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  • Mice  (307)
  • United States  (87)
  • Rats, Inbred Strains
  • American Association for the Advancement of Science (AAAS)  (447)
  • 1985-1989  (266)
  • 1980-1984  (181)
Collection
Keywords
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  • American Association for the Advancement of Science (AAAS)  (447)
  • Springer  (5)
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Year
  • 1
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    The MHC-binding and gp120-binding functions of CD4 are separable (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-08-18
    Description: CD4 is a cell surface glycoprotein that is thought to interact with nonpolymorphic determinants of class II major histocompatibility (MHC) molecules. CD4 is also the receptor for the human immunodeficiency virus (HIV), binding with high affinity to the HIV-1 envelope glycoprotein, gp120. Homolog-scanning mutagenesis was used to identify CD4 regions that are important in class II MHC binding and to determine whether the gp120 and class II MHC binding sites of CD4 are related. Class II MHC binding was abolished by mutations in each of the first three immunoglobulin-like domains of CD4. The gp120 binding could be abolished without affecting class II MHC binding and vice versa, although at least one mutation examined reduced both functions significantly. These findings indicate that, while there may be overlap between the gp120 and class II MHC binding sites of CD4, these sites are distinct and can be separated. Thus it should be possible to design CD4 analogs that can block HIV infectivity but intrinsically lack the ability to affect the normal immune response by binding to class II MHC molecules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lamarre, D -- Ashkenazi, A -- Fleury, S -- Smith, D H -- Sekaly, R P -- Capon, D J -- New York, N.Y. -- Science. 1989 Aug 18;245(4919):743-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire d'Immunologie, Institut de Recherches Cliniques de Montreal, Quebec, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2549633" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, Surface ; Binding Sites ; DNA, Recombinant ; HIV/*metabolism ; HIV Envelope Protein gp120 ; HLA-DP Antigens/immunology ; Histocompatibility Antigens Class II/*immunology ; Humans ; Hybridomas ; Mice ; Molecular Sequence Data ; Mutation ; Receptors, HIV ; Receptors, Virus/genetics/immunology/*metabolism ; Retroviridae Proteins/immunology/*metabolism ; Rosette Formation ; Structure-Activity Relationship ; T-Lymphocytes/immunology/metabolism ; Transfection
    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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    Monoclonal antibodies reveal the structural basis of antibody diversity (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-11-18
    Description: Hybridoma technology has made it possible to introduce into continuous culture normal antibody-forming cells and to obtain large amounts of the immunoglobulin produced by each of these cells. Examination of the structure of a number of monoclonal antibodies that react with a single antigen has provided new information on the structural basis of the specificity and affinity of antibodies. Comparisons of families of monoclonal antibodies derived from a single germ line gene revealed the importance of somatic mutation in generating antibody diversity. Monoclonal antibodies that react with variable regions of other monoclonals allow the further dissection and modulation of the immune response. Finally, the continued somatic instability of immunoglobulin genes in cultured antibody-forming cells makes it possible to determine the rate of somatic mutation and to generate mutant monoclonal antibodies that may be more effective serological reagents.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Teillaud, J L -- Desaymard, C -- Giusti, A M -- Haseltine, B -- Pollock, R R -- Yelton, D E -- Zack, D J -- Scharff, M D -- 5T32GM7288/GM/NIGMS NIH HHS/ -- AI05231/AI/NIAID NIH HHS/ -- AI10702/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1983 Nov 18;222(4625):721-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6356353" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies, Monoclonal/genetics/*immunology ; *Antibody Diversity ; Antibody Specificity ; Genes ; Hybridomas/immunology ; Immunoglobulin Idiotypes/immunology ; Immunoglobulin Variable Region/genetics ; Mice ; Mutation ; Protein Conformation ; Structure-Activity Relationship
    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
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    Autoimmunity and increased c-myb transcription (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-11-30
    Description: A single recessive gene, lpr, induces an autoimmune-lymphoproliferative syndrome in several strains of mice. The lymphoid organs of lpr/lpr mice contained cells with increased amounts of myb RNA, which codes for a protein found in the nucleus. A similar human lymphoproliferative disorder also had an increase in c-myb expression. Mouse T cells induced by mitogens to proliferate did not express large amounts of myb RNA, indicating that marked myb expression is not a general feature of lymphocyte activation and proliferation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mountz, J D -- Steinberg, A D -- Klinman, D M -- Smith, H R -- Mushinski, J F -- New York, N.Y. -- Science. 1984 Nov 30;226(4678):1087-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6494925" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoantibodies/*genetics ; Autoimmune Diseases/*genetics ; Female ; *Genes, Recessive ; Lymphocytes/immunology ; Lymphoproliferative Disorders/*genetics ; Mice ; Mice, Inbred Strains ; Nucleic Acid Hybridization ; *Oncogenes ; Species Specificity ; Spleen/immunology ; *Transcription, Genetic
    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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  • 4
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    Hypoxic coordinate regulation of mitochondrial enzymes in mammalian cells (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-02-17
    Description: The effect of hypoxic exposure on various mitochondrial enzymes and on cell mitochondrial genomic content was studied in two types of mammalian cells. Hypoxia depressed the activity of six enzymes to the same degree. The kinetics of depression and of recovery during reexposure to normoxia were statistically similar for three marker enzymes. Despite the global and symmetrical decrease in enzyme activities, mitochondrial DNA remained constant. This suggests either symmetrical loss of mitochondrial enzymes from all mitochondria or complete loss of enzymes from a subpopulation of mitochondria with retention of an intact mitochondrial genome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Murphy, B J -- Robin, E D -- Tapper, D P -- Wong, R J -- Clayton, D A -- 5 R01 HL23701-14/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1984 Feb 17;223(4637):707-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6320368" target="_blank"〉PubMed〈/a〉
    Keywords: Aerobiosis ; Anaerobiosis ; Animals ; Anoxia/physiopathology ; Citrate (si)-Synthase/genetics/*metabolism ; DNA, Mitochondrial/*genetics ; Electron Transport Complex IV/genetics/*metabolism ; Macrophages/*enzymology ; Mice ; Mitochondria/*enzymology ; Mitochondria, Muscle/*enzymology ; Oxidoreductases/genetics/*metabolism ; Oxo-Acid-Lyases/*metabolism ; Rats
    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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  • 5
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    Concerted nonsyntenic allelic loss in human colorectal carcinoma (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-08-19
    Description: Familial polyposis coli (FPC) is caused by an autosomal dominant gene on chromosome 5, and it has been proposed that colorectal cancer in the general population arises from loss or inactivation of the FPC gene, analogous to recessive tumor genes in retinoblastoma and Wilms' tumor. Since allelic loss can be erroneously scored in nonhomogeneous samples, tumor cell populations were first microdissected from 24 colorectal carcinomas, an additional nine cancers were engrafted in nude mice, and nuclei were flow-sorted from an additional two. Of 31 cancers informative for chromosome 5 markers, only 6 (19%) showed loss of heterozygosity of chromosome 5 alleles, compared to 19 of 34 (56%) on chromosome 17, and 17 of 33 (52%) on chromosome 18. Therefore, it appears that (i) FPC is a true dominant for adenomatosis but not a common recessive gene for colon cancer; and (ii) simple Mendelian models involving loss of alleles at a single locus may be inappropriate for understanding common human solid tumors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Law, D J -- Olschwang, S -- Monpezat, J P -- Lefrancois, D -- Jagelman, D -- Petrelli, N J -- Thomas, G -- Feinberg, A P -- New York, N.Y. -- Science. 1988 Aug 19;241(4868):961-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of Michigan Medical School, Ann Arbor 48109.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2841761" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/genetics ; Adenoma/genetics ; Adenomatous Polyposis Coli/*genetics ; *Alleles ; Animals ; Chromosomes, Human, Pair 17 ; Chromosomes, Human, Pair 18 ; Chromosomes, Human, Pair 5 ; Colonic Neoplasms/*genetics ; DNA, Neoplasm/analysis ; Genes, Dominant ; *Genetic Linkage ; Humans ; Mice ; Precancerous Conditions/genetics ; Rectal Neoplasms/*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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    T-cell receptor beta-chain expression: dependence on relatively few variable region genes (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-08-09
    Description: Fifteen independently isolated complementary DNA clones that contain T-cell receptor (TCR) V beta genes were sequenced and found to represent 11 different V beta genes. When compared with known sequences, 14 different V beta genes could be defined from a total of 25 complementary DNA's; 11 clones therefore involved repeated usage of previously identified V beta's. Based on these data, we calculate a maximum likelihood estimate of the number of expressed germline V beta genes to be 18 with an upper 95 percent confidence bound of 30 genes. Southern blot analysis has shown that most of these genes belong to single element subfamilies which show very limited interstrain polymorphism. The TCR beta-chain diversity appears to be generated from a limited V beta gene pool primarily by extensive variability at the variable-diversity-joining (V-D-J) junctional site, with no evidence for the involvement of somatic hypermutation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Behlke, M A -- Spinella, D G -- Chou, H S -- Sha, W -- Hartl, D L -- Loh, D Y -- GM07200/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1985 Aug 9;229(4713):566-70.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3875151" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Base Sequence ; Chromosome Mapping ; Cloning, Molecular ; Dna ; Gene Pool ; *Genetic Variation ; Humans ; Hybridomas ; Immunoglobulin Variable Region/genetics ; Mice ; Mice, Inbred BALB C/genetics ; Mice, Inbred C57BL/genetics ; Mice, Inbred Strains/genetics ; Receptors, Antigen, T-Cell/*genetics ; Species Specificity ; Spleen ; T-Lymphocytes ; Thymus Gland
    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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    Germline organization of the murine T cell receptor beta-chain genes (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-10-23
    Description: The complete germline organization of the beta-chain genes of the murine T cell receptor was elucidated in order to obtain the structural basis for understanding the mechanisms of somatic DNA rearrangements. Twenty of the 22 known variable (V beta) genes are clustered within 250 kilobases of DNA 5' to the constant region (C beta) genes. These V beta genes share the same transcriptional orientation as the diversity (D beta), joining (J beta), and C beta genes, which implies that chromosomal deletion is the mechanism for most V beta to D beta-J beta rearrangements. Within this V beta cluster, the distance between the most proximal V beta gene and the D beta-J beta-C beta cluster is 320 kilobases, as determined by field-inversion gel electrophoresis. The large distance between V beta and D beta, relative to that between D beta and J beta, may have significant implications for the ordered rearrangement of the T cell receptor beta-chain genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chou, H S -- Nelson, C A -- Godambe, S A -- Chaplin, D D -- Loh, D Y -- GM07067/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Oct 23;238(4826):545-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2821625" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Deletion ; Chromosome Mapping ; DNA/genetics ; DNA Restriction Enzymes ; Electrophoresis ; Macromolecular Substances ; Mice ; Mice, Inbred BALB C ; Mice, Mutant Strains ; Nucleic Acid Hybridization ; Receptors, Antigen, T-Cell/*genetics ; Transcription, Genetic
    Print ISSN: 0036-8075
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  • 8
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    Effects on Trichinella spiralis of host responses to purified antigens (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-02-22
    Description: Purification of two antigens (48-kilodalton polypeptide and a group with major subunits of 50 and 55 kilodaltons) from the infective larvae of the parasitic nematode Trichinella spiralis was recently reported. Immunization of mice with either of these antigens induces strong resistance to a subsequent challenge infection. In the study reported here the mechanism of this resistance was investigated by monitoring the parasite's life cycle in mice immunized with the antigens. Immunized mice were able to expel intestinal adult worms and to inhibit the fecundity of adult female worms at an accelerated rate compared to control mice. Accelerated expulsion and inhibition of fecundity may account entirely for the level of resistance induced by immunization. Although the effects of the immune response apparently are exerted on adult worms, the target antigens are expressed only by developing larvae. This suggests that immune effector mechanisms act on intestinal larvae in such a way that they develop into defective adults.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Silberstein, D S -- Despommier, D D -- New York, N.Y. -- Science. 1985 Feb 22;227(4689):948-50.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3969571" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Helminth/immunology/*isolation & purification ; Female ; Immunization ; Larva ; Male ; Mice ; Trichinella/growth & development/*immunology ; Trichinellosis/immunology
    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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    Loss of M2 muscarine receptors in the cerebral cortex in Alzheimer's disease and experimental cholinergic denervation (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-05-31
    Description: Cerebral cortex samples from patients with Alzheimer's disease and from rats after experimental cholinergic denervation of the cerebral cortex exhibited reductions in the presynaptic marker choline acetyltransferase activity and in the number of M2 muscarine receptors, with no change in the number of M1 receptors. These results are in keeping with evidence that M2 receptors function in cholinergic nerve terminals to regulate the release of acetylcholine, whereas M1 receptors are located on postsynaptic cells and facilitate cellular excitation. New M1-selective agonists and M2-selective antagonists directed at post- or presynaptic sites deserve consideration as potential agents for the treatment of the disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mash, D C -- Flynn, D D -- Potter, L T -- HLO-7188/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1985 May 31;228(4703):1115-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3992249" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Alzheimer Disease/*metabolism ; Animals ; Cerebral Cortex/*metabolism ; Choline O-Acetyltransferase/*metabolism ; Cholinergic Fibers/physiology ; Denervation ; Humans ; Male ; Oxotremorine ; Quinuclidinyl Benzilate ; Rats ; Rats, Inbred Strains ; Receptors, Muscarinic/*metabolism ; Synaptic Membranes/*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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    Effect of prior immunization on induction of cervial cancer in mice by herpes simplex virus type 2 (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-12-09
    Description: Previous studies at this laboratory showed that repeated application of inactivated herpes simplex virus type 2 to the mouse cevix produced premalignant and malignant lesions. In the present study mice were inoculated with inactivated herpes simplex virus type 2 or control solution and Freund's adjuvant by intraperitoneal and subcuaneous routes before exposure of the cervix to inactivated virus. It appears that immunization with inactivated virus conferred a protection against the induction of cervical carcinoma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wentz, W B -- Heggie, A D -- Anthony, D D -- Reagan, J W -- CA-31973/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1983 Dec 9;222(4628):1128-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6316503" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; Herpes Simplex/*complications ; Immunization ; Mice ; Simplexvirus/immunology ; Uterine Cervical Neoplasms/microbiology/pathology/*prevention & control
    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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