Atlas Journal

Total Page:16

File Type:pdf, Size:1020Kb

Atlas Journal Atlas of Genetics and Cytogenetics in Oncology and Haematology Home Genes Leukemias Solid Tumours Cancer-Prone Deep Insight Portal Teaching X Y 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 NA Atlas Journal Atlas Journal versus Atlas Database: the accumulation of the issues of the Journal constitutes the body of the Database/Text-Book. TABLE OF CONTENTS Volume 11, Number 3, Jul-Sep 2007 Previous Issue / Next Issue Genes MSH6 (mutS homolog 6 (E. Coli)) (2p16). Sreeparna Banerjee. Atlas Genet Cytogenet Oncol Haematol 2006; 9 11 (3): 289-297. [Full Text] [PDF] URL : http://atlasgeneticsoncology.org/Genes/MSH6ID344ch2p16.html LDB1 (10q24). Takeshi Setogawa, Testu Akiyama. Atlas Genet Cytogenet Oncol Haematol 2006; 11 (3): 298-301.[Full Text] [PDF] URL : http://atlasgeneticsoncology.org/Genes/LDB1ID41135ch10q24.html INTS6 (integrator complex subunit 6) (13q14.3). Ilse Wieland. Atlas Genet Cytogenet Oncol Haematol 2006; 11 (3): 302-306.[Full Text] [PDF] URL : http://atlasgeneticsoncology.org/Genes/INTS6ID40287ch13q14.html EPHA7 (EPH receptor A7) (6q16.1). Haruhiko Sugimura, Hiroki Mori, Tomoyasu Bunai, Masaya Suzuki. Atlas Genet Cytogenet Oncol Haematol 2007; 11 (3): 307-312. [Full Text] [PDF] Atlas Genet Cytogenet Oncol Haematol 2007;3 -I URL : http://atlasgeneticsoncology.org/Genes/EPHA7ID40466ch6q16.html RNASET2 (ribonuclease T2) (6q27). Francesco Acquati, Paola Campomenosi. Atlas Genet Cytogenet Oncol Haematol 2007; 11 (3): 313-317. [Full Text] [PDF] URL : http://atlasgeneticsoncology.org/Genes/RNASET2ID518ch6q27.html RHOB (ras homolog gene family, member B) (2p24.1). Minzhou Huang, Lisa D Laury-Kleintop, George Prendergast. Atlas Genet Cytogenet Oncol Haematol 2007; 11 (3): 318-323. [Full Text] [PDF] URL : http://atlasgeneticsoncology.org/Genes/RHOBID42108ch2p24.html RBM5 (RNA binding motif protein 5) (3p21.3). Mirna Mourtada-Maarabouni. Atlas Genet Cytogenet Oncol Haematol 2007; 11 (3): 324-331. [Full Text] [PDF] URL : http://atlasgeneticsoncology.org/Genes/RBM5ID42069ch3p21.html RAC3 (ras-related C3 botulinum toxin substrate 3 (rho family, small GTP binding protein Rac3)) (17q25.3). Nora C. Heisterkamp. Atlas Genet Cytogenet Oncol Haematol 2007; 11 (3): 332-338. [Full Text] [PDF] URL : http://atlasgeneticsoncology.org/Genes/RAC3ID42022ch17q25.html NUT (nuclear protein in testis) (15q14). Anna Collin. Atlas Genet Cytogenet Oncol Haematol 2007; 11 (3): 339-342. [Full Text] [PDF] URL : http://atlasgeneticsoncology.org/Genes/NUTID41595ch15q14.html MUC4 (mucin 4, cell surface associated) (3q29). Nicolas Moniaux, Pallavi Chaturvedi, Isabelle Van Seuningen, Nicole Porchet, Ajay P. Singh, Surinder K. Batra. Atlas Genet Cytogenet Oncol Haematol 2007; 11 (3): 343-354. [Full Text] [PDF] URL : http://atlasgeneticsoncology.org/Genes/MUC4ID41459ch3q29.html JAG2 (Human Jagged2) (14q32). Atlas Genet Cytogenet Oncol Haematol 2007;3 -II Pushpankur Ghoshal, Lionel J Coignet. Atlas Genet Cytogenet Oncol Haematol 2007; 11 (3): 355-359. [Full Text] [PDF] URL : http://atlasgeneticsoncology.org/Genes/JAG2ID41030ch14q32.html HSPH1 (heat shock 105kDa/110kDa protein 1) (13q12.3). Takumi Hatayama, Nobuyuki Yamagishi. Atlas Genet Cytogenet Oncol Haematol 2007; 11 (3): 360-364. [Full Text] [PDF] URL : http://atlasgeneticsoncology.org/Genes/HSPH1ID40891ch13q12.html HSPD1 (Heat Shock 60kDa Protein 1) (2q33.1). Ahmad Faried, Leri S Faried. Atlas Genet Cytogenet Oncol Haematol 2007; 11 (3): 365-371. [Full Text] [PDF] URL : http://atlasgeneticsoncology.org/Genes/HSPD1ID40888ch2q33.html HIC1 (Hypermethylated in Cancer 1) (17p13.3). Dominique Leprince. Atlas Genet Cytogenet Oncol Haematol 2007; 11 (3): 372-377. [Full Text] [PDF] URL : http://atlasgeneticsoncology.org/Genes/HIC1ID40819ch17p13.html FLCN (folliculin gene) (17p11.2). Laura S Schmidt. Atlas Genet Cytogenet Oncol Haematol 2007; 11 (3): 378-385. [Full Text] [PDF] URL : http://atlasgeneticsoncology.org/Genes/FLCNID789ch17p11.html ENPP2 (ectonucleotide pyrophosphatase/phosphodiesterase 2) (8q24.12). Mary L. Stracke, Timothy Clair. Atlas Genet Cytogenet Oncol Haematol 2007; 11 (3): 386-395. [Full Text] [PDF] URL : http://atlasgeneticsoncology.org/Genes/ENPP2ID40455ch8q24.html BRD4 (bromodomain containing 4) (19p13). Anna Collin. Atlas Genet Cytogenet Oncol Haematol 2007; 11 (3): 396-400. [Full Text] [PDF] URL : http://atlasgeneticsoncology.org/Genes/BRD4ID837ch19p13.html Atlas Genet Cytogenet Oncol Haematol 2007;3 -III BCL6 (B-Cell Lymphoma 6) (3q27) - updated. Stevan Knezevich. Atlas Genet Cytogenet Oncol Haematol 2007; 11 (3): 401-407. [Full Text] [PDF] URL : http://atlasgeneticsoncology.org/Genes/BCL6ID20.html BARD1 (BRCA1 associated RING domain 1) (2q35). Irmgard Irminger-Finger. Atlas Genet Cytogenet Oncol Haematol 2007; 11 (3): 408-418. [Full Text] [PDF] URL : http://atlasgeneticsoncology.org/Genes/BARD1ID756ch2q35.html RAF1 (v-raf-1 murine leukemia viral oncogene homolog 1) (3p25). Max Cayo, David Yu Greentblatt, Muthusamy Kunnimalaiyaan, Herbert Chen. Atlas Genet Cytogenet Oncol Haematol 2007; 11 (3): 419-434. [Full Text] [PDF] URL : http://atlasgeneticsoncology.org/Genes/RAF1ID42032ch3p25.html PSIP1 (PC4 and SFRS1 interacting protein 1) (9p22.3). Cristina Morerio, Claudio Panarello. Atlas Genet Cytogenet Oncol Haematol 2007; 11 (3): 435-439. [Full Text] [PDF] URL : http://atlasgeneticsoncology.org/Genes/PSIP1ID405ch9q22.html MIRN21 (microRNA 21) (17q23.1). Sadan Duygu Selcuklu, Mustafa Cengiz Yakicier, Ayse Elif Erson. Atlas Genet Cytogenet Oncol Haematol 2007; 11 (3): 440-447. [Full Text] [PDF] URL : http://atlasgeneticsoncology.org/Genes/MIRN21ID44019ch17q23.html KLF6 (Krüppel like factor 6) (10p15.1). Scott L. Friedman, Goutham Narla, John A. Martignetti. Atlas Genet Cytogenet Oncol Haematol 2007; 11 (3): 448-455. [Full Text] [PDF] URL : http://atlasgeneticsoncology.org/Genes/KLF6ID44002ch10p15.html IL6 (interleukin 6 (interferon beta 2)) (7p15.3). Stefan Nagel, Roderick A F MacLeod. Atlas Genet Cytogenet Oncol Haematol 2007; 11 (3): 456-464. [Full Text] [PDF] Atlas Genet Cytogenet Oncol Haematol 2007;3 -IV URL : http://atlasgeneticsoncology.org/Genes/IL6ID519ch7p15.html ALOX12 (Arachidonate 12-Lipoxygenase) Homo sapiens (17p13.1). Sreeparna Banerjee, Asli Erdog. Atlas Genet Cytogenet Oncol Haematol 2007; 11 (3): 465-473. [Full Text] [PDF] URL : http://atlasgeneticsoncology.org/Genes/ALOX12ID620ch17p13.html Leukaemias t(5;12)(q31;p13) in MDS, AML and AEL. Maria D. Odero. Atlas Genet Cytogenet Oncol Haematol 2007; 11 (3): 474-476. [Full Text] [PDF] URL : http://atlasgeneticsoncology.org/Anomalies/t0512q31p13ID1344.html i(8)(q10) in acute myeloid leukaemia. David Betts. Atlas Genet Cytogenet Oncol Haematol 2007; 11 (3): 477-478. [Full Text] [PDF] URL : http://atlasgeneticsoncology.org/Anomalies/i8q10ID1334.html Solid Tumours Vulva and Vagina tumors: an overview. Roberta Vanni, Giuseppina Parodo. Atlas Genet Cytogenet Oncol Haematol 2007;11 (3): 479-484. [Full Text] [PDF] URL : http://atlasgeneticsoncology.org/Tumors/VulVaginaCarcID5274.html Carcinoma with t(15;19) translocation. Anna Collin. Atlas Genet Cytogenet Oncol Haematol 2007; 11 (3): 485-488. [Full Text] [PDF] URL : http://atlasgeneticsoncology.org/Tumors/Carcinot1519q14p13ID5474.html Cancer Prone Diseases Diamond-Blackfan anemia (DBA) - updated. Hanna T. Gazda. Atlas Genet Cytogenet Oncol Haematol 2007; 11 (3): 489-492. [Full Text] [PDF] Atlas Genet Cytogenet Oncol Haematol 2007;3 -V URL : http://atlasgeneticsoncology.org/Kprones/DiamondBlackfanID10040.html Deep Insights Case Reports t(16;21)(q24;q22) in therapy-related acute myelogenous leukemia arising from myelodysplastic syndrome . Paola Dal Cin, Karim Ouahchi. Atlas Genet Cytogenet Oncol Haematol 2007; 11 (3): 493-495. [Full Text] [PDF] URL : http://atlasgeneticsoncology.org/Reports/1621DalCinID100022.html A de novo AML with a t(1;21)(p36;q22) in an elderly patient. Paola Dal Cin, Andrew J Yee, Bimalangshu Dey. Atlas Genet Cytogenet Oncol Haematol 2007; 11 (3): 496-498. [Full Text] [PDF] URL : http://atlasgeneticsoncology.org/Reports/0121DalCinID100021.html Educational Items © Atlas of Genetics and Cytogenetics in Oncology and Haematology X Y 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 NA Home Genes Leukemias Solid Tumours Cancer-Prone Deep Insight Portal Teaching For comments and suggestions or contributions, please contact us [email protected]. Atlas Genet Cytogenet Oncol Haematol 2007;3 -VI Atlas of Genetics and Cytogenetics in Oncology and Haematology MSH6 (mutS homolog 6 (E. Coli)) Identity Other names GTBP HSAP HNPCC5 Hugo MSH6 Location 2p16 Genes flanking MSH6 in centromere to telomere direction on 2p16 are: HTLF (2p22-p16) (human T-cell leukemia virus enhancer factor) FBXO11 (2p16.3) (F-box protein 11) Local_order MSH6 (2p16) (mutS homolog 6 (E. coli)) LOC285053 (2p16.3) (similar to ribosomal protein L18a). KCNK12 (2p22-p21) (potassium channel, subfamily K, member 12). MSH2 (2p22-p21) (mutS homolog 2, colon cancer, nonpolyposis type 1 (E. coli)). DNA/RNA Note The genes for MSH2 and MSH6 which form the major mismatch recognition MutSalpha complex functional in the mismatch repair (MMR) pathway are located within 1 Mb of each other. MSH2 and MSH6 may have been produced by duplication of a primordial mutS repair gene. Exons are represented by gray boxes (in scale) with exon numbers on the bottom. The arrows show the ATG and the stop codons respectively. Description MSH6 gene maps to NC_000002.10 and spans a region of 23.8 kilo bases. MSH6 has 10 exons, the sizes being 347, 197, 170, 2545, 266, 119, 89, 155, 200 and 176 bps. Transcription
Recommended publications
  • University of California, San Diego
    UNIVERSITY OF CALIFORNIA, SAN DIEGO The post-terminal differentiation fate of RNAs revealed by next-generation sequencing A dissertation submitted in partial satisfaction of the requirements for the degree Doctor of Philosophy in Biomedical Sciences by Gloria Kuo Lefkowitz Committee in Charge: Professor Benjamin D. Yu, Chair Professor Richard Gallo Professor Bruce A. Hamilton Professor Miles F. Wilkinson Professor Eugene Yeo 2012 Copyright Gloria Kuo Lefkowitz, 2012 All rights reserved. The Dissertation of Gloria Kuo Lefkowitz is approved, and it is acceptable in quality and form for publication on microfilm and electronically: __________________________________________________________________ __________________________________________________________________ __________________________________________________________________ __________________________________________________________________ __________________________________________________________________ Chair University of California, San Diego 2012 iii DEDICATION Ma and Ba, for your early indulgence and support. Matt and James, for choosing more practical callings. Roy, my love, for patiently sharing the ups and downs of this journey. iv EPIGRAPH It is foolish to tear one's hair in grief, as though sorrow would be made less by baldness. ~Cicero v TABLE OF CONTENTS Signature Page .............................................................................................................. iii Dedication ....................................................................................................................
    [Show full text]
  • A Disease Spectrum for ITPA Variation: Advances in Biochemical and Clinical Research Nicholas E
    Burgis Journal of Biomedical Science (2016) 23:73 DOI 10.1186/s12929-016-0291-y REVIEW Open Access A disease spectrum for ITPA variation: advances in biochemical and clinical research Nicholas E. Burgis Abstract Human ITPase (encoded by the ITPA gene) is a protective enzyme which acts to exclude noncanonical (deoxy) nucleoside triphosphates ((d)NTPs) such as (deoxy)inosine 5′-triphosphate ((d)ITP), from (d)NTP pools. Until the last few years, the importance of ITPase in human health and disease has been enigmatic. In 2009, an article was published demonstrating that ITPase deficiency in mice is lethal. All homozygous null offspring died before weaning as a result of cardiomyopathy due to a defect in the maintenance of quality ATP pools. More recently, a whole exome sequencing project revealed that very rare, severe human ITPA mutation results in early infantile encephalopathy and death. It has been estimated that nearly one third of the human population has an ITPA status which is associated with decreased ITPase activity. ITPA status has been linked to altered outcomes for patients undergoing thiopurine or ribavirin therapy. Thiopurine therapy can be toxic for patients with ITPA polymorphism, however, ITPA polymorphism is associated with improved outcomes for patients undergoing ribavirin treatment. ITPA polymorphism has also been linked to early-onset tuberculosis susceptibility. These data suggest a spectrum of ITPA-related disease exists in human populations. Potentially, ITPA status may affect a large number of patient outcomes, suggesting that modulation of ITPase activity is an important emerging avenue for reducing the number of negative outcomes for ITPA-related disease.
    [Show full text]
  • Bayesian Hierarchical Modeling of High-Throughput Genomic Data with Applications to Cancer Bioinformatics and Stem Cell Differentiation
    BAYESIAN HIERARCHICAL MODELING OF HIGH-THROUGHPUT GENOMIC DATA WITH APPLICATIONS TO CANCER BIOINFORMATICS AND STEM CELL DIFFERENTIATION by Keegan D. Korthauer A dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy (Statistics) at the UNIVERSITY OF WISCONSIN–MADISON 2015 Date of final oral examination: 05/04/15 The dissertation is approved by the following members of the Final Oral Committee: Christina Kendziorski, Professor, Biostatistics and Medical Informatics Michael A. Newton, Professor, Statistics Sunduz Kele¸s,Professor, Biostatistics and Medical Informatics Sijian Wang, Associate Professor, Biostatistics and Medical Informatics Michael N. Gould, Professor, Oncology © Copyright by Keegan D. Korthauer 2015 All Rights Reserved i in memory of my grandparents Ma and Pa FL Grandma and John ii ACKNOWLEDGMENTS First and foremost, I am deeply grateful to my thesis advisor Christina Kendziorski for her invaluable advice, enthusiastic support, and unending patience throughout my time at UW-Madison. She has provided sound wisdom on everything from methodological principles to the intricacies of academic research. I especially appreciate that she has always encouraged me to eke out my own path and I attribute a great deal of credit to her for the successes I have achieved thus far. I also owe special thanks to my committee member Professor Michael Newton, who guided me through one of my first collaborative research experiences and has continued to provide key advice on my thesis research. I am also indebted to the other members of my thesis committee, Professor Sunduz Kele¸s,Professor Sijian Wang, and Professor Michael Gould, whose valuable comments, questions, and suggestions have greatly improved this dissertation.
    [Show full text]
  • Analysis of Gene Expression Data for Gene Ontology
    ANALYSIS OF GENE EXPRESSION DATA FOR GENE ONTOLOGY BASED PROTEIN FUNCTION PREDICTION A Thesis Presented to The Graduate Faculty of The University of Akron In Partial Fulfillment of the Requirements for the Degree Master of Science Robert Daniel Macholan May 2011 ANALYSIS OF GENE EXPRESSION DATA FOR GENE ONTOLOGY BASED PROTEIN FUNCTION PREDICTION Robert Daniel Macholan Thesis Approved: Accepted: _______________________________ _______________________________ Advisor Department Chair Dr. Zhong-Hui Duan Dr. Chien-Chung Chan _______________________________ _______________________________ Committee Member Dean of the College Dr. Chien-Chung Chan Dr. Chand K. Midha _______________________________ _______________________________ Committee Member Dean of the Graduate School Dr. Yingcai Xiao Dr. George R. Newkome _______________________________ Date ii ABSTRACT A tremendous increase in genomic data has encouraged biologists to turn to bioinformatics in order to assist in its interpretation and processing. One of the present challenges that need to be overcome in order to understand this data more completely is the development of a reliable method to accurately predict the function of a protein from its genomic information. This study focuses on developing an effective algorithm for protein function prediction. The algorithm is based on proteins that have similar expression patterns. The similarity of the expression data is determined using a novel measure, the slope matrix. The slope matrix introduces a normalized method for the comparison of expression levels throughout a proteome. The algorithm is tested using real microarray gene expression data. Their functions are characterized using gene ontology annotations. The results of the case study indicate the protein function prediction algorithm developed is comparable to the prediction algorithms that are based on the annotations of homologous proteins.
    [Show full text]
  • Molecular and Physiological Basis for Hair Loss in Near Naked Hairless and Oak Ridge Rhino-Like Mouse Models: Tracking the Role of the Hairless Gene
    University of Tennessee, Knoxville TRACE: Tennessee Research and Creative Exchange Doctoral Dissertations Graduate School 5-2006 Molecular and Physiological Basis for Hair Loss in Near Naked Hairless and Oak Ridge Rhino-like Mouse Models: Tracking the Role of the Hairless Gene Yutao Liu University of Tennessee - Knoxville Follow this and additional works at: https://trace.tennessee.edu/utk_graddiss Part of the Life Sciences Commons Recommended Citation Liu, Yutao, "Molecular and Physiological Basis for Hair Loss in Near Naked Hairless and Oak Ridge Rhino- like Mouse Models: Tracking the Role of the Hairless Gene. " PhD diss., University of Tennessee, 2006. https://trace.tennessee.edu/utk_graddiss/1824 This Dissertation is brought to you for free and open access by the Graduate School at TRACE: Tennessee Research and Creative Exchange. It has been accepted for inclusion in Doctoral Dissertations by an authorized administrator of TRACE: Tennessee Research and Creative Exchange. For more information, please contact [email protected]. To the Graduate Council: I am submitting herewith a dissertation written by Yutao Liu entitled "Molecular and Physiological Basis for Hair Loss in Near Naked Hairless and Oak Ridge Rhino-like Mouse Models: Tracking the Role of the Hairless Gene." I have examined the final electronic copy of this dissertation for form and content and recommend that it be accepted in partial fulfillment of the requirements for the degree of Doctor of Philosophy, with a major in Life Sciences. Brynn H. Voy, Major Professor We have read this dissertation and recommend its acceptance: Naima Moustaid-Moussa, Yisong Wang, Rogert Hettich Accepted for the Council: Carolyn R.
    [Show full text]
  • DNA·RNA Triple Helix Formation Can Function As a Cis-Acting Regulatory
    DNA·RNA triple helix formation can function as a cis-acting regulatory mechanism at the human β-globin locus Zhuo Zhoua, Keith E. Gilesa,b,c, and Gary Felsenfelda,1 aLaboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892; bUniversity of Alabama at Birmingham Stem Cell Institute, University of Alabama at Birmingham, Birmingham, AL 35294; and cDepartment of Biochemistry and Molecular Genetics, University of Alabama at Birmingham, Birmingham, AL 35294 Contributed by Gary Felsenfeld, February 4, 2019 (sent for review January 4, 2019; reviewed by James Douglas Engel and Sergei M. Mirkin) We have identified regulatory mechanisms in which an RNA tran- of the criteria necessary to establish the presence of a triplex script forms a DNA duplex·RNA triple helix with a gene or one of its structure, we first describe and characterize triplex formation at regulatory elements, suggesting potential auto-regulatory mecha- the FAU gene in human erythroid K562 cells. FAU encodes a nisms in vivo. We describe an interaction at the human β-globin protein that is a fusion containing fubi, a ubiquitin-like protein, locus, in which an RNA segment embedded in the second intron of and ribosomal protein S30. Although fubi function is unknown, the β-globin gene forms a DNA·RNA triplex with the HS2 sequence posttranslational processing produces S30, a component of the within the β-globin locus control region, a major regulator of glo- 40S ribosome. We used this system to refine methods necessary bin expression. We show in human K562 cells that the triplex is to detect triplex formation and to distinguish it from R-loop stable in vivo.
    [Show full text]
  • Ldb1 Is Essential for Development of Nkx2.1 Lineage Derived Gabaergic and Cholinergic Neurons in the Telencephalon
    Developmental Biology 385 (2014) 94–106 Contents lists available at ScienceDirect Developmental Biology journal homepage: www.elsevier.com/locate/developmentalbiology Ldb1 is essential for development of Nkx2.1 lineage derived GABAergic and cholinergic neurons in the telencephalon Yangu Zhao a,n,1, Pierre Flandin b,2, Daniel Vogt b, Alexander Blood a, Edit Hermesz a,3, Heiner Westphal a, John L. R. Rubenstein b,nn a Program on Genomics of Differentiation, Eunice Kennedy Shriver National Institute of Child Health and Human Development, NIH, Bethesda, MD 20892, USA b Department of Psychiatry and the Nina Ireland Laboratory of Developmental Neurobiology, University of California San Francisco, San Francisco, CA 94143, USA article info abstract Article history: The progenitor zones of the embryonic mouse ventral telencephalon give rise to GABAergic and cholinergic Received 1 June 2013 neurons. We have shown previously that two LIM-homeodomain (LIM-HD) transcription factors, Lhx6 and Received in revised form Lhx8, that are downstream of Nkx2.1, are critical for the development of telencephalic GABAergic and 8 October 2013 cholinergic neurons. Here we investigate the role of Ldb1, a nuclear protein that binds directly to all LIM-HD Accepted 9 October 2013 factors, in the development of these ventral telencephalon derived neurons. We show that Ldb1 is expressed Available online 21 October 2013 in the Nkx2.1 cell lineage during embryonic development and in mature neurons. Conditional deletion of Ldb1 Keywords: causes defects in the expression of a series of genes in the ventral telencephalon and severe impairment in the Differentiation tangential migration of cortical interneurons from the ventral telencephalon.
    [Show full text]
  • Datasheet BA0931 Anti-HSPH1 Antibody
    Product datasheet Anti-HSPH1 Antibody Catalog Number: BA0931 BOSTER BIOLOGICAL TECHNOLOGY Special NO.1, International Enterprise Center, 2nd Guanshan Road, Wuhan, China Web: www.boster.com.cn Phone: +86 27 67845390 Fax: +86 27 67845390 Email: [email protected] Basic Information Product Name Anti-HSPH1 Antibody Gene Name HSPH1 Source Rabbit IgG Species Reactivity human,rat,mouse Tested Application WB,IHC-P,ICC/IF,FCM Contents 500ug/ml antibody with PBS ,0.02% NaN3 , 1mg BSA and 50% glycerol. Immunogen A synthetic peptide corresponding to a sequence at the C-terminus of human Hsp105(713-733aa EVMEWMNNVMNAQAKKSLDQD), different from the related mouse sequence by one amino acid, and different from the related rat sequence by two amino acids. Purification Immunogen affinity purified. Observed MW 110KD Dilution Ratios Western blot: 1:500-2000 Immunohistochemistry in paraffin section IHC-(P): 1:50-400 Immunocytochemistry/Immunofluorescence (ICC/IF): 1:50-400 Flow cytometry (FCM): 1-3μg/1x106 cells (Boiling the paraffin sections in 10mM citrate buffer,pH6.0,or PH8.0 EDTA repair liquid for 20 mins is required for the staining of formalin/paraffin sections.) Optimal working dilutions must be determined by end user. Storage 12 months from date of receipt,-20℃ as supplied.6 months 2 to 8℃ after reconstitution. Avoid repeated freezing and thawing Background Information HSP105(HEAT-SHOCK 105/110-KD PROTEIN 1), also called HSPH1 or HSP110, is a protein that in humans is encoded by the HSPH1 gene. Immunohistochemical analysis localizes HSP105 mainly in the cytoplasm. Database analysis indicates that both HSP105 isoforms are highly conserved during evolution.
    [Show full text]
  • Fnip1 Regulates Skeletal Muscle Fiber Type Specification, Fatigue Resistance, and Susceptibility to Muscular Dystrophy
    Fnip1 regulates skeletal muscle fiber type specification, fatigue resistance, and susceptibility to muscular dystrophy Nicholas L. Reyesa, Glen B. Banksb, Mark Tsanga, Daciana Margineantuc, Haiwei Gud, Danijel Djukovicd, Jacky Chana, Michelle Torresa, H. Denny Liggitta, Dinesh K. Hirenallur-Sa, David M. Hockenberyc, Daniel Rafteryd,e, and Brian M. Iritania,1 aThe Department of Comparative Medicine, University of Washington, Seattle, WA 98195-7190; bDepartment of Neurology, University of Washington, Seattle, WA 98195; cClinical Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109-1024; dDepartment of Anesthesiology and Pain Medicine, Mitochondria and Metabolism Center, Northwest Metabolomics Research Center, University of Washington, Seattle, WA 98109-8057; and ePublic Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109-1024 Edited* by Robert N. Eisenman, Fred Hutchinson Cancer Research Center, Seattle, WA, and approved December 8, 2014 (received for review July 14, 2014) Mammalian skeletal muscle is broadly characterized by the presence moderate strength and improved resistance to fatigue. Because of two distinct categories of muscle fibers called type I “red” slow slow twitch fibers use predominantly fatty acid oxidation for twitch and type II “white” fast twitch, which display marked differ- energy production, increasing the representation of type I fibers ences in contraction strength, metabolic strategies, and susceptibil- provides increased protection against obesity and related meta- ity to fatigue. The relative representation of each fiber type can bolic disorders including diabetes (2–5). Hence, identifying mol- have major influences on susceptibility to obesity, diabetes, and ecules that regulate fiber type conversion can profoundly impact muscular dystrophies. However, the molecular factors controlling susceptibility to metabolic diseases and can influence the patho- fiber type specification remain incompletely defined.
    [Show full text]
  • (Ubl-Ptms): Small Peptides with Huge Impact in Liver Fibrosis
    cells Review Ubiquitin-Like Post-Translational Modifications (Ubl-PTMs): Small Peptides with Huge Impact in Liver Fibrosis 1 1, 1, Sofia Lachiondo-Ortega , Maria Mercado-Gómez y, Marina Serrano-Maciá y , Fernando Lopitz-Otsoa 2, Tanya B Salas-Villalobos 3, Marta Varela-Rey 1, Teresa C. Delgado 1,* and María Luz Martínez-Chantar 1 1 Liver Disease Lab, CIC bioGUNE, Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), 48160 Derio, Spain; [email protected] (S.L.-O.); [email protected] (M.M.-G.); [email protected] (M.S.-M.); [email protected] (M.V.-R.); [email protected] (M.L.M.-C.) 2 Liver Metabolism Lab, CIC bioGUNE, 48160 Derio, Spain; fl[email protected] 3 Department of Biochemistry and Molecular Medicine, School of Medicine, Autonomous University of Nuevo León, Monterrey, Nuevo León 66450, Mexico; [email protected] * Correspondence: [email protected]; Tel.: +34-944-061318; Fax: +34-944-061301 These authors contributed equally to this work. y Received: 6 November 2019; Accepted: 1 December 2019; Published: 4 December 2019 Abstract: Liver fibrosis is characterized by the excessive deposition of extracellular matrix proteins including collagen that occurs in most types of chronic liver disease. Even though our knowledge of the cellular and molecular mechanisms of liver fibrosis has deeply improved in the last years, therapeutic approaches for liver fibrosis remain limited. Profiling and characterization of the post-translational modifications (PTMs) of proteins, and more specifically NEDDylation and SUMOylation ubiquitin-like (Ubls) modifications, can provide a better understanding of the liver fibrosis pathology as well as novel and more effective therapeutic approaches.
    [Show full text]
  • DRE-1/FBXO11, a Conserved F Box Protein, Regulates Apoptosis in C
    Rockefeller University Digital Commons @ RU Student Theses and Dissertations 2011 DRE-1/FBXO11, A Conserved F Box Protein, Regulates Apoptosis in C. elegans and is Mutated in Human Lymphoma Michael Chiorazzi Follow this and additional works at: http://digitalcommons.rockefeller.edu/ student_theses_and_dissertations Part of the Life Sciences Commons Recommended Citation Chiorazzi, Michael, "DRE-1/FBXO11, A Conserved F Box Protein, Regulates Apoptosis in C. elegans and is Mutated in Human Lymphoma" (2011). Student Theses and Dissertations. Paper 139. This Thesis is brought to you for free and open access by Digital Commons @ RU. It has been accepted for inclusion in Student Theses and Dissertations by an authorized administrator of Digital Commons @ RU. For more information, please contact [email protected]. DRE-1/FBXO11, A CONSERVED F BOX PROTEIN, REGULATES APOPTOSIS IN C. ELEGANS AND IS MUTATED IN HUMAN LYMPHOMA A Thesis Presented to the Faculty of The Rockefeller University in Partial Fulfillment of the Requirements for the degree of Doctor of Philosophy by Michael Chiorazzi June 2011 © Copyright by Michael Chiorazzi 2011 DRE-1/FBXO11, a conserved F box protein, regulates apoptosis in C. elegans and is mutated in human lymphoma Michael Chiorazzi, Ph.D. The Rockefeller University 2011 In the course of metazoan embryonic and post-embryonic development, more cells are generated than exist in the mature organism, and these cells are deleted by the process of programmed cell death. In addition, cells can be pushed toward death when they accumulate genetic errors, are virally-infected or are otherwise deemed potentially-harmful to the overall organism. Caenorhabditis elegans has proved to be an excellent model system for elucidating the genetic underpinnings of cell death, and research has shown that the core machinery, made up of the egl-1, ced-9, ced-4 and ced-3 genes, is conserved across metazoans, and their homologues are crucial for such diseases as cancer, neurodegeneration and autoimmunity.
    [Show full text]
  • Biochemical Mechanisms of Thyroid Hormone Deiodination
    THYROID Volume 15, Number 8, 2005 © Mary Ann Liebert, Inc. Biochemical Mechanisms of Thyroid Hormone Deiodination George G.J.M. Kuiper, Monique H.A. Kester, Robin P. Peeters, and Theo J. Visser Deiodination is the foremost pathway of thyroid hormone metabolism not only in quantitative terms but also because thyroxine (T4) is activated by outer ring deiodination (ORD) to 3,3’,5-triiodothyronine (T3), whereas both T4 and T3 are inactivated by inner ring deiodination (IRD) to 3,3’,5-triiodothyronine and 3,3’- diiodothyronine, respectively. These reactions are catalyzed by three iodothyronine deiodinases, D1-3. Although they are homologous selenoproteins, they differ in important respects such as catalysis of ORD and/or IRD, deiodination of sulfated iodothyronines, inhibition by the thyrostatic drug propylthiouracil, and regulation during fetal and neonatal development, by thyroid state, and during illness. In this review we will briefly discuss recent developments in these different areas. These have resulted in the emerging view that the biological activity of thyroid hormone is regulated locally by tissue-specific regulation of the different deiodinases. HYROID HORMONE is essential for growth, development, thyrostatic drug 6-propyl-2-thiouracil (PTU). D1 activity is Tand regulation of energy metabolism (1–3). Amphibian positively regulated by T3, reflecting regulation of D1 ex- metamorphosis is an important example of thyroid hormone pression by T3 at the pretranslational level. actions on development (4). Equally well known is the crit- In humans, D2 activity is found in brain, anterior pitu- ical role of thyroid hormone in development and function itary, placenta, thyroid and skeletal muscle, and D2 mRNA of the human central nervous system (5,6).
    [Show full text]