https://www.selleckchem.com/products/ly333531.html
The Tyr576/577 in FAK played an important role in the interaction between FAK and SHP-1. Knockdown of SHP-1 dramatically increased the spontaneous contraction of HUSMCs, which was reversed by co-infection of a FAK-knockdown lentivirus. PGF2a downregulated SHP-1 via PLCβ-PKC-NF-kB or PI3K-NF-kB pathways, suggesting the regenerative downregulation of SHP-1 enhances the uterine remodeling and plasticity by activating FAK and subsequent focal adhesion pathway, which eventually facilitates myometrium contraction and leads to labor. The stud
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