Results 81 to 90 of about 59,918 (258)

Identification of a Shiga toxin A‐derived peptide internalized into Gb3 receptor‐bearing cells via interaction with the Shiga toxin B subunit

open access: yesFEBS Letters, EarlyView.
The process of internalization of the Shiga toxin A subunit via formation of a complex with the Shiga toxin B subunit, which specifically binds to the Gb3 receptor. The peptide is designed to act as a carrier of drugs into cancer cells. Here, we explored the potential of peptides derived from the catalytic A subunit of Shiga toxin (STxA) to be drug ...
Giulia Opassi   +6 more
wiley   +1 more source

DNA Damage Induced by Alkylating Agents and Repair Pathways

open access: yesJournal of Nucleic Acids, 2010
The cytotoxic effects of alkylating agents are strongly attenuated by cellular DNA repair processes, necessitating a clear understanding of the repair mechanisms. Simple methylating agents form adducts at N- and O-atoms.
Natsuko Kondo   +3 more
doaj   +1 more source

Microbiome‐blood–brain barrier interactions in aging — mechanisms and therapeutic potential

open access: yesFEBS Letters, EarlyView.
Aging reshapes the gut microbiome (↓SCFA‐producing commensals; ↑pro‐inflammatory outputs), shifting circulating metabolites (↓SCFAs; ↑LPS, ↑TMAO, ↑PAA) that act at the BBB to increase nonspecific transcytosis, alter transport, and promote astrocyte reactivity, heightening brain vulnerability.
Daniel Cuervo‐Zanatta   +3 more
wiley   +1 more source

Alkyladenine DNA glycosylase associates with transcription elongation to coordinate DNA repair with gene expression

open access: yesNature Communications, 2019
How genome stability is maintained at regions of active transcription is currently not entirely clear. Here, the authors reveal an association between base excision repair factors and transcription elongation to modulate DNA repair.
Nicola P. Montaldo   +15 more
doaj   +1 more source

Mitochondrial DNA damage and impaired base excision repair during epileptogenesis

open access: yesNeurobiology of Disease, 2008
Oxidative stress and mitochondrial dysfunction are acute consequences of status epilepticus (SE). However, the role of mitochondrial oxidative stress and genomic instability during epileptogenesis remains unknown.
Stuart G. Jarrett   +4 more
doaj   +1 more source

An epithelial GPR35 isoform supports tumor‐associated transcriptional and metabolic phenotypes

open access: yesFEBS 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

Discerning protein pools by selective staining with self‐labeling tags

open access: yesFEBS Letters, EarlyView.
Cell surface proteins have an intra‐ and extracellular pool. Combining genetic fusion to self‐labeling tags that can be addressed with small molecule fluorophores allows separating these pools. We highlight recent developments and techniques for state‐of‐the‐art interrogation of cell surface proteins in the complex tissue setting.
Kati Fischermanns, Johannes Broichhagen
wiley   +1 more source

Peripheral lysosomes recruit PLEKHG3 to focal adhesions and restrain protrusion dynamics

open access: yesFEBS Letters, EarlyView.
Proximity‐dependent labeling at the LAMTOR complex revealed the Rho GEF PLEKHG3 as a lysosome‐proximal protein directing the study toward the influence of lysosome positioning on actin dynamics and cell motility. We show that PLEKHG3 colocalizes with lysosomes at focal adhesion sites and observe that forced peripheral dispersion of lysosomes hinders ...
Rainer Ettelt   +8 more
wiley   +1 more source

Mammalian Base Excision Repair: Functional Partnership between PARP-1 and APE1 in AP-Site Repair.

open access: yesPLoS ONE, 2015
The apurinic/apyrimidinic- (AP-) site in genomic DNA arises through spontaneous base loss and base removal by DNA glycosylases and is considered an abundant DNA lesion in mammalian cells.
Rajendra Prasad   +3 more
doaj   +1 more source

Epigenetic reprogramming of lineage switching in cancer

open access: yesFEBS Letters, EarlyView.
Cancer cells rarely commit to a single identity. Epigenetic mechanisms and tumor microenvironment cues push epithelial cells toward flexible, hybrid states that can shift into mesenchymal, neuroendocrine, or stem‐like fates, driving metastasis, drug resistance, and tumor heterogeneity. Targeting the epigenetic regulators behind these transitions, using
Ezgi Boyvatlı   +4 more
wiley   +1 more source

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