We have identified a new transcription initiation site in the 5'-flanking regulatory region of the rat insulin II gene. This site is located on the opposite strand with respect to the insulin gene promoter, upstream of the insulin gene transcriptional enhancer. The cell-specific activity of this reverse promoter element is demonstrated in two lineages of transgenic mice, in which it directs expression of simian virus 40 T antigen specifically to the beta cells of the endocrine pancreas, resulting in development of pancreatic tumors. Analysis of RNA from the tumor cells demonstrates bidirectional transcription from the insulin regulatory region of the transgene. These data raise the possibility that bidirectional activity is a quality of the regulatory region of the insulin gene in its natural genomic context.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC365056PMC
http://dx.doi.org/10.1128/mcb.7.1.192-198.1987DOI Listing

Publication Analysis

Top Keywords

insulin gene
16
regulatory region
12
bidirectional activity
8
rat insulin
8
transgenic mice
8
insulin
6
activity rat
4
insulin 5'-flanking
4
region
4
5'-flanking region
4

Similar Publications

Childhood obesity increases the risk of developing metabolic diseases in adulthood, since environmental stimuli during critical windows of development can impact on adult metabolic health. Studies demonstrating the effect of prepubertal diet on adult metabolic disease risk are still limited. We hypothesized that a prepubertal control diet (CD) protects the adult metabolic phenotype from diet-induced obesity (DIO), while a high-fat diet (HFD) would predispose to adult metabolic alterations.

View Article and Find Full Text PDF

Homeobox C4 transcription factor promotes adipose tissue thermogenesis.

Diabetes

January 2025

Department of Pharmacology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, China.

The homeobox (HOX) family has shown potential in adipose development and function, yet the specific HOX proteins fueling adipose thermogenesis remain elusive. In this study, we uncovered the novel function of HOXC4 in stimulating adipose thermogenesis. Our bioinformatic analysis indicated an enrichment of Hoxc4 co-expressed genes in metabolic pathways and linked HOXC4 polymorphisms to metabolic parameters, suggesting its involvement in metabolic regulation.

View Article and Find Full Text PDF

PPARγ is the pharmacological target of thiazolidinediones (TZDs), potent insulin sensitizers that prevent metabolic disease morbidity but are accompanied by side effects such as weight gain, in part due to non-physiological transcriptional agonism. Using high throughput genome engineering, we targeted nonsense mutations to every exon of PPARG, finding an ATG in Exon 2 (chr3:12381414, CCDS2609 c.A403) that functions as an alternative translational start site.

View Article and Find Full Text PDF

Background: The breakthrough discovery of novel biomarkers with prognostic and diagnostic value enables timely medical intervention for the survival of patients diagnosed with gastric cancer (GC). Typically, in studies focused on biomarker analysis, highly connected nodes (hubs) within the protein-protein interaction network (PPIN) are proposed as potential biomarkers. However, this study revealed an unexpected finding following the clustering of network nodes.

View Article and Find Full Text PDF

The developmental theory of ageing proposes that age-specific decline in the force of natural selection results in suboptimal levels of gene expression in adulthood, leading to functional senescence. This theory explicitly predicts that optimising gene expression in adulthood can ameliorate functional senescence and improve fitness. Reduced insulin/IGF-1 signalling (rIIS) extends the reproductive lifespan of Caenorhabditis elegans at the cost of reduced reproduction.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!