Results 201 to 210 of about 4,554,738 (310)
DNA Methylation Analysis of Buds from Two Peach Varieties with Distinct Chilling Requirements During the Dormancy Induction Period. [PDF]
Biology (Basel)Jiang X +6 more
europepmc +1 more source
Molecular Oncology, EarlyView.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
Kinetic Control of Condensate Function: How the Formation Dynamics of APBs Influence ALT Cancer Telomere Length Heterogeneity. [PDF]
BioessaysZhang H.
europepmc +1 more source
Unraveling the epigenetic code in cancer cell–tumor microenvironment crosstalk
Molecular Oncology, EarlyView.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
Current state: Assessing DNA results considering transfer. [PDF]
Forensic Sci Int SynergKennedy JR, Champod C.
europepmc +1 more source
Molecular Oncology, EarlyView.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
Mechanisms and therapeutic opportunities of the ribotoxic stress response in cancer
Molecular Oncology, EarlyView.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