Leptin is a four-helix bundle: secondary structure by NMR.

Leptin is a signaling protein that in its mutant forms has been associated with obesity and Type II diabetes. The lack of sequence similarity has precluded analogies based on structural resemblance to known systems. Backbone NMR signals for mouse leptin (13C/15N -labeled) have been assigned and its secondary structure reveals it to be a four-helix bundle cytokine.

Enantioselective reduction of 3,4-methylene-dioxyphenylacetone using Candida famata and Zygosaccharomyces rouxii.

In an effort to prepare 3,4-methylene-dioxyphenyl-(S)-isopropanol from 3,4-methylene-dioxyphenylacetone, an initial screen of microbes indicated that Candida famata could catalyze this reaction efficiently at low substrate concentration. A dilute, large-scale process was developed to provide experimental material for the chemical synthesis to be explored. However, the productivity number of this process [0.

Isolation of BPgp70, a fibroblast receptor for the envelope antigen of Rauscher murine leukemia virus.

A protein that avidly binds gp70, the envelope antigen of Rauscher murine leukemia virus (RMuLV), has been purified from the culture medium used for growth of BALB/c 3T3 mouse cells. Gel filtration chromatrography revealed the apparent Mr 10,000 BPgp70 was efficiently labeled when BALB/c 3T3 cells were grown in medium containing [3H]leucine, indicating a cellular origin for BPpg70. Metabolically labeled [3H]BPgp70 was not immunoprecipitated by IgG-anti RMuLV-gp&) alone, but was immunoprecipitated when gp70 was added, an indicaton of BPgp70 x gp70 complex formation.

Molecular identification and properties of two cell surface receptors playing roles in mitogenesis and epigenesis.

Studies leading to the identification of cell surface receptor macromolecules which specifically recognize a hormone, epidermal growth factor (EGF), or gp70, the coat antigen of the C-type RNA tumor viruses, have been described. EGF receptors are internalized and processed by lysosomal protease action after interaction of receptor and EGF. Other hormones, which resemble EGF in their ability to trigger mitogenesis in cultured cells, interact with the EGF receptor in a yet to be defined, but probably indirect way, decreasing the number of EGF binding sites on the cell surface.

Protease activity on the surface of HSV-infected cells.

Monolayers of primary rabbit kidney cells infected with HSV type I bound lymphoblastoid (Raji) cells, to which the third component (C3) of the complement system had been attached (Raji-C3). This induction of cell contact did not occur on non-infected monolayers and was dependent on C3. The interaction could be suppressed by the presence of protease inhibitors (1 mM-TLCK or-PMSF).

Complement receptor analogous factors in human serum: I. Isolation of a molecule inhibitory for complement dependent rosette formation, its identification as alpha 1-antitrypsin and its functional characterization.

A glycoprotein was isolated from human plasma which partially inhibited C3 carrying erythrocytes from binding to complement receptor cells (CR+C). Based on its physicochemical characteristics and its antigenicity this glycoprotein was identified as alpha 1-antitrypsin (alpha 1-AT). The activity of alpha 1-AT towards C3 and its fragments was unaffected by heating but it was destroyed by periodic acid.

Identity of C3- and C5-receptors on lymphoid cells.

Tannic acid-treated SRBC, incubated with increasing concentrations of C5 (Etan-C5) can be attached to C3 receptor-carrying (Raji) cells. This binding is dependent on the amount of C5 on Etan-C5 and can be inhibited by pretreatment on the Raji cells with either C5 or C3. Similar inhibition by soluble C3 and C5, respectively, is obtained for the interaction between Raji cells and Etan-C3.

C3-mediated cytoadherence. II. Dependence of cell attachment on similar topographic distribution of the receptors (for C3) and the ligands (C3/C3b).

Particles carrying C3 in a random distribution (Etan-C3) bound to C3 receptor (Raji+) cells independent of temperature and irrespective of whether the Raji cells were fixed with glutardialdehyde. In contrast, the reactivity of EAC43b, having grouped C3b in clusters, was dependent on temperature. The interaction with Raji cells was inhibited if the latter were treated with a fixative.

Complement bridges between cells analysis of a possible cell-cell interaction mechanism.

Different leukocytes (Raji, Daudi, Rael lymphoid cells; human peripheral blood lymphocytes, and guinea pig granulocytes), which had been coated with C3 by incubation of 37 degrees C for 20 min in a C3 solution, were demonstrated to form rosettes with erythrocytes coated with complement components (EAC142). The percentage of rosettes was dependent of the amount of C3 present on the cells. Loading of the lymphoid cells with C3 was a time- and temperature-dependent process.