Results 191 to 200 of about 112,765 (306)
Defining RNA oligonucleotides that reverse deleterious phase transitions of RNA-binding proteins with prion-like domains. [PDF]
Guo L +32 more
europepmc +1 more source
Beyond its role in immune evasion, this study identified that CD47 drives tumor‐intrinsic signaling in non‐small cell lung cancer (NSCLC). Transcriptomic profiling and functional studies revealed that CD47 regulates cell adhesion, migration, and metastasis through an ERK–EMT signaling axis.
Asa P.Y. Lau +8 more
wiley +1 more source
Electro-encephalographic surrogate measures fail to describe the pharmacodynamic interaction between ketamine and propofol. [PDF]
Mortier, Eric +2 more
core +1 more source
Biochemistry and applications of Aprotimin, the kallikrein inhibitor from bovine organs. [PDF]
Fritz, Hans, Wunderer, G.
core +1 more source
Disease trajectories and end of life care in a Norwegian ALS cohort. [PDF]
Johansen H +3 more
europepmc +1 more source
KDM7A and KDM1A inhibition suppresses tumour promoting pathways in prostate cancer
Treatment resistance is a major challenge for patients with advanced prostate cancer. This study examined an alternative approach to target the major prostate cancer‐promoting pathway by targeting epigenetic factors, whose levels are higher in tumours.
Jennie N Jeyapalan +16 more
wiley +1 more source
G-Quadruplexes Abet Neuronal Burnout in ALS and FTD. [PDF]
Herbert A.
europepmc +1 more source
EXOSC10, an essential nuclear RNA exosome‐associated 3′‐5′ exoribonuclease, is inhibited by the anticancer drug 5‐fluorouracil (5‐FU), and EXOSC10 depletion increases 5‐FU sensitivity. The colon‐cancer variant EXOSC10S402T, located in a proteolysis motif, is stable and nuclear but nonfunctional in vivo.
Radhika Sain +10 more
wiley +1 more source
Brain organoids as precision models for neurodegenerative diseases: from disease modeling to drug discovery. [PDF]
Zheng Y, Zhou W, Chang H, Zheng K.
europepmc +1 more source
We analyze cisplatin–DNA adducts (CDAs) and double‐strand breaks (DSBs) in a cell‐cycle‐dependent manner. We find that CDAs form similarly across all cell cycle phases. DSBs arise only in S‐phase. CDAs might not directly impair DSB repair, but S‐phase DSB lesions evolve in the presence of CDAs and disrupt repair in G2, also causing radiosensitization ...
Ye Qiu +10 more
wiley +1 more source

