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Structure and cell-specific expression of a cloned human retinol binding protein gene: the 5\'-flanking region contains hepatoma specific transcriptional signals.
No full textStructure and cell-specific expression of a cloned human retinol binding protein gene: the 5\'-flanking region contains hepatoma specific transcriptional signals.
No full textRegulation of insulin-like-growth-factor-II gene expression in rat liver cells.
No full textThe rat insulin-like-growth-factor-(IGF)-II gene is expressed at high levels during embryonic and fetal life and at low levels in adult animals. To study the regulation of IGF-II gene expression, we analyzed the synthesis and localization of the IGF-II transcripts in cultured rat liver cells either expressing (BRL3A cells) or not expressing (BRL30E and FAO cells) the IGF-II mRNA. The IGF-II gene is transcribed at a similar rate in expressing and non-expressing cells, whereas its nuclear and cytoplasmic RNA levels are diversely distributed in the cells. IGF-II RNA is more abundant in the cytoplasmic than in the nuclear RNA fraction of BRL3A cells and is present in the nucleus but not in the cytoplasm of the FAO cells. However, both precursor and mature IGF-II nuclear RNA levels are reduced in FAO cells. Our data indicate that the IGF-II gene expression is regulated by mechanisms affecting the subcellular distribution and the abundance of the transcripts
Negative control of liver-specific gene expression: cloned human retinol-binding protein gene is repressed in HeLa cells.
No full textDefective mutant of sindbis virus with a smaller-molecular-weight form of the E1 glycoprotein
No full textMutations in the extracellular domain cause RET loss of function by a dominant negative mechanism
No full textThe RET proto-oncogene encodes a tyrosine kinase receptor expressed in neuroectoderm-derived cells. Mutations in specific regions of the gene are responsible for the tumor syndromes multiple endocrine neoplasia types 2A and 2B (MEN 2A and 2B), while mutations along the entire gene are involved in a developmental disorder of the gastrointestinal tract, Hirschsprung's disease (HSCR disease). Two mutants in the extracellular domain of RET, one associated with HSCR disease and one carrying a flag epitope, were analyzed to investigate the impact of the mutations on RET function. Both mutants were impeded in their maturation, resulting in the lack of the 170-kDa mature form and the accumulation of the 150-kDa immature form in the endoplasmic reticulum. Although not exposed on the cell surface, the 150-kDa species formed dimers and aggregates; this was more pronounced in a double mutant bearing a MEN 2A mutation. Tyrosine phosphorylation and the transactivation potential were drastically reduced in single and double mutants. Finally, in cotransfection experiments both mutants exerted a dominant negative effect over protoRET and RET2A through the formation of a heteromeric complex that prevents their maturation and function. These results suggest that HSCR mutations in the extracellular region cause RET loss of function through a dominant negative mechanism
Negative control of liver-specific gene expression: cloned human retinol-binding protein gene is repressed in HeLa cells.
No full textTimeless Link Between Circadian Patterns and Disease
No full textThe Timeless (Tim) gene, originally identified in Drosophila melanogaster and subsequently in mammals, is involved in the molecular clockwork that drives 24. h periodicity in physiology and behavior. The Tim protein is involved not only in circadian rhythmicity but also in embryonic development, cell cycle progression, DNA replication, and the DNA damage response (DDR). It is thus a multifaceted factor implicated in the maintenance of many cellular processes, tissue functions, and ultimately homeostasis of various organisms, from insects to humans. This review highlights the current knowledge of Tim functions, especially the most recent achievements, and illustrates the possible roles that this factor plays in the physiological preservation of health, as well as in the pathogenic mechanisms of related diseases. The Timeless (Tim) gene is evolutionarily conserved from insects to mammals. The Drosophila melanogaster Tim gene is involved in circadian rhythmicity, but the role mammalian Tim plays in this process is still debated.Tim, however, has been implicated in additional and distinct cellular processes comprising DNA replication and the DDR, telomere length and integrity maintenance, as well as cell cycle progression.The precise mechanisms of action of Tim in these processes, or Tim interactions with various protein partners, however, have not been completely elucidated.Tim plays a role in embryonic development and developmental apoptosis, suggesting a potential involvement in mechanisms of tissue regeneration, which could be exploited in translational research and regenerative medicine.Owing to the wide range of functions, Tim has drawn attention for its possible involvement in the pathogenesis of diverse diseases ranging from tumors to psychiatric conditions hallmarked by genetic mutations, alterations of circadian rhythmicity, and other so far unidentified events. Thus, Tim may well represent a therapeutic target in such conditions
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