Results 151 to 160 of about 5,803,880 (315)

Pharmacological inhibition of the PERK pathway modulates hepatocellular carcinoma growth and immune signaling

open access: yesFEBS Open Bio, EarlyView.
Pharmacological inhibition of PERK in a DEN‐induced mouse model of liver cancer does not reduce tumor burden but alters cellular stress signaling. Despite blocking PERK activity, downstream stress responses, including CHOP expression, remain active, suggesting compensatory mechanisms within the unfolded protein response that may influence tumor ...
Ada Lerma‐Clavero   +5 more
wiley   +1 more source

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

Accounting Information, Disclosure, and the Cost of Capital

open access: yes, 2007
Richard A. Lambert   +2 more
semanticscholar   +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

Hyperosmotic stress‐induced redistribution of pre‐mRNA cleavage factor I subunits is associated with shifts in alternative polyadenylation

open access: yesFEBS Open Bio, EarlyView.
Hyperosmotic stress triggers the relocation of the CFIm complex from the nucleus to the cytoplasm. This shift creates a nuclear ‘stoichiometric bottleneck’, limiting CFIm availability for mRNA processing. Consequently, specific mRNAs like NUDT21 and DICER1 undergo targeted 3′UTR shortening, demonstrating how spatial protein dynamics drive rapid ...
Hitomi Soumiya   +2 more
wiley   +1 more source

Loss of AMBRA1 activates MAPK and angiogenesis signaling pathways in melanoma cells

open access: yesFEBS Open Bio, EarlyView.
Loss of AMBRA1 in melanoma cells activates multiple oncogenic pathways associated with tumor progression. Transcriptomic and protein network analyses revealed that AMBRA1 depletion enhances MAPK/ERK signaling, angiogenesis, TGF‐β/EMT signaling, and Wnt/axon guidance pathways.
Milad Ibrahim   +4 more
wiley   +1 more source

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