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U Weiss

Publications and source records attributed to U Weiss.

At least 73 records · Page 4Linked to original sources
PubMed1989

Structure of elsinochrome A: a perylenequinone metabolite.

trans-1,2-Diacetyl-1,2-dihydro-5,10-dihydroxy-3,7,8,12- tetramethoxybenzo[ghi]perylene-4,11-dione, C30H24O10, Mr = 544.51, orthorhombic, P2(1)2(1)2(1), Z = 4, a = 12.428 (3), b = 13.048 (3), c = 14.933 (3) A, V = 2421.5 (9) A3, Dx = 1.494, Dm (by flotation) = 1.48 g cm-3, lambda(Mo K alpha) = 0.71069 A, mu = 1.057 cm-1, F(000) = 1136, T = 293 K, R = 0.046 (2065 observed reflections). Elsinochrome A is shown to exist in the solid state as a nonplanar quinone tautomer; the pigment adopts a helical conformation, in analogy with the related cercosporin, but the perylenequinone moiety in elsinochrome A appears to be significantly less skewed.

Benz(a)Anthracenes↗
PubMed1989

Effects of nicks on repair of single-stranded loops in heteroduplex DNA in mammalian cells.

Heteroduplexes that contain single-stranded loops are repaired very efficiently in mammalian cells. The strand that does not contain the loop is used as the template strand for repair nearly twice as often as the looped strand. In this study we tested the influence of nearby nicks on the choice of template strand. We find that strand selection in repair of heteroduplexes with single-stranded loops is influenced by the presence of a nick located 71 or 125 base pairs from the loop, but only to a minor degree. Thus the loop itself is a stronger signal for repair than is a nearby nick. On the other hand, if a break is introduced into the single strand that forms the loop, the looped strand is marked for excision and rarely, if ever, is used as the template for repair.

Animals↗
PubMed1989

An antibody against secretogranin I (chromogranin B) is packaged into secretory granules.

We have investigated the sorting and packaging of secretory proteins into secretory granules by an immunological approach. An mAb against secretogranin I (chromogranin B), a secretory protein costored with various peptide hormones and neuropeptides in secretory granules of many endocrine cells and neurons, was expressed by microinjection of its mRNA into the secretogranin I-producing cell line PC12. An mAb against the G protein of vesicular stomatitis virus--i.e., against an antigen not present in PC12 cells--was expressed as a control. The intracellular localization and the secretion of the antibodies was studied by double-labeling immunofluorescence using the conventional and the confocal microscope, as well as by pulse-chase experiments. The secretogranin I antibody, like the control antibody, was transported along the secretory pathway to the Golgi complex. However, in contrast to the control antibody, which was secreted via the constitutive pathway, the secretogranin I antibody formed an immunocomplex with secretogranin I, was packaged into secretory granules, and was released by regulated exocytosis. Our results show that a constitutive secretory protein, unaltered by genetic engineering, can be diverted to the regulated pathway of secretion by its protein-protein interaction with a regulated secretory protein. The data also provide the basis for immunologically studying the role of luminally exposed protein domains in the biogenesis and function of regulated secretory vesicles.

Ammonium Chloride↗
PubMed1988

Heteroduplex-induced mutagenesis in mammalian cells.

We have shown previously that heteroduplexes containing single-stranded loops are repaired efficiently in monkey cells, but not always correctly: 2% of the repair products acquired mutations within a 350 base-pair target (Weiss, U. and Wilson, J.H., Proc. Natl. Acad. Sci. USA 87:1123-1126, 1987). The structures of the mutant genomes, which are described here, are consistent with an error-prone repair system. The spectrum of mutations includes about 25% point mutations and 75% rearrangements, which consist of deletions, duplications, and substitutions. The mutations are clustered in the vicinity of single-stranded loops in the original heteroduplex. The high frequency of mutation, their clustering, and the positions of rearrangement endpoints suggest that the mutations were generated during repair of the heteroduplexes.

Animals↗
PubMed1987

Repair of single-stranded loops in heteroduplex DNA transfected into mammalian cells.

Repair of heteroduplex DNA, generated between two interacting DNA molecules during homologous recombination, has been implicated as a contributing factor in the process of gene conversion. To assess patterns of heteroduplex repair in mammalian cells, we constructed 13 different heteroduplexes from simian virus 40 wild-type and deletion mutant DNAs. Each heteroduplex contained one or multiple single-stranded loops in the intron of the gene for large tumor antigen, which is not essential during lytic infection. After transfection into cultured monkey cells, cellular repair was evaluated by restriction analysis of the amplified viral progeny from 1123 individual plaques, each representing the clonal expansion of a single repair event. Single-stranded loops were corrected prior to replication with an overall efficiency of 90%. At the position of a loop, one of the two heteroduplex strands served as a template for accurate repair 98% of the time. Repair of single-stranded loops was biased nearly 2 to 1 in favor of the strand without the loop. The efficiency, accuracy, and strand bias of repair were unaffected by loop size within the tested range, which was 25-247 nucleotides. The excision tract associated with repair of single-stranded loops rarely exceeds 200-400 nucleotides in length.

Cell Line↗