Results 221 to 230 of about 416,724 (298)
Partial inhibition of focal adhesion kinase (FAK) can paradoxically promote tumor growth, rather than simply producing a weaker antitumor effect than that observed with strong FAK suppression. In breast cancer and melanoma models, targeting p110δ PI3K, particularly in macrophages, counteracted these tumor‐promoting effects, highlighting the importance ...
Lydia Xenou +4 more
wiley +1 more source
Reader reception of translation strategies for Li Bai's "Yu Jie Yuan": Empirical evidence from a mixed-methods study. [PDF]
Chang H, Zhao J, Sun Y, Ding H.
europepmc +1 more source
Unraveling the epigenetic code in cancer cell–tumor microenvironment crosstalk
Epigenetic regulation is a key driver of cancer development and progression. Diverse epigenetic alterations in cancer cells and components of the tumor microenvironment (TME) orchestrate their communication through multiple mechanisms. We discuss how the epigenetic code coordinates bidirectional cancer cell–TME crosstalk to promote cancer progression ...
Ji Hoon Park, Mi‐Young Kim
wiley +1 more source
A multi-segment underwater acoustic array telemetry dataset with depth, heading, pitch, and roll time series. [PDF]
Huang F, Zhao L.
europepmc +1 more source
Arginine methylation can be viewed as a persistence‐prone post‐translational modification regulated by a network of PRMTs. Competitive and compensatory interactions among PRMTs can redistribute methylation across substrate pools shaped by sequence, structural, spatial, and environmental layers, reinforcing RNA‐processing, chromatin, and signaling ...
So Hyun Kwon, Ji Min Lee
wiley +1 more source
Overseas reception of English translations of Journey to the West: Temporal dynamics, cross-platform sentiment patterns, and topic modeling. [PDF]
Jia N, Xin J, Wang Y.
europepmc +1 more source
Mechanisms and therapeutic opportunities of the ribotoxic stress response in cancer
Cancer cells' high translational demand creates opportunities to therapeutically target ribosome function. Ribosome stalling and collisions activate ZAKα and the ribotoxic stress response (RSR), which can trigger rapid, p53‐independent apoptosis in cancer.
Anastassiya Kim +7 more
wiley +1 more source

