E-GuARD: expert-guided augmentation for the robust detection of compounds interfering with biological assays. [PDF]
Palmacci V +5 more
europepmc +1 more source
Dimensional distribution control of elongate mineral particles for their use in biological assays. [PDF]
Vigliaturo R +3 more
europepmc +1 more source
Dual activity inhibition of threonine aspartase 1 by a single bisphosphate ligand. [PDF]
Höing A +8 more
europepmc +1 more source
Annual Report - Marine Biological Laboratory, 1952
Annual report of the Marine Biological Laboratory in Woods Hole. 1952.
Marine Biological Laboratory (Woods Hole MA)
core
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
Exploring Schiff base bromhexine derivatives: study on synthesis, characterization, biological assays, molecular docking. [PDF]
Yasmeen Z +10 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
Molecular docking, derivatization, characterization and biological assays of amantadine. [PDF]
Yasmeen Z +6 more
europepmc +1 more source
Tetrazole and acylsulfonamide bioisosteric replacements of the carboxylic acid in a dual MCL-1/BCL-xL inhibitor are tolerated. [PDF]
Chen L, Lowe B, Fletcher S.
europepmc +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

