Results 81 to 90 of about 5,567,373 (294)
The Shewanella oneidensis Fic enzyme SoFic targets the switch‐I region of EF‐Tu for AMPylation
FEBS Letters, EarlyView.Fic enzymes mediate diverse post‐translational modifications across all domains of life, including AMPylation. Prokaryotic EF‐Tu can be AMPylated and deAMPylated by the conserved Fic enzyme SoFic. Structural and biochemical approaches were used to characterize the effect of AMPylation on EF‐Tu, SoFic's enzymatic activities, and the enzyme‐target ...
Svenja Runge +6 more
wiley +1 more source
Prospecting the protein design landscape
FEBS Letters, EarlyView.This review outlines the current state of various protein design approaches. We discuss the current possibilities enabled by recently released tools, highlight future avenues to pursue in protein design, and underscore the crucial role of key databases and resources for successful protein design workflows.
Jakob R. Riccabona +4 more
wiley +1 more source
The role of miR‐335‐5p in the redifferentiation of BRAF p.V600E thyroid cancers
Molecular Oncology, EarlyView.The BRAF p.V600E mutation promotes thyroid cancer dedifferentiation and radioiodine resistance. Using a network approach, we identified miR‐335‐5p as a key regulator of BRAF‐mutated thyroid tumors. Restoring miR‐335‐5p increased thyroid‐specific gene expression and iodine uptake in cells and organoids.
Valeria Pecce +11 more
wiley +1 more source
Molecular Oncology, EarlyView.This study shows that lung adenocarcinomas exploit developmental branching morphogenesis to acquire a therapy resistant basal‐like tumour cell state. This process was found to be regulated by combined TP53 loss‐of‐function and type‐I interferon signalling, identifying a novel axis for biomarker and therapeutic target discovery.
Kamila J Bienkowska +13 more
wiley +1 more source
Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining
Molecular 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
, 1991 These proceedings reflect the extensive fundamental and applied research efforts that are currently being made on the conversion of gas, in particular on the direct conversion of methane.
Jens, K.-J.(Klaus-J.) +3 more
core
Molecular 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
MITF maintains genome stability in nonmelanocyte lineages
Molecular Oncology, EarlyView.MITF is essential for melanocyte survival and acts as an oncogene in 10%–20% of melanomas. We show that MITF depletion causes genome instability in nonmelanocytic cells, leading to LATS2‐mediated P53 activation, cell cycle arrest, and apoptosis. This study highlights the role of MITF as a genome maintenance factor beyond the melanocyte lineage. Created
Drifa H. Gudmundsdottir +13 more
wiley +1 more source
Oncogenic DMTF1β promotes cancer cell motility by regulating autophagy through ULK1 stabilization
Molecular Oncology, EarlyView.In the current study, we demonstrate that the oncogene DMTF1β regulates ULK1 stability by reducing its proteasomal degradation in cancer cells. This stabilization enables ULK1 to induce autophagy, which in turn facilitates cancer cell migration. Consequently, reduced DMTF1β levels lead to decreased autophagy and impaired cancer cell migration.
Jun Xu +13 more
wiley +1 more source