http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Branko Jovcic,Iris Bertani,Vittorio Venturi,Ljubisa Topisirovic,Milan Kojic 한국미생물학회 2008 The journal of microbiology Vol.46 No.1
The σS subunit of RNA polymerase is a central regulator which governs the expression of a host of stationary phase-induced and osmotically regulated genes in Gram-negative bacteria. The Pseudomonas putida rpoS gene is transcribed as a monocistronic rpoS mRNA with a 368 nucleotide-long 5’untranslated region (5’UTR). In this study, we investigate the posttranscriptional control of RpoS synthesis using rpoS-lacZ transcriptional and translational fusions consisting of the native promoter and deletions of 5’ UTR or insertion into UTR. The differing activity of constructed translational fusions strongly indicated that the 5’ UTR is involved in the translational regulation of RpoS expression in the stationary phase. The results obtained herein demonstrated that the structure of UTR performs an important function in the translational regulation of the rpoS gene.
S6K1 Plays a Critical Role in Early Adipocyte Differentiation
Carnevalli, Larissa S.,Masuda, Kouhei,Frigerio, Francesca,Le Bacquer, Olivier,Um, Sung Hee,Gandin, Valentina,Topisirovic, Ivan,Sonenberg, Nahum,Thomas, George,Kozma, Sara C. Elsevier 2010 Developmental cell Vol.18 No.5
<P><B>Summary</B></P><P>Earlier, we reported that <I>S6K1</I><SUP>−/−</SUP> mice have reduced body fat mass, have elevated rates of lipolysis, have severely decreased adipocyte size, and are resistant to high fat diet (HFD)-induced obesity. Here we report that adipocytes of <I>S6K1</I><SUP>−/−</SUP> mice on a HFD have the capacity to increase in size to a degree comparable to that of wild-type (WT) mice, but not in number, indicating an unexpected lesion in adipogenesis. Tracing this lesion revealed that S6K1 is dispensable for terminal adipocyte differentiation, but is involved in the commitment of embryonic stem cells to early adipocyte progenitors. We further show that absence of S6K1 attenuates the upregulation of transcription factors critical for commitment to adipogenesis. These results led to the conclusion that a lack of S6K1 impairs the generation of de novo adipocytes when mice are challenged with a HFD, consistent with a reduction in early adipocyte progenitors.</P> <P><B>Graphical Abstract</B></P><P><ce:figure></ce:figure></P>