Biomedical subjects

A Ubasawa

Publications and source records attributed to A Ubasawa.

3 recordsLinked to original sources

PubMed1991

A variant database.

Variant biomacromolecules, either natural or artificially created, are proving to be useful in determining structure-function relationships. Research in this field would be facilitated by the compilation of data of variants into a central and widely available repository. The Variant Database acts as a repository for data concerning variant molecules. It complements the Biological Activity and the Physicochemical Property Databases as well as provides variant sequences.

Amino Acid Sequence↗

PubMed1986

Oligonucleotide duplexes containing inosine, 7-deazainosine, tubercidin, nebularine and 7-deazanebularine as substrates for restriction endonucleases HindII, SalI and TaqI.

Synthetic hexadecanucleotide duplexes containing a single purine nucleotide analogue in the recognition sites of the restriction endonucleases HindII, SalI and TaqI were used to investigate the restriction site determinants required by these enzymes for sequence recognition and phosphodiester bond cleavage. The enzymes were, in general, unaffected by changes introduced into the minor groove of the helix. SalI was found to be inhibited by the major groove modifications introduced into the fourth position of its recognition sequence GTCGAC. HindII and TaqI were, by contrast, able to cleave the sites containing the analogues at this position. TaqI and, to a lesser extent, HindII could also be shown to tolerate "mismatch analogues" at this site.

Base Sequence↗

PubMed1986

Guanine and adenine analogues as tools in the investigation of the mechanisms of mismatch repair in E. coli.

The efficiency of in vivo correction of five "mismatch analogues", incorporated into M13mp9 DNA, was studied in an attempt to elucidate the structural determinants required for mismatch recognition by the repair machinery of E. coli. Inosine was efficiently removed from an I/T mismatch, presumably by the action of hypoxanthine glycosylase. The mismatch analogues DI/T (DI = 7-deazainosine), Tu/C (Tu = tubercidin), N/C (N = nebularine) and DN/C (DN = 7-deazanebularine) were left largely unrepaired, giving rise to high yields of mutant phenotype. The efficiency of correction of these mismatch analogues could be correlated with their structure within the base-pair.

Adenine↗