GSE212474
TGFß signaling in the uterine epithelium controls endometrial cell homeostasis and regeneration [CUT&RUN]
In this study, we define the epithelial-specific contribution of SMAD2/3 to endometrial function by conditionally ablating the Smad2 and Smad3 transcription factors using Lactoferrin-iCre (Ltf-cre). Using epithelial organoid cultures from the endometrium, we uncover the signaling mechanisms downstream of TGFß that control endometrial cell regeneration and are critical for endometrial regeneration and homeostasis. Overall design: We performed Cleavage Under Targets & Release Using Nuclease (CUT&RUN-seq) for SMAD4 in the mouse endometrial epithelium organoids.