Results 51 to 60 of about 1,587 (196)
Ligand‐dependent transcriptional heterogeneity in cell cycle gene expression delays G1/S entry
EGF and HRG induce distinct G1/S progression programs in ErbB2‐amplified BT474 breast cancer cells. Despite activating the potent ErbB2–ErbB3 heterodimer, HRG does not accelerate cell‐cycle entry. Instead, EGF promotes earlier restriction‐point passage via ERK–FOS signaling, whereas HRG activates the AKT–MYC axis, driving transcriptional heterogeneity ...
Ririn Rahmala Febri +5 more
wiley +1 more source
Mycobacterial 3‐methylcrotonyl‐CoA carboxylase uses a mobile biotin‐carrying domain to shuttle a carboxyl group between two catalytic sites, enabling carboxylation of 3‐methylcrotonyl‐CoA during leucine breakdown. Cryo‐electron microscopy captures the carrier at both sites and reveals an inward loop movement that may prevent futile rebinding to the ...
Ajit Yadav +2 more
wiley +1 more source
How do genomes gain new functional parts? In eukaryotes, which tend to evolve under weak selection, much of the genome is junk. Palazzo and Qiu borrow the logic of Markov chains to show how non‐functional DNA becomes functional through the appearance of intermediate states, which arise due to epistasis, buffering, and biochemical messiness, allowing ...
Alexander F. Palazzo, Yi Qiu
wiley +1 more source
Heterodimeric amino acid transporters consist of SLC7 and SLC3 family proteins arranged in a conserved structural organization. They regulate nutrient transport across cell membranes, supporting essential cellular functions. These transporters also contribute to xenobiotic/drug uptake and distribution.
Mariafrancesca Scalise +5 more
wiley +1 more source
Metastatic niche shaped by host factors influences disseminated cancer cell fate
Metastasis is shaped not only by cancer cells but also by the environments they encounter. This review explores how factors such as aging, diet, the microbiome, lifestyle, and environmental exposures remodel organ‐specific niches in the lung, liver, bone, and brain, influencing where metastatic cells survive, remain dormant, or grow, and ultimately ...
Gwennan Delyth Ward +2 more
wiley +1 more source
Tumour–host interactions in Drosophila: mechanisms in the tumour micro‐ and macroenvironment
This review examines how tumour–host crosstalk takes place at multiple levels of biological organisation, from local cell competition and immune crosstalk to organism‐wide metabolic and physiological collapse. Here, we integrate findings from Drosophila melanogaster studies that reveal conserved mechanisms through which tumours hijack host systems to ...
José Teles‐Reis, Tor Erik Rusten
wiley +1 more source
Hijacking emergency granulopoiesis: Neutrophil ontogeny and reprogramming in cancer
Neutrophils are highly plastic innate immune cells; their functions in cancer extend beyond the tumour microenvironment. This Review summarises current understanding of neutrophil maturation and heterogeneity and highlights tumour‐induced granulopoiesis as a systemic programme that expands immature, immunosuppressive neutrophils via tumour‐derived ...
Gabriela Marinescu, Yi Feng
wiley +1 more source
Dormant cancer cells can hide in distant organs for years, evading treatment and the immune system. This review highlights how signals from the surrounding tissue and immune environment keep these cells inactive or trigger their reawakening. Understanding these mechanisms may help develop therapies to eliminate or control dormant cells and prevent ...
Kanishka Tiwary +1 more
wiley +1 more source
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
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

