Vargheese M. Chennathukuzhi

RE-1 silencing transcription factor is reduced in endometriosis and uterine deletion in mice alters progesterone responsiveness

This study shows REST is reduced in endometriosis and its deletion in mice causes progesterone resistance, subfertility, and larger endometriotic lesions.

Regulatory Role for Tumor Suppressor REST on Estrogen Receptor (ESR1) Expression and Leiomyoma Pathophysiology

This study identifies REST as a regulator of ESR1 expression and highlights its role in leiomyoma pathophysiology through epigenetic mechanisms.

Loss of PRICKLE1 leads to abnormal endometrial epithelial architecture, decreased embryo implantation, and reduced fertility in mice.

This study shows that loss of PRICKLE1 in mouse endometrial epithelium causes abnormal architecture, reduced implantation, and infertility by disrupting cell polarity, cytokinesis, and epithelial-mesenchymal transition.

Loss of PRICKLE1 in the myometrium leads to reduced fertility, abnormal myometrial architecture, and aberrant extracellular matrix deposition in mice.

This study shows that loss of Prickle1 in mouse myometrium causes uterine leiomyoma-like features, including altered collagen, ECM deposition, and Wnt/PCP signaling disruption.

Estrogen receptor alpha mediated repression of PRICKLE1 destabilizes REST and promotes uterine fibroid pathogenesis

This study identifies a mechanism by which estrogen receptor alpha suppresses PRICKLE1, leading to REST loss and promoting uterine fibroid development.