IndraLab
Statements
sparser
"Importantly, deleting the putative motif 66PDSST 70 (ΔPDSST) impaired the interaction between Nanog and SPOP both in cells and in vitro ( xref , xref , and xref ), leading to acquired resistance to SPOP-mediated destruction ( xref – xref ) and poly-ubiquitination in cells and in vitro ( xref and xref )."
sparser
"Clinically, cancer-associated mutations in the MATH domain of SPOP disrupt the interaction between SPOP and NANOG, thereby preventing SPOP-mediated destruction of NANOG, stabilizing NANOG from AMPK-BRAF-signaling-axis-induced phosphorylation, and consequently promoting the maintenance of PCa stem-like cells."
sparser
"In prostate cancer, tumor suppressor SPOP interacts with Nanog and promotes Nanog poly-ubiquitination and subsequent degradation, but Pin1 functions as an upstream Nanog regulator and impairs its recognition by SPOP, stabilizing Nanog to promote the cancer stem cell traits and tumor progression ( xref )."