18 April 2019 |       Share
 
 
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NEWS

PPRE-Luc mouse model
In a recent publication: “LT175 is a novel ...
A novel insights on our repTOP ERE-Luc mouse model
In a recent publication: “Estrogen receptor...
Join TOP srl at the 12th FELASA and 12th SECAL joint congress entitled: ‘Animal Research: Better Science from Fewer Animals’ (10-13 June 2013 Barcelona)
This year at the FELASA meeting, TOP srl will...
Join TOP srl at the American Association for Cancer Research (AACR) Annual Meeting 2013 (April 6-10 2013 Washington DC)
This year at the AACR meeting, TOP srl will p...

Technology which makes a difference

Tight regulation and ubiquitous expression of the reporter gene in transgenic repTOP™ mice is possible thanks to our proprietary technology (EP 1913813A1; US patent pending).

This technology consists in two molecular genetic features:


Site-specific transgene integration

In conventional transgenesis random integration of the DNA construct into the host genome leads to unforeseen outcomes on transgene expression due to positional effects. These range from complete transcriptional silencing to constitutive abnormal expression.

TOP integrates reporter transgenes into the mouse genome by homologous recombination in few selected sites, which have been previously identified and characterized as constitutive transcriptionally open regions.

 

Prevention of epigenetic modifications

Even in a constitutively open locus, transgene expression can be modified by epigenetic mechanisms. These effects are prevented by the use of insulator elements in the reporter transgene.


We have selected the most effective insulator elements for that purpose.




Structure of a typical repTOP™ transgene. A reporter gene encoding a surrogate marker is under the transcriptional control of an artificial promoter containing a responsive element (RE) regulated by the physiological stimulus or the drug to be studied. Reporter synthesis in all cells is proportional to drug activity. The presence of insulator sequences prevents interference by unrelated enhancers, silencers, or epigenetic modifications.