiologie, Hamburg Prof. Dr. Tim Beißbarth, Institut f¨urMedizinische Statistik, Universit¨atsmedizin, Korreferent: Georg-August Universit¨at,G¨ottingen Prof. Dr. Burkhard Morgenstern, Weitere Mitglieder Institut f¨urMikrobiologie und Genetik Abtl. Bioinformatik, der Pr¨ufungskommission: Georg-August Universit¨at,G¨ottingen Prof. Dr. Carsten Damm, Institut f¨urInformatik, Georg-August Universit¨at,G¨ottingen Prof. Dr. Florentin W¨org¨otter, Physikalisches Institut Biophysik, Georg-August-Universit¨at,G¨ottingen Prof. Dr. Stephan Waack, Institut f¨urInformatik, Georg-August Universit¨at,G¨ottingen Tag der m¨undlichen Pr¨ufung: der 30. M¨arz2018 -
Transdifferentiation of Human Mesenchymal Stem Cells
Transdifferentiation of Human Mesenchymal Stem Cells Dissertation zur Erlangung des naturwissenschaftlichen Doktorgrades der Julius-Maximilians-Universität Würzburg vorgelegt von Tatjana Schilling aus San Miguel de Tucuman, Argentinien Würzburg, 2007 Eingereicht am: Mitglieder der Promotionskommission: Vorsitzender: Prof. Dr. Martin J. Müller Gutachter: PD Dr. Norbert Schütze Gutachter: Prof. Dr. Georg Krohne Tag des Promotionskolloquiums: Doktorurkunde ausgehändigt am: Hiermit erkläre ich ehrenwörtlich, dass ich die vorliegende Dissertation selbstständig angefertigt und keine anderen als die von mir angegebenen Hilfsmittel und Quellen verwendet habe. Des Weiteren erkläre ich, dass diese Arbeit weder in gleicher noch in ähnlicher Form in einem Prüfungsverfahren vorgelegen hat und ich noch keinen Promotionsversuch unternommen habe. Gerbrunn, 4. Mai 2007 Tatjana Schilling Table of contents i Table of contents 1 Summary ........................................................................................................................ 1 1.1 Summary.................................................................................................................... 1 1.2 Zusammenfassung..................................................................................................... 2 2 Introduction.................................................................................................................... 4 2.1 Osteoporosis and the fatty degeneration of the bone marrow..................................... 4 2.2 Adipose and bone -
Entrez ID Gene Name Fold Change Q-Value Description
Entrez ID gene name fold change q-value description 4283 CXCL9 -7.25 5.28E-05 chemokine (C-X-C motif) ligand 9 3627 CXCL10 -6.88 6.58E-05 chemokine (C-X-C motif) ligand 10 6373 CXCL11 -5.65 3.69E-04 chemokine (C-X-C motif) ligand 11 405753 DUOXA2 -3.97 3.05E-06 dual oxidase maturation factor 2 4843 NOS2 -3.62 5.43E-03 nitric oxide synthase 2, inducible 50506 DUOX2 -3.24 5.01E-06 dual oxidase 2 6355 CCL8 -3.07 3.67E-03 chemokine (C-C motif) ligand 8 10964 IFI44L -3.06 4.43E-04 interferon-induced protein 44-like 115362 GBP5 -2.94 6.83E-04 guanylate binding protein 5 3620 IDO1 -2.91 5.65E-06 indoleamine 2,3-dioxygenase 1 8519 IFITM1 -2.67 5.65E-06 interferon induced transmembrane protein 1 3433 IFIT2 -2.61 2.28E-03 interferon-induced protein with tetratricopeptide repeats 2 54898 ELOVL2 -2.61 4.38E-07 ELOVL fatty acid elongase 2 2892 GRIA3 -2.60 3.06E-05 glutamate receptor, ionotropic, AMPA 3 6376 CX3CL1 -2.57 4.43E-04 chemokine (C-X3-C motif) ligand 1 7098 TLR3 -2.55 5.76E-06 toll-like receptor 3 79689 STEAP4 -2.50 8.35E-05 STEAP family member 4 3434 IFIT1 -2.48 2.64E-03 interferon-induced protein with tetratricopeptide repeats 1 4321 MMP12 -2.45 2.30E-04 matrix metallopeptidase 12 (macrophage elastase) 10826 FAXDC2 -2.42 5.01E-06 fatty acid hydroxylase domain containing 2 8626 TP63 -2.41 2.02E-05 tumor protein p63 64577 ALDH8A1 -2.41 6.05E-06 aldehyde dehydrogenase 8 family, member A1 8740 TNFSF14 -2.40 6.35E-05 tumor necrosis factor (ligand) superfamily, member 14 10417 SPON2 -2.39 2.46E-06 spondin 2, extracellular matrix protein 3437 -
Novel Therapeutic Approach for Regulating the Susceptibility
NOVEL THERAPEUTIC APPROACH FOR REGULATING THE SUSCEPTIBILITY OF EPITHELIA TO ADENOVIRUS INFECTION A Dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy By Mahmoud S Alghamri B.Pharm, Alazhar University, Gaza, Palestine M.S., Wright State University, Dayton, USA 2016 Wright State University COPYRIGHT BY MAHMOUD S ALGHAMRI 2016 WRIGHT STATE UNIVERSITY GRADUATE SCHOOL August 1, 2016 I HEREBY RECOMMEND THAT THE DISSERTATION PREPARED UNDER MY SUPERVISION BY Mahmoud S Alghamri ENTITLED Novel Therapeutic Approach for Regulating the Susceptibility of Epithelia to Adenovirus Infection BE ACCEPTED IN PARTIAL FULFILMENT OF THE REQUIREMENTS FOR THE DEGREE OF Doctor of Philosophy Katherine J.D.A. Excoffon, Ph.D. Dissertation Director Mill W. Miller, Ph.D. Director, Biomedical Sciences Ph.D program Robert E. W. Fyffe, Ph.D. Vice President for Research and Dean of the Committee on Final Examination Graduate School David R. Cool, Ph.D. David R. Ladle, Ph.D. Quan Zhong, Ph.D. Weiwen Long, Ph.D. Abstract Mahmoud S Alghamri Ph.D. Biomedical Sciences Ph.D. Program. Wright State University, 2016. Novel therapeutic approach for regulating the susceptibility of epithelia to adenovirus infection. Human Adenoviruses (AdVs) are etiologic agents for respiratory tract, digestive tract, heart, and eye infections. Although most AdV infections are self-resolving, some infections progress to acute respiratory disease with up to 50% mortality, particularly in immunosuppressed people. Except for vaccines for serotypes, 4 and 7, serotypes that are prevalent in the military, no vaccines or therapeutics that specifically prevent or treat AdV infection exist. On the other hand, AdV remains the most common vector system used in gene therapy clinical trials worldwide and several AdV vectors show promise in phase III clinical trials. -
Dissecting the Genetic Etiology of Lupus at ETS1 Locus
Dissecting the Genetic Etiology of Lupus at ETS1 Locus A dissertation submitted to the Graduate School of the University of Cincinnati in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Immunobiology of the College of Medicine 2017 by Xiaoming Lu B.S. Sun Yat-sen University, P.R. China June 2011 Dissertation Committee: John B. Harley, MD, PhD Harinder Singh, PhD Leah C. Kottyan, PhD Matthew T. Weirauch, PhD Kasper Hoebe, PhD Lili Ding, PhD i Abstract Systemic lupus erythematosus (SLE) is a complex autoimmune disease with strong evidence for genetics factor involvement. Genome-wide association studies have identified 84 risk loci associated with SLE. However, the specific genotype-dependent (allelic) molecular mechanisms connecting these lupus-genetic risk loci to immunological dysregulation are mostly still unidentified. ~ 90% of these loci contain variants that are non-coding, and are thus likely to act by impacting subtle, comparatively hard to predict mechanisms controlling gene expression. Here, we developed a strategic approach to prioritize non-coding variants, and screen them for their function. This approach involves computational prioritization using functional genomic databases followed by experimental analysis of differential binding of transcription factors (TFs) to risk and non-risk alleles. For both electrophoretic mobility shift assay (EMSA) and DNA affinity precipitation assay (DAPA) analysis of genetic variants, a synthetic DNA oligonucleotide (oligo) is used to identify factors in the nuclear lysate of disease or phenotype-relevant cells. This strategic approach was then used for investigating SLE association at ETS1 locus. Genetic variants at chromosomal region 11q23.3, near the gene ETS1, have been associated with systemic lupus erythematosus (SLE), or lupus, in independent cohorts of Asian ancestry. -
SANTA CRUZ BIOTECHNOLOGY, INC. FCHSD2 Sirna (M): Sc-145151
SANTA CRUZ BIOTECHNOLOGY, INC. FCHSD2 siRNA (m): sc-145151 BACKGROUND STORAGE AND RESUSPENSION FCHSD2 (FCH and double SH3 domains protein 2) is a 740 amino acid protein Store lyophilized siRNA duplex at -20° C with desiccant. Stable for at least that contains one FCH domain and two SH3 domains. FCHSD2 exists as three one year from the date of shipment. Once resuspended, store at -20° C, isoforms as a result of alternative splicing events, and is expressed in liver, avoid contact with RNAses and repeated freeze thaw cycles. brain, heart, placenta, skeletal muscle, pancreas, lung and kidney. The gene Resuspend lyophilized siRNA duplex in 330 µl of the RNAse-free water encoding FCHSD2 maps to chromosome 11, which makes up around 4% of provided. Resuspension of the siRNA duplex in 330 µl of RNAse-free water human genomic DNA and is considered a gene and disease association dense makes a 10 µM solution in a 10 µM Tris-HCl, pH 8.0, 20 mM NaCl, 1 mM chromosome. The chromosome 11 encoded Atm gene is important for regu- EDTA buffered solution. lation of cell cycle arrest and apoptosis following double strand DNA breaks. Atm mutation leads to the disorder known as ataxia-telangiectasia. The blood APPLICATIONS disorders Sickle cell anemia and β thalassemia are caused by HBB gene muta- tions. Wilms’ tumors, WAGR syndrome and Denys-Drash syndrome are asso- FCHSD2 siRNA (m) is recommended for the inhibition of FCHSD2 expression ciated with mutations of the WT1 gene. Jervell and Lange-Nielsen syndrome, in mouse cells. Jacobsen syndrome, Niemann-Pick disease, hereditary angioedema and Smith- Lemli-Opitz syndrome are also associated with defects in chromosome 11. -
Identification of a Systemic Lupus Erythematosus Risk Locus Spanning ATG16L2, FCHSD2, and P2RY2 in Koreans
ARTHRITIS & RHEUMATOLOGY Vol. 68, No. 5, May 2016, pp 1197–1209 DOI 10.1002/art.39548 VC 2016, American College of Rheumatology Identification of a Systemic Lupus Erythematosus Risk Locus Spanning ATG16L2, FCHSD2, and P2RY2 in Koreans Christopher J. Lessard,1 Satria Sajuthi,2 Jian Zhao,3 Kwangwoo Kim,4 John A. Ice,1 He Li,5 Hannah Ainsworth,2 Astrid Rasmussen,1 Jennifer A. Kelly,1 Miranda Marion,2 So-Young Bang,4 Young Bin Joo,4 Jeongim Choi,4 Hye-Soon Lee,4 Young Mo Kang,6 Chang-Hee Suh,7 Won Tae Chung,8 Soo-Kon Lee,9 Jung-Yoon Choe,10 Seung Cheol Shim,11 Ji Hee Oh,12 Young Jin Kim,12 Bok-Ghee Han,12 Nan Shen,13 Hwee Siew Howe,14 Edward K. Wakeland,15 Quan-Zhen Li,15 Yeong Wook Song,16 Patrick M. Gaffney,1 Marta E. Alarcon-Riquelme, 17 Lindsey A. Criswell,18 Chaim O. Jacob,19 Robert P. Kimberly,20 Timothy J. Vyse,21 John B. Harley,22 Kathy L. Sivils,5 Sang-Cheol Bae,4 Carl D. Langefeld,2 and Betty P. Tsao3 Objective. Systemic lupus erythematosus (SLE) is unbiased genome-wide association (GWA) scan and rep- a chronic autoimmune disorder whose etiology is incom- lication analysis, we sought to identify the genetic loci pletely understood, but likely involves environmental associated with SLE in a Korean population. triggers in genetically susceptible individuals. Using an Methods. A total of 1,174 SLE cases and 4,246 pop- ulation controls from Korea were genotyped and analyzed The contents of this article are solely the responsibility of the with a GWA scan to identify single-nucleotide polymor- authors and do not necessarily represent the official views of the phisms (SNPs) significantly associated with SLE, after National Institutes of Health. -
Estrogen's Impact on the Specialized Transcriptome, Brain, and Vocal
Estrogen’s Impact on the Specialized Transcriptome, Brain, and Vocal Learning Behavior of a Sexually Dimorphic Songbird by Ha Na Choe Department of Molecular Genetics & Microbiology Duke University Date:_____________________ Approved: ___________________________ Erich D. Jarvis, Supervisor ___________________________ Hiroaki Matsunami ___________________________ Debra Silver ___________________________ Dong Yan ___________________________ Gregory Crawford Dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Molecular Genetics & Microbiology in the Graduate School of Duke University 2020 ABSTRACT Estrogen’s Impact on the Specialized Transcriptome, Brain, and Vocal Learning Behavior of a Sexually Dimorphic Songbird by Ha Na Choe Department of Molecular Genetics & Microbiology Duke University Date:_________________________ Approved: ___________________________ Erich D. Jarvis, Supervisor ___________________________ Hiroaki Matsunami ___________________________ Debra Silver ___________________________ Dong Yan ___________________________ Gregory Crawford Dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Molecular Genetics & Microbiology in the Graduate School of Duke University 2020 Copyright by Ha Na Choe 2020 Abstract The song system of the zebra finch (Taeniopygia guttata) is highly sexually dimorphic, where only males develop the neural structures necessary to learn and produce learned vocalizations -
LNX1/LNX2 Proteins: Functions in Neuronal Signalling and Beyond
Neuronal Signaling (2018) 2 NS20170191 https://doi.org/10.1042/NS20170191 Review Article LNX1/LNX2 proteins: functions in neuronal signalling and beyond Paul W. Young School of Biochemistry and Cell Biology, Cork Neuroscience Centre, SynBioCentre, University College Cork, Cork, Ireland Correspondence: Paul W. Young ([email protected]) Ligand of NUMB Protein X1 and X2 (LNX1 and LNX2) are E3 ubiquitin ligases, named for their ability to interact with and promote the degradation of the cell fate determinant protein NUMB. On this basis they are thought to play a role in modulating NUMB/NOTCH signalling during processes such as cortical neurogenesis. However, LNX1/2 proteins can bind, via their four PDZ (PSD95, DLGA, ZO-1) domains, to an extraordinarily large number of other proteins besides NUMB. Many of these interactions suggest additional roles for LNX1/2 proteins in the nervous system in areas such as synapse formation, neurotransmission and regulating neuroglial function. Twenty years on from their initial discovery, I discuss here the putative neuronal functions of LNX1/2 proteins in light of the anxiety-related phenotype of double knockout mice lacking LNX1 and LNX2 in the central nervous system (CNS). I also review what is known about non-neuronal roles of LNX1/2 proteins, including their roles in embryonic patterning and pancreas development in zebrafish and their possible involvement in colorectal cancer (CRC), osteoclast differentiation and immune function in mammals. The emerging picture places LNX1/2 proteins as potential regulators of multiple cellular signalling processes, but in many cases the physiological significance of such roles remains only partly validated and needs to be considered in the context of the tight control of LNX1/2 protein levels in vivo.