Results 201 to 210 of about 7,011,032 (315)

Soman induces endoplasmic reticulum stress and apoptosis of cerebral organoids via the GRP78‐ATF6‐CHOP signaling pathway

open access: yesFEBS Open Bio, EarlyView.
Cerebral organoids were employed as a novel model to explore the neurotoxicity of soman. Soman inhibited acetylcholinesterase activity, increased cell apoptosis and upregulated endoplasmic reticulum (ER) stress markers glucose‐regulated protein 78 (GRP78), activating transcription factor 6 (ATF6) and C/EBP homologous protein (CHOP).
Yue Wei   +7 more
wiley   +1 more source

EVENT STUDY METHODOLOGY IN CONDUCTING RESEARCH [PDF]

open access: yes, 2013
Ivanova, T., Martynyuk, A.
core  

Advanced glycation end products promote the release of endothelial cell‐derived mitocytosis

open access: yesFEBS Open Bio, EarlyView.
Under diabetic conditions, AGEs induce mitochondrial damage in HUVECs, activating migrasome‐mediated mitocytosis. Migrasomes encapsulate damaged mitochondria and are released into the extracellular space, facilitating intercellular mitochondrial transfer.
Rong Liu   +6 more
wiley   +1 more source

Co‐expression of HSV‐1 ICP34.5 enhances the expression of gene delivered by self‐amplifying RNA and mitigates its immunogenicity

open access: yesFEBS Open Bio, EarlyView.
ICP34.5 is one of the most important antihost response proteins. The saRNA‐encoding HSV‐1 neurovirulence protein ICP34.5 clearly mediated the eukaryotic initiation factor 2 alpha subunit (eIF2α) dephosphorylation and significant suppression of innate immune responses in vitro, leading to enhanced expression of the saRNA‐encoded gene.
Xuemin Lu   +6 more
wiley   +1 more source

Gut alterations in a chronic kidney disease rat model with diet‐induced vascular calcification

open access: yesFEBS Open Bio, EarlyView.
Chronic kidney disease (CKD) patients often suffer from intestinal and/or mineral and bone disorders. Using a rat model, we showed that uremic vascular calcification is associated with gut barrier alterations (decreased gut mucus production and Nlrp6 gene expression, increased gut inflammation), and plasma retention of gut‐origin uremic toxins (indoxyl
Piotr Bartochowski   +13 more
wiley   +1 more source

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