Results 211 to 220 of about 19,772 (299)

Cyclic azapeptide CD36 ligand attenuates cardiac injury and reduces long‐chain fatty acid accumulation after myocardial ischemia–reperfusion in mice

open access: yesFEBS Open Bio, EarlyView.
In a murine model of myocardial ischemia and reperfusion (MI/R), the CD36 azapeptide ligand MPE‐298 reduces cardiac injury and transiently lowers left ventricular long‐chain fatty acids (LCFAs) accumulation 3 h after reperfusion, accompanied by a decrease of oxidative stress and inflammation‐associated genes' expression in the heart and adipose tissue.
Jade Gauvin   +12 more
wiley   +1 more source

Directed evolution of enzymes at the crossroads of tradition and innovation

open access: yesFEBS Open Bio, EarlyView.
An iterative cycle of data‐driven enzyme optimization comprising four stages: genetic diversification of a template enzyme, expression of protein variants, high‐throughput evaluation, and machine‐learning‐guided redesign of the next variant library.
Maria Tomkova   +2 more
wiley   +1 more source

Small RNA pathways in mammalian oocytes

open access: yesFEBS Open Bio, EarlyView.
Three distinct small RNA pathways operate in mammalian oocytes: RNAi interference (RNAi), the microRNA (miRNA) pathway, and the PIWI‐associated RNA (piRNA) pathway. These pathways use small RNAs to guide sequence‐specific repression and contribute to oocyte biology by targeting genes and mobile elements or appear insignificant since different ...
Petr Svoboda, Josef Pasulka
wiley   +1 more source

Transcripts enriched in codons that trigger P‐site tRNA‐mediated mRNA decay possess stable mRNA

open access: yesFEBS Open Bio, EarlyView.
PTMD codons were first described by Mendel et al. as mediators of an mRNA decay pathway dependent on the human protein CNOT3, homologous to yeast Not5. Our findings confirm that PTMD codons destabilize transcripts; however, unlike in yeast, the human pathway specifically targets and slightly destabilizes primarily stable mRNAs.
Rodolfo Lopes Carneiro   +1 more
wiley   +1 more source

Evaluating the involvement of autolysosomes in the nuclear translocation of fluorescent proteins

open access: yesFEBS Open Bio, EarlyView.
Endogenously expressed fluorescent proteins can be degraded by autophagy and transported to cell nuclei via the nuclear pore complex. But in some cell lines, for example, HeLa cells which are positive for immunoreactivity of a receptor ligand, such as UCN I, in cell nuclei, fusion of autolysosome with the nuclear envelope is involved in the nuclear ...
Keiichi Ikeda
wiley   +1 more source

MagmaFlow: A desktop platform for artificial intelligence‐driven expression analysis

open access: yesFEBS Open Bio, EarlyView.
MagmaFlow is a free, no‐code platform for gene expression analysis. It generates interactive volcano plots, links genes to literature, pathways, and diseases, prioritizes candidates using millions of publications, identifies affected biological processes, builds network diagrams, and exports publication‐ready figures and reports for macOS and Windows ...
Carlos E. Buss   +7 more
wiley   +1 more source

A new flow chip in combination with multiphoton microscopy as a protocol for longitudinal 3D imaging of tissue calcification under shear stress

open access: yesFEBS Open Bio, EarlyView.
Miniaturized flow chip platform enabling continuous perfusion and longitudinal multiphoton 3D imaging of vascular smooth muscle cell constructs under physiological flow. Brightfield imaging guides region selection, while CellTracker Green and mRuby‐labeled fetuin‐A visualize cells and mineral deposition, respectively. Magnesium supplementation markedly
Vytautas Kučikas   +6 more
wiley   +1 more source

Mutant NPM1 in Acute Myeloid Leukemia Initiation and Maintenance

open access: yesAging and Cancer, EarlyView.
NPM1 mutations drive acute myeloid leukemia by acting as neomorphic transcriptional regulators that cooperate with Menin–MLL and XPO1 to sustain HOX/MEIS1 expression and block differentiation. Targeting these mutant‐specific transcriptional dependencies provides a rational therapeutic strategy for NPM1‐mutated AML.
Yanan Jiang   +3 more
wiley   +1 more source

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