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  • 1
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    BLM heterozygosity and the risk of colorectal cancer (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-09-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gruber, Stephen B -- Ellis, Nathan A -- Scott, Karen K -- Almog, Ronit -- Kolachana, Prema -- Bonner, Joseph D -- Kirchhoff, Tomas -- Tomsho, Lynn P -- Nafa, Khedoudja -- Pierce, Heather -- Low, Marcelo -- Satagopan, Jaya -- Rennert, Hedy -- Huang, Helen -- Greenson, Joel K -- Groden, Joanna -- Rapaport, Beth -- Shia, Jinru -- Johnson, Stephen -- Gregersen, Peter K -- Harris, Curtis C -- Boyd, Jeff -- Rennert, Gad -- Offit, Kenneth -- R01CA81488/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2002 Sep 20;297(5589):2013.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Internal Medicine and Epidemiology, University of Michigan, Ann Arbor, MI 48109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12242432" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphatases/*genetics ; Alleles ; Animals ; Bloom Syndrome/genetics ; Case-Control Studies ; Colorectal Neoplasms/*genetics ; DNA Helicases/*genetics ; Female ; Genes, APC ; *Genetic Predisposition to Disease ; *Heterozygote ; Humans ; Israel ; Jews/genetics ; Male ; Mice ; Mutation ; New York ; RecQ Helicases ; Risk Factors
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Human chromosome 7: DNA sequence and biology (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-04-12
    Description: DNA sequence and annotation of the entire human chromosome 7, encompassing nearly 158 million nucleotides of DNA and 1917 gene structures, are presented. To generate a higher order description, additional structural features such as imprinted genes, fragile sites, and segmental duplications were integrated at the level of the DNA sequence with medical genetic data, including 440 chromosome rearrangement breakpoints associated with disease. This approach enabled the discovery of candidate genes for developmental diseases including autism.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2882961/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2882961/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scherer, Stephen W -- Cheung, Joseph -- MacDonald, Jeffrey R -- Osborne, Lucy R -- Nakabayashi, Kazuhiko -- Herbrick, Jo-Anne -- Carson, Andrew R -- Parker-Katiraee, Layla -- Skaug, Jennifer -- Khaja, Razi -- Zhang, Junjun -- Hudek, Alexander K -- Li, Martin -- Haddad, May -- Duggan, Gavin E -- Fernandez, Bridget A -- Kanematsu, Emiko -- Gentles, Simone -- Christopoulos, Constantine C -- Choufani, Sanaa -- Kwasnicka, Dorota -- Zheng, Xiangqun H -- Lai, Zhongwu -- Nusskern, Deborah -- Zhang, Qing -- Gu, Zhiping -- Lu, Fu -- Zeesman, Susan -- Nowaczyk, Malgorzata J -- Teshima, Ikuko -- Chitayat, David -- Shuman, Cheryl -- Weksberg, Rosanna -- Zackai, Elaine H -- Grebe, Theresa A -- Cox, Sarah R -- Kirkpatrick, Susan J -- Rahman, Nazneen -- Friedman, Jan M -- Heng, Henry H Q -- Pelicci, Pier Giuseppe -- Lo-Coco, Francesco -- Belloni, Elena -- Shaffer, Lisa G -- Pober, Barbara -- Morton, Cynthia C -- Gusella, James F -- Bruns, Gail A P -- Korf, Bruce R -- Quade, Bradley J -- Ligon, Azra H -- Ferguson, Heather -- Higgins, Anne W -- Leach, Natalia T -- Herrick, Steven R -- Lemyre, Emmanuelle -- Farra, Chantal G -- Kim, Hyung-Goo -- Summers, Anne M -- Gripp, Karen W -- Roberts, Wendy -- Szatmari, Peter -- Winsor, Elizabeth J T -- Grzeschik, Karl-Heinz -- Teebi, Ahmed -- Minassian, Berge A -- Kere, Juha -- Armengol, Lluis -- Pujana, Miguel Angel -- Estivill, Xavier -- Wilson, Michael D -- Koop, Ben F -- Tosi, Sabrina -- Moore, Gudrun E -- Boright, Andrew P -- Zlotorynski, Eitan -- Kerem, Batsheva -- Kroisel, Peter M -- Petek, Erwin -- Oscier, David G -- Mould, Sarah J -- Dohner, Hartmut -- Dohner, Konstanze -- Rommens, Johanna M -- Vincent, John B -- Venter, J Craig -- Li, Peter W -- Mural, Richard J -- Adams, Mark D -- Tsui, Lap-Chee -- 38103/Canadian Institutes of Health Research/Canada -- P01 GM061354/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2003 May 2;300(5620):767-72. Epub 2003 Apr 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics and Genomic Biology, The Hospital for Sick Children, Toronto, Ontario, Canada, M5G 1X8. steve@genet.sickkids.on.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12690205" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autistic Disorder/genetics ; Chromosome Aberrations ; Chromosome Fragile Sites ; Chromosome Fragility ; Chromosome Mapping ; Chromosomes, Human, Pair 7/*genetics ; Computational Biology ; Congenital Abnormalities/genetics ; CpG Islands ; DNA, Complementary ; Databases, Genetic ; Euchromatin/genetics ; Expressed Sequence Tags ; Gene Duplication ; Genes, Overlapping ; Genetic Diseases, Inborn/genetics ; Genomic Imprinting ; Humans ; In Situ Hybridization, Fluorescence ; Limb Deformities, Congenital/genetics ; Mice ; Molecular Sequence Data ; Mutation ; Neoplasms/genetics ; Pseudogenes ; RNA/genetics ; Retroelements ; *Sequence Analysis, DNA ; Williams Syndrome/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Electronic Resource
    Electronic Resource
    A novel interstitial deletion of KAL1 in a Japanese family with Kallmann syndrome (2000)
    Springer
    Journal of human genetics 45 (2000), S. 237-240 
    Details
    ISSN: 1435-232X
    Keywords: Key words Kallmann syndrome ; KAL1 ; Mutation ; Anosmia ; Hypogonadism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract We identified a novel interstitial deletion that spanned from exons 5 to 10 of KAL1 in two Japanese brothers with X-linked Kallmann syndrome (KS; MIM no. 308700). Both brothers had hypogonadism, unilateral renal agenesis, and disturbance of the sense of smell, but they had no other neurological manifestations, including mental disturbance. Their mother was confirmed to be an asymptomatic carrier, by use of a comparative multiplex polymerase chain reaction (PCR) analysis. The present patients are further examples of patients with KS without mental disturbance caused by a mutation confined to KAL1.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s100380070033
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  • 4
    Electronic Resource
    Electronic Resource
    Fibrillin gene (FBN1) mutations in Japanese patients with Marfan syndrome (2000)
    Springer
    Journal of human genetics 45 (2000), S. 115-118 
    Details
    ISSN: 1435-232X
    Keywords: Key words Marfan syndrome ; FBN1 ; Fibrillin-1 ; Japanese ; Mutation ; Gene
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Marfan syndrome (MFS; MIM #154700) is a connective tissue disorder characterized by cardiovascular, skeletal, and ocular abnormalities. The fibrillin-1 gene (FBN1; MIM no. 134797) on chromosome 15 was revealed to be the cause of Marfan syndrome. To date over 137 types of FBN1 mutations have been reported. In this study, two novel mutations and a recurrent de-novo mutation were identified in patients with MFS by means of single-strand conformational polymorphism (SSCP) analysis. The two novel mutations are a 4-bp deletion at nucleotide 2820-2823 and a G-to-T transversion at nucleotide 1421 (C474F), located on exon 23 and exon 11, respectively. A previously reported mutation at the splicing donor site of intron 2 (IVS2 G + 1A), which is predicted to cause exon skipping, was identified in a sporadic patient with classical MFS.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s100380050027
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  • 5
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    Complete genome sequence of Neisseria meningitidis serogroup B strain MC58 (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-03-10
    Description: The 2,272,351-base pair genome of Neisseria meningitidis strain MC58 (serogroup B), a causative agent of meningitis and septicemia, contains 2158 predicted coding regions, 1158 (53.7%) of which were assigned a biological role. Three major islands of horizontal DNA transfer were identified; two of these contain genes encoding proteins involved in pathogenicity, and the third island contains coding sequences only for hypothetical proteins. Insights into the commensal and virulence behavior of N. meningitidis can be gleaned from the genome, in which sequences for structural proteins of the pilus are clustered and several coding regions unique to serogroup B capsular polysaccharide synthesis can be identified. Finally, N. meningitidis contains more genes that undergo phase variation than any pathogen studied to date, a mechanism that controls their expression and contributes to the evasion of the host immune system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tettelin, H -- Saunders, N J -- Heidelberg, J -- Jeffries, A C -- Nelson, K E -- Eisen, J A -- Ketchum, K A -- Hood, D W -- Peden, J F -- Dodson, R J -- Nelson, W C -- Gwinn, M L -- DeBoy, R -- Peterson, J D -- Hickey, E K -- Haft, D H -- Salzberg, S L -- White, O -- Fleischmann, R D -- Dougherty, B A -- Mason, T -- Ciecko, A -- Parksey, D S -- Blair, E -- Cittone, H -- Clark, E B -- Cotton, M D -- Utterback, T R -- Khouri, H -- Qin, H -- Vamathevan, J -- Gill, J -- Scarlato, V -- Masignani, V -- Pizza, M -- Grandi, G -- Sun, L -- Smith, H O -- Fraser, C M -- Moxon, E R -- Rappuoli, R -- Venter, J C -- New York, N.Y. -- Science. 2000 Mar 10;287(5459):1809-15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Institute for Genomic Research (TIGR), 9712 Medical Center Drive, Rockville, MD 20850, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10710307" target="_blank"〉PubMed〈/a〉
    Keywords: Antigenic Variation ; Antigens, Bacterial/immunology ; Bacteremia/microbiology ; Bacterial Capsules/genetics ; Bacterial Proteins/genetics/physiology ; DNA Transposable Elements ; Evolution, Molecular ; Fimbriae, Bacterial/genetics ; *Genome, Bacterial ; Humans ; Meningitis, Meningococcal/microbiology ; Meningococcal Infections/microbiology ; Molecular Sequence Data ; Mutation ; Neisseria meningitidis/classification/*genetics/*pathogenicity/physiology ; Open Reading Frames ; Operon ; Phylogeny ; Recombination, Genetic ; *Sequence Analysis, DNA ; Serotyping ; Transformation, Bacterial ; Virulence/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Regulation of spermatogenesis by testis-specific, cytoplasmic poly(A) polymerase TPAP (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-12-10
    Description: Spermatogenesis is a highly specialized process of cellular differentiation to produce spermatozoa. This differentiation process accompanies morphological changes that are controlled by a number of genes expressed in a stage-specific manner during spermatogenesis. Here we show that in mice, the absence of a testis-specific, cytoplasmic polyadenylate [poly(A)] polymerase, TPAP, results in the arrest of spermiogenesis. TPAP-deficient mice display impaired expression of haploid-specific genes that are required for the morphogenesis of germ cells. The TPAP deficiency also causes incomplete elongation of poly(A) tails of particular transcription factor messenger RNAs. Although the overall cellular level of the transcription factor TAF10 is unaffected, TAF10 is insufficiently transported into the nucleus of germ cells. We propose that TPAP governs germ cell morphogenesis by modulating specific transcription factors at posttranscriptional and posttranslational levels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kashiwabara, Shin-Ichi -- Noguchi, Junko -- Zhuang, Tiangang -- Ohmura, Ko -- Honda, Arata -- Sugiura, Shin -- Miyamoto, Kiyoko -- Takahashi, Satoru -- Inoue, Kimiko -- Ogura, Atsuo -- Baba, Tadashi -- New York, N.Y. -- Science. 2002 Dec 6;298(5600):1999-2002.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Applied Biochemistry, Institute of Basic Medical Sciences, University of Tsukuba, Tsukuba Science City, Ibaraki 305-8572, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12471261" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Cytoplasm/enzymology ; Female ; Gene Expression Regulation, Developmental ; Gene Targeting ; In Situ Nick-End Labeling ; Male ; Mice ; Mice, Inbred C57BL ; Mutation ; Nuclear Proteins/genetics/metabolism ; Organ Size ; Poly A/metabolism ; Polynucleotide Adenylyltransferase/genetics/*metabolism ; Protein Biosynthesis ; RNA, Messenger/*metabolism ; Spermatids/physiology ; Spermatocytes/physiology ; *Spermatogenesis ; Spermatozoa/*physiology ; Testis/*enzymology/metabolism ; Transcription Factors/genetics/metabolism ; Transcription, Genetic ; mRNA Cleavage and Polyadenylation Factors/genetics/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Recent origin of Plasmodium falciparum from a single progenitor (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-07-21
    Description: Genetic variability of Plasmodium falciparum underlies its transmission success and thwarts efforts to control disease caused by this parasite. Genetic variation in antigenic, drug resistance, and pathogenesis determinants is abundant, consistent with an ancient origin of P. falciparum, whereas DNA variation at silent (synonymous) sites in coding sequences appears virtually absent, consistent with a recent origin of the parasite. To resolve this paradox, we analyzed introns and demonstrated that these are deficient in single-nucleotide polymorphisms, as are synonymous sites in coding regions. These data establish the recent origin of P. falciparum and further provide an explanation for the abundant diversity observed in antigen and other selected genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Volkman, S K -- Barry, A E -- Lyons, E J -- Nielsen, K M -- Thomas, S M -- Choi, M -- Thakore, S S -- Day, K P -- Wirth, D F -- Hartl, D L -- New York, N.Y. -- Science. 2001 Jul 20;293(5529):482-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Harvard-Oxford Malaria Genome Diversity Project, Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11463913" target="_blank"〉PubMed〈/a〉
    Keywords: Africa ; Agriculture ; Alternative Splicing ; Animals ; Base Sequence ; *Biological Evolution ; Genes, Protozoan ; *Genetic Variation ; Humans ; *Introns ; Malaria, Falciparum/epidemiology/parasitology/transmission ; *Microsatellite Repeats ; Molecular Sequence Data ; Mutation ; Plasmodium/genetics ; Plasmodium falciparum/*genetics ; *Polymorphism, Single Nucleotide
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Role of histone H3 lysine 27 methylation in X inactivation (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-03-22
    Description: The Polycomb group (PcG) protein Eed is implicated in regulation of imprinted X-chromosome inactivation in extraembryonic cells but not of random X inactivation in embryonic cells. The Drosophila homolog of the Eed-Ezh2 PcG protein complex achieves gene silencing through methylation of histone H3 on lysine 27 (H3-K27), which suggests a role for H3-K27 methylation in imprinted X inactivation. Here we demonstrate that transient recruitment of the Eed-Ezh2 complex to the inactive X chromosome (Xi) occurs during initiation of X inactivation in both extraembryonic and embryonic cells and is accompanied by H3-K27 methylation. Recruitment of the complex and methylation on the Xi depend on Xist RNA but are independent of its silencing function. Together, our results suggest a role for Eed-Ezh2-mediated H3-K27 methylation during initiation of both imprinted and random X inactivation and demonstrate that H3-K27 methylation is not sufficient for silencing of the Xi.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Plath, Kathrin -- Fang, Jia -- Mlynarczyk-Evans, Susanna K -- Cao, Ru -- Worringer, Kathleen A -- Wang, Hengbin -- de la Cruz, Cecile C -- Otte, Arie P -- Panning, Barbara -- Zhang, Yi -- New York, N.Y. -- Science. 2003 Apr 4;300(5616):131-5. Epub 2003 Mar 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, University of California San Francisco, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12649488" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/metabolism/*physiology ; Cell Differentiation ; Cell Nucleus/metabolism ; Cells, Cultured ; *Dosage Compensation, Genetic ; Female ; Fluorescent Antibody Technique ; Genomic Imprinting ; HeLa Cells ; Histones/*metabolism ; Humans ; In Situ Hybridization, Fluorescence ; Lysine/metabolism ; Male ; Methylation ; Mice ; Mutation ; Polycomb Repressive Complex 2 ; RNA, Long Noncoding ; RNA, Untranslated/genetics/metabolism ; Repressor Proteins/metabolism ; Stem Cells/metabolism/*physiology ; Transgenes ; Trophoblasts/*physiology ; X Chromosome/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Cell corpse engulfment mediated by C. elegans phosphatidylserine receptor through CED-5 and CED-12 (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-04
    Description: During apoptosis, phosphatidylserine, which is normally restricted to the inner leaflet of the plasma membrane, is exposed on the surface of apoptotic cells and has been suggested to act as an "eat-me" signal to trigger phagocytosis. It is unclear how phagocytes recognize phosphatidylserine. Recently, a putative phosphatidylserine receptor (PSR) was identified and proposed to mediate recognition of phosphatidylserine and phagocytosis. We report that psr-1, the Caenorhabditis elegans homolog of PSR, is important for cell corpse engulfment. In vitro PSR-1 binds preferentially phosphatidylserine or cells with exposed phosphatidylserine. In C. elegans, PSR-1 acts in the same cell corpse engulfment pathway mediated by intracellular signaling molecules CED-2 (homologous to the human CrkII protein), CED-5 (DOCK180), CED-10 (Rac GTPase), and CED-12 (ELMO), possibly through direct interaction with CED-5 and CED-12. Our findings suggest that PSR-1 is likely an upstream receptor for the signaling pathway containing CED-2, CED-5, CED-10, and CED-12 proteins and plays an important role in recognizing phosphatidylserine during phagocytosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Xiaochen -- Wu, Yi-Chun -- Fadok, Valerie A -- Lee, Ming-Chia -- Gengyo-Ando, Keiko -- Cheng, Li-Chun -- Ledwich, Duncan -- Hsu, Pei-Ken -- Chen, Jia-Yun -- Chou, Bin-Kuan -- Henson, Peter -- Mitani, Shohei -- Xue, Ding -- New York, N.Y. -- Science. 2003 Nov 28;302(5650):1563-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular, Cellular, and Developmental Biology, University of Colorado, Boulder, CO 80309, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14645848" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Amino Acid Sequence ; Animals ; *Apoptosis ; Caenorhabditis elegans/cytology/embryology/metabolism/*physiology ; Caenorhabditis elegans Proteins/genetics/*metabolism ; Carrier Proteins/genetics/*metabolism ; *Cytoskeletal Proteins ; Embryo, Nonmammalian/cytology/metabolism ; Embryonic Development ; Humans ; Jumonji Domain-Containing Histone Demethylases ; Membrane Proteins/genetics/*metabolism ; Molecular Sequence Data ; Mutation ; *Phagocytosis ; Phosphatidylserines/metabolism ; Protein Binding ; Receptors, Cell Surface/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Recombinant Proteins/metabolism ; Signal Transduction ; rac GTP-Binding Proteins/genetics/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    Identification of signal peptide peptidase, a presenilin-type aspartic protease (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-06-22
    Description: Signal peptide peptidase (SPP) catalyzes intramembrane proteolysis of some signal peptides after they have been cleaved from a preprotein. In humans, SPP activity is required to generate signal sequence-derived human lymphocyte antigen-E epitopes that are recognized by the immune system, and to process hepatitis C virus core protein. We have identified human SPP as a polytopic membrane protein with sequence motifs characteristic of the presenilin-type aspartic proteases. SPP and potential eukaryotic homologs may represent another family of aspartic proteases that promote intramembrane proteolysis to release biologically important peptides.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weihofen, Andreas -- Binns, Kathleen -- Lemberg, Marius K -- Ashman, Keith -- Martoglio, Bruno -- New York, N.Y. -- Science. 2002 Jun 21;296(5576):2215-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Biochemistry, Swiss Federal Institute of Technology (ETH), ETH-Hoenggerberg, 8093 Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12077416" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Amino Acid Sequence ; Amyloid Precursor Protein Secretases ; Animals ; Aspartic Acid Endopeptidases/*chemistry/genetics/isolation & ; purification/*metabolism ; Azirines/chemical synthesis/pharmacology ; Binding Sites ; Biotin/analogs & derivatives/chemical synthesis/pharmacology ; Cloning, Molecular ; Conserved Sequence ; Endopeptidases/metabolism ; Endoplasmic Reticulum/enzymology ; Glycosylation ; Humans ; Membrane Proteins/*chemistry/genetics/isolation & purification/*metabolism ; Molecular Sequence Data ; Mutation ; Presenilin-1 ; Presenilin-2 ; Protease Inhibitors/chemical synthesis/pharmacology ; Recombinant Proteins/chemistry/metabolism ; Saccharomyces cerevisiae/genetics ; Sequence Alignment ; Sequence Homology, Amino Acid
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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