GLANDULAR DEFECTS IN THE MOUSE UTERUS WITH SUSTAINED ACTIVATION OF TGF-BETA SIGNALING IS ASSOCIATED WITH ALTERED DIFFERENTIATION OF ENDOMETRIAL STROMAL CELLS AND FORMATION OF STROMAL COMPARTMENT.

Glandular defects in the mouse uterus with sustained activation of TGF-beta signaling is associated with altered differentiation of endometrial stromal cells and formation of stromal compartment.

Uterine gland development, also known as adenogenesis, is a key uterine morphogenic process indispensable for normal uterine function and fertility.Our earlier studies have reported that overactivation of TGFB receptor 1 (TGFBR1) in the mouse uterus using progesterone receptor (Pgr)-Cre recombinase causes female infertility, defective decidualizati

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