Results 41 to 50 of about 207,488 (262)
FEBS Letters, EarlyView.Septin 9 polybasic domains couple phosphoinositide‐rich membrane binding to centrosome positioning, Golgi organization, and microtubule acetylation to control epithelial polarity. Their loss disrupts this axis, causing centrosome mispositioning, Golgi fragmentation, reduced microtubule acetylation, and polarity inversion via upregulation of the ...
Ting ting Cai +4 more
wiley +1 more source
Tumor Biology, 2017 Epithelial–mesenchymal transition is a crucial event for metastasis and could be mediated by several pathways such as phosphoinositide 3-kinase/Akt, mitogen-activated protein kinases, as well as many epigenetic regulators.
Hakan Kucuksayan, Hakan Akca
doaj +1 more source
Novel insights from a multiomics dissection of the Hayflick limit
eLife, 2022 The process wherein dividing cells exhaust proliferative capacity and enter into replicative senescence has become a prominent model for cellular aging in vitro.
Michelle Chan +19 more
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From mice to humans—divergent strategies for intestinal homeostasis and regeneration
FEBS Letters, EarlyView.Recent advances such as organoid genome editing, xenotransplantation, imaging, and whole‐genome sequencing have enabled direct studies of human intestinal stem cells (ISCs). These studies reveal species‐specific features, including slower ISC proliferation, distinct injury responses, slower somatic mutation accumulation in humans, and an inverse ...
Keiko Ishikawa +2 more
wiley +1 more source
Cancer spreading patterns based on epithelial-mesenchymal plasticity
Frontiers in Cell and Developmental BiologyIntroduction: Metastasis is a major cause of cancer-related deaths, underscoring the necessity to discern the rules and patterns of cancer cell spreading. Epithelial-mesenchymal plasticity contributes to cancer aggressiveness and metastasis.
Rui Wang, Zhaopeng Yan
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FEBS Letters, EarlyView.Cancer progression is regulated by the dynamic matrix code of the tumor microenvironment, which influences cellular behavior and disease development. Importantly, matrix remodeling in three‐dimensional cancer models more accurately reflects in vivo conditions compared to conventional two‐dimensional systems.
Sylvia Mangani +3 more
wiley +1 more source
An epithelial GPR35 isoform supports tumor‐associated transcriptional and metabolic phenotypes
FEBS Letters, EarlyView.GPR35 generates two functionally distinct isoforms with previously unresolved roles. GPR35‐short mediates immune‐cell chemotaxis, while GPR35‐long is enriched in colorectal cancer epithelium, where it supports increased metabolism, proliferation, and tumor‐associated transcriptional programs.
Jørgen D. Rønneberg +14 more
wiley +1 more source
Structure‐forward targeting of claudins with synthetic binders
FEBS Letters, EarlyView.Claudins form the paracellular barriers between epithelial and endothelial tissues at tight junctions and are targets for molecular binders with the goal of modulating barrier permeability. Claudin‐binding molecules are relevant in drug delivery or in altering claudin interactions with disease‐causing proteins.
Alex J. Vecchio
wiley +1 more source
eLife, 2022 Many of the features associated with senescence appear steadily over time before cells stop dividing.
Na Yang, Payel Sen
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Metabolic reprogramming and epithelial‐to‐mesenchymal transition in cancer [PDF]
The FEBS Journal, 2017 Several lines of evidence indicate that during transformation epithelial cancer cells can acquire mesenchymal features via a process called epithelial‐to‐mesenchymal transition (EMT). This process endows cancer cells with increased invasive and migratory capacity, enabling tumour dissemination and metastasis.
Sciacovelli, M, Frezza, C
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