Mechanisms and therapeutic opportunities of the ribotoxic stress response in cancer
Molecular Oncology, EarlyView.Cancer cells' high translational demand creates opportunities to therapeutically target ribosome function. Ribosome stalling and collisions activate ZAKα and the ribotoxic stress response (RSR), which can trigger rapid, p53‐independent apoptosis in cancer.
Anastassiya Kim +7 more
wiley +1 more source
Impact of feeding by Arenicola marina (L.) and ageing of faecal material on fatty acid distribution and bacterial community structure in marine sediments: An experimental approach [PDF]
, 2006 The fate of ingested eukaryotic photoautotrophic fatty acids during gut transit in the lugwormArenicolamarina (L.) and the influence of A. marina's faeces on the evolution of fatty acid distribution and bacterial community structure in superficial ...
Caradec, S +11 more
core +1 more source
Molecular Oncology, EarlyView.This study integrates publicly available transcriptomic datasets to identify molecular signatures associated with response to neoadjuvant chemoradiotherapy in locally advanced rectal cancer. By analyzing a combination of multiple cohorts with bioinformatics approaches, we reveal biological pathways and immune‐related features that may improve ...
Aleksandra Stanojevic +10 more
wiley +1 more source
Molecular basis for SMC rod formation and its dissolution upon DNA binding. [PDF]
, 2015 SMC condensin complexes are central modulators of chromosome superstructure in all branches of life. Their SMC subunits form a long intramolecular coiled coil, which connects a constitutive "hinge" dimerization domain with an ATP-regulated "head ...
Soh, Young-Min +69 more
core +1 more source
Multiple gene sequence analysis using genes of the bacterial DNA repair pathway
Brazilian Archives of Biology and Technology, 2015 The ability to recognize and repair abnormal DNA structures is common to all forms of life. Physiological studies and genomic sequencing of a variety of bacterial species have identified an incredible diversity of DNA repair pathways.
Miguel Rotelok Neto +6 more
doaj +1 more source
The VHL tumor suppressor at the crossroad of protein folding, aggregation, and cancer
Molecular Oncology, EarlyView.Mutations, environmental stress, and chaperone dysfunction can destabilize pVHL, promoting its conversion from the native folded state into amyloid‐like assemblies. This transition may contribute to protein storage, cell dormancy, survival, and drug resistance.
Lara Abad +2 more
wiley +1 more source
Structure of the N-terminal gyrase B fragment in complex with ADP⋅Pi reveals rigid-body motion induced by ATP hydrolysis [PDF]
, 2014 Type II DNA topoisomerases are essential enzymes that catalyze topological rearrangement of double-stranded DNA using the free energy generated by ATP hydrolysis.
Stanger, Frédéric V. +9 more
core +1 more source
Gut microbiota alterations in patients with non‐small‐cell lung cancer undergoing chemoradiotherapy
Molecular Oncology, EarlyView.We investigated the impact of concurrent chemoradiotherapy (CRT) on the gut microbiota in patients with locally advanced non‐small‐cell lung cancer. Overall gut microbiota composition remained largely stable throughout CRT while antibiotic exposure may influence microbial diversity.
Hanne Marte Nymoen +19 more
wiley +1 more source
Mutant p53R273H disrupts PDPK1 homodimerization and contributes to PDPK1 activation
Molecular Oncology, EarlyView.How mutant p53R273H drives AKT signaling is unclear. We show that p53R273H, but not wild‐type, directly binds PDPK1 via a mutation‐dependent conformational change. This interaction disrupts inhibitory PDPK1 homodimerization and enhances AKT phosphorylation.
Mei Chee Lim +11 more
wiley +1 more source
Targeting the EpCAM‐AXL axis to overcome drug resistance in lung cancer
Molecular Oncology, EarlyView.Lung cancer cells often evade therapy by hijacking signaling pathways. We reveal that cleaved EpCAM (sEpCAM) stabilizes the oncogenic protein AXL, driving NF‐κB and STAT3‐mediated chemoresistance. This EpCAM‐AXL axis identifies a high‐risk patient subset with poor prognosis.
Alexa Guerrero‐Alba +5 more
wiley +1 more source