Results 301 to 310 of about 27,156,344 (411)
Combining osimertinib with the STING agonist ADU‐S100 activates innate and adaptive immunity to overcome the non‐inflamed microenvironment of Egfr‐mutant lung cancer. This combination increases NK and CD8+ T‐cell infiltration, associated with activation of the STING‐IRF3 pathway and local immunogenic cell death.
Jun Nishimura +19 more
wiley +1 more source
Accelerated Photogenerated Charge Separation Driven Synergistically by the Interfacial Electric Field and Work Function in Z-Scheme Zn-Ni<sub>2</sub>P/G-C<sub>3</sub>N<sub>4</sub> for Efficient Photocatalytic Hydrogen Evolution. [PDF]
Chen Q +8 more
europepmc +1 more source
Erratum: Reproducibility of work ability and work functioning instruments [PDF]
openaire +2 more sources
Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining
IGF‐1R promotes radioresistance by facilitating DNA‐PKcs recruitment to chromatin, enabling non‐homologous end‐joining (NHEJ) repair of double‐strand breaks. Inhibition or loss of IGF‐1R disrupts this recruitment to damage sites, driving compensatory reliance on microhomology‐mediated end‐joining (MMEJ) repair.
Matthew O. Ellis +3 more
wiley +1 more source
Reduced subthreshold swing in a vertical tunnel FET using a low-work-function live metal strip and a low-k material at the drain. [PDF]
Kanagarajan KS, Sadhasivan DK.
europepmc +1 more source
Quantitative electronic structure and work-function changes of liquid water induced by solute.
Credidio B +7 more
europepmc +1 more source
We identify USP29 as the only DUB mirroring CA9 expression, a marker of hypoxia and HIF pathway activation associated with PCA aggressiveness. USP29 stabilizes HIF‐1α and HIF‐2α via a noncanonical mechanism that is independent of PHD/pVHL activity yet relies on proteasomal regulation, establishing USP29 as a previously unrecognized regulator of hypoxic
Amelie S Schober +16 more
wiley +1 more source
Finding novel vulnerabilities of hypomorphic BRCA1 alleles
Synthetic lethality screens performed to identify novel vulnerabilities often model complete gene loss, thereby overlooking patient‐derived hypomorphic mutations. In this study, we have performed genome‐wide CRISPR screens on BRCA1 hypomorphic mutations, showing BRCA1I26A behaves like wild‐type, while BRCA1R1699Q mimics deficiency. Furthermore, we have
Anne Schreuder +10 more
wiley +1 more source

