Results 91 to 100 of about 12,215,662 (215)
Inhibition of dipeptidyl peptidase 7 impairs lysophagy in LLOMe‐treated HepG2 cells
FEBS Letters, EarlyView.DPP7 inhibition delays ubiquitin‐dependent lysophagy by attenuating ubiquitin accumulation and the recruitment of SQSTM1 and LC3 to damaged lysosomes, resulting in delayed clearance of damaged lysosomes and impaired restoration of lysosomal homeostasis. Created using FigureLabs (Certificate ID: FL‐PUB‐20260922‐Z99XNX).
Na Yeon Park +8 more
wiley +1 more source
DNA ligase LigE increases bacterial transformation with damaged extracellular DNA
FEBS Letters, EarlyView.The DNA ligase LigE from the naturally competent Gram‐negative bacterium Neisseria gonorrhoaea increases transformation with cut extracellular DNA. This process is ATP‐dependent and relies on the catalytic activity of LigE; it also requires that LigE contains an intact periplasmic localisation sequence, indicating that ligE functions in the periplasm ...
Jolyn Pan +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.Cytarabine is a key therapy for acute myeloid leukaemia (AML), but its efficacy is limited by the dNTPase SAMHD1, which hydrolyses its active metabolite. Screening nucleotide biosynthesis inhibitors revealed that IMPDH inhibitors selectively sensitise SAMHD1‐proficient AML cells to cytarabine.
Miriam Yagüe‐Capilla +9 more
wiley +1 more source
KDM7A and KDM1A inhibition suppresses tumour promoting pathways in prostate cancer
Molecular Oncology, EarlyView.Treatment resistance is a major challenge for patients with advanced prostate cancer. This study examined an alternative approach to target the major prostate cancer‐promoting pathway by targeting epigenetic factors, whose levels are higher in tumours.
Jennie N Jeyapalan +16 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
Molecular Oncology, EarlyView.Pair‐wise comparison of the CellSearch and FETCH enrichment technologies for circulating tumor cells (CTCs) from metastatic breast, prostate, and small cell lung cancer patients shows an increased capture of CTCs using FETCH enrichment. The clinical implementation of circulating tumor cells (CTCs) as a predictive tool for therapy efficacy in the ...
Michiel Stevens +6 more
wiley +1 more source
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
Finding novel vulnerabilities of hypomorphic BRCA1 alleles
Molecular 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