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Biomedical subjects

R Esteban

Publications and source records attributed to R Esteban.

At least 55 records · Page 3Linked to original sources
PubMed1988

Site-specific binding of viral plus single-stranded RNA to replicase-containing open virus-like particles of yeast.

X double-stranded RNA is a deletion mutant of L-A double-stranded RNA and is encapsidated in viral particles by the L-A-encoded major coat protein. X double-stranded RNA has all the cis sites necessary to be transcribed, encapsidated, and replicated. We have cloned X double-stranded RNA and sequenced it. The complete X double-stranded RNA sequence deduced indicates that the first 25 bases of the X plus-strand 5' end originated from the 5' end of the L-A plus strand and that most, if not all, of the rest comes from the 3' end of the L-A plus strand. The X plus strand made by X double-stranded RNA-containing virus-like particles binds specifically to empty open virus-like particles and is converted by these particles to X double-stranded RNA. RNA transcripts of the X complementary DNA clones and deletion derivatives thereof were made in vitro by T7 and T3 RNA polymerases and tested for specific binding to the virus-like particles. The results suggest that the binding is due to the sequence UUUGGCCAGG, 370 bases upstream from the X plus-strand 3' end. This sequence is also present in the M1 plus strand 140 bases from its 3' end.

Amino Acid Sequence↗
PubMed1988

A deletion mutant of L-A double-stranded RNA replicates like M1 double-stranded RNA.

X double-stranded RNA (dsRNA) is a 0.52-kilobase dsRNA molecule that arose spontaneously in a nonkiller strain of Saccharomyces cerevisiae originally containing L-A and L-BC dsRNAs (L-BC is the same size as L-A but shares no homology with it). X hybridized with L-A, and direct RNA sequencing of X showed that the first 5' 25 base pairs (of the X positive strand) and at least the last 110 base pairs of the 3' end were identical to the ends of L-A dsRNA. X showed cytoplasmic inheritance and, like M1, was dependent on L-A for its maintenance. X was encapsidated in viruslike particles whose major coat protein was provided by L-A (as is true for M1), and X was found in viruslike particles with one to eight X molecules per particle. This finding confirms our "head-full replication" model originally proposed for M1 and M2. Like M1 or M2, X lowers the copy number of L-A, especially in a ski host. Surprisingly, X requires many chromosomal MAK genes that are necessary for M1 but not for L-A.

Base Sequence↗
PubMed1987

Anti-HD IgM as a marker of chronic delta infection.

The value of anti-HD IgM as a marker of chronic delta infection was evaluated by correlating its presence in serum with that of HD-Ag in liver cells and with the degree of inflammatory activity. Thirty-six patients with HBsAg-positive chronic hepatitis and anti-HD at high titers were studied. Overall, the liver cells of 26 patients contained HD-Ag and 27 were positive for IgM anti-HD. The correlation between both markers was excellent: 25 cases were positive for both serum anti-HD IgM and intrahepatic HD-Ag and 8 were negative for both markers. There was only 1 HD-Ag-positive patient, who was anti-HD IgM-negative. Two patients were anti-HD IgM-positive and HD-Ag-negative. Histological damage was more severe in anti-HD IgM-positive cases than in those negative for this marker (Knodell's index 13.5 vs 11.9, P less than 0.01). We conclude that anti-HD IgM is a good marker of chronic active delta infection.

Adolescent↗
PubMed1987

A new non-mendelian genetic element of yeast that increases cytopathology produced by M1 double-stranded RNA in ski strains.

The Saccharomyces cerevisiae SKI (superkiller) genes are repressors of replication of M, L-A, and L-BC double-stranded (ds) RNAs; ski strains have an increased M dsRNA copy number and, as a result, are cold-sensitive for growth at 8 degrees. Growth is normal, however, at higher temperatures. We have found a new cytoplasmic genetic element [D] (for disease) that makes M1 dsRNA-containing superkiller strains grow slowly at 30 degrees, not at all at 37 degrees, and only very poorly at 20 degrees. These growth defects require three factors: a chromosomal ski mutation, the presence of M1 dsRNA, and the presence of the new cytoplasmic factor, [D]. We have isolated mutants unable to maintain [D] (mad), at least one of which is due to mutation of a single chromosomal locus. Further, [D] can be cured by growth at 37-39 degrees. We present evidence that [D] is not M, L-A, L-BC or W dsRNAs or mitochondrial DNA, 2 mu DNA, or [psi], but [D] depends on L-A for its maintenance. We also show that [D] is distinct from [B], a cytoplasmic element that allows M1 dsRNA to be stably replicated and maintained in spite of defects in certain chromosomal MAK genes that would otherwise be necessary. [D] activity is blocked by the presence of another extrachromosomal element, called [DIN] (for [D] interference). [D] and [DIN] may be different natural variants of the same molecule.

Genes, Fungal↗