![]() TP53 deletion causes abnormal ciliogenesis in neural rosettes. ![]() Genome-wide CRISPR screen reveals requirements of ciliogenesis and sonic hedgehog (Shh) pathways for hESC differentiation into NPCs. TP53 −/− hESCs exhibit increased proliferation rates, mitotic errors, and low-grade structural aneuploidy produce poorly differentiated immature teratomas in mice and fail to differentiate into neural progenitor cells (NPCs) in vitro. Here, we probe the potential links among these cancer traits by inactivating TP53 in human embryonic stem cells (hESCs). Aneuploidy, defective differentiation, and inactivation of the tumor suppressor TP53 all occur frequently during tumorigenesis.
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