SigalLab

It’s been a blast! Thanks for the opportunity to talk about my previous research about the role of P53 in #regeneration #reprogramming and #carcinogenesis @nyscf conference! Happy to have connected within NYC‘s stem cell community! #organoids #research #stemcells

New paper from the Sigal lab: nature.com/articles/s4146…

We are very proud to announce that yesterday our PhD Student Kimberly @KimberlyHartl_ successfully defended her thesis. Congratulations Dr Hartl! 🎓 We wish you all the best for your future career 🥳 #AcademicTwitter #PhDone

For more info see: bit.ly/greenlabcert

Proud to share that our department @ChariteBerlin was awarded Platinum level certification by @My_Green_Lab! Thx to @Flt3Linda & @KimberlyHartl_ for taking the lead! The #GreenLabCertification is the international gold standard in #lab #sustainability best practices!

During the last month we had to say goodbye to two wonderful colleagues! @LCLiu17 and @KimberlyHartl_ , we wish you both a brilliant future ahead! #AcademicTwitter

Menschen mit Colitis ulcerosa haben ein höheres Darmkrebsrisiko. Die Rolle des Gens p53 dabei und wie man Krebsvorläufer möglicherweise früh medikamentös ausschalten könnte, beschreiben Forschende der #CharitéBerlin und des @MDC_Berlin in @ScienceAdvances. charite.de/forschung/pape…

Our study gives a first explanation how cells that lack p53 signaling could outcompete healthy bystander cells and thus become fixed in the mucosa. They can be targeted metabolically, which could be used for preventive and diagnostic measures.

Those cells also fail to re-establish homeostasis metabolically and show an increased glycolytic flux - and can be targeted by a small-molecule glycolysis inhibitor.

We're thrilled to announce our latest study led by @KimberlyHartl_ has now been published in @ScienceAdvances! Together with colleagues at @ChariteBerlin and @BIMSB_MDC we unravel the role of p53 in #UlcerativeColitis! A 🧵- full paper here: science.org/doi/full/10.11… @MDC_Berlin

However, when p53 signaling is lost, injured epithelial fails to return to a healthy, homestatic state and is "locked" in the regenerative, fetal-like state with high YAP signaling.

During regeneration, when there is a Wnt burst, we see upregulation of p53 in both model systems. P53 acttvation then in turn leads to downregulation of Wnt targets again.