STK40 inhibits trophoblast fusion by mediating COP1 ubiquitination to degrade P57^Kip2.

ABSTRACT:

Background

The syncytiotrophoblast (SCT) layer in the placenta serves as a crucial physical barrier separating maternal-fetal circulation, facilitating essential signal and substance exchange between the mother and fetus. Any abnormalities in its formation or function can result in various maternal syndromes, such as preeclampsia. The transition of proliferative villous cytotrophoblasts (VCT) from the mitotic cell cycle to the G0 phase is a prerequisite for VCT differentiation and their fusion into SCT. The imprinting gene P57^Kip2, specifically expressed in intermediate VCT capable of fusion, plays a pivotal role in driving this key event. Moreover, aberrant expression of P57^Kip2 has been linked to pathological placental conditions and adverse fetal outcomes.<

SUBMITTER: Li X 

PROVIDER: S-EPMC11414097 | biostudies-literature | 2024 Sep

REPOSITORIES: biostudies-literature