Ibrahim I. Taskiran
@ibrahimihsan
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https://t.co/2JG3hG5Bhk Previously PhD student at @steinaerts lab and Research Scientist Intern at @GoogleDeepMind. Interested in genomics and ai
Leuven, Belgium
Joined April 2010
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RT @sj_marzi: I'm sure you've all been keenly awaiting the lineup for the @UKDRI #neurogenomics seminars in 2024, so here it is 🥳🧠🧬 Excite…
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RT @deAlmeida_BP: Very happy to see my final PhD paper on designing synthetic enhancers for selected tissues in vivo using #AI out in @Natu…
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@deAlmeida_BP @Nature Thanks so much Bernardo, yours is as well! It is cool to be back-to-back :)
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As this research chapter closes with the publication of our paper, I'm proud to announce I've completed my Ph.D. and am currently exploring opportunities where I can contribute my expertise to new and exciting challenges. Open to discussions and opportunities! [14/14]
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Our research underscores the critical role of repressor binding site elimination. Introducing repressors into active enhancers (without disrupting activator binding sites) destroys the activity of enhancers. [7/n]
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Network-explaining techniques allowed us to trace the impact of each mutation and decode its contribution to the resulting enhancer activity. [6/n]
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Reciprocally, we demonstrated that the code of a second cell-type can be deleted from an enhancer that is active in multiple cell-types to restrict its spatial activity. [5/n]
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Starting from the same random DNA sequence, we could evolve it into different cell type-specific enhancers by directing the mutation selection. [3/n]
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Our findings reveal that only a small number of targeted mutations are needed to transform random sequences or inactive genomic regions into enhancers that drive specific cell-type activities. [2/n]
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