Results 191 to 200 of about 3,956,990 (303)

Dual activity inhibition of threonine aspartase 1 by a single bisphosphate ligand. [PDF]

open access: yesRSC Adv, 2022
Höing A   +8 more
europepmc   +1 more source

Annual Report - Marine Biological Laboratory, 1952

open access: yes, 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

open access: yesMolecular Oncology, EarlyView.
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]

open access: yesFuture Med Chem
Yasmeen Z   +10 more
europepmc   +1 more source

USP29‐regulated noncanonical stabilization of the hypoxia‐inducible factor‐α in aggressive prostate cancer

open access: yesMolecular Oncology, EarlyView.
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]

open access: yesFuture Med Chem
Yasmeen Z   +6 more
europepmc   +1 more source

Finding novel vulnerabilities of hypomorphic BRCA1 alleles

open access: yesMolecular Oncology, EarlyView.
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

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