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
    Antisense gene inhibition by oligonucleotides containing C-5 propyne pyrimidines (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-04
    Description: Phosphorothioate oligodeoxynucleotides containing the C-5 propyne analogs of uridine and cytidine bind RNA with high affinity and are potent antisense inhibitors of gene expression. In a cellular assay, gene-specific antisense inhibition occurred at nanomolar concentrations of oligonucleotide, was dose-dependent and exquisitely sensitive to sequence mismatches, and was correlated with the melting temperature and length of oligonucleotide. Activity was independent of RNA target site and cell type but was detectable only when the oligonucleotides were microinjected or delivered with cell-permeabilizing agents. These oligonucleotides may have important applications in therapy and in studies of gene function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wagner, R W -- Matteucci, M D -- Lewis, J G -- Gutierrez, A J -- Moulds, C -- Froehler, B C -- New York, N.Y. -- Science. 1993 Jun 4;260(5113):1510-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gilead Sciences, Inc., Foster City, CA 94404.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7684856" target="_blank"〉PubMed〈/a〉
    Keywords: Alkynes/pharmacology ; Animals ; Base Sequence ; Cell Line ; Cercopithecus aethiops ; Humans ; Molecular Sequence Data ; Oligonucleotides, Antisense/pharmacokinetics/*pharmacology ; Pyrimidine Nucleotides/pharmacokinetics/*pharmacology ; RNA/*drug effects ; Rats ; Thionucleotides/pharmacokinetics/*pharmacology
    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
    Specific association of human telomerase activity with immortal cells and cancer (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-12-23
    Description: Synthesis of DNA at chromosome ends by telomerase may be necessary for indefinite proliferation of human cells. A highly sensitive assay for measuring telomerase activity was developed. In cultured cells representing 18 different human tissues, 98 of 100 immortal and none of 22 mortal populations were positive for telomerase. Similarly, 90 of 101 biopsies representing 12 human tumor types and none of 50 normal somatic tissues were positive. Normal ovaries and testes were positive, but benign tumors such as fibroids were negative. Thus, telomerase appears to be stringently repressed in normal human somatic tissues but reactivated in cancer, where immortal cells are likely required to maintain tumor growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, N W -- Piatyszek, M A -- Prowse, K R -- Harley, C B -- West, M D -- Ho, P L -- Coviello, G M -- Wright, W E -- Weinrich, S L -- Shay, J W -- AG07992/AG/NIA NIH HHS/ -- CA50195/CA/NCI NIH HHS/ -- CA65178/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1994 Dec 23;266(5193):2011-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Geron Corporation, Menlo Park, CA 94025.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7605428" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Cell Division ; Cell Line ; Cell Line, Transformed/enzymology ; DNA Nucleotidylexotransferase/*metabolism ; Enzyme Activation ; Enzyme Repression ; Female ; Humans ; Male ; Molecular Sequence Data ; Neoplasms/*enzymology ; Ovary/enzymology ; Polymerase Chain Reaction ; Testis/enzymology ; Tumor Cells, Cultured
    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
    Down-regulation of LFA-1 adhesion receptors by C-myc oncogene in human B lymphoblastoid cells (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-11-02
    Description: The function of the c-myc gene and its role in tumorigenesis are poorly understood. In order to elucidate the role of c-myc oncogene activation in B cell malignancy, the phenotypic changes caused by the expression of c-myc oncogenes in human B lymphoblastoid cells immortalized by Epstein-Barr virus were analyzed. C-myc oncogenes caused the down-regulation of lymphocyte function-associated antigen-1 (LFA-1) adhesion molecules (alpha L/beta 2 integrin) and loss of homotypic B cell adhesion in vitro. Down-regulation of LFA-1 occurred by (i) posttranscriptional modulation of LFA-1 alpha L-chain RNA soon after acute c-myc induction, and (ii) transcriptional modulation in cells that chronically express c-myc oncogenes. Analogous reductions in LFA-1 expression were detectable in Burkitt lymphoma cells carrying activated c-myc oncogenes. Since LFA-1 is involved in B cell adhesion to cytotoxic T cells, natural killer cells, and vascular endothelium, these results imply functions for c-myc in normal B cell development and lymphomagenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Inghirami, G -- Grignani, F -- Sternas, L -- Lombardi, L -- Knowles, D M -- Dalla-Favera, R -- CA 37165/CA/NCI NIH HHS/ -- CA 37295/CA/NCI NIH HHS/ -- CA 48236/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1990 Nov 2;250(4981):682-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, College of Physicians and Surgeons, Columbia University, New York, NY 10032.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2237417" target="_blank"〉PubMed〈/a〉
    Keywords: B-Lymphocytes/*immunology ; Cell Line ; Cell Transformation, Neoplastic ; Down-Regulation ; Humans ; Lymphocyte Function-Associated Antigen-1/*analysis/genetics/physiology ; Plasminogen Inactivators ; Proto-Oncogene Proteins c-myc/*genetics ; *Proto-Oncogenes
    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
    Interaction of p107 with cyclin A independent of complex formation with viral oncoproteins (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-01-03
    Description: The p107 protein and the retinoblastoma protein (RB) both bind specifically to two viral oncoproteins, the SV40 T antigen (T) and adenoviral protein E1A (E1A). Like RB, p107 contains a segment (the pocket) that, alone, can bind specifically to T, E1A, and multiple cellular proteins. Cyclin A bound to the p107 pocket, but not the RB pocket. Although both pockets contain two, related collinear subsegments (A and B), the unique sequence in the p107 pocket that occupies the space between A and B is required for the interaction with cyclin A.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ewen, M E -- Faha, B -- Harlow, E -- Livingston, D M -- New York, N.Y. -- Science. 1992 Jan 3;255(5040):85-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dana-Farber Cancer Institute, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1532457" target="_blank"〉PubMed〈/a〉
    Keywords: Adenovirus Early Proteins ; Amino Acid Sequence ; Antigens, Polyomavirus Transforming/*metabolism ; Base Sequence ; Binding Sites ; Cell Line ; Cloning, Molecular ; Cyclins/*metabolism ; Escherichia coli/genetics ; Eye Neoplasms ; Glutathione Transferase/genetics/metabolism ; Humans ; Molecular Sequence Data ; Mutagenesis, Site-Directed ; *Nuclear Proteins ; Oligodeoxyribonucleotides ; Oncogene Proteins, Viral/genetics/*metabolism ; Protein Conformation ; Proteins/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Retinoblastoma ; Retinoblastoma Protein/genetics/*metabolism ; Retinoblastoma-Like Protein p107 ; Structure-Activity Relationship
    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
  • 5
    facet.materialart.
    Unknown
    Interaction between human cyclin A and adenovirus E1A-associated p107 protein (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-01-03
    Description: The products of the adenovirus early region 1A (E1A) gene are potent oncoproteins when tested in standard transformation and immortalization assays. Many of the changes induced by E1A may be due to its interaction with cellular proteins. Four of these cellular proteins are the retinoblastoma protein (pRB), p107, cyclin A, and p33cdk2. The pRB and p107 proteins are structurally related and have several characteristics in common, including that they both bind to the SV40 large T oncoprotein as well as to E1A. Cyclin A and p33cdk2 are thought to function in the control of the cell cycle. They bind to one another, forming a kinase that closely resembles the cell cycle-regulating complexes containing p34cdc2. Cyclin A is now shown to bind to p107 in the absence of E1A. The association of p107 with cyclin A suggests a direct link between cell cycle control and the function of p107.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Faha, B -- Ewen, M E -- Tsai, L H -- Livingston, D M -- Harlow, E -- CA 13106/CA/NCI NIH HHS/ -- CA 55339/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1992 Jan 3;255(5040):87-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Massachusetts General Hospital Cancer Center, Charlestown 02129.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1532458" target="_blank"〉PubMed〈/a〉
    Keywords: Adenovirus Early Proteins ; Amino Acid Sequence ; Antibodies, Monoclonal ; CDC2 Protein Kinase/metabolism ; Cell Line ; Cyclins/immunology/isolation & purification/*metabolism ; Electrophoresis, Polyacrylamide Gel ; Glutathione Transferase/genetics/isolation & purification ; Humans ; Methionine/metabolism ; Molecular Sequence Data ; *Nuclear Proteins ; Oncogene Proteins, Viral/*metabolism ; Proteins/genetics/*metabolism ; Recombinant Fusion Proteins/isolation & purification ; Retinoblastoma Protein/metabolism ; Retinoblastoma-Like Protein p107
    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
  • 6
    facet.materialart.
    Unknown
    The receptor for ciliary neurotrophic factor (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-07-05
    Description: Although neurotrophic factors were originally isolated on the basis of their ability to support the survival of neurons, these molecules are now thought to influence many aspects of the development and maintenance of the nervous system. Identifying the receptors for these neurotrophic factors should aid in identifying the cells on which these factors act and in understanding their precise mechanisms of action. A "tagged-ligand panning" procedure was used to clone a receptor for ciliary neurotrophic factor (CNTF). This receptor is expressed exclusively within the nervous system and skeletal muscle. The CNTF receptor has a structure unrelated to the receptors utilized by the nerve growth factor family of neurotrophic molecules, but instead is most homologous to the receptor for a cytokine, interleukin-6. This similarity suggestes that the CNTF receptor, like the interleukin-6 receptor, requires a second, signal-transducing component. In contrast to all known receptors, the CNTF receptor is anchored to cell membranes by a glycosyl-phosphatidylinositol linkage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Davis, S -- Aldrich, T H -- Valenzuela, D M -- Wong, V V -- Furth, M E -- Squinto, S P -- Yancopoulos, G D -- New York, N.Y. -- Science. 1991 Jul 5;253(5015):59-63.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Regeneron Pharmaceuticals, Inc., Tarrytown, NY 10591.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1648265" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Blotting, Northern ; Cell Line ; Cloning, Molecular ; Electrophoresis, Agar Gel ; Gene Expression ; Humans ; In Vitro Techniques ; Molecular Sequence Data ; Muscles/metabolism ; Nervous System/metabolism ; Neuroblastoma/metabolism ; Rats ; Receptor, Ciliary Neurotrophic Factor ; Receptors, Cell Surface/blood/*genetics ; Sequence Homology, Nucleic Acid ; 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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 7
    facet.materialart.
    Unknown
    Production of the Alzheimer amyloid beta protein by normal proteolytic processing (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-10-02
    Description: The 4-kilodalton (39 to 43 amino acids) amyloid beta protein (beta AP), which is deposited as amyloid in the brains of patients with Alzheimer's diseases, is derived from a large protein, the amyloid beta protein precursor (beta APP). Human mononuclear leukemic (K562) cells expressing a beta AP-bearing, carboxyl-terminal beta APP derivative released significant amounts of a soluble 4-kilodalton beta APP derivative essentially identical to the beta AP deposited in Alzheimer's disease. Human neuroblastoma (M17) cells transfected with constructs expressing full-length beta APP and M17 cells expressing only endogenous beta APP also released soluble 4-kilodalton beta AP, and a similar, if not identical, fragment was readily detected in cerebrospinal fluid from individuals with Alzheimer's disease and normal individuals. Thus cells normally produce and release soluble 4-kilodalton beta AP that is essentially identical to the 4-kilodalton beta AP deposited as insoluble amyloid fibrils in Alzheimer's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shoji, M -- Golde, T E -- Ghiso, J -- Cheung, T T -- Estus, S -- Shaffer, L M -- Cai, X D -- McKay, D M -- Tintner, R -- Frangione, B -- AG05891/AG/NIA NIH HHS/ -- AG06656/AG/NIA NIH HHS/ -- AR02594/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 1992 Oct 2;258(5079):126-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Gunma University, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1439760" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*cerebrospinal fluid ; Amino Acid Sequence ; Amyloid beta-Peptides/*biosynthesis ; Amyloid beta-Protein Precursor/metabolism ; Animals ; Base Sequence ; Cell Line ; Immunoblotting ; Leukemia, Myeloid/*metabolism ; Molecular Sequence Data ; Neuroblastoma/*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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 8
    facet.materialart.
    Unknown
    Transcriptional repression mediated by the WT1 Wilms tumor gene product (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-10-07
    Description: The wt1 gene, a putative tumor suppressor gene located at the Wilms tumor (WT) locus on chromosome 11p13, encodes a zinc finger-containing protein that binds to the same DNA sequence as EGR-1, a mitogen-inducible immediate-early gene product that activates transcription. The transcriptional regulatory potential of WT1 has not been demonstrated. In transient transfection assays, the WT1 protein functioned as a repressor of transcription when bound to the EGR-1 site. The repression function was mapped to the glutamine- and proline-rich NH2-terminus of WT1; fusion of this domain to the zinc finger region of EGR-1 converted EGR-1 into a transcriptional repressor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Madden, S L -- Cook, D M -- Morris, J F -- Gashler, A -- Sukhatme, V P -- Rauscher, F J 3rd -- CA-0917-15/CA/NCI NIH HHS/ -- CA-23413/CA/NCI NIH HHS/ -- CA-52009/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1991 Sep 27;253(5027):1550-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wistar Institute of Anatomy and Biology, Philadelphia, PA 19104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1654597" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Cell Line ; Chromosomes, Human, Pair 11 ; DNA/genetics ; DNA-Binding Proteins/*genetics ; Gene Expression Regulation ; *Genes, Tumor Suppressor ; Humans ; Kidney Neoplasms/*genetics ; Molecular Sequence Data ; Repressor Proteins/*genetics ; *Transcription, Genetic ; Wilms Tumor/*genetics ; Zinc Fingers/*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
  • 9
    facet.materialart.
    Unknown
    Enhancement of HIV-1 cytocidal effects in CD4+ lymphocytes by the AIDS-associated mycoplasma (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-03-01
    Description: Coinfection with Mycoplasma fermentans (incognitus strain) enhances the ability of human immunodeficiency virus type-1 (HIV-1) to induce cytopathic effects on human T lymphocytes in vitro. Syncytium formation of HIV-infected T cells was essentially eliminated in the presence of M. fermentans (incognitus strain), despite prominent cell death. However, replication and production of HIV-1 particles continued during the coinfection. Furthermore, the supernatant from cultures coinfected with HIV-1 and the mycoplasma contained a factor that inhibited the standard reverse transcriptase enzyme assay. The modification of the biological properties of HIV-1 by coinfection with mycoplasma may be involved in the pathogenesis of acquired immunodeficiency syndrome (AIDS).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lo, S C -- Tsai, S -- Benish, J R -- Shih, J W -- Wear, D J -- Wong, D M -- New York, N.Y. -- Science. 1991 Mar 1;251(4997):1074-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Infections and Parasitic Diseases Pathology, Armed Forces Institute of Pathology, Washington, DC 20306.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1705362" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*microbiology ; CD4-Positive T-Lymphocytes/*microbiology ; Cell Fusion ; Cell Line ; Cytopathogenic Effect, Viral ; HIV-1/*pathogenicity ; Humans ; In Vitro Techniques ; Mycoplasma/*pathogenicity ; Mycoplasma Infections/*complications ; RNA-Directed DNA Polymerase/metabolism ; Virus Replication
    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
  • 10
    facet.materialart.
    Unknown
    Treatment of established renal cancer by tumor cells engineered to secrete interleukin-4 (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-11-01
    Description: The generation of antigen-specific antitumor immunity is the ultimate goal in cancer immunotherapy. When cells from a spontaneously arising murine renal cell tumor were engineered to secrete large doses of interleukin-4 (IL-4) locally, they were rejected in a predominantly T cell-independent manner. However, animals that rejected the IL-4-transfected tumors developed T cell-dependent systemic immunity to the parental tumor. This systemic immunity was tumor-specific and primarily mediated by CD8+ T cells. Established parental tumors could be cured by the systemic immune response generated by injection of the genetically engineered tumors. These results provide a rationale for the use of lymphokine gene-transfected tumor cells as a modality for cancer therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Golumbek, P T -- Lazenby, A J -- Levitsky, H I -- Jaffee, L M -- Karasuyama, H -- Baker, M -- Pardoll, D M -- New York, N.Y. -- Science. 1991 Nov 1;254(5032):713-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Johns Hopkins University, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1948050" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinoma, Renal Cell/genetics/immunology/pathology/*therapy ; Cell Division ; Cell Line ; *Immunotherapy ; Interleukin-4/*genetics/secretion ; Kidney Neoplasms/genetics/immunology/pathology/*therapy ; Lymphocyte Depletion ; Mice ; Mice, Inbred BALB C ; Mice, SCID ; Neoplasm Transplantation ; *Protein Engineering ; T-Lymphocyte Subsets/immunology ; 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)
    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...