Genetic Control of Protein Structure

Yanofsky, Charles

doi:10.1016/b978-0-12-395555-5.50007-4

Cited by 6 publications

(1 citation statement)

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“…Both EMS and MNNG effectively induce bacterial nonsense mutations (GAREN and SIDDIQI 1962). Since missense mutations may result in mutant proteins with residual activity, and nonsense mutations usually result in total loss of enzyme activity, the percentage of nonsense mutants in our extreme negative group of mutants is expected to be high (WHITFIELD, MARTIN and AMES 1966;GAREN 1968;YANOFSKY 1963). Some naturally occurring mutants of man (Lesch-Nyhan syndrome) have no detectable erythrocyte HGPRTase activity, but extracts of these cells react readily with antibody (CRM+) prepared to normal human red cell HGPRTase (RUBIN et al 1971).…”

Section: -Azaguanine Resistance 249mentioning

confidence: 99%

8-Azaguanine Resistance in Mammalian Cells I. Hypoxanthine-Guanine Phosphoribosyltransferase

et al. 1972

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Chinese hamster cells were treated with ethyl methanesulfonate or N-methyl-N'-nitro-N-nitrosoguanidine, and mutants resistant to 8-azaguanine were selected and characterized. Hypoxanthine-guanine phosphoribosyltransferase activity of sixteen mutants is extremely negative, making them suitable for reversion to HGPRTase+. Ten of the extremely negative mutants revert at a frequency higher than 10-7 suggesting their point mutational character. The remaining mutants have demonstrable HGPRTase activity and are not useful for reversion analysis. Five of these mutants have < 2% HGPRTase and are presumably also HGPRTase point mutants. The remaining 14 mutants utilize exogenous hypoxanthine for nucleic acid synthesis poorly, and possess 20-150% of wild-type HGPRTase activity in in vitro. Their mechanism of 8-azaguanine resistance is not yet defined.

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Section: -Azaguanine Resistance 249mentioning

confidence: 99%