ZMYND10 Functions in a Chaperone Relay During Axonemal Dynein
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Compression of Large Sets of Sequence Data Reveals Fine Diversification of Functional Profiles in Multigene Families of Proteins
Technical note Compression of Large Sets of Sequence Data Reveals Fine Diversification of Functional Profiles in Multigene Families of Proteins: A Study for Peptidyl-Prolyl cis/trans Isomerases (PPIase) Andrzej Galat Retired from: Service d’Ingénierie Moléculaire des Protéines (SIMOPRO), CEA-Université Paris-Saclay, France; [email protected]; Tel.: +33-0164465072 Received: 21 December 2018; Accepted: 21 January 2019; Published: 11 February 2019 Abstract: In this technical note, we describe analyses of more than 15,000 sequences of FK506- binding proteins (FKBP) and cyclophilins, also known as peptidyl-prolyl cis/trans isomerases (PPIases). We have developed a novel way of displaying relative changes of amino acid (AA)- residues at a given sequence position by using heat-maps. This type of representation allows simultaneous estimation of conservation level in a given sequence position in the entire group of functionally-related paralogues (multigene family of proteins). We have also proposed that at least two FKBPs, namely FKBP36, encoded by the Fkbp6 gene and FKBP51, encoded by the Fkbp5 gene, can form dimers bound via a disulfide bridge in the nucleus. This type of dimer may have some crucial function in the regulation of some nuclear complexes at different stages of the cell cycle. Keywords: FKBP; cyclophilin; PPIase; heat-map; immunophilin 1 Introduction About 30 years ago, an exciting adventure began in finding some correlations between pharmacological activities of macrocyclic hydrophobic drugs, namely the cyclic peptide cyclosporine A (CsA), and two macrolides, namely FK506 and rapamycin, which have profound and clinically useful immunosuppressive effects, especially in organ transplantations and in combating some immune disorders. -
ZMYND10 Functions in a Chaperone Relay During Axonemal Dynein Assembly
bioRxiv preprint doi: https://doi.org/10.1101/233718; this version posted December 13, 2017. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity.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 ZMYND10 functions in a chaperone relay during axonemal dynein assembly. 2 3 Girish R Mali1,9 , Patricia Yeyati1, Seiya Mizuno2, Margaret A Keighren1, Petra zur Lage3, Amaya 4 Garcia-Munoz4, Atsuko Shimada5, Hiroyuki Takeda5, Frank Edlich6, Satoru Takahashi2,7, Alex von 5 Kreigsheim4,8, Andrew Jarman3 and Pleasantine Mill1,*. 6 7 1. MRC Human Genetics Unit, Institute of Genetics and Molecular Medicine, University of 8 Edinburgh, Edinburgh, UK, EH4 2XU 9 2. Laboratory Animal Resource Centre, University of Tsukuba, Tsukuba, Japan, 305-8575 10 3. Centre for Integrative Physiology, University of Edinburgh, Edinburgh, UK, EH8 9XD 11 4. Systems Biology Ireland, University College Dublin, Dublin, Ireland 12 5. Department of Biological Sciences, University of Tokyo, Tokyo, Japan, 113-0033 13 6. Institute for Biochemistry and Molecular Biology, University of Freiburg, Freiburg, Germany, 14 79104 15 7. Department of Anatomy and Embryology, Faculty of Medicine, University of Tsukuba, Tsukuba, 16 Japan, 305-8575 17 8. Edinburgh Cancer Research UK Centre, Institute of Genetics and Molecular Medicine, University 18 of Edinburgh, Edinburgh, UK, EH4 2XU 19 9. Current address: MRC Laboratory of Molecular Biology, Cambridge, UK, CB2 0QH 20 * Corresponding author: [email protected] 21 22 23 24 25 26 27 28 29 30 31 1 bioRxiv preprint doi: https://doi.org/10.1101/233718; this version posted December 13, 2017. -
Ventral Hindgut and Bladder Development
Ventral Hindgut and Bladder Development by Wei CHENG A thesis submitted in conformity with the requirements For the degree of PhD Graduate Department of Institute of Medical Science University of Toronto © Copyright by Wei Cheng, 2008 Library and Bibliotheque et 1*1 Archives Canada Archives Canada Published Heritage Direction du Branch Patrimoine de I'edition 395 Wellington Street 395, rue Wellington Ottawa ON K1A0N4 Ottawa ON K1A0N4 Canada Canada Your file Votre reference ISBN: 978-0-494-40009-8 Our file Notre reference ISBN: 978-0-494-40009-8 NOTICE: AVIS: The author has granted a non L'auteur a accorde une licence non exclusive exclusive license allowing Library permettant a la Bibliotheque et Archives and Archives Canada to reproduce, Canada de reproduire, publier, archiver, publish, archive, preserve, conserve, sauvegarder, conserver, transmettre au public communicate to the public by par telecommunication ou par Plntemet, prefer, telecommunication or on the Internet, distribuer et vendre des theses partout dans loan, distribute and sell theses le monde, a des fins commerciales ou autres, worldwide, for commercial or non sur support microforme, papier, electronique commercial purposes, in microform, et/ou autres formats. paper, electronic and/or any other formats. The author retains copyright L'auteur conserve la propriete du droit d'auteur ownership and moral rights in et des droits moraux qui protege cette these. this thesis. Neither the thesis Ni la these ni des extraits substantiels de nor substantial extracts from it celle-ci ne doivent etre imprimes ou autrement may be printed or otherwise reproduits sans son autorisation. reproduced without the author's permission. -
A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus
Page 1 of 781 Diabetes A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes Mellitus Robert N. Bone1,6,7, Olufunmilola Oyebamiji2, Sayali Talware2, Sharmila Selvaraj2, Preethi Krishnan3,6, Farooq Syed1,6,7, Huanmei Wu2, Carmella Evans-Molina 1,3,4,5,6,7,8* Departments of 1Pediatrics, 3Medicine, 4Anatomy, Cell Biology & Physiology, 5Biochemistry & Molecular Biology, the 6Center for Diabetes & Metabolic Diseases, and the 7Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; 2Department of BioHealth Informatics, Indiana University-Purdue University Indianapolis, Indianapolis, IN, 46202; 8Roudebush VA Medical Center, Indianapolis, IN 46202. *Corresponding Author(s): Carmella Evans-Molina, MD, PhD ([email protected]) Indiana University School of Medicine, 635 Barnhill Drive, MS 2031A, Indianapolis, IN 46202, Telephone: (317) 274-4145, Fax (317) 274-4107 Running Title: Golgi Stress Response in Diabetes Word Count: 4358 Number of Figures: 6 Keywords: Golgi apparatus stress, Islets, β cell, Type 1 diabetes, Type 2 diabetes 1 Diabetes Publish Ahead of Print, published online August 20, 2020 Diabetes Page 2 of 781 ABSTRACT The Golgi apparatus (GA) is an important site of insulin processing and granule maturation, but whether GA organelle dysfunction and GA stress are present in the diabetic β-cell has not been tested. We utilized an informatics-based approach to develop a transcriptional signature of β-cell GA stress using existing RNA sequencing and microarray datasets generated using human islets from donors with diabetes and islets where type 1(T1D) and type 2 diabetes (T2D) had been modeled ex vivo. To narrow our results to GA-specific genes, we applied a filter set of 1,030 genes accepted as GA associated. -
FKBP8 Antibody Cat
FKBP8 Antibody Cat. No.: 62-126 FKBP8 Antibody With HepG2 cell line lysate, the resolved proteins were electrophoretically transferred to PVDF membrane and incubated sequentially with primary antibody FKBP38 (1:1000, 4˚C,overnight ) and horseradish peroxidase–conjugated second antibody. After washing, the bound antibody complex was detected using an ECL chemiluminescence reagentand XAR film (Kodak). Specifications HOST SPECIES: Rabbit SPECIES REACTIVITY: Human HOMOLOGY: Predicted species reactivity based on immunogen sequence: Mouse, Rat This FKBP8 antibody is generated from rabbits immunized with a KLH conjugated IMMUNOGEN: synthetic peptide between 199-226 amino acids from the Central region of human FKBP8. TESTED APPLICATIONS: WB APPLICATIONS: For WB starting dilution is: 1:1000 PREDICTED MOLECULAR 45 kDa WEIGHT: September 28, 2021 1 https://www.prosci-inc.com/fkbp8-antibody-62-126.html Properties This antibody is purified through a protein A column, followed by peptide affinity PURIFICATION: purification. CLONALITY: Polyclonal ISOTYPE: Rabbit Ig CONJUGATE: Unconjugated PHYSICAL STATE: Liquid BUFFER: Supplied in PBS with 0.09% (W/V) sodium azide. CONCENTRATION: batch dependent Store at 4˚C for three months and -20˚C, stable for up to one year. As with all antibodies STORAGE CONDITIONS: care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures. Additional Info OFFICIAL SYMBOL: FKBP8 Peptidyl-prolyl cis-trans isomerase FKBP8, PPIase FKBP8, 38 kDa FK506-binding protein, ALTERNATE NAMES: 38 kDa FKBP, FKBP-38, hFKBP38, FK506-binding protein 8, FKBP-8, FKBPR38, Rotamase, FKBP8, FKBP38 ACCESSION NO.: Q14318 PROTEIN GI NO.: 193806337 GENE ID: 23770 USER NOTE: Optimal dilutions for each application to be determined by the researcher. -
Naringenin Regulates FKBP4/NR3C1/TMEM173 Signaling Pathway in Autophagy and Proliferation of Breast Cancer and Tumor-Infltrating Dendritic Cell Maturation
Naringenin Regulates FKBP4/NR3C1/TMEM173 Signaling Pathway in Autophagy and Proliferation of Breast Cancer and Tumor-Inltrating Dendritic Cell Maturation Hanchu Xiong ( [email protected] ) Zhejiang Provincial People's Hospital https://orcid.org/0000-0001-6075-6895 Zihan Chen First Hospital of Zhejiang Province: Zhejiang University School of Medicine First Aliated Hospital Baihua Lin Zhejiang Provincial People's Hospital Cong Chen Zhejiang University School of Medicine Sir Run Run Shaw Hospital Zhaoqing Li Zhejiang University School of Medicine Sir Run Run Shaw Hospital Yongshi Jia Zhejiang Provincial People's Hospital Linbo Wang Zhejiang University School of Medicine Sir Run Run Shaw Hospital Jichun Zhou Zhejiang University School of Medicine Sir Run Run Shaw Hospital Research Keywords: FKBP4, TMEM173, Autophagy, Exosome, Dendritic cell, Breast cancer Posted Date: July 7th, 2021 DOI: https://doi.org/10.21203/rs.3.rs-659646/v1 License: This work is licensed under a Creative Commons Attribution 4.0 International License. Read Full License Page 1/38 Abstract Background TMEM173 is a pattern recognition receptor detecting cytoplasmic nucleic acids and transmits cGAS related signals that activate host innate immune responses. It has also been found to be involved in tumor immunity and tumorigenesis. Methods Bc-GenExMiner, PROMO and STRING database were used for analyzing clinical features and interplays of FKBP4, TMEM173 and NR3C1. Transient transfection, western blotting, quantitative real-time PCR, luciferase reporter assay, immunouorescence and nuclear and cytoplasmic fractionation were used for regulation of FKBP4, TMEM173 and NR3C1. Both knockdown and overexpression of FKBP4, TMEM173 and NR3C1 were used to analyze effects on autophagy and proliferation of breast cancer (BC) cells. -
Translational Activity of the Splicing Factor SRSF1 Is Required for Development and Cilia Function
bioRxiv preprint doi: https://doi.org/10.1101/2020.09.04.263251; this version posted September 4, 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-ND 4.0 International license. Haward, Maslon, Yeyati et al. Translational activity of the splicing factor SRSF1 is required for development and cilia function Fiona Haward,1,5,6 Magdalena M. Maslon,1,6 Patricia L. Yeyati,1,6 Nicolas Bellora,2 Jan N. Hansen,3 Stuart Aitken,1 Jennifer Lawson,1 Alex von Kriegsheim,4 Dagmar Wachten,3 Pleasantine Mill,1,* Ian R. Adams1,* and Javier F. Cáceres1,7,* 1MRC Human Genetics Unit, Institute of Genetics and Molecular Medicine, University of Edinburgh, Crewe Road South, Edinburgh EH4 2XU, UK 2IPATEC, ConseJo Nacional de Investigaciones, Científicas y Técnicas (CONICET)- Universidad Nacional del Comahue, 8400, Bariloche, Argentina. 3Institute of Innate Immunity, Biophysical Imaging, Medical Faculty, University of Bonn, Bonn, Germany 4Edinburgh Cancer Research UK Centre, Institute of Genetics and Molecular Medicine, University of Edinburgh, Crewe Road South, Edinburgh EH4 2XU, UK 5Present address: Centre for Gene Regulation and Expression, School of Life Sciences, University of Dundee, Dundee DD1 5EH, UK 6These authors contributed equally to this work 7Lead contact *Correspondence: [email protected]; [email protected]; [email protected] Running title: Nucleo-cytoplasmic shuttling of SR proteins [Key Words: SR proteins; SRSF1; alternative splicing; mRNA translation; cilia] 1 bioRxiv preprint doi: https://doi.org/10.1101/2020.09.04.263251; this version posted September 4, 2020. -
SI Appendix Table of Contents
SI Appendix Contact-ID, a tool for profiling organelle-membrane contact sites, reveals regulatory proteins of mitochondrial-associated membrane formation Chulhwan Kwak1,2†, Sanghee Shin3,4,†, Jong-Seok Park2,†, Minkyo Jung5, Truong Thi My Nhung6, Myeong-Gyun Kang1,2, Chaiheon Lee2, Tae-Hyuk Kwon2, Sang Ki Park6,*, Ji Young Mun5,*, Jong-Seo Kim3,4,*, and Hyun-Woo Rhee1,4* 1Department of Chemistry, Seoul National University, Seoul, 08826, Korea 2Department of Chemistry, Ulsan National Institute of Science and Technology (UNIST), Ulsan, 44919, Korea 3Center for RNA Research, Institute of Basic Science (IBS), Seoul, 08826, Korea 4School of Biological Sciences, Seoul National University, Seoul, 08826, Korea 5Department of Structure and Function of Neural Network, Korea Brain Research Institute, Daegu, 41062, South Korea 6 Department of Life Sciences, Pohang University of Science and Technology (POSTECH), 37673, Pohang, Republic of Korea. *Corresponding authors: [email protected] (H.-W.R.), [email protected] (J.-S.K.), [email protected] (J. Y. M.), [email protected] (S. K. P.) † These authors equally contributed to this work. Table of Contents Table S1------------------------------------------------------------------------------------------------------------------------------------------------S3 Figure S1-17------------------------------------------------------------------------------------------------------------------------------S4-32 Movie S1-4& dataset S1-5 legends-------------------------------------------------------------------------------------------------------S33 -
Test Catalogue August 2019
Test Catalogue August 2019 www.centogene.com/catalogue Table of Contents CENTOGENE CLINICAL DIAGNOSTIC PRODUCTS AND SERVICES › Whole Exome Testing 4 › Whole Genome Testing 5 › Genome wide CNV Analysis 5 › Somatic Mutation Analyses 5 › Biomarker Testing, Biochemical Testing 6 › Prenatal Testing 7 › Additional Services 7 › Metabolic Diseases 9 - 21 › Neurological Diseases 23 - 47 › Ophthalmological Diseases 49 - 55 › Ear, Nose and Throat Diseases 57 - 61 › Bone, Skin and Immune Diseases 63 - 73 › Cardiological Diseases 75 - 79 › Vascular Diseases 81 - 82 › Liver, Kidney and Endocrinological Diseases 83 - 89 › Reproductive Genetics 91 › Haematological Diseases 93 - 96 › Malformation and/or Retardation Syndromes 97 - 107 › Oncogenetics 109 - 113 ® › CentoXome - Sequencing targeting exonic regions of ~20.000 genes Test Test name Description code CentoXome® Solo Medical interpretation/report of WES findings for index 50029 CentoXome® Solo - Variants Raw data; fastQ, BAM, Vcf files along with variant annotated file in xls format for index 50028 CentoXome® Solo - with CNV Medical interpretation/report of WES including CNV findings for index 50103 Medical interpretation/report of WES in index, package including genome wide analyses of structural/ CentoXome® Solo - with sWGS 50104 large CNVs through sWGS Medical interpretation/report of WES in index, package including genome wide analyses of structural/ CentoXome® Solo - with aCGH 750k 50122 large CNVs through 750k microarray Medical interpretation/report of WES in index, package including genome -
Mouse Cfap298 Conditional Knockout Project (CRISPR/Cas9)
https://www.alphaknockout.com Mouse Cfap298 Conditional Knockout Project (CRISPR/Cas9) Objective: To create a Cfap298 conditional knockout Mouse model (C57BL/6J) by CRISPR/Cas-mediated genome engineering. Strategy summary: The Cfap298 gene (NCBI Reference Sequence: NM_026502.2 ; Ensembl: ENSMUSG00000022972 ) is located on Mouse chromosome 16. 7 exons are identified, with the ATG start codon in exon 1 and the TGA stop codon in exon 7 (Transcript: ENSMUST00000023694). Exon 2~3 will be selected as conditional knockout region (cKO region). Deletion of this region should result in the loss of function of the Mouse Cfap298 gene. To engineer the targeting vector, homologous arms and cKO region will be generated by PCR using BAC clone RP24-100B13 as template. Cas9, gRNA and targeting vector will be co-injected into fertilized eggs for cKO Mouse production. The pups will be genotyped by PCR followed by sequencing analysis. Note: Exon 2 starts from about 16.09% of the coding region. The knockout of Exon 2~3 will result in frameshift of the gene. The size of intron 1 for 5'-loxP site insertion: 3420 bp, and the size of intron 3 for 3'-loxP site insertion: 2407 bp. The size of effective cKO region: ~1746 bp. The cKO 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 2 3 7 Targeting vector Targeted allele Constitutive KO allele (After Cre recombination) Legends Exon of mouse Cfap298 Homology arm cKO region loxP site Page 2 of 8 https://www.alphaknockout.com Overview of the Dot Plot Window size: 10 bp Forward Reverse Complement Sequence 12 Note: The sequence of homologous arms and cKO region is aligned with itself to determine if there are tandem repeats. -
FKBP8 and the Autophagy-Inducing Class-III PI3K Complex Roles of LIR Dependent Interactions
Faculty of Health Science Department of Medical Biology FKBP8 and the autophagy-inducing Class-III PI3K Complex Roles of LIR dependent interactions Zambarlal Bhujabal A dissertation for the degree of Philosophiae Doctor – June 2017 FKBP8 and the autophagy-inducing Class-III PI3K Complex Roles of LIR dependent interactions Zambarlal Baban Bhujabal A dissertation for the degree of Philosophiae Doctor UiT The Artic University of Norway Faculty of Health Science Department of Medical Biology Molecular Cancer Research Group June 2017 Table of Contents Acknowledgement ....................................................................................................................... I Abbreviation ...............................................................................................................................II Summary .................................................................................................................................. IV List of papers ............................................................................................................................. V Introduction ................................................................................................................................ 1 Ubiquitin Proteasome System (UPS) ..................................................................................... 1 Autophagy .............................................................................................................................. 2 Initiation ............................................................................................................................. -
Altered Metabotropic Glutamate Receptor 5 Markers in PTSD: in Vivo and Postmortem Evidence,” by Sophie E
Correction NEUROSCIENCE Correction for “Altered metabotropic glutamate receptor 5 markers in PTSD: In vivo and postmortem evidence,” by Sophie E. Holmes, Matthew J. Girgenti, Margaret T. Davis, Robert H. Pietrzak, Nicole DellaGioia, Nabeel Nabulsi, David Matuskey, Steven Southwick, Ronald S. Duman, Richard E. Carson, John H. Krystal, Irina Esterlis, and the Traumatic Stress Brain Study Group, which was first pub- lished July 17, 2017; 10.1073/pnas.1701749114 (Proc Natl Acad Sci USA 114:8390–8395). The authors note that the affiliation for c should instead appear as National Center for PTSD, Clinical Neurosciences Division, West Haven, CT 06516. The authors also note that this affiliation should be applied to Steven Southwick, in addition to affiliations a and b. The corrected author and affiliation lines appear below. The online version has been corrected. Sophie E. Holmesa,b, Matthew J. Girgentia,b,c,MargaretT. Davisa,b, Robert H. Pietrzaka,b,c, Nicole DellaGioiaa,b, Nabeel Nabulsia,b, David Matuskeya,b, Steven Southwicka,b,c, Ronald S. Dumana,b,c, Richard E. Carsona,b, John H. Krystala,b,c, Irina Esterlisa,b,c, and the Traumatic Stress Brain Study Group aDepartment of Psychiatry, Yale University School of Medicine, New Haven, CT 06519; bDepartment of Radiology and Biomedical Imaging, Yale University School of Medicine, New Haven, CT 06519; and cNational Center for PTSD, Clinical Neurosciences Division, West Haven, CT 06516 www.pnas.org/cgi/doi/10.1073/pnas.1714425114 E7852 | PNAS | September 12, 2017 | vol. 114 | no. 37 www.pnas.org Downloaded by guest on September 29, 2021 Altered metabotropic glutamate receptor 5 markers in PTSD: In vivo and postmortem evidence Sophie E.