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      Positional cloning of the mouse obese gene and its human homologue

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      Nature

      Springer Science and Business Media LLC

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          Abstract

          The mechanisms that balance food intake and energy expenditure determine who will be obese and who will be lean. One of the molecules that regulates energy balance in the mouse is the obese (ob) gene. Mutation of ob results in profound obesity and type II diabetes as part of a syndrome that resembles morbid obesity in humans. The ob gene product may function as part of a signalling pathway from adipose tissue that acts to regulate the size of the body fat depot.

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          Most cited references 35

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          DNA sequencing with chain-terminating inhibitors

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            Isolation of biologically active ribonucleic acid from sources enriched in ribonuclease

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              Point mutations define a sequence flanking the AUG initiator codon that modulates translation by eukaryotic ribosomes.

              By analyzing the effects of single base substitutions around the ATG initiator codon in a cloned preproinsulin gene, I have identified ACCATGG as the optimal sequence for initiation by eukaryotic ribosomes. Mutations within that sequence modulate the yield of proinsulin over a 20-fold range. A purine in position -3 (i.e., 3 nucleotides upstream from the ATG codon) has a dominant effect; when a pyrimidine replaces the purine in position -3, translation becomes more sensitive to changes in positions -1, -2, and +4. Single base substitutions around an upstream, out-of-frame ATG codon affect the efficiency with which it acts as a barrier to initiating at the downstream start site for preproinsulin. The optimal sequence for initiation defined by mutagenesis is identical to the consensus sequence that emerged previously from surveys of translational start sites in eukaryotic mRNAs. The mechanism by which nucleotides flanking the ATG codon might exert their effect is discussed.
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                Author and article information

                Journal
                Nature
                Nature
                Springer Science and Business Media LLC
                0028-0836
                1476-4687
                December 1994
                December 1994
                : 372
                : 6505
                : 425-432
                Article
                10.1038/372425a0
                7984236
                © 1994

                http://www.springer.com/tdm

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