ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    facet.materialart.
    Unknown
    Characterization of a novel coronavirus associated with severe acute respiratory syndrome (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-05-06
    Description: In March 2003, a novel coronavirus (SARS-CoV) was discovered in association with cases of severe acute respiratory syndrome (SARS). The sequence of the complete genome of SARS-CoV was determined, and the initial characterization of the viral genome is presented in this report. The genome of SARS-CoV is 29,727 nucleotides in length and has 11 open reading frames, and its genome organization is similar to that of other coronaviruses. Phylogenetic analyses and sequence comparisons showed that SARS-CoV is not closely related to any of the previously characterized coronaviruses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rota, Paul A -- Oberste, M Steven -- Monroe, Stephan S -- Nix, W Allan -- Campagnoli, Ray -- Icenogle, Joseph P -- Penaranda, Silvia -- Bankamp, Bettina -- Maher, Kaija -- Chen, Min-Hsin -- Tong, Suxiong -- Tamin, Azaibi -- Lowe, Luis -- Frace, Michael -- DeRisi, Joseph L -- Chen, Qi -- Wang, David -- Erdman, Dean D -- Peret, Teresa C T -- Burns, Cara -- Ksiazek, Thomas G -- Rollin, Pierre E -- Sanchez, Anthony -- Liffick, Stephanie -- Holloway, Brian -- Limor, Josef -- McCaustland, Karen -- Olsen-Rasmussen, Melissa -- Fouchier, Ron -- Gunther, Stephan -- Osterhaus, Albert D M E -- Drosten, Christian -- Pallansch, Mark A -- Anderson, Larry J -- Bellini, William J -- New York, N.Y. -- Science. 2003 May 30;300(5624):1394-9. Epub 2003 May 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, GA 30333, USA. prota@cdc.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12730500" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Conserved Sequence ; Coronavirus/classification/genetics ; DNA, Complementary ; Endopeptidases/chemistry/genetics ; *Genome, Viral ; Humans ; Membrane Glycoproteins/chemistry/genetics ; Molecular Sequence Data ; Nucleocapsid Proteins/chemistry/genetics ; Open Reading Frames ; Phylogeny ; Polyproteins/chemistry/genetics ; RNA Replicase/chemistry/genetics ; RNA, Messenger/genetics/metabolism ; RNA, Viral/*genetics ; Regulatory Sequences, Nucleic Acid ; SARS Virus/chemistry/classification/*genetics/isolation & purification ; Sequence Analysis, DNA ; Severe Acute Respiratory Syndrome/virology ; Spike Glycoprotein, Coronavirus ; Transcription, Genetic ; Viral Envelope Proteins/chemistry/genetics ; Viral Matrix Proteins/chemistry/genetics ; Viral Proteins/chemistry/*genetics
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 2
    facet.materialart.
    Unknown
    Activating mutations of NOTCH1 in human T cell acute lymphoblastic leukemia (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-10-09
    Description: Very rare cases of human T cell acute lymphoblastic leukemia (T-ALL) harbor chromosomal translocations that involve NOTCH1, a gene encoding a transmembrane receptor that regulates normal T cell development. Here, we report that more than 50% of human T-ALLs, including tumors from all major molecular oncogenic subtypes, have activating mutations that involve the extracellular heterodimerization domain and/or the C-terminal PEST domain of NOTCH1. These findings greatly expand the role of activated NOTCH1 in the molecular pathogenesis of human T-ALL and provide a strong rationale for targeted therapies that interfere with NOTCH signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weng, Andrew P -- Ferrando, Adolfo A -- Lee, Woojoong -- Morris, John P 4th -- Silverman, Lewis B -- Sanchez-Irizarry, Cheryll -- Blacklow, Stephen C -- Look, A Thomas -- Aster, Jon C -- CA109901/CA/NCI NIH HHS/ -- CA21765/CA/NCI NIH HHS/ -- CA68484/CA/NCI NIH HHS/ -- CA82308/CA/NCI NIH HHS/ -- CA94233/CA/NCI NIH HHS/ -- CA98093/CA/NCI NIH HHS/ -- P01 CA109901/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2004 Oct 8;306(5694):269-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15472075" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Alleles ; Amino Acid Sequence ; Amyloid Precursor Protein Secretases ; Aspartic Acid Endopeptidases ; Cell Cycle ; Cell Line, Tumor ; Child ; Dimerization ; Endopeptidases/metabolism ; Frameshift Mutation ; Humans ; Leukemia-Lymphoma, Adult T-Cell/*genetics/metabolism ; Molecular Sequence Data ; *Mutation ; Mutation, Missense ; Point Mutation ; Protease Inhibitors/pharmacology ; Protein Structure, Tertiary ; Receptor, Notch1 ; Receptors, Cell Surface/chemistry/*genetics/metabolism ; Sequence Deletion ; Signal Transduction ; Transcription Factors/chemistry/*genetics/metabolism
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 3
    facet.materialart.
    Unknown
    Cassette of eight exons shared by genes for LDL receptor and EGF precursor (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-05-17
    Description: The amino acid sequences of the human low-density lipoprotein (LDL) receptor and the human precursor for epidermal growth factor (EGF) show 33 percent identity over a stretch of 400 residues. This region of homologous is encoded by eight contiguous exons in each respective gene. Of the nine introns that separate these exons, five are located in identical positions in the two protein sequences. This finding suggests that the homologous region may have resulted from a duplication of an ancestral gene and that the two genes evolved further by recruitment of exons from other genes, which provided the specific functional domains of the LDL receptor and the EGF precursor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sudhof, T C -- Russell, D W -- Goldstein, J L -- Brown, M S -- Sanchez-Pescador, R -- Bell, G I -- HL 01287/HL/NHLBI NIH HHS/ -- HL 20948/HL/NHLBI NIH HHS/ -- HL 31346/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1985 May 17;228(4701):893-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3873704" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; *Base Sequence ; Biological Evolution ; Cloning, Molecular ; Epidermal Growth Factor/*genetics ; Genes ; Humans ; Protein Precursors/genetics ; Receptors, LDL/*genetics ; Repetitive Sequences, Nucleic Acid
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 4
    facet.materialart.
    Unknown
    Nucleotide sequence and expression of an AIDS-associated retrovirus (ARV-2) (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-02-01
    Description: The nucleotide sequence of molecular clones of DNA from a retrovirus, ARV-2, associated with the acquired immune deficiency syndrome (AIDS) was determined. Proviral DNA of ARV-2 (9737 base pairs) has long terminal repeat structures (636 base pairs) and long open reading frames encoding gag (506 codons), pol (1003 codons), and env (863 codons) genes. Two additional open reading frames were identified. Significant amino acid homology with several other retroviruses was noted in the predicted product of gag and pol, but ARV-2 was as closely related to murine and avian retroviruses as it was to human T-cell leukemia viruses (HTLV-I and HTLV-II). By means of an SV-40 vector in transfected simian cells, the cloned gag and env genes of ARV-2 were shown to express viral proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sanchez-Pescador, R -- Power, M D -- Barr, P J -- Steimer, K S -- Stempien, M M -- Brown-Shimer, S L -- Gee, W W -- Renard, A -- Randolph, A -- Levy, J A -- New York, N.Y. -- Science. 1985 Feb 1;227(4686):484-92.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2578227" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*microbiology ; Amino Acid Sequence ; Base Sequence ; Cloning, Molecular ; Codon ; DNA, Viral/*genetics ; Deltaretrovirus/genetics ; Gene Products, gag ; Genes, Viral ; Humans ; Nucleic Acid Conformation ; RNA-Directed DNA Polymerase/biosynthesis/genetics ; Repetitive Sequences, Nucleic Acid ; Retroviridae/*genetics ; Viral Envelope Proteins/biosynthesis/genetics ; Viral Proteins/biosynthesis/*genetics
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...