Results 221 to 230 of about 254,775 (306)
Glucose deprivation in the primary CNS lymphoma (PCNSL) tumor microenvironment drives SLC2A5 (encoding GLUT5)‐dependent fructose metabolism in tumor cells, while hypoxia induces HIF‐mediated SLC2A5 expression in tumor‐supportive macrophages, revealing SLC2A5‐driven fructose utilization as a shared and targetable metabolic vulnerability across malignant
Qiaoli Wu +13 more
wiley +1 more source
CRISPR-MBTF: a multi-branch transformer fusion framework for CRISPR-Cas9 off-target prediction. [PDF]
Jahangiri-Sisakht A +2 more
europepmc +1 more source
Radioresistance arises partly from tumor cells evading cuproptosis via unknown defenses. This study reveals that the PRMT5‐VPS34 axis acts as a radiation‐activated anticuproptotic mechanism: PRMT5 methylates VPS34 at Arg174, recruiting USP10 to remove K48‐linked ubiquitination and prevent degradation.
Wei Chen +17 more
wiley +1 more source
CRISPR/Cas9-mediated targeted editing of GmSH2 enhances sugar accumulation in vegetable soybean. [PDF]
Li C +10 more
europepmc +1 more source
ABSTRACT Background Therapeutic resistance limits durable survival in advanced/metastatic renal cell carcinoma (RCC) treated with first‐line tyrosine kinase inhibitor (TKI) plus immune checkpoint inhibitor (ICI). We sought to define key resistance drivers and actionable targets.
Jinchen Luo +16 more
wiley +1 more source
Engineered AcrIIA5 for optogenetic control of CRISPR-Cas9-based genome editing. [PDF]
Chen Q +5 more
europepmc +1 more source
Astrocytic FABP5 promotes mitochondrial stress, cGAS‐STING pathway activation, pyroptosis, and neuroinflammation in epilepsy, contributing to seizure pathology. Genetic targeting of FABP5 or pharmacological inhibition of STING alleviates epileptic phenotypes, highlighting a potential therapeutic strategy for epilepsy.
Chen Chen +10 more
wiley +1 more source
Suppression of HBV replication and expression by CRISPR/Cas9 ribonucleoproteins. [PDF]
Hill AC +16 more
europepmc +1 more source
PDGFA/PDGFRα signaling recruits CAFs to OSCC nests, and CAF‐OSCC contact drives tumor budding invasion. Mechanistically, heterotypic adhesion via E‐cadherin/integrin α2β1 activates YAP signaling in OSCC cells, inducing EMT. Concurrently, CAFs transfer mitochondria through TNTs, supplying ATP to fuel invasion.
Yufang Liu +17 more
wiley +1 more source

