ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

feed icon rss

Your email was sent successfully. Check your inbox.

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

Proceed reservation?

Export
Filter
  • Mice  (2)
  • Molecular Sequence Data  (2)
  • Transfection  (2)
  • Adoptive Transfer  (1)
  • American Association for the Advancement of Science (AAAS)  (5)
Collection
Publisher
Years
  • 1
    Publication Date: 2003-04-12
    Description: The CD8+ cytotoxic T cell response to pathogens is thought to be CD4+ helper T cell independent because infectious agents provide their own inflammatory signals. Mice that lack CD4+ T cells mount a primary CD8 response to Listeria monocytogenes equal to that of wild-type mice and rapidly clear the infection. However, protective memory to a challenge is gradually lost in the former animals. Memory CD8+ T cells from normal mice can respond rapidly, but memory CD8+ T cells that are generated without CD4 help are defective in their ability to respond to secondary encounters with antigen. The results highlight a previously undescribed role for CD4 help in promoting protective CD8 memory development.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2778341/" 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/PMC2778341/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sun, Joseph C -- Bevan, Michael J -- AI 19335/AI/NIAID NIH HHS/ -- R01 AI019335/AI/NIAID NIH HHS/ -- R01 AI019335-19/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2003 Apr 11;300(5617):339-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology and the Howard Hughes Medical Institute, University of Washington, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12690202" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Animals ; CD8-Positive T-Lymphocytes/*immunology/transplantation ; Cytotoxicity, Immunologic ; Genes, MHC Class II ; Immunization ; *Immunologic Memory ; Interferon-gamma/biosynthesis ; Listeria monocytogenes/genetics/immunology ; Listeriosis/*immunology ; Mice ; Mice, Inbred C57BL ; Ovalbumin/biosynthesis/genetics/immunology ; T-Lymphocyte Subsets/immunology ; T-Lymphocytes, Helper-Inducer/*immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 2
    Publication Date: 2001-08-25
    Description: In mammals, the canonical nuclear factor kappaB (NF-kappaB) signaling pathway activated in response to infections is based on degradation of IkappaB inhibitors. This pathway depends on the IkappaB kinase (IKK), which contains two catalytic subunits, IKKalpha and IKKbeta. IKKbeta is essential for inducible IkappaB phosphorylation and degradation, whereas IKKalpha is not. Here we show that IKKalpha is required for B cell maturation, formation of secondary lymphoid organs, increased expression of certain NF-kappaB target genes, and processing of the NF-kappaB2 (p100) precursor. IKKalpha preferentially phosphorylates NF-kappaB2, and this activity requires its phosphorylation by upstream kinases, one of which may be NF-kappaB-inducing kinase (NIK). IKKalpha is therefore a pivotal component of a second NF-kappaB activation pathway based on regulated NF-kappaB2 processing rather than IkappaB degradation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Senftleben, U -- Cao, Y -- Xiao, G -- Greten, F R -- Krahn, G -- Bonizzi, G -- Chen, Y -- Hu, Y -- Fong, A -- Sun, S C -- Karin, M -- AI434477/AI/NIAID NIH HHS/ -- AI45045/AI/NIAID NIH HHS/ -- ESO4151/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 2001 Aug 24;293(5534):1495-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Gene Regulation and Signal Transduction, Department of Pharmacology, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11520989" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/immunology/*physiology ; Bone Marrow Cells/metabolism ; Evolution, Molecular ; Female ; Gene Expression Regulation ; Germinal Center ; I-kappa B Kinase ; I-kappa B Proteins/metabolism ; Immunoglobulin D/analysis ; Lipopolysaccharides/pharmacology ; Lymph Nodes/cytology/immunology ; Lymphoid Tissue/*physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; NF-kappa B/*metabolism ; NF-kappa B p52 Subunit ; Phosphorylation ; Protein Processing, Post-Translational ; Protein-Serine-Threonine Kinases/*metabolism ; Radiation Chimera ; Recombinant Proteins/metabolism ; *Signal Transduction ; Spleen/cytology/immunology ; Transcription, Genetic ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 3
    Publication Date: 1990-12-21
    Description: Insects have an efficient defense system against infections. Their antibacterial immune proteins have been well characterized. However, the molecular mechanisms by which insects recognize foreignness are not yet known. Data are presented showing that hemolin (previously named P4), a bacteria-inducible hemolymph protein of the giant silk moth Hyalophora cecropia, belongs to the immunoglobulin superfamily. Functional analyses indicate that hemolin is one of the first hemolymph components to bind to the bacterial surface, taking part in a protein complex formation that is likely to initiate the immune response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sun, S C -- Lindstrom, I -- Boman, H G -- Faye, I -- Schmidt, O -- New York, N.Y. -- Science. 1990 Dec 21;250(4988):1729-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, University of Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2270488" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; DNA/genetics ; *Genes, Immunoglobulin ; Hemolymph/immunology ; Immunoglobulins ; Insect Proteins ; Molecular Sequence Data ; Moths/genetics/*immunology ; *Multigene Family ; Proteins/*genetics ; Sequence Homology, Nucleic Acid
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 4
    Publication Date: 1993-03-26
    Description: The eukaryotic transcription factor nuclear factor-kappa B (NF-kappa B) participates in many parts of the genetic program mediating T lymphocyte activation and growth. Nuclear expression of NF-kappa B occurs after its induced dissociation from its cytoplasmic inhibitor I kappa B alpha. Phorbol ester and tumor necrosis factor-alpha induction of nuclear NF-kappa B is associated with both the degradation of performed I kappa B alpha and the activation of I kappa B alpha gene expression. Transfection studies indicate that the I kappa B alpha gene is specifically induced by the 65-kilodalton transactivating subunit of NF-kappa B. Association of the newly synthesized I kappa B alpha with p65 restores intracellular inhibition of NF-kappa B DNA binding activity and prolongs the survival of this labile inhibitor. Together, these results show that NF-kappa B controls the expression of I kappa B alpha by means of an inducible autoregulatory pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sun, S C -- Ganchi, P A -- Ballard, D W -- Greene, W C -- 5T32CA09111/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Mar 26;259(5103):1912-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gladstone Institute of Virology and Immunology, University of California, San Francisco.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8096091" target="_blank"〉PubMed〈/a〉
    Keywords: CD4-Positive T-Lymphocytes/metabolism ; Cell Line ; Cell Nucleus/metabolism ; Cycloheximide/pharmacology ; Cytoplasm/metabolism ; DNA/metabolism ; DNA-Binding Proteins/*genetics ; *Gene Expression Regulation ; Humans ; *I-kappa B Proteins ; Immunoblotting ; Kinetics ; Molecular Weight ; Mutagenesis ; NF-kappa B/*antagonists & inhibitors/genetics/*physiology ; RNA, Messenger/biosynthesis ; Tetradecanoylphorbol Acetate/pharmacology ; Trans-Activators/pharmacology ; Transfection ; Tumor Necrosis Factor-alpha/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 5
    Publication Date: 2010-10-12
    Description: Culex quinquefasciatus (the southern house mosquito) is an important mosquito vector of viruses such as West Nile virus and St. Louis encephalitis virus, as well as of nematodes that cause lymphatic filariasis. C. quinquefasciatus is one species within the Culex pipiens species complex and can be found throughout tropical and temperate climates of the world. The ability of C. quinquefasciatus to take blood meals from birds, livestock, and humans contributes to its ability to vector pathogens between species. Here, we describe the genomic sequence of C. quinquefasciatus: Its repertoire of 18,883 protein-coding genes is 22% larger than that of Aedes aegypti and 52% larger than that of Anopheles gambiae with multiple gene-family expansions, including olfactory and gustatory receptors, salivary gland genes, and genes associated with xenobiotic detoxification.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3740384/" 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/PMC3740384/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arensburger, Peter -- Megy, Karine -- Waterhouse, Robert M -- Abrudan, Jenica -- Amedeo, Paolo -- Antelo, Beatriz -- Bartholomay, Lyric -- Bidwell, Shelby -- Caler, Elisabet -- Camara, Francisco -- Campbell, Corey L -- Campbell, Kathryn S -- Casola, Claudio -- Castro, Marta T -- Chandramouliswaran, Ishwar -- Chapman, Sinead B -- Christley, Scott -- Costas, Javier -- Eisenstadt, Eric -- Feschotte, Cedric -- Fraser-Liggett, Claire -- Guigo, Roderic -- Haas, Brian -- Hammond, Martin -- Hansson, Bill S -- Hemingway, Janet -- Hill, Sharon R -- Howarth, Clint -- Ignell, Rickard -- Kennedy, Ryan C -- Kodira, Chinnappa D -- Lobo, Neil F -- Mao, Chunhong -- Mayhew, George -- Michel, Kristin -- Mori, Akio -- Liu, Nannan -- Naveira, Horacio -- Nene, Vishvanath -- Nguyen, Nam -- Pearson, Matthew D -- Pritham, Ellen J -- Puiu, Daniela -- Qi, Yumin -- Ranson, Hilary -- Ribeiro, Jose M C -- Roberston, Hugh M -- Severson, David W -- Shumway, Martin -- Stanke, Mario -- Strausberg, Robert L -- Sun, Cheng -- Sutton, Granger -- Tu, Zhijian Jake -- Tubio, Jose Manuel C -- Unger, Maria F -- Vanlandingham, Dana L -- Vilella, Albert J -- White, Owen -- White, Jared R -- Wondji, Charles S -- Wortman, Jennifer -- Zdobnov, Evgeny M -- Birren, Bruce -- Christensen, Bruce M -- Collins, Frank H -- Cornel, Anthony -- Dimopoulos, George -- Hannick, Linda I -- Higgs, Stephen -- Lanzaro, Gregory C -- Lawson, Daniel -- Lee, Norman H -- Muskavitch, Marc A T -- Raikhel, Alexander S -- Atkinson, Peter W -- HHSN266200400001C/PHS HHS/ -- HHSN266200400039C/AI/NIAID NIH HHS/ -- HHSN266200400039C/PHS HHS/ -- N01-AI-30071/AI/NIAID NIH HHS/ -- N01AI30071/AI/NIAID NIH HHS/ -- ZIA AI000810-13/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2010 Oct 1;330(6000):86-8. doi: 10.1126/science.1191864.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Disease Vector Research, University of California Riverside, Riverside, CA 92521, USA. arensburger@gmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20929810" target="_blank"〉PubMed〈/a〉
    Keywords: Aedes/genetics ; Animals ; Anopheles gambiae/genetics ; Chromosome Mapping ; Chromosomes/*genetics ; Culex/classification/*genetics/physiology ; DNA Transposable Elements ; *Genes, Insect ; *Genome ; Insect Proteins/genetics/physiology ; Insect Vectors/genetics ; Molecular Sequence Data ; Multigene Family ; Phylogeny ; Receptors, Odorant/genetics ; Retroelements ; *Sequence Analysis, DNA
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...