Kabat
Mostrando 13-24 de 47 artigos, teses e dissertações.
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13. AN ELECTROPHORETIC STUDY OF THE PROTEIN COMPONENTS IN CEREBROSPINAL FLUID AND THEIR RELATIONSHIP TO THE SERUM PROTEINS 1
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14. Effect of public smoking ban in Helena, Montana: When results look too good to be true, they probably are
BMJ Publishing Group Ltd..
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15. Comparison of invariant residues in the variable and constant regions of human K, human L, and mouse K Bence-Jones proteins.
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16. The paucity of species-specific amino acid residues in the variable regions of human and mouse Bence-Jones proteins and its evolutionary and genetic implications.
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17. Resolution of hypervariable regions in T-cell receptor beta chains by a modified Wu-Kabat index of amino acid diversity.
The Wu-Kabat variability coefficient is a well-established descriptor of the susceptibility of an amino acid position to evolutionary replacements. It conveniently highlights stretches of accentuated amino acid variation that, for example, in an antibody molecule account for most of the antigen contacts (complementarity-determining regions). Diverse opinion
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18. The Ets-related transcription factor PU.1 immortalizes erythroblasts.
In vivo studies of Friend virus erythroleukemia have implied that proviral integrations adjacent to the gene for the Ets-related transcription factor PU.1 may inhibit the commitment of erythroblasts to differentiate and cause their capability for indefinite transplantation (C. Spiro, B. Gliniak, and D. Kabat, J. Virol. 62:4129-4135, 1988; R. Paul, S. Schuetz
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19. Immunoselection of mutants deficient in cell surface glycoproteins encoded by murine erythroleukemia viruses.
We have described a heterogeneously processed glycoprotein with an apparent molecular weight of 55,000 (gp55) that is encoded by the Friend spleen focus-forming virus, an acute erythroleukemia virus [Dresler, S., Ruta, M., Murray, M.J. & Kabat, D. (1976) J. Virol. 30, 564-573]. Several lines of evidence suggest that a small proportion of the gp55 in infected
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20. A common site for immortalizing proviral integrations in Friend erythroleukemia: molecular cloning and characterization.
By using a tagged derivative of Friend spleen focus-forming virus, we previously obtained evidence that proviral integration(s) in the host genome can cause erythroblast immortality by abrogating the commitment of the cell to differentiate (C. Spiro, B. Gliniak, and D. Kabat, J. Virol. 62:4129-4135, 1988). Exploiting the fact that each leukemia was a single
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21. Some correlations between specificity and sequence of the first complementarity-determining segments of human kappa light chains.
Examination of the sequences of the first complementarity-determining segments of the light chains of two IgM cold agglutinins agains blood group I, four monoclonal IgM antibodies against IgG proteins, and of three Bence Jones proteins provides clues for predicting which residues contribute to antibody specificity and indicates that these predictions may be
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22. A very limited number of keywords (main patterns) describes all sequences of the human variable heavy (VH) and κ (Vκ) domains
Sequences of the variable heavy (VH) and κ (Vκ) domains of Ig structures were divided into 21 fragments that correspond to strands, loops, or parts of these structural units of the variable domains. Amino acid sequences of fragments (termed “words”) were collected from the 1,172 human heavy and 668 human κ chains available in the Kabat database. Stati
The National Academy of Sciences of the USA.
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23. Role of the PU.1 transcription factor in controlling differentiation of Friend erythroleukemia cells.
Both viral and cellular genes have been directly implicated in pathogenesis of Friend viral erythroleukemia. The virus-encoded gp55 glycoprotein binds to erythropoietin receptors to cause mitogenesis and differentiation of erythroblasts. However, if the provirus integrates adjacent to the gene for the PU.1 transcription factor, the cell loses its commitment
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24. Further Comparison of Predicted and Experimentally Determined Structure of Adenylate Kinase
An analysis is made of various predictive methods used to locate α-helices and β-sheets in proteins. The analysis is based on attempts to locate the α-helices and β-sheets in adenylate kinase (ATP:AMP phosphotransferase EC 2.7.4.3) from the sequence without prior knowledge of the x-ray findings. Specification of the β-sheet breaking and α-helix breakin